PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33784509-8	2021	Furthermore, rapid reduction of cyclin D1 upon DNA damage was attributed to proteasomal degradation, as evidenced by data showing that proteasomal inhibition by MG132 blocked cyclin D1 reduction while cycloheximide facilitated it.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-166	cyclin D1	Homo sapiens	32-41
33617988-3	2021	Here, we demonstrate that mitofusins (Mfn1/2) are post-translationally modified by SUMO2 (Small Ubiquitin-related Modifier 2) in Human embryonic kidney 293 (Hek293) cells treated with protonophore CCCP and proteasome inhibitor MG132, both known mitochondrial stressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	mitofusin 1	Homo sapiens	38-44
33617988-3	2021	Here, we demonstrate that mitofusins (Mfn1/2) are post-translationally modified by SUMO2 (Small Ubiquitin-related Modifier 2) in Human embryonic kidney 293 (Hek293) cells treated with protonophore CCCP and proteasome inhibitor MG132, both known mitochondrial stressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	small ubiquitin like modifier 2	Homo sapiens	83-88
33617988-3	2021	Here, we demonstrate that mitofusins (Mfn1/2) are post-translationally modified by SUMO2 (Small Ubiquitin-related Modifier 2) in Human embryonic kidney 293 (Hek293) cells treated with protonophore CCCP and proteasome inhibitor MG132, both known mitochondrial stressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	small ubiquitin like modifier 2	Homo sapiens	90-124
33617988-4	2021	SUMOylation of Mfn1/2 is not for their proteasomal degradation but facilitate mitochondrial congression at the perinuclear region in CCCP- and MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	mitofusin 1	Homo sapiens	15-21
33848640-0	2021	In depth proteomic analysis of proteasome inhibitors bortezomib, carfilzomib and MG132 reveals that mortality factor 4-like 1 (MORF4L1) protein ubiquitylation is negatively impacted.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	mortality factor 4 like 1	Homo sapiens	100-125
33848640-0	2021	In depth proteomic analysis of proteasome inhibitors bortezomib, carfilzomib and MG132 reveals that mortality factor 4-like 1 (MORF4L1) protein ubiquitylation is negatively impacted.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	mortality factor 4 like 1	Homo sapiens	127-134
33784509-8	2021	Furthermore, rapid reduction of cyclin D1 upon DNA damage was attributed to proteasomal degradation, as evidenced by data showing that proteasomal inhibition by MG132 blocked cyclin D1 reduction while cycloheximide facilitated it.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-166	cyclin D1	Homo sapiens	175-184
33529913-8	2021	In vitro, IL-1beta stimulation downregulated eNOS expression levels in human aortic endothelial cells (HAECs) in a concentration- and time-dependent manner, while pretreatment with 1 microM of the proteasome inhibitor MG132 reversed this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	218-223	interleukin 1 alpha	Homo sapiens	10-18
34006831-12	2021	MG132 (proteasome inhibitor) administration manifested that AdipoR1 was ubiquitinated, while inhibited SOCS3 rescued the reduced AdipoR1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	adiponectin receptor 1	Homo sapiens	60-67
34006831-12	2021	MG132 (proteasome inhibitor) administration manifested that AdipoR1 was ubiquitinated, while inhibited SOCS3 rescued the reduced AdipoR1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	suppressor of cytokine signaling 3	Homo sapiens	103-108
34006831-12	2021	MG132 (proteasome inhibitor) administration manifested that AdipoR1 was ubiquitinated, while inhibited SOCS3 rescued the reduced AdipoR1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	adiponectin receptor 1	Homo sapiens	129-136
33974963-4	2021	Treatment with MG132 or 3MA significantly increased the clinical hanging wire score and exacerbated alpha-motor neuron loss at 18 weeks in G93A mice, and increased the amount of ubiquitin, p62 aggregates, and BAG3 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	nucleoporin 62	Mus musculus	189-192
33974963-4	2021	Treatment with MG132 or 3MA significantly increased the clinical hanging wire score and exacerbated alpha-motor neuron loss at 18 weeks in G93A mice, and increased the amount of ubiquitin, p62 aggregates, and BAG3 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	BCL2-associated athanogene 3	Mus musculus	209-213
33864412-4	2021	In cultured mouse PCT cells treated with high glucose, CBS protein and activity was reduced while ubiquitinated CBS was increased, which was abolished by a proteasome inhibitor MG132 at 1 hour; high glucose drove CBS colocalized with proteasome 26S subunit ATPase6, indicating an involvement of ubiquitination proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	cystathionine beta-synthase	Mus musculus	55-58
33864412-4	2021	In cultured mouse PCT cells treated with high glucose, CBS protein and activity was reduced while ubiquitinated CBS was increased, which was abolished by a proteasome inhibitor MG132 at 1 hour; high glucose drove CBS colocalized with proteasome 26S subunit ATPase6, indicating an involvement of ubiquitination proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	cystathionine beta-synthase	Mus musculus	112-115
33864412-4	2021	In cultured mouse PCT cells treated with high glucose, CBS protein and activity was reduced while ubiquitinated CBS was increased, which was abolished by a proteasome inhibitor MG132 at 1 hour; high glucose drove CBS colocalized with proteasome 26S subunit ATPase6, indicating an involvement of ubiquitination proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	cystathionine beta-synthase	Mus musculus	112-115
33864412-4	2021	In cultured mouse PCT cells treated with high glucose, CBS protein and activity was reduced while ubiquitinated CBS was increased, which was abolished by a proteasome inhibitor MG132 at 1 hour; high glucose drove CBS colocalized with proteasome 26S subunit ATPase6, indicating an involvement of ubiquitination proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	proteasome (prosome, macropain) 26S subunit, ATPase, 6	Mus musculus	234-264
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	cyclin dependent kinase 2	Homo sapiens	96-100
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	cyclin dependent kinase 4	Homo sapiens	102-106
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	BCL2 like 1	Homo sapiens	108-114
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	BCL2 apoptosis regulator	Homo sapiens	120-125
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	H3 histone pseudogene 16	Homo sapiens	201-204
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	proteasome 26S subunit, non-ATPase 9	Homo sapiens	206-209
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	tumor protein p53	Homo sapiens	211-214
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	tumor protein p53	Homo sapiens	218-221
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	caspase 3	Homo sapiens	266-275
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	caspase 7	Homo sapiens	277-286
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	caspase 9	Homo sapiens	288-297
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	collagen type XI alpha 2 chain	Homo sapiens	303-307
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	forkhead box O3	Homo sapiens	313-318
34002651-10	2021	Interestingly, MG132 downregulated the phosphorylation of Akt and Erk.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	AKT serine/threonine kinase 1	Homo sapiens	58-61
34002651-10	2021	Interestingly, MG132 downregulated the phosphorylation of Akt and Erk.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	mitogen-activated protein kinase 1	Homo sapiens	66-69
33529913-8	2021	In vitro, IL-1beta stimulation downregulated eNOS expression levels in human aortic endothelial cells (HAECs) in a concentration- and time-dependent manner, while pretreatment with 1 microM of the proteasome inhibitor MG132 reversed this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	218-223	nitric oxide synthase 3	Homo sapiens	45-49
33529913-9	2021	In addition, treatment with 10 mg/kg MG132 also prevented the proteolysis of eNOS and improved endothelium-dependent vascular relaxation in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	nitric oxide synthase 3	Homo sapiens	77-81
31204209-10	2021	After pretreated with MG132, the expression of SOCS3 protein was increased which lead to attenuate the STAT3 phosphorylation and APP gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	suppressor of cytokine signaling 3	Homo sapiens	47-52
31204209-10	2021	After pretreated with MG132, the expression of SOCS3 protein was increased which lead to attenuate the STAT3 phosphorylation and APP gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	signal transducer and activator of transcription 3	Homo sapiens	103-108
33502336-11	2021	Following over-expression, AKR1D1-001 and AKR1D1-006 protein levels were lower than AKR1D1-002, but significantly increased following treatment with the proteasomal inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	aldo-keto reductase family 1 member D1	Homo sapiens	27-33
33482188-7	2021	MG-132 dose-dependently inhibited the growth of HPFs, induced G2/M phase arrest of cell cycle at a certain dose, and also caused cell apoptosis, with the levels of cleaved caspase3, cleaved PARP, Bax and p21 increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 3	Homo sapiens	172-180
33482188-7	2021	MG-132 dose-dependently inhibited the growth of HPFs, induced G2/M phase arrest of cell cycle at a certain dose, and also caused cell apoptosis, with the levels of cleaved caspase3, cleaved PARP, Bax and p21 increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	collagen type XI alpha 2 chain	Homo sapiens	190-194
33482188-7	2021	MG-132 dose-dependently inhibited the growth of HPFs, induced G2/M phase arrest of cell cycle at a certain dose, and also caused cell apoptosis, with the levels of cleaved caspase3, cleaved PARP, Bax and p21 increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	BCL2 associated X, apoptosis regulator	Homo sapiens	196-199
33482188-7	2021	MG-132 dose-dependently inhibited the growth of HPFs, induced G2/M phase arrest of cell cycle at a certain dose, and also caused cell apoptosis, with the levels of cleaved caspase3, cleaved PARP, Bax and p21 increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	H3 histone pseudogene 16	Homo sapiens	204-207
33540066-10	2021	Inhibiting proteasome activity with MG132 prevented CDH1 and beta2M degradation, indicating that MARCH8 might be targeting CDH1 and beta2M for proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	cadherin 1	Homo sapiens	52-56
33540066-10	2021	Inhibiting proteasome activity with MG132 prevented CDH1 and beta2M degradation, indicating that MARCH8 might be targeting CDH1 and beta2M for proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	alpha-2-macroglobulin	Homo sapiens	61-67
33540066-10	2021	Inhibiting proteasome activity with MG132 prevented CDH1 and beta2M degradation, indicating that MARCH8 might be targeting CDH1 and beta2M for proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	cadherin 1	Homo sapiens	123-127
33540066-10	2021	Inhibiting proteasome activity with MG132 prevented CDH1 and beta2M degradation, indicating that MARCH8 might be targeting CDH1 and beta2M for proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	alpha-2-macroglobulin	Homo sapiens	132-138
33828480-5	2021	In vitro, expression of phosphorylated-IkBalpha, MIF and M2 cytokines (Ym-1, Fizz-1, arginase-1) in IL-4-induced macrophages decreased upon exposure to the NF-kB inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-178	interleukin 4	Mus musculus	100-104
33828480-5	2021	In vitro, expression of phosphorylated-IkBalpha, MIF and M2 cytokines (Ym-1, Fizz-1, arginase-1) in IL-4-induced macrophages decreased upon exposure to the NF-kB inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-178	nuclear factor kappa B subunit 1	Rattus norvegicus	156-161
33502336-11	2021	Following over-expression, AKR1D1-001 and AKR1D1-006 protein levels were lower than AKR1D1-002, but significantly increased following treatment with the proteasomal inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	aldo-keto reductase family 1 member D1	Homo sapiens	42-48
33529121-8	2021	Furthermore, after treatment with MG-132, the relative protein level of Smad4 significantly increased in NSCLC cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	SMAD family member 4	Homo sapiens	72-77
33536006-14	2021	MRCKbeta could phosphorylate Siah2 but itself got ubiquitinated from this interaction leading to the proteasomal degradation of MRCKbeta and use of proteasomal inhibitor MG132 could rescue MRCKbeta from Siah2-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	CDC42 binding protein kinase beta	Mus musculus	0-8
33536006-14	2021	MRCKbeta could phosphorylate Siah2 but itself got ubiquitinated from this interaction leading to the proteasomal degradation of MRCKbeta and use of proteasomal inhibitor MG132 could rescue MRCKbeta from Siah2-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	siah E3 ubiquitin protein ligase 2	Mus musculus	29-34
33536006-14	2021	MRCKbeta could phosphorylate Siah2 but itself got ubiquitinated from this interaction leading to the proteasomal degradation of MRCKbeta and use of proteasomal inhibitor MG132 could rescue MRCKbeta from Siah2-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	CDC42 binding protein kinase beta	Mus musculus	128-136
33536006-14	2021	MRCKbeta could phosphorylate Siah2 but itself got ubiquitinated from this interaction leading to the proteasomal degradation of MRCKbeta and use of proteasomal inhibitor MG132 could rescue MRCKbeta from Siah2-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	CDC42 binding protein kinase beta	Mus musculus	128-136
33536006-14	2021	MRCKbeta could phosphorylate Siah2 but itself got ubiquitinated from this interaction leading to the proteasomal degradation of MRCKbeta and use of proteasomal inhibitor MG132 could rescue MRCKbeta from Siah2-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	siah E3 ubiquitin protein ligase 2	Mus musculus	203-208
33648539-12	2021	Specifically, SIRT7 is shown to interact with the CRL4-DCAF1 complex, and expression of Vpr in HEK293T cells results in SIRT7 degradation, which is partially rescued by CRL inhibitor MNL4924 and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-221	sirtuin 7	Homo sapiens	14-19
33648539-12	2021	Specifically, SIRT7 is shown to interact with the CRL4-DCAF1 complex, and expression of Vpr in HEK293T cells results in SIRT7 degradation, which is partially rescued by CRL inhibitor MNL4924 and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-221	Vpr	Human immunodeficiency virus 1	88-91
33671709-7	2021	Furthermore, cell pretreatment with proteasome inhibitor MG132 completely abrogates the effect of Olaparib, suggesting that PARP1 acts with NF-kappaB in the same regulatory pathway, which controls pro-inflammatory cytokine transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	poly(ADP-ribose) polymerase 1	Homo sapiens	124-129
33671709-7	2021	Furthermore, cell pretreatment with proteasome inhibitor MG132 completely abrogates the effect of Olaparib, suggesting that PARP1 acts with NF-kappaB in the same regulatory pathway, which controls pro-inflammatory cytokine transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	nuclear factor kappa B subunit 1	Homo sapiens	140-149
33359671-9	2021	The HIF-1alpha plasmid reversed the inhibition of balanophorin B on glycolysis, and the proteasome inhibitor MG132 attenuated the effect of balanophorin B on HIF-1alpha protein expression, suggesting that balanophorin B might post-transcriptionally affect HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	hypoxia inducible factor 1 subunit alpha	Homo sapiens	158-168
33359671-9	2021	The HIF-1alpha plasmid reversed the inhibition of balanophorin B on glycolysis, and the proteasome inhibitor MG132 attenuated the effect of balanophorin B on HIF-1alpha protein expression, suggesting that balanophorin B might post-transcriptionally affect HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	hypoxia inducible factor 1 subunit alpha	Homo sapiens	158-168
33461598-10	2021	We further found that alpha-syn overexpression decreased mGluR5 expression via a lysosomal pathway, as evidenced by the lysosomal inhibitor, NH4Cl, by blocking mGluR5 degradation, which was not evident with the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	233-238	synuclein, alpha	Mus musculus	22-31
33534085-4	2021	Further investigation showed that proteasome inhibitor MG132 rescued ATP1B3-mediated envelope proteins degradation, demonstrating that proteasome-dependent pathway is involved in ATP1B3-induced degradation of envelope proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	ATPase Na+/K+ transporting subunit beta 3	Homo sapiens	69-75
33534085-4	2021	Further investigation showed that proteasome inhibitor MG132 rescued ATP1B3-mediated envelope proteins degradation, demonstrating that proteasome-dependent pathway is involved in ATP1B3-induced degradation of envelope proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	ATPase Na+/K+ transporting subunit beta 3	Homo sapiens	179-185
33527027-11	2021	Proteasome inhibitor MG132 abolished PARK2 overexpression-induced down-regulation of NLRP3 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	parkin RBR E3 ubiquitin protein ligase	Homo sapiens	37-42
33527027-11	2021	Proteasome inhibitor MG132 abolished PARK2 overexpression-induced down-regulation of NLRP3 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	NLR family pyrin domain containing 3	Homo sapiens	85-90
33177203-5	2021	Addition of the proteasomal inhibitor, MG132, to culture media stabilized NID1 in virus-infected cells, implicating infection-activated proteasomal degradation of NID1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nidogen 1	Homo sapiens	74-78
33177203-5	2021	Addition of the proteasomal inhibitor, MG132, to culture media stabilized NID1 in virus-infected cells, implicating infection-activated proteasomal degradation of NID1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nidogen 1	Homo sapiens	163-167
33152381-10	2021	MG132, a proteasome inhibitor, decreased CBP degradation and restored the IFN-beta production induced by gE.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	CREB binding protein	Homo sapiens	41-44
33439458-4	2021	Proteasome inhibitor MG132 but not autophagy inhibitor chloroquine could suppress the Hsp90 inhibitor STA-9090-induced reduction of Ikaros, which is accompanied with the increased ubiquitination of Ikaros.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	heat shock protein 90 alpha family class A member 1	Homo sapiens	86-91
33439458-4	2021	Proteasome inhibitor MG132 but not autophagy inhibitor chloroquine could suppress the Hsp90 inhibitor STA-9090-induced reduction of Ikaros, which is accompanied with the increased ubiquitination of Ikaros.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	IKAROS family zinc finger 1	Homo sapiens	132-138
33439458-4	2021	Proteasome inhibitor MG132 but not autophagy inhibitor chloroquine could suppress the Hsp90 inhibitor STA-9090-induced reduction of Ikaros, which is accompanied with the increased ubiquitination of Ikaros.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	IKAROS family zinc finger 1	Homo sapiens	198-204
33440835-9	2021	Intriguingly, si-FAM188B treatment increased EGFR mRNA levels but decreased its protein levels, which was reversed by treatment with the proteasomal inhibitor MG132, indicating that FAM188B regulates EGFR levels via the proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	MINDY lysine 48 deubiquitinase 4	Homo sapiens	17-24
33440835-9	2021	Intriguingly, si-FAM188B treatment increased EGFR mRNA levels but decreased its protein levels, which was reversed by treatment with the proteasomal inhibitor MG132, indicating that FAM188B regulates EGFR levels via the proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	epidermal growth factor receptor	Homo sapiens	45-49
33440835-9	2021	Intriguingly, si-FAM188B treatment increased EGFR mRNA levels but decreased its protein levels, which was reversed by treatment with the proteasomal inhibitor MG132, indicating that FAM188B regulates EGFR levels via the proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	MINDY lysine 48 deubiquitinase 4	Homo sapiens	182-189
33440835-9	2021	Intriguingly, si-FAM188B treatment increased EGFR mRNA levels but decreased its protein levels, which was reversed by treatment with the proteasomal inhibitor MG132, indicating that FAM188B regulates EGFR levels via the proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	epidermal growth factor receptor	Homo sapiens	200-204
33461174-7	2021	Functional analysis indicated overexpression of praja2 inhibited the proliferation, migration and invasion of MKN-45 cells, while MG132 or FGF2 treatment removed the inhibitory effects of praja2 on GC progression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	praja ring finger ubiquitin ligase 2	Homo sapiens	188-194
33152381-10	2021	MG132, a proteasome inhibitor, decreased CBP degradation and restored the IFN-beta production induced by gE.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	IFN1@	Homo sapiens	74-82
33067759-7	2021	We also found no experimental evidence that, at a fixed temperature, chronic RF exposure for 24 h at a SAR of 1.5 and 6 W/kg altered the potency or the maximal capability of the proteasome inhibitor MG132 to activate HSF1, whatever signal used.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	199-204	heat shock transcription factor 1	Homo sapiens	217-221
33243462-4	2021	Overexpression of HRD1 promoted SERT ubiquitination, the effect of which was augmented by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	synoviolin 1	Homo sapiens	18-22
33243462-4	2021	Overexpression of HRD1 promoted SERT ubiquitination, the effect of which was augmented by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	solute carrier family 6 member 4	Homo sapiens	32-36
33243462-5	2021	Immunoprecipitation studies revealed that HRD1 interacts with SERT in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	synoviolin 1	Homo sapiens	42-46
33243462-5	2021	Immunoprecipitation studies revealed that HRD1 interacts with SERT in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	solute carrier family 6 member 4	Homo sapiens	62-66
32869129-3	2021	In this study, we investigated this phenomenon in various cell lines and found that HSP90 was cleaved by treatment with SAHA or MG132 in 6 out of 16 solid tumor cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	heat shock protein 90 alpha family class A member 1	Homo sapiens	84-89
32869129-5	2021	In the K562 and Mia-PaCa-2 cell lines expressing HSP90beta D294A, the cleavage of HSP90 by the treatment with SAHA or MG132 was reduced compared with the K562 and Mia-PaCa-2 cell lines expressing HSP90beta WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	heat shock protein 90 alpha family class A member 1	Homo sapiens	49-58
32869129-5	2021	In the K562 and Mia-PaCa-2 cell lines expressing HSP90beta D294A, the cleavage of HSP90 by the treatment with SAHA or MG132 was reduced compared with the K562 and Mia-PaCa-2 cell lines expressing HSP90beta WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	heat shock protein 90 alpha family class A member 1	Homo sapiens	49-54
33381997-7	2021	Also, VCP/p97 interacts with XPB upon treatment of spironolactone and proteasome inhibitor MG132, while the VCP/p97 adaptor UBXD7 binds XPB and its ubiquitin conjugates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	valosin containing protein	Homo sapiens	6-13
32869129-5	2021	In the K562 and Mia-PaCa-2 cell lines expressing HSP90beta D294A, the cleavage of HSP90 by the treatment with SAHA or MG132 was reduced compared with the K562 and Mia-PaCa-2 cell lines expressing HSP90beta WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	heat shock protein 90 alpha family class A member 1	Homo sapiens	196-205
33381997-7	2021	Also, VCP/p97 interacts with XPB upon treatment of spironolactone and proteasome inhibitor MG132, while the VCP/p97 adaptor UBXD7 binds XPB and its ubiquitin conjugates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	valosin containing protein	Homo sapiens	6-9
33381997-7	2021	Also, VCP/p97 interacts with XPB upon treatment of spironolactone and proteasome inhibitor MG132, while the VCP/p97 adaptor UBXD7 binds XPB and its ubiquitin conjugates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	valosin containing protein	Homo sapiens	10-13
33381997-7	2021	Also, VCP/p97 interacts with XPB upon treatment of spironolactone and proteasome inhibitor MG132, while the VCP/p97 adaptor UBXD7 binds XPB and its ubiquitin conjugates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	UBX domain protein 7	Homo sapiens	124-129
33381997-7	2021	Also, VCP/p97 interacts with XPB upon treatment of spironolactone and proteasome inhibitor MG132, while the VCP/p97 adaptor UBXD7 binds XPB and its ubiquitin conjugates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	ERCC excision repair 3, TFIIH core complex helicase subunit	Homo sapiens	29-32
33381997-7	2021	Also, VCP/p97 interacts with XPB upon treatment of spironolactone and proteasome inhibitor MG132, while the VCP/p97 adaptor UBXD7 binds XPB and its ubiquitin conjugates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	ERCC excision repair 3, TFIIH core complex helicase subunit	Homo sapiens	136-139
32510596-1	2021	Proteasome inhibitor MG132 was shown to enhance the secretion of interleukin 8 (IL-8) by various cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	C-X-C motif chemokine ligand 8	Homo sapiens	80-84
33388604-6	2021	Retention of E2F2 in the nucleus of cancer cells upon MG132 combination with 17AAG has suggested that Hsp90 is required for E2F2 stability and function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	heat shock protein HSP 90-beta	Xenopus laevis	102-107
32510596-4	2021	The purpose of the present study was to explore the combinations of the AP-1 family proteins that contribute to MG132-driven IL-8 secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	C-X-C motif chemokine ligand 8	Homo sapiens	125-129
32510596-6	2021	IL-8 secretion was augmented by MG132 in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
32510596-8	2021	The influence of MG132 stimulation on c-Jun and c-Fos expression was further examined by western blot analysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	38-43
32510596-9	2021	c-Jun expression was increased by MG132 stimulation, whereas c-Fos expression was not detected even after MG132 stimulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
32510596-12	2021	In contrast to our expectations, MG132-induced IL-8 secretion was significantly reduced in all the transfectants suggesting that other c-Jun members might form homodimers with c-Jun and contribute to IL-8 enhancement.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	C-X-C motif chemokine ligand 8	Homo sapiens	47-51
32510596-12	2021	In contrast to our expectations, MG132-induced IL-8 secretion was significantly reduced in all the transfectants suggesting that other c-Jun members might form homodimers with c-Jun and contribute to IL-8 enhancement.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	135-140
32510596-12	2021	In contrast to our expectations, MG132-induced IL-8 secretion was significantly reduced in all the transfectants suggesting that other c-Jun members might form homodimers with c-Jun and contribute to IL-8 enhancement.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	176-181
32510596-12	2021	In contrast to our expectations, MG132-induced IL-8 secretion was significantly reduced in all the transfectants suggesting that other c-Jun members might form homodimers with c-Jun and contribute to IL-8 enhancement.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	C-X-C motif chemokine ligand 8	Homo sapiens	200-204
32979864-5	2021	RESULTS: The reduction of the protein levels of FLI1 and ERG in response to IFNalpha or Poly:(IC) was reversed by blocking either lysosomal (leupeptin and Cathepsin B inhibitor) or proteosomal degradation (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	Fli-1 proto-oncogene, ETS transcription factor	Homo sapiens	48-52
32979864-5	2021	RESULTS: The reduction of the protein levels of FLI1 and ERG in response to IFNalpha or Poly:(IC) was reversed by blocking either lysosomal (leupeptin and Cathepsin B inhibitor) or proteosomal degradation (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	ETS transcription factor ERG	Homo sapiens	57-60
32979864-5	2021	RESULTS: The reduction of the protein levels of FLI1 and ERG in response to IFNalpha or Poly:(IC) was reversed by blocking either lysosomal (leupeptin and Cathepsin B inhibitor) or proteosomal degradation (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	interferon alpha 1	Homo sapiens	76-84
32979864-6	2021	MG132, leupeptin or CTSB-(i) also counteracted the anti-angiogenic effects of Poly:(IC) or IFNalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interferon alpha 1	Homo sapiens	91-99
32580819-8	2020	MG-132 at a low concentration (0.5 uM) diminished c-Met levels in H441 cells, while neither a low nor high concentration (~20 uM) altered c-Metlevels in A549 and H460 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	50-55
33436154-9	2021	Enhanced degradation of Smad7 protein in the fibroblasts of hypertrophic scars was prevented by proteasome inhibitors MG132 / MG115.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	SMAD family member 7	Homo sapiens	24-29
33091444-9	2021	MG-132 could reverse the decrease in endothelial nitric oxide synthase expression and improve nitric oxide-dependent vasodilator dysfunction in septic mice arteries.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nitric oxide synthase 3, endothelial cell	Mus musculus	37-70
33414721-8	2020	KDM3A upregulation in vitro by a proteasome inhibitor MG132 comparably dampened the inhibitory role of MF in inflammatory response and fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	lysine demethylase 3A	Rattus norvegicus	0-5
33488293-4	2020	Interestingly, MG-132, a proteasome inhibitor reducing the degradation of MCPIP-1, further facilitated neutrophils to express MCPIP-1 in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	zinc finger CCCH-type containing 12A	Homo sapiens	74-81
33488293-4	2020	Interestingly, MG-132, a proteasome inhibitor reducing the degradation of MCPIP-1, further facilitated neutrophils to express MCPIP-1 in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	zinc finger CCCH-type containing 12A	Homo sapiens	126-133
33488293-6	2020	Consistently, the same functional changes were observed in neutrophils from mice with myeloid-targeted overexpression of MCPIP-1 as MG-132 did.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-138	zinc finger CCCH type containing 12A	Mus musculus	121-128
33488293-8	2020	MG-132 may partially modulate the function of neutrophils via the induction of MCPIP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	zinc finger CCCH type containing 12A	Mus musculus	79-86
33318468-8	2020	Further, we identified FN1 degradation through the lysosome-dependent degradation pathway using the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	fibronectin 1	Homo sapiens	23-26
33322385-7	2020	Furthermore, MG132 inhibited the reduction of HA-ARF6 level by ABA and 4  C treatments, suggesting that these treatments decrease HA-ARF6 level through 26S proteasome-mediated protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	auxin response factor 6	Arabidopsis thaliana	49-53
33322385-7	2020	Furthermore, MG132 inhibited the reduction of HA-ARF6 level by ABA and 4  C treatments, suggesting that these treatments decrease HA-ARF6 level through 26S proteasome-mediated protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	auxin response factor 6	Arabidopsis thaliana	133-137
32580819-9	2020	A higher concentration of MG-132 (5 uM) was required fordecreasing c-Met levels in H1299 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	67-72
30663414-5	2020	We initially confirmed that BMP7 protein, but not mRNA, is downregulated when cultured under high glucose mimicking DN conditions, which was rescued by MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	bone morphogenetic protein 7	Rattus norvegicus	28-32
33376855-6	2020	We validated the decreased protein expression of DNA-directed RNA polymerase II subunit RPB2 (POLR2B) in both human cataract capsule tissues and UVB-treated SRA01/04 cells and found that treatment with proteasome inhibitor (MG-132) could reverse the protein level of POLR2B in UVB-irradiated SRA01/04 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-230	RNA polymerase II subunit B	Homo sapiens	49-92
33376855-6	2020	We validated the decreased protein expression of DNA-directed RNA polymerase II subunit RPB2 (POLR2B) in both human cataract capsule tissues and UVB-treated SRA01/04 cells and found that treatment with proteasome inhibitor (MG-132) could reverse the protein level of POLR2B in UVB-irradiated SRA01/04 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-230	RNA polymerase II subunit B	Homo sapiens	94-100
33376855-6	2020	We validated the decreased protein expression of DNA-directed RNA polymerase II subunit RPB2 (POLR2B) in both human cataract capsule tissues and UVB-treated SRA01/04 cells and found that treatment with proteasome inhibitor (MG-132) could reverse the protein level of POLR2B in UVB-irradiated SRA01/04 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-230	RNA polymerase II subunit B	Homo sapiens	267-273
33147870-0	2020	Proteasome Inhibitor MG132 is Toxic and Inhibits the Proliferation of Rat Neural Stem Cells but Increases BDNF Expression to Protect Neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	brain-derived neurotrophic factor	Rattus norvegicus	106-110
33168592-6	2020	We found that TGFbeta1, chloroquine and MG132 had little effect on ATG protein levels but increased LC3 lipidation, LC3 puncta formation and autophagosome-lysosome co-localization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	100-103
33168592-6	2020	We found that TGFbeta1, chloroquine and MG132 had little effect on ATG protein levels but increased LC3 lipidation, LC3 puncta formation and autophagosome-lysosome co-localization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	116-119
33147870-6	2020	In addition, MG132 treatment induced cAMP response element-binding protein phosphorylation and increased the expression of brain-derived neurotrophic factor transcripts and proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	brain-derived neurotrophic factor	Rattus norvegicus	123-156
32693013-11	2020	However, inhibition of p65 activation by MG132 reduced the co-localization of phos-p65/ PGC-1alpha and significantly increased the Mfn-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	RELA proto-oncogene, NF-kB subunit	Homo sapiens	23-26
32693013-11	2020	However, inhibition of p65 activation by MG132 reduced the co-localization of phos-p65/ PGC-1alpha and significantly increased the Mfn-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	PPARG coactivator 1 alpha	Homo sapiens	88-98
32693013-11	2020	However, inhibition of p65 activation by MG132 reduced the co-localization of phos-p65/ PGC-1alpha and significantly increased the Mfn-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	mitofusin 1	Homo sapiens	131-136
33707392-6	2020	The effect of the pathogenic PRKN variants on a drug (MG-132) induced loss of mitochondrial membrane potential ( PsiM) was measured by a fluorescent dye tetramethylrhodamine methyl ester (TMRM).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-60	parkin RBR E3 ubiquitin protein ligase	Homo sapiens	29-33
32745765-8	2020	The proteasome inhibitor MG132 stabilized HIF-1a expression, but not PGC-1alpha or SIRT3, and dramatically restrained BMSCs survival under hypoxia combined with curcumin condition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	hypoxia inducible factor 1, alpha subunit	Mus musculus	42-48
32745765-9	2020	MG132 also increased mitochondrial superoxide and intracellular hydrogen peroxide (H2O2) production and caspase-3 activation in hypoxia combined with curcumin-treated BMSCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Mus musculus	104-113
32679125-7	2020	ALA accelerated Twist1 degradation in the presence of cycloheximide, whereas the ubiquitination and degradation of Twist1 by ALA was suppressed by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-153	twist family bHLH transcription factor 1	Homo sapiens	115-121
33149608-8	2020	Conversely, RNF126 overexpression downregulated p53 and p21 but promoted pRb expression, which was reversed by a classic proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	ring finger protein 126	Homo sapiens	12-18
33149608-8	2020	Conversely, RNF126 overexpression downregulated p53 and p21 but promoted pRb expression, which was reversed by a classic proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	tumor protein p53	Homo sapiens	48-51
33149608-8	2020	Conversely, RNF126 overexpression downregulated p53 and p21 but promoted pRb expression, which was reversed by a classic proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	RB transcriptional corepressor 1	Homo sapiens	73-76
33149608-13	2020	Conversely, MG132 inhibited RNF126 overexpression-promoted above cell biology in HCT-8 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	ring finger protein 126	Homo sapiens	28-34
33490882-11	2021	In keeping with this mechanism, DEX"s inhibitory effect on SNAT2 transport activity was significantly blunted by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	solute carrier family 38, member 2	Rattus norvegicus	59-64
33101541-9	2020	CMTM2 degradation could be attributed to HBx-activated Lys48 (K48)-linked polyubiquitination, which was abolished by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	157-162	CKLF like MARVEL transmembrane domain containing 2	Homo sapiens	0-5
32720982-5	2020	MG132 treatment largely abolished Cu-induced degradation of COPT1, implying a link between the proteasome and COPT1 activity in modulating copper uptake.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	copper transporter 1	Arabidopsis thaliana	60-65
32720982-5	2020	MG132 treatment largely abolished Cu-induced degradation of COPT1, implying a link between the proteasome and COPT1 activity in modulating copper uptake.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	copper transporter 1	Arabidopsis thaliana	110-115
32720982-6	2020	Coimmunoprecipitation analyses revealed that COPT1 cannot be ubiquitinated in the presence of excess copper and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	copper transporter 1	Arabidopsis thaliana	45-50
33116878-9	2020	Furthermore, MG132 treatment enhanced the protein levels and ubiquitination of Spry2, suggesting that Spry2 protein expression can be regulated via the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	sprouty RTK signaling antagonist 2	Homo sapiens	79-84
33116878-9	2020	Furthermore, MG132 treatment enhanced the protein levels and ubiquitination of Spry2, suggesting that Spry2 protein expression can be regulated via the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	sprouty RTK signaling antagonist 2	Homo sapiens	102-107
32480040-8	2020	The proteasome inhibitor, MG-132, prevented the iron chelator-mediated decrease in ADI1 expression, while the lysosomotropic agent, chloroquine, had no effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	acireductone dioxygenase 1	Homo sapiens	83-87
32722981-7	2021	The macroautophagy/autophagy inhibitor 3-MA and the proteasome inhibitor MG132 were used in cerebral ischemic brains to identify how BNIP3L was reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	BCL2 interacting protein 3 like	Homo sapiens	133-139
33101052-7	2020	Proteasome inhibitor MG-132 blocked the ouabain-induced suppression of the total STAT3, but did not prevent the dephosphorylation of STAT3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	signal transducer and activator of transcription 3	Homo sapiens	81-86
32819607-8	2020	The expression level of Axin significantly decreased in OA chondrocytes with UBE2M overexpression and increased after MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	axin 1	Homo sapiens	24-28
32130656-5	2020	Proteasome inhibitor MG-132 could reverse the decrease of SynGAP protein level in wild-type mice following cerebral ischemia reperfusion through inhibiting SynGAP ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	synaptic Ras GTPase activating protein 1 homolog (rat)	Mus musculus	58-64
32130656-5	2020	Proteasome inhibitor MG-132 could reverse the decrease of SynGAP protein level in wild-type mice following cerebral ischemia reperfusion through inhibiting SynGAP ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	synaptic Ras GTPase activating protein 1 homolog (rat)	Mus musculus	156-162
32616662-7	2020	RHD3 is degraded more slowly in the absence of LNPs, as well as in the presence of MG132 and Concanamycin A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	Root hair defective 3 GTP-binding protein (RHD3)	Arabidopsis thaliana	0-4
32860670-4	2020	The reductions of CDK4, CDK6 and p-Rb were reversed by proteasome inhibitor MG132; similarly, the upregulation of 26S proteasome by SFN-Cys was reversed by PD98059.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	cyclin dependent kinase 4	Homo sapiens	18-22
32860670-4	2020	The reductions of CDK4, CDK6 and p-Rb were reversed by proteasome inhibitor MG132; similarly, the upregulation of 26S proteasome by SFN-Cys was reversed by PD98059.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	cyclin dependent kinase 6	Homo sapiens	24-28
32860670-4	2020	The reductions of CDK4, CDK6 and p-Rb were reversed by proteasome inhibitor MG132; similarly, the upregulation of 26S proteasome by SFN-Cys was reversed by PD98059.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	RNA exonuclease 2	Homo sapiens	132-135
32848167-5	2020	This binding induced MG132-sensitive reduction of AIF expression in the presence of E6 derived from HPV16 (16E6), a cancer-causing type of HPV.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	apoptosis inducing factor mitochondria associated 1	Homo sapiens	50-53
32722981-8	2021	We found that MG132 blocked the loss of BNIP3L and subsequently promoted mitophagy in ischemic brains.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	BCL2 interacting protein 3 like	Homo sapiens	40-46
32248569-10	2020	Furthermore, the influence of WWP2 on cell proliferation and apoptosis was rescued by MG132 (proteasome inhibitor) treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	WW domain containing E3 ubiquitin protein ligase 2	Homo sapiens	30-34
32447485-11	2020	The results of cycloheximide (CHX) and MG-132 assays indicated that SHCBP1 knockdown could attenuate the degradation of TP53 by the proteasome, prolong the half-life of TP53, and enhance the stabilization of TP53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	SHC binding and spindle associated 1	Homo sapiens	68-74
32464781-6	2020	This was partially reversed by proteasome inhibitor MG132 for AhR but not for PXR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	aryl hydrocarbon receptor	Homo sapiens	62-65
32714042-7	2020	We observed that the levels of miR-424, let-7c, miR-222, miR-200b were upregulated when hepatoma cells were treated with MG132, and this increase was negatively correlated with the levels of PBX3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	PBX homeobox 3	Homo sapiens	191-195
32487733-7	2020	Cotreatment of EMD with proteasome inhibitor MG132 reversed its c-Myc targeting effect, suggesting the involvement of ubiquitin-mediated proteasomal degradation in the process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-69
32714042-0	2020	MG132 inhibits the expression of PBX3 through miRNAs by targeting Argonaute2 in hepatoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	PBX homeobox 3	Homo sapiens	33-37
32884739-3	2020	Therefore, this article investigated the effects of small molecular weight SBP on MG132-induced apoptosis in RAW264.7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	spermine binding protein	Mus musculus	75-78
32714042-0	2020	MG132 inhibits the expression of PBX3 through miRNAs by targeting Argonaute2 in hepatoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	argonaute RISC catalytic component 2	Homo sapiens	66-76
32714042-5	2020	However, when we treated hepatoma cells using the proteasome inhibitor MG132, found the levels of PBX3 protein and mRNA were significantly downregulated, suggesting that PBX3 protein is not degraded by the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	PBX homeobox 3	Homo sapiens	98-102
32714042-5	2020	However, when we treated hepatoma cells using the proteasome inhibitor MG132, found the levels of PBX3 protein and mRNA were significantly downregulated, suggesting that PBX3 protein is not degraded by the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	PBX homeobox 3	Homo sapiens	170-174
32714042-6	2020	Our study aims to investigate the mechanism of MG132 regulation of PBX3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	PBX homeobox 3	Homo sapiens	67-71
32714042-7	2020	We observed that the levels of miR-424, let-7c, miR-222, miR-200b were upregulated when hepatoma cells were treated with MG132, and this increase was negatively correlated with the levels of PBX3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	microRNA 424	Homo sapiens	31-38
32714042-7	2020	We observed that the levels of miR-424, let-7c, miR-222, miR-200b were upregulated when hepatoma cells were treated with MG132, and this increase was negatively correlated with the levels of PBX3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	microRNA let-7c	Homo sapiens	40-46
32714042-7	2020	We observed that the levels of miR-424, let-7c, miR-222, miR-200b were upregulated when hepatoma cells were treated with MG132, and this increase was negatively correlated with the levels of PBX3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	microRNA 222	Homo sapiens	48-55
32714042-7	2020	We observed that the levels of miR-424, let-7c, miR-222, miR-200b were upregulated when hepatoma cells were treated with MG132, and this increase was negatively correlated with the levels of PBX3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	microRNA 200b	Homo sapiens	57-65
32884739-4	2020	SBP inhibited MG132-induced apoptosis of RAW264.7 cells in a dose-dependent manner by flow cytometry.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	spermine binding protein	Mus musculus	0-3
32884739-6	2020	These results indicated the protective effect of SBP on MG132-induced apoptosis in RAW264.7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	spermine binding protein	Mus musculus	49-52
32246947-7	2020	In PC12-CerK-HA cells, serum withdrawal caused ubiquitination of CerK-HA protein and down-regulated both CerK-HA protein and C1P formation within 6 h, and these down-regulations were abolished by co-treatments with NGF or proteasome inhibitors such as MG132 and clasto-lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	252-257	nerve growth factor	Rattus norvegicus	215-218
33693264-5	2020	The proteasome inhibitors MG132 and lactacystine increased levels of hMCT9-FLAG protein expression with enhanced ubiquitination, prolonged their half-life, and decreased [14C]-urate uptake.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	solute carrier family 16 member 9	Homo sapiens	69-79
32242227-7	2020	Finally, RAD23B was found to promote the degradation of KRP1 in vivo, which was accumulated following treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	Rad23 UV excision repair protein family	Arabidopsis thaliana	9-15
32242227-7	2020	Finally, RAD23B was found to promote the degradation of KRP1 in vivo, which was accumulated following treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	Cyclin-dependent kinase inhibitor family protein	Arabidopsis thaliana	56-60
32714200-8	2020	Similarly, pretreatment of HEK293 cells with either the lysosomal inhibitor bafilomycin A1 or the proteasomal inhibitor MG132 reversed the inhibitory effects of SPAK knockdown on BK expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	serine/threonine kinase 39	Homo sapiens	161-165
32564010-8	2020	HK2 protein levels were reduced in KCNQ1OT1 knockdown CRC cells, but were restored by treatment with the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	hexokinase 2	Homo sapiens	0-3
32669967-6	2020	Further, acidic pHi could activate the ubiquitin-proteasome system and inhibiting proteasome activity by MG132 prevented cells entering quiescence.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	glucose-6-phosphate isomerase	Homo sapiens	16-19
32581820-11	2020	The proteasome inhibitor MG132 attenuated the effects of icariin on PTEN protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	phosphatase and tensin homolog	Homo sapiens	68-72
32626542-12	2020	We found that after treatment with proteasomal inhibitor MG132 and lysosomal inhibitor bafilomycin A1, MDR3 expression of V399L was significantly increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	ATP binding cassette subfamily B member 4	Homo sapiens	103-107
32278272-0	2020	MG-132 attenuates cardiac deterioration of viral myocarditis via AMPK pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	65-69
32582037-6	2020	Since the activation of ISGs is controlled by the JAK-STAT signal pathway, we next examined the effect of MG132 on the expression and localization of key molecular STAT1 in the infected cells using Western blot and confocal laser scanning microscopy, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	signal transducer and activator of transcription 1	Homo sapiens	164-169
32582037-7	2020	Results showed that CSFV infection and viral NS4A protein decreased the protein level of STAT1, and MG132 promoted the accumulation of STAT1 in the nucleus of cells adjacent to the CSFV-infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	signal transducer and activator of transcription 1	Homo sapiens	135-140
32278272-3	2020	MG-132, a proteasome inhibitor, regulates mitochondrial-mediated intrinsic myocardial apoptosis and downregulates NF-kappaB-mediated inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor kappa B subunit 1	Homo sapiens	114-123
32278272-4	2020	Here, we determined whether AMPK pathway participates in MG-132-mediated myocardial protection in viral-induced myocarditis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-63	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	28-32
32278272-10	2020	CONCLUSION: MG-132 modulated apoptosis and inflammation, improved hemodynamics, and inhibited the structural remodeling of ventricles in a myocarditis mouse model via regulation of the AMPK signal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-18	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	185-189
31945194-5	2020	Treatment with cycloheximide reduced the levels of Zwint-1 while treatment with MG132 to inhibit endogenous ubiquitin-proteasome elevated the levels of Zwint-1 in HEK293T cells or Hela cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	ZW10 interacting kinetochore protein	Homo sapiens	152-159
31945194-7	2020	Furthermore, induction of cell-division cycle protein 20 (Cdc20) overexpression decreased the levels of Zwint-1, which was abrogated by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	cell division cycle 20	Homo sapiens	58-63
31945194-7	2020	Furthermore, induction of cell-division cycle protein 20 (Cdc20) overexpression decreased the levels of Zwint-1, which was abrogated by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	ZW10 interacting kinetochore protein	Homo sapiens	104-111
32234809-3	2020	The current study showed that the ubiquitinated OAT1 accumulated in the presence of the proteasomal inhibitors MG132 and ALLN rather than the lysosomal inhibitors leupeptin and pepstatin A, suggesting that ubiquitinated OAT1 degrades through proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	solute carrier family 22 member 6	Homo sapiens	48-52
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	caspase 3	Homo sapiens	59-67
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	116-120
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	cyclin D2	Homo sapiens	122-131
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	136-141
31954175-7	2020	SKi also enhanced the stimulatory effect of the proteasome inhibitor, MG132 on the expression of the pro-survival protein XBP-1s and this was reduced by siRNA knockdown of SK2 and increased by knockdown of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	SKI proto-oncogene	Homo sapiens	0-3
32457708-6	2020	We further found that this reduction of gamma-catenin protein is a result of ubiquitin proteasome-mediated degradation, since the addition of proteasome inhibitor MG132 inhibited gamma-catenin downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	junction plakoglobin	Mus musculus	40-53
32457708-6	2020	We further found that this reduction of gamma-catenin protein is a result of ubiquitin proteasome-mediated degradation, since the addition of proteasome inhibitor MG132 inhibited gamma-catenin downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	junction plakoglobin	Mus musculus	179-192
31891806-7	2020	Moreover, MG132 preserved mitochondrial mass, prevented mitochondrial network fragmentation, and abolished IR-induced reductions in Mfn2 levels in heart tissue and cultured cardiomyocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	mitofusin 2	Rattus norvegicus	132-136
32323732-8	2020	PEDF reduced CMPK2 protein levels but did not affect the mRNA levels, and treatment with the proteasomal inhibitor MG132 significantly reversed this reduction in CMPK2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	cytidine/uridine monophosphate kinase 2	Homo sapiens	13-18
32323732-8	2020	PEDF reduced CMPK2 protein levels but did not affect the mRNA levels, and treatment with the proteasomal inhibitor MG132 significantly reversed this reduction in CMPK2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	cytidine/uridine monophosphate kinase 2	Homo sapiens	162-167
32323732-9	2020	Furthermore, a ubiquitination assay of immunoprecipitation demonstrated that CMPK2 was polyubiquitinated in the presence of LPS, PEDF and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	cytidine/uridine monophosphate kinase 2	Homo sapiens	77-82
32351584-8	2020	Ubiquitination-IP and the treatment of MG132 and CHX were used to detect the ubiquitylation level of NFRKB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nuclear factor related to kappaB binding protein	Homo sapiens	101-106
32046856-7	2020	MG-132 but not doxycycline significantly restored telmisartan-inhibited MLCK expression and p-MLC-Ser19.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	myosin light chain kinase	Rattus norvegicus	72-76
32046856-12	2020	Furthermore, the telmisartan-inhibited vessel contraction in the aortas was significantly reversed by MG-132 or compound C. In conclusion, we demonstrated that telmisartan inhibits VSMC contractility and vessel contraction by activating AMPK/proteasome/MLCK degradation signaling axis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	237-241
32046856-12	2020	Furthermore, the telmisartan-inhibited vessel contraction in the aortas was significantly reversed by MG-132 or compound C. In conclusion, we demonstrated that telmisartan inhibits VSMC contractility and vessel contraction by activating AMPK/proteasome/MLCK degradation signaling axis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	myosin light chain kinase	Rattus norvegicus	253-257
32301004-9	2020	After MG132 or PSMB5-siRNA pretreatment, and then L-02 cells were treated with NaAsO2, the gene expression of PSMB remarkably decreased; however, the protein expression of SOD1 and GPx1 increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	superoxide dismutase 1	Homo sapiens	172-176
32301004-9	2020	After MG132 or PSMB5-siRNA pretreatment, and then L-02 cells were treated with NaAsO2, the gene expression of PSMB remarkably decreased; however, the protein expression of SOD1 and GPx1 increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	glutathione peroxidase 1	Homo sapiens	181-185
32134157-13	2020	Furthermore, CSN6-mediated downregulation of PD-L1 was inhibited by MG132, a proteasome inhibitor in U87 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	COP9 signalosome subunit 6	Homo sapiens	13-17
32134157-13	2020	Furthermore, CSN6-mediated downregulation of PD-L1 was inhibited by MG132, a proteasome inhibitor in U87 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	CD274 molecule	Homo sapiens	45-50
32317666-0	2020	MG132 exerts anti-viral activity against HSV-1 by overcoming virus-mediated suppression of the ERK signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 1	Homo sapiens	95-98
32317666-7	2020	Importantly, the proteasome inhibitor MG132 inhibited HSV-1 replication by reversing ERK suppression in infected cells, inhibiting lytic genes (ICP5, ICP27 and UL42) expression, and overcoming the downregulation of Ras-GRF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	mitogen-activated protein kinase 1	Homo sapiens	85-88
32317666-7	2020	Importantly, the proteasome inhibitor MG132 inhibited HSV-1 replication by reversing ERK suppression in infected cells, inhibiting lytic genes (ICP5, ICP27 and UL42) expression, and overcoming the downregulation of Ras-GRF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	DNA polymerase processivity subunit	Human alphaherpesvirus 1	160-164
32317666-7	2020	Importantly, the proteasome inhibitor MG132 inhibited HSV-1 replication by reversing ERK suppression in infected cells, inhibiting lytic genes (ICP5, ICP27 and UL42) expression, and overcoming the downregulation of Ras-GRF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	Ras protein specific guanine nucleotide releasing factor 2	Homo sapiens	215-223
32317666-9	2020	Given that ERK activation by MG132 exhibits anti-HSV-1 activity, these results suggest that the proteasome inhibitor could serve as a novel therapeutic agent against HSV-1 infection.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	mitogen-activated protein kinase 1	Homo sapiens	11-14
31954175-7	2020	SKi also enhanced the stimulatory effect of the proteasome inhibitor, MG132 on the expression of the pro-survival protein XBP-1s and this was reduced by siRNA knockdown of SK2 and increased by knockdown of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	X-box binding protein 1	Homo sapiens	122-127
31954175-7	2020	SKi also enhanced the stimulatory effect of the proteasome inhibitor, MG132 on the expression of the pro-survival protein XBP-1s and this was reduced by siRNA knockdown of SK2 and increased by knockdown of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	sphingosine kinase 2	Homo sapiens	172-175
31954175-7	2020	SKi also enhanced the stimulatory effect of the proteasome inhibitor, MG132 on the expression of the pro-survival protein XBP-1s and this was reduced by siRNA knockdown of SK2 and increased by knockdown of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	tumor protein p53	Homo sapiens	206-209
32101771-11	2020	The inhibition of proteolysis by MG132, a proteasoma inhibitor, restored Nrf2 and YAP protein expressions, suggesting that the Aila effect was at post-translational level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	NFE2 like bZIP transcription factor 2	Homo sapiens	73-77
32101771-11	2020	The inhibition of proteolysis by MG132, a proteasoma inhibitor, restored Nrf2 and YAP protein expressions, suggesting that the Aila effect was at post-translational level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	Yes1 associated transcriptional regulator	Homo sapiens	82-85
31891772-6	2020	A proteasome inhibitor, MG-132, inhibited DGKdelta-dependent SERT degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	diacylglycerol kinase, delta	Mus musculus	42-50
32368563-4	2020	Significant loss of overexpressed TP during erythroid differentiation can be reduced by addition of the ubiquitination inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	thymidine phosphorylase	Homo sapiens	34-36
32210081-5	2020	Protein synthesis, as assessed by puromycin incorporation in neo-synthesized polypeptides, was inhibited already after 1 h of FK506 treatment, while the use of a proteasome inhibitor MG132 (1 muM) shows that GLAST protein degradation was only suppressed after 7 days of FK506 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	183-188	latexin	Homo sapiens	192-195
32210081-5	2020	Protein synthesis, as assessed by puromycin incorporation in neo-synthesized polypeptides, was inhibited already after 1 h of FK506 treatment, while the use of a proteasome inhibitor MG132 (1 muM) shows that GLAST protein degradation was only suppressed after 7 days of FK506 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	183-188	solute carrier family 1 member 3	Homo sapiens	208-213
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	cyclin dependent kinase 7	Homo sapiens	84-88
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	cyclin dependent kinase 7	Homo sapiens	150-154
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	cyclin dependent kinase 13	Homo sapiens	159-164
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	jagged canonical Notch ligand 2	Homo sapiens	213-217
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	dedicator of cytokinesis 4	Homo sapiens	247-252
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	dedicator of cytokinesis 9	Homo sapiens	257-262
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	Rac family small GTPase 1	Homo sapiens	283-287
32143485-5	2020	In addition, the protein degradation inhibitor MG132 reversed the effect of THZ1, a CDK7 inhibitor which could decrease the cell number and amount of CDK7 and CDK13, accompanied by a reduction in the level of CTD Ser2 and Ser5 phosphorylation and DOCK4 and DOCK9 (the activators for Rac1 and Cdc42, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	cell division cycle 42	Homo sapiens	292-297
31891772-6	2020	A proteasome inhibitor, MG-132, inhibited DGKdelta-dependent SERT degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	solute carrier family 6 (neurotransmitter transporter, serotonin), member 4	Mus musculus	61-65
31489637-7	2020	The proteasome inhibitor MG132 blocked Cdh1-mediated PECAM-1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cadherin 1	Homo sapiens	39-43
31302751-10	2020	In contrast, treatment with MG132 increased abundance of AQP2-L137P but not AQP2-WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	aquaporin 2	Homo sapiens	57-62
31302751-10	2020	In contrast, treatment with MG132 increased abundance of AQP2-L137P but not AQP2-WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	aquaporin 2	Homo sapiens	57-61
31489637-7	2020	The proteasome inhibitor MG132 blocked Cdh1-mediated PECAM-1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	platelet and endothelial cell adhesion molecule 1	Homo sapiens	53-60
32092124-6	2020	We now demonstrate that proteasomal inhibition by MG132 induces EBNA3C degradation both in EBV transformed B-lymphocytes and ectopic-expression systems.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	EBNA-3C	Human gammaherpesvirus 4	64-70
32184710-7	2020	This decrease in FMRP was suppressed by the ubiquitin-activating enzyme E1 enzyme inhibitor PYR-41 and proteasome inhibitor MG132, suggesting that the ubiquitin-proteasome pathway is involved in Sema3A-induced FMRP degradation in growth cones.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	fragile X messenger ribonucleoprotein 1	Homo sapiens	17-21
32184710-7	2020	This decrease in FMRP was suppressed by the ubiquitin-activating enzyme E1 enzyme inhibitor PYR-41 and proteasome inhibitor MG132, suggesting that the ubiquitin-proteasome pathway is involved in Sema3A-induced FMRP degradation in growth cones.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	semaphorin 3A	Homo sapiens	195-201
32092124-7	2020	Interestingly, MG132 treatment promotes degradation of two EBNA3 family oncoproteins-EBNA3A and EBNA3C, but not the viral tumor suppressor protein EBNA3B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	EBNA3A	Human gammaherpesvirus 4	85-91
32092124-7	2020	Interestingly, MG132 treatment promotes degradation of two EBNA3 family oncoproteins-EBNA3A and EBNA3C, but not the viral tumor suppressor protein EBNA3B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	EBNA-3C	Human gammaherpesvirus 4	96-102
32110043-11	2020	BRD4 downregulation could repress DUB3-induced EZH2 production, and MG132 reversed DUB3 decreasing-mediated BRD4 downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	ubiquitin specific peptidase 17 like family member 2	Homo sapiens	83-87
32110043-11	2020	BRD4 downregulation could repress DUB3-induced EZH2 production, and MG132 reversed DUB3 decreasing-mediated BRD4 downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	bromodomain containing 4	Homo sapiens	108-112
31390480-5	2020	Furthermore, the increase in acetylation by LBH589 could inhibit the degradation and improve the accumulation of BmApoLp-III in BmN cells treated with cycloheximide and MG132 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	apolipophorins	Bombyx mori	113-124
31209364-8	2020	Interestingly, the degradation could be almost fully rescued by a non-specific LONP1 and proteasome inhibitor, MG132, in mutant mitochondria.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	lon peptidase 1, mitochondrial	Mus musculus	79-84
31390677-5	2020	Interestingly, by performing Q-PCR, HDAC6 inhibition did not cause a down-regulation of MKK7 mRNA level, whereas the suppressive effects on MKK7 protein can be efficiently blocked by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	209-214	mitogen-activated protein kinase kinase 7	Mus musculus	140-144
32966974-0	2020	HDAC3 Silencing Enhances Acute B Lymphoblastic Leukaemia Cells Sensitivity to MG-132 by Inhibiting the JAK/Signal Transducer and Activator of Transcription 3 Signaling Pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	histone deacetylase 3	Homo sapiens	0-5
32966974-0	2020	HDAC3 Silencing Enhances Acute B Lymphoblastic Leukaemia Cells Sensitivity to MG-132 by Inhibiting the JAK/Signal Transducer and Activator of Transcription 3 Signaling Pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	signal transducer and activator of transcription 3	Homo sapiens	107-157
32966974-9	2020	When we treated Sup-B15 and CCRF-SB cells with siHDAC3 and MG-132 for 24 h, silencing HDAC3 enhanced the apoptosis rate induced by MG-132 in B-ALL cells and further inhibited the JAK/STAT3 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	signal transducer and activator of transcription 3	Homo sapiens	183-188
32966974-9	2020	When we treated Sup-B15 and CCRF-SB cells with siHDAC3 and MG-132 for 24 h, silencing HDAC3 enhanced the apoptosis rate induced by MG-132 in B-ALL cells and further inhibited the JAK/STAT3 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-137	histone deacetylase 3	Homo sapiens	49-54
32966974-9	2020	When we treated Sup-B15 and CCRF-SB cells with siHDAC3 and MG-132 for 24 h, silencing HDAC3 enhanced the apoptosis rate induced by MG-132 in B-ALL cells and further inhibited the JAK/STAT3 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-137	signal transducer and activator of transcription 3	Homo sapiens	183-188
32966974-10	2020	Furthermore, MG-132 was observed to cause G2/M phase arrest in B-ALL cells and inhibited the JAK/STAT3 pathway, leading to apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	signal transducer and activator of transcription 3	Homo sapiens	97-102
32966974-11	2020	CONCLUSIONS: Silencing of HDAC3 enhanced the sensitivity of B-ALL cells to MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	histone deacetylase 3	Homo sapiens	26-31
31470364-8	2020	In this study, we identified that RAW264.7 preosteoclast cells treated with proteasome inhibitor (MG-132) suppress RANK receptor expression essential for OCL differentiation, but no effect on TRAF-6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	occludin	Mus musculus	154-157
31470364-13	2020	MG-132 inhibited RANKL induced proteasome activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	17-22
31470364-16	2020	In-addition, mouse bone marrow cultures treated with MG-132 suppress OCL formation and bone resorption activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	occludin	Mus musculus	69-72
32568195-7	2020	LiCl, MG132, CHX, and IGF-1 treatment were used to research the signaling pathways which regulated by HO-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	heme oxygenase 1	Mus musculus	102-106
31789395-5	2020	Pre-treatment of the cells with the proteasome inhibitor, MG132, to confirm the inhibition of melanogenesis through the beta-catenin pathway by TQ treatment resulted in an increase in the expression of beta-catenin that was initially reduced by TQ, and the expression and activity of MITF and tyrosinase also increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	catenin (cadherin associated protein), beta 1	Mus musculus	202-214
31789395-5	2020	Pre-treatment of the cells with the proteasome inhibitor, MG132, to confirm the inhibition of melanogenesis through the beta-catenin pathway by TQ treatment resulted in an increase in the expression of beta-catenin that was initially reduced by TQ, and the expression and activity of MITF and tyrosinase also increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	melanogenesis associated transcription factor	Mus musculus	284-288
31789395-5	2020	Pre-treatment of the cells with the proteasome inhibitor, MG132, to confirm the inhibition of melanogenesis through the beta-catenin pathway by TQ treatment resulted in an increase in the expression of beta-catenin that was initially reduced by TQ, and the expression and activity of MITF and tyrosinase also increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	tyrosinase	Mus musculus	293-303
31563647-5	2019	Notably, administration of proteasome inhibitor MG132 significantly inhibited the expression of cullin7 and up-regulated the expression of p53 in pulmonary arteries concomitantly with improvement of hypoxia-induced pulmonary vascular remodeling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	cullin 7	Homo sapiens	96-103
31842909-10	2019	In orthotopic mouse model, NQO1 knock-out inhibited tumor growth and induced apoptosis while this effect was effectively rescued by SIRT6 overexpression or MG132 treatment partially.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-161	NAD(P)H dehydrogenase, quinone 1	Mus musculus	27-31
31850806-17	2019	MG132 and DHB significantly blocked the MeHg-induced decrease in HIF-1alpha expression (p<0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	65-75
31563647-5	2019	Notably, administration of proteasome inhibitor MG132 significantly inhibited the expression of cullin7 and up-regulated the expression of p53 in pulmonary arteries concomitantly with improvement of hypoxia-induced pulmonary vascular remodeling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	tumor protein p53	Homo sapiens	139-142
31148189-6	2019	Mechanistically, forced expression of KPC1 promoted Bax protein degradation, which was abolished by proteasome inhibitor MG132, suggesting that KPC1 promoted proteasomal degradation of Bax.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	ring finger protein 123	Homo sapiens	38-42
31148189-6	2019	Mechanistically, forced expression of KPC1 promoted Bax protein degradation, which was abolished by proteasome inhibitor MG132, suggesting that KPC1 promoted proteasomal degradation of Bax.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	BCL2 associated X, apoptosis regulator	Rattus norvegicus	52-55
31148189-6	2019	Mechanistically, forced expression of KPC1 promoted Bax protein degradation, which was abolished by proteasome inhibitor MG132, suggesting that KPC1 promoted proteasomal degradation of Bax.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	BCL2 associated X, apoptosis regulator	Rattus norvegicus	185-188
31853378-13	2019	The inhibitory effect of AEG-1 on SOCS1 was weakened after the addition of MG-132 (p < 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	metadherin	Mus musculus	25-30
30929966-19	2019	The effect of MARCKS knockdown on KIS stability was abrogated by the 26s proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-100	myristoylated alanine rich protein kinase C substrate	Homo sapiens	14-20
30929966-19	2019	The effect of MARCKS knockdown on KIS stability was abrogated by the 26s proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-100	U2AF homology motif kinase 1	Homo sapiens	34-37
31319135-4	2019	Their transcriptional, as well as translational blockage of Nrf2 expression, was verified by using a proteasomal inhibitor (MG132) and well-known Nrf2 activator (alpha-lipoic acid (ALA)).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	NFE2 like bZIP transcription factor 2	Homo sapiens	60-64
31853378-13	2019	The inhibitory effect of AEG-1 on SOCS1 was weakened after the addition of MG-132 (p < 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	suppressor of cytokine signaling 1	Mus musculus	34-39
31521246-11	2019	Treatment with hemin and MG132 enhanced Cd-mediated increases in HO-1 and polyUb-p62 levels, resulting in increased apoptosis, which indicated that Cd-induced HO-1 accumulation is associated with polyUb-p62 formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	sequestosome 1	Mus musculus	81-84
31521246-11	2019	Treatment with hemin and MG132 enhanced Cd-mediated increases in HO-1 and polyUb-p62 levels, resulting in increased apoptosis, which indicated that Cd-induced HO-1 accumulation is associated with polyUb-p62 formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	sequestosome 1	Mus musculus	203-206
31491427-10	2019	Further analysis using proteasome inhibitors revealed that degradation of immature SLC4A11 was delayed after treatment with the proteasome inhibitors, MG-132 and bortezomib, and was mediated by poly-ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-157	solute carrier family 4 member 11	Homo sapiens	83-90
31377397-11	2019	In line with this model of mutation-induced instability of SHIP1-F28L, treatment of cells with proteasomal inhibitor MG132 was able to rescue expression of SHIP1-F28L.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	inositol polyphosphate-5-phosphatase D	Homo sapiens	59-64
31377397-11	2019	In line with this model of mutation-induced instability of SHIP1-F28L, treatment of cells with proteasomal inhibitor MG132 was able to rescue expression of SHIP1-F28L.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	inositol polyphosphate-5-phosphatase D	Homo sapiens	156-161
31462568-9	2019	PRRSV-induced STAT2 degradation could be restored by treatment with the proteasome inhibitor MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	signal transducer and activator of transcription 2	Homo sapiens	14-19
31129810-4	2019	In primary mixed neuronal and glial cell cultures (MNGCs) from transgenic mice expressing wild-type Sho from the PrP gene promoter (Tg.Sprn mice), lactacystin- and MG132-mediated inhibition of proteasomal activity shifted the repertoire of Sho species towards unglycosylated forms appearing in the nuclei; conversely, the autophagic modulators NH4Cl and 3-MA did not affect Sho or PrPC glycosylation patterns.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	prion protein	Mus musculus	381-385
31687087-6	2019	Treatment with the proteasome inhibitor, MG132, on SCA3-iPSC-derived neurons downregulated proteasome activity, increased production of radical oxygen species (ROS), and upregulated the cleaved caspase 3 level and caspase 3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	caspase 3	Homo sapiens	194-203
31687087-6	2019	Treatment with the proteasome inhibitor, MG132, on SCA3-iPSC-derived neurons downregulated proteasome activity, increased production of radical oxygen species (ROS), and upregulated the cleaved caspase 3 level and caspase 3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	caspase 3	Homo sapiens	214-223
31291699-4	2019	Treatment with cycloheximide and MG132 indicated that endogenous CREB3 is a proteasome substrate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	cAMP responsive element binding protein 3	Homo sapiens	65-70
31165943-4	2019	Meanwhile, we observed that the clearance of alpha-Syn by astrocytes was abolished by proteasome inhibitor MG132 and autophagy inhibitor 3-methyladenine (3MA).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	synuclein alpha	Homo sapiens	45-54
31165943-5	2019	We further showed that intracellular alpha-Syn was reduced after ginkgolide B (GB) and bilobalide (BB) treatment, and the decrease was reversed by MG132 and 3MA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	synuclein alpha	Homo sapiens	37-46
31250983-3	2019	Treatment with proteasome inhibitor MG-132 has been shown to increase misfolded dysferlin in fibroblasts, allowing them to recover their membrane resealing function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	dysferlin	Homo sapiens	80-89
31555373-1	2019	Effects of ubiquitin-proteasome system (UPS) inhibitor MG-132 on the expression levels of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in mice with viral myocarditis were investigated to analyze the correlation of myocardial tissue score of mice between TNF-alpha and TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	tumor necrosis factor	Mus musculus	90-117
31555373-1	2019	Effects of ubiquitin-proteasome system (UPS) inhibitor MG-132 on the expression levels of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in mice with viral myocarditis were investigated to analyze the correlation of myocardial tissue score of mice between TNF-alpha and TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	tumor necrosis factor	Mus musculus	119-128
31555373-1	2019	Effects of ubiquitin-proteasome system (UPS) inhibitor MG-132 on the expression levels of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in mice with viral myocarditis were investigated to analyze the correlation of myocardial tissue score of mice between TNF-alpha and TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	transforming growth factor, beta 1	Mus musculus	134-166
31555373-1	2019	Effects of ubiquitin-proteasome system (UPS) inhibitor MG-132 on the expression levels of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in mice with viral myocarditis were investigated to analyze the correlation of myocardial tissue score of mice between TNF-alpha and TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	transforming growth factor, beta 1	Mus musculus	168-177
31555373-6	2019	The expression levels of myocardial histopathological scores, mRNA and protein of TNF-alpha and TGF-beta1 in the blank and control group were significantly lower than those in the VMC and the MG-132 group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-198	tumor necrosis factor	Mus musculus	82-91
31555373-7	2019	The myocardial histopathological scores, mRNA and TNF-alpha and TGF-beta1 protein in the MG-132 group were significantly lower than those in the VMC group (P<0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-95	tumor necrosis factor	Mus musculus	50-59
31555373-7	2019	The myocardial histopathological scores, mRNA and TNF-alpha and TGF-beta1 protein in the MG-132 group were significantly lower than those in the VMC group (P<0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-95	transforming growth factor, beta 1	Mus musculus	64-73
31323531-4	2019	The proteasome inhibitor MG132 used as an activator of MCPIP1 overexpression, and we showed that MG132 can indeed increase the expression of MCPIP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	zinc finger CCCH type containing 12A	Mus musculus	55-61
31323531-4	2019	The proteasome inhibitor MG132 used as an activator of MCPIP1 overexpression, and we showed that MG132 can indeed increase the expression of MCPIP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	zinc finger CCCH type containing 12A	Mus musculus	141-147
31323531-4	2019	The proteasome inhibitor MG132 used as an activator of MCPIP1 overexpression, and we showed that MG132 can indeed increase the expression of MCPIP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	zinc finger CCCH type containing 12A	Mus musculus	55-61
31323531-4	2019	The proteasome inhibitor MG132 used as an activator of MCPIP1 overexpression, and we showed that MG132 can indeed increase the expression of MCPIP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	zinc finger CCCH type containing 12A	Mus musculus	141-147
31323531-5	2019	MCPIP1 overexpression induced by MG132 alleviated sepsis-induced pathologic changes, water content and protein leakage in the lungs, and induction of systemic inflammatory mediators, and improved the 7-day mortality rate in the model rats.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	zinc finger CCCH type containing 12A	Rattus norvegicus	0-6
31889041-9	2019	Amylin expression/oligomerization with melatonin treatment was significantly decreased in the thapsigargin- or tunicamycin-combined Bafilomycin A1 or MG132 treatments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	islet amyloid polypeptide	Rattus norvegicus	0-6
31362890-7	2019	Blocking CRM1-dependent nuclear export with leptomycin B augmented PINK1 levels in the nucleus of MG132-treated cells but not in normal cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	exportin 1	Homo sapiens	9-13
31362890-7	2019	Blocking CRM1-dependent nuclear export with leptomycin B augmented PINK1 levels in the nucleus of MG132-treated cells but not in normal cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	PTEN induced kinase 1	Homo sapiens	67-72
31131398-8	2019	Of the five chemical chaperones tested, only the proteasomal inhibitor MG132 markedly increased the amount of mutant LAL secreted.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	lipase A, lysosomal acid type	Homo sapiens	117-120
31495089-5	2019	m6A-IP-qPCR method was applied to confirm whether HNRNPA2B1 RNA in Daoy cells was modified with m6A.Western blot was used to detect the effect of MG132 treatment on the HNRNPA2B1 protein level in Daoy cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	50-59
31514384-9	2019	We observed that the increase in the alpha-Syn PFF-induced aggregation in the DNAJB6 KO cells compared with the parental cells was strongly diminished upon the incubation of the cells with the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	215-220	synuclein alpha	Homo sapiens	37-46
31514384-9	2019	We observed that the increase in the alpha-Syn PFF-induced aggregation in the DNAJB6 KO cells compared with the parental cells was strongly diminished upon the incubation of the cells with the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	215-220	DnaJ heat shock protein family (Hsp40) member B6	Homo sapiens	78-84
31495089-5	2019	m6A-IP-qPCR method was applied to confirm whether HNRNPA2B1 RNA in Daoy cells was modified with m6A.Western blot was used to detect the effect of MG132 treatment on the HNRNPA2B1 protein level in Daoy cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	169-178
31495089-9	2019	The HNRNPA2B1 protein level in Daoy cells increased upon MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	4-13
30980109-4	2019	Preincubation with a proteasome or lysosome inhibitor (MG132, 3 MA or CQ) mainly led to IGF-1Rbeta degradation via the lysosome degradation pathway, rather than the proteasome-dependent pathway, after PC cells were treated with 922 for 24 h. These results might be associated with the inhibition of pancreatic cellular chymotrypsin-peptidase activity by 922 for 24 h. Interestingly, 922 induced autophagic flux by increasing LC3II expression and puncta formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	insulin like growth factor 1	Homo sapiens	88-93
31502579-0	2019	Down-regulation effects of IFN-alpha on p11, 5-htr1b and 5-HTR4 protein levels were affected by NH4CL or MG132 treatment in SH-sy5y cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	interferon alpha 1	Homo sapiens	27-36
31220549-8	2019	UVB irradiation induced Nrf2 degradation is inhibited by co-treatment of cells with W-7, cyclosporin A, SB-216763 or MG-132, which are inhibitors of calmodulin, calcineurin, GSK3beta and the proteasome, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	GA binding protein transcription factor subunit alpha	Homo sapiens	24-28
31220549-8	2019	UVB irradiation induced Nrf2 degradation is inhibited by co-treatment of cells with W-7, cyclosporin A, SB-216763 or MG-132, which are inhibitors of calmodulin, calcineurin, GSK3beta and the proteasome, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	calmodulin 1	Homo sapiens	149-159
31220549-8	2019	UVB irradiation induced Nrf2 degradation is inhibited by co-treatment of cells with W-7, cyclosporin A, SB-216763 or MG-132, which are inhibitors of calmodulin, calcineurin, GSK3beta and the proteasome, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	glycogen synthase kinase 3 alpha	Homo sapiens	174-182
31502579-0	2019	Down-regulation effects of IFN-alpha on p11, 5-htr1b and 5-HTR4 protein levels were affected by NH4CL or MG132 treatment in SH-sy5y cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	5-hydroxytryptamine receptor 4	Homo sapiens	59-63
31502579-6	2019	MG132 could recover the protein levels of 5-HT1b and 5-HT4 in p11 knock-down cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	5-hydroxytryptamine receptor 1B	Homo sapiens	42-48
31502579-6	2019	MG132 could recover the protein levels of 5-HT1b and 5-HT4 in p11 knock-down cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	endonuclease, poly(U) specific	Homo sapiens	62-65
31050353-6	2019	We found that UBP12/UBP13 can deubiquitinate polyubiquitinated ORE1 in vitro and increase the stability of ORE1 in vivo in MG132/cycloheximide-chase experiments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	ubiquitin-specific protease 12	Arabidopsis thaliana	14-19
31415587-6	2019	The infected-mice were treated with proteasomal activity inhibitor MG132 by 1.5 and 3.0 mg/kg/day, which resulted in significantly reduced protein levels of phosphorylated IkappaBalpha (P<0.05) compared with the untreated control.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	172-184
31415587-8	2019	In addition, MMP-9 activity and occludin degradation were reduced because of MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	matrix metallopeptidase 9	Mus musculus	13-18
31415587-8	2019	In addition, MMP-9 activity and occludin degradation were reduced because of MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	occludin	Mus musculus	32-40
31306228-11	2019	Podocytes treated with MG132 showed remarkably increased intra-cellular expression of the COL4A3 c.4317delA mutation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	collagen type IV alpha 3 chain	Homo sapiens	90-96
31306228-12	2019	MG132 intervention improved higher ERS and apoptosis levels in the COL4A3 c.4317delA group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	collagen type IV alpha 3 chain	Homo sapiens	67-73
31194565-6	2019	Interestingly, PP2-mediated suppression of hASBT protein expression was rescued by the proteasome inhibitor MG132, suggesting that dephosphorylation impacts protein stability with the subsequent proteasome-dependent degradation of hASBT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	neuropeptide Y receptor Y6 (pseudogene)	Homo sapiens	15-18
31194565-6	2019	Interestingly, PP2-mediated suppression of hASBT protein expression was rescued by the proteasome inhibitor MG132, suggesting that dephosphorylation impacts protein stability with the subsequent proteasome-dependent degradation of hASBT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	solute carrier family 10 member 2	Homo sapiens	43-48
31194565-6	2019	Interestingly, PP2-mediated suppression of hASBT protein expression was rescued by the proteasome inhibitor MG132, suggesting that dephosphorylation impacts protein stability with the subsequent proteasome-dependent degradation of hASBT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	solute carrier family 10 member 2	Homo sapiens	231-236
31214877-8	2019	Further, RTS could accumulate PML/RARalpha into the nuclear bodies and then execute degradation, which could be reversed by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	PML nuclear body scaffold	Homo sapiens	30-33
31214877-8	2019	Further, RTS could accumulate PML/RARalpha into the nuclear bodies and then execute degradation, which could be reversed by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	retinoic acid receptor alpha	Homo sapiens	34-42
31406108-8	2019	The inhibition of macroautophagy induction in MG132-treated NCM increased CLU mRNA and m-CLU levels, but not s-CLU compared to NCM only treated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	clusterin	Rattus norvegicus	74-77
31406108-8	2019	The inhibition of macroautophagy induction in MG132-treated NCM increased CLU mRNA and m-CLU levels, but not s-CLU compared to NCM only treated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	clusterin	Rattus norvegicus	89-92
31406108-8	2019	The inhibition of macroautophagy induction in MG132-treated NCM increased CLU mRNA and m-CLU levels, but not s-CLU compared to NCM only treated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	clusterin	Rattus norvegicus	89-92
31406108-11	2019	However, the overexpression of CLU secreted isoform in H9c2 cells, but not in NCM decreased apoptosis after MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	clusterin	Rattus norvegicus	31-34
30783947-6	2019	However, cotreatment with a proteasome inhibitor, MG132, restored Herp expression only to a limited extent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	66-70
31257950-5	2019	Inhibition of the proteasome with MG132 also prevented the loss of the PRDX1 dimer, suggesting that the decrease is due to a NO-activated proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	peroxiredoxin 1	Mus musculus	71-76
31366881-17	2019	CONCLUSIONS Our study suggested that MG-132 was able to protect against acute lung injury via inhibition of HIF-1alpha mediated mTOR/4EBP1/EIF4E pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	108-118
31366881-17	2019	CONCLUSIONS Our study suggested that MG-132 was able to protect against acute lung injury via inhibition of HIF-1alpha mediated mTOR/4EBP1/EIF4E pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	mechanistic target of rapamycin kinase	Rattus norvegicus	128-132
31366881-17	2019	CONCLUSIONS Our study suggested that MG-132 was able to protect against acute lung injury via inhibition of HIF-1alpha mediated mTOR/4EBP1/EIF4E pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	133-138
31366881-17	2019	CONCLUSIONS Our study suggested that MG-132 was able to protect against acute lung injury via inhibition of HIF-1alpha mediated mTOR/4EBP1/EIF4E pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	eukaryotic translation initiation factor 4E	Rattus norvegicus	139-144
31332289-6	2019	Treatment of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuate the SOX7 promoted BIM degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	SRY-box transcription factor 7	Homo sapiens	114-118
31332289-6	2019	Treatment of either a proteasome inhibitor MG132 or bortezomib, or with a p-ERK/MEK inhibitor U0126 attenuate the SOX7 promoted BIM degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	BCL2 like 11	Homo sapiens	128-131
31050353-6	2019	We found that UBP12/UBP13 can deubiquitinate polyubiquitinated ORE1 in vitro and increase the stability of ORE1 in vivo in MG132/cycloheximide-chase experiments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	ubiquitin-specific protease 13	Arabidopsis thaliana	20-25
31050353-6	2019	We found that UBP12/UBP13 can deubiquitinate polyubiquitinated ORE1 in vitro and increase the stability of ORE1 in vivo in MG132/cycloheximide-chase experiments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	NAC domain containing protein 6	Arabidopsis thaliana	107-111
30926361-5	2019	Moreover, TP significantly induced Nrf2 degradation by ubiquitination, which was blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	NFE2 like bZIP transcription factor 2	Rattus norvegicus	35-39
30819007-7	2019	We monitored the stability of beta-catenin with the proteasomal inhibitor, MG132, in DU145 cells and found that MG132 reversed KHC-4-induced proteasomal beta-catenin degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	catenin beta 1	Homo sapiens	30-42
31071385-5	2019	The proteasome inhibitor MG132 could restore the RP2 Q158P protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	RP2 activator of ARL3 GTPase	Homo sapiens	49-52
31337730-4	2019	The role of USF-1 in the regulation of the A20 promoter in HCV-infected cells was confirmed by the chromatin immunoprecipitation (ChIP) assay, and its depletion was apparently mediated by proteasomes, as USF-1 could be stabilized by the proteasome inhibitor MG132 to suppress the A20 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	258-263	upstream transcription factor 1	Homo sapiens	12-17
31337730-4	2019	The role of USF-1 in the regulation of the A20 promoter in HCV-infected cells was confirmed by the chromatin immunoprecipitation (ChIP) assay, and its depletion was apparently mediated by proteasomes, as USF-1 could be stabilized by the proteasome inhibitor MG132 to suppress the A20 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	258-263	TNF alpha induced protein 3	Homo sapiens	43-46
30980919-8	2019	A proteasome inhibitor and a lysosome inhibitor, MG132 and chloroquine, respectively, partly inhibited DGKdelta degradation, suggesting that myristic acid prevents, at least in part, the degradation of DGKdelta by the ubiquitin-proteasome system and the autophagy-lysosome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	diacylglycerol kinase, delta	Mus musculus	103-111
30980919-8	2019	A proteasome inhibitor and a lysosome inhibitor, MG132 and chloroquine, respectively, partly inhibited DGKdelta degradation, suggesting that myristic acid prevents, at least in part, the degradation of DGKdelta by the ubiquitin-proteasome system and the autophagy-lysosome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	diacylglycerol kinase, delta	Mus musculus	202-210
31329620-7	2019	This complex of ubiquitinated Apaf-1 and p62 induces caspase-9 activation following MG132 treatment of HEK293T cells that stably express bcl-xl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	apoptotic peptidase activating factor 1	Homo sapiens	30-36
31329620-7	2019	This complex of ubiquitinated Apaf-1 and p62 induces caspase-9 activation following MG132 treatment of HEK293T cells that stably express bcl-xl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	nucleoporin 62	Homo sapiens	41-44
31329620-7	2019	This complex of ubiquitinated Apaf-1 and p62 induces caspase-9 activation following MG132 treatment of HEK293T cells that stably express bcl-xl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	caspase 9	Homo sapiens	53-62
31329620-7	2019	This complex of ubiquitinated Apaf-1 and p62 induces caspase-9 activation following MG132 treatment of HEK293T cells that stably express bcl-xl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	BCL2 like 1	Homo sapiens	137-143
30819007-7	2019	We monitored the stability of beta-catenin with the proteasomal inhibitor, MG132, in DU145 cells and found that MG132 reversed KHC-4-induced proteasomal beta-catenin degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	catenin beta 1	Homo sapiens	30-42
30819007-7	2019	We monitored the stability of beta-catenin with the proteasomal inhibitor, MG132, in DU145 cells and found that MG132 reversed KHC-4-induced proteasomal beta-catenin degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	catenin beta 1	Homo sapiens	153-165
30968125-8	2019	Using a reversible inhibitor of the 26S proteasome, MG132, we find that sand rat and mouse Pdx1 are both degraded through the ubiquitin proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	pancreatic and duodenal homeobox 1	Mus musculus	91-95
31142735-5	2019	By co-treating cells with cycloheximide and MG-132, we proved that CANA promoted proteasomal degradation of beta-catenin protein by increasing phosphorylation of beta-catenin, and CANA-induced inactivation of protein phosphatase 2A was identified being responsible for this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	catenin beta 1	Homo sapiens	108-120
31084929-6	2019	Treatment with the proteasome inhibitor MG132 and mutation of Lys48 to Arg in ubiquitin successfully blunted the inhibitory effects of AngII on the endogenous H2S/CSE pathway in vascular endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	angiotensinogen	Homo sapiens	135-140
31084929-6	2019	Treatment with the proteasome inhibitor MG132 and mutation of Lys48 to Arg in ubiquitin successfully blunted the inhibitory effects of AngII on the endogenous H2S/CSE pathway in vascular endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	163-166
31050072-9	2019	Besides, the proteasome inhibitor MG132 upregulated the expression of the mature CTR1 in U-2OS and MG-63 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	solute carrier family 31 member 1	Homo sapiens	81-85
31142735-5	2019	By co-treating cells with cycloheximide and MG-132, we proved that CANA promoted proteasomal degradation of beta-catenin protein by increasing phosphorylation of beta-catenin, and CANA-induced inactivation of protein phosphatase 2A was identified being responsible for this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	catenin beta 1	Homo sapiens	162-174
32884994-9	2020	Vps34 indeed was subjected to proteasomal or lysosomal degradation, as prolonged treatment of proteasomal inhibitor MG132 or lysosomal inhibitor chloroquine elevated Vps34 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	0-5
30857762-7	2019	Treatment of human atrial myofibroblasts with cycloheximide had no effect on this outcome; however, treatment of cells with MG132 enhanced BNP-induced MMP-2 expression, indicating that protein stability and inhibition of proteasome-mediated protein degradation pathways are potentially involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	natriuretic peptide B	Homo sapiens	139-142
30857762-7	2019	Treatment of human atrial myofibroblasts with cycloheximide had no effect on this outcome; however, treatment of cells with MG132 enhanced BNP-induced MMP-2 expression, indicating that protein stability and inhibition of proteasome-mediated protein degradation pathways are potentially involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	matrix metallopeptidase 2	Homo sapiens	151-156
32884994-9	2020	Vps34 indeed was subjected to proteasomal or lysosomal degradation, as prolonged treatment of proteasomal inhibitor MG132 or lysosomal inhibitor chloroquine elevated Vps34 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	phosphatidylinositol 3-kinase catalytic subunit type 3	Mus musculus	166-171
30890561-8	2019	Notably, HSP90 inhibition promoted apoptosis of eEF2K-/- MEFs under proteostatic stress induced by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	heat shock protein, 2	Mus musculus	9-14
31117253-11	2019	When MG132, a potent selective proteasome inhibitor, was utilized, it could restore the Mcl-1 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	5-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	88-93
31083332-8	2019	MG-132 reversed the fluoride-mediated p21 decrease, indicating that fluoride facilitates p21 proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	38-41
31083332-8	2019	MG-132 reversed the fluoride-mediated p21 decrease, indicating that fluoride facilitates p21 proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	89-92
30890561-8	2019	Notably, HSP90 inhibition promoted apoptosis of eEF2K-/- MEFs under proteostatic stress induced by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	eukaryotic elongation factor-2 kinase	Mus musculus	48-53
30868765-6	2019	Combined with LiCl or MG-132 treatment, SPINK5 can inhibit GSK3beta phosphorylation and promote beta-catenin protein degradation, thus inhibit Wnt/beta-catenin signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	serine peptidase inhibitor Kazal type 5	Homo sapiens	40-46
30868765-6	2019	Combined with LiCl or MG-132 treatment, SPINK5 can inhibit GSK3beta phosphorylation and promote beta-catenin protein degradation, thus inhibit Wnt/beta-catenin signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	glycogen synthase kinase 3 beta	Homo sapiens	59-67
30868765-6	2019	Combined with LiCl or MG-132 treatment, SPINK5 can inhibit GSK3beta phosphorylation and promote beta-catenin protein degradation, thus inhibit Wnt/beta-catenin signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	catenin beta 1	Homo sapiens	96-108
30868765-6	2019	Combined with LiCl or MG-132 treatment, SPINK5 can inhibit GSK3beta phosphorylation and promote beta-catenin protein degradation, thus inhibit Wnt/beta-catenin signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	catenin beta 1	Homo sapiens	147-159
30905731-7	2019	Treatment with proteasome inhibitor MG132 markedly inhibited the IRE1/XBP1-mediated loss of Sp1 and SOD, suggesting the involvement of proteasome-dependent ER-associated degradation (ERAD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	65-69
30905731-7	2019	Treatment with proteasome inhibitor MG132 markedly inhibited the IRE1/XBP1-mediated loss of Sp1 and SOD, suggesting the involvement of proteasome-dependent ER-associated degradation (ERAD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	X-box binding protein 1	Homo sapiens	70-74
30905731-7	2019	Treatment with proteasome inhibitor MG132 markedly inhibited the IRE1/XBP1-mediated loss of Sp1 and SOD, suggesting the involvement of proteasome-dependent ER-associated degradation (ERAD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	Sp1 transcription factor	Homo sapiens	92-103
30647455-3	2019	Here, we observed that AGR2 expression is significantly suppressed by proteasome inhibitor MG132/bortezomib at mRNA and protein levels in lung cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	23-27
30647455-4	2019	MG132-mediated repression of AGR2 transcription was independent of ROS generation and ER stress induction, but partially resulted from the downregulated E2F1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	29-33
30647455-4	2019	MG132-mediated repression of AGR2 transcription was independent of ROS generation and ER stress induction, but partially resulted from the downregulated E2F1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	E2F transcription factor 1	Homo sapiens	153-157
30647455-5	2019	Further investigation revealed that MG132 facilitated polyubiquitinated AGR2 degradation through activation of autophagy, as evidenced by predominant restoration of AGR2 level in cells genetic depletion of Atg5 and Atg7, or by autophagy inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	72-76
30647455-5	2019	Further investigation revealed that MG132 facilitated polyubiquitinated AGR2 degradation through activation of autophagy, as evidenced by predominant restoration of AGR2 level in cells genetic depletion of Atg5 and Atg7, or by autophagy inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	165-169
30647455-5	2019	Further investigation revealed that MG132 facilitated polyubiquitinated AGR2 degradation through activation of autophagy, as evidenced by predominant restoration of AGR2 level in cells genetic depletion of Atg5 and Atg7, or by autophagy inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	autophagy related 5	Homo sapiens	206-210
30647455-5	2019	Further investigation revealed that MG132 facilitated polyubiquitinated AGR2 degradation through activation of autophagy, as evidenced by predominant restoration of AGR2 level in cells genetic depletion of Atg5 and Atg7, or by autophagy inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	autophagy related 7	Homo sapiens	215-219
30647455-8	2019	In addition, an autophagy receptor NBR1 was demonstrated to be important in polyubiquitinated AGR2 clearance in response to MG132 or bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	NBR1 autophagy cargo receptor	Homo sapiens	35-39
30647455-8	2019	In addition, an autophagy receptor NBR1 was demonstrated to be important in polyubiquitinated AGR2 clearance in response to MG132 or bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	94-98
31017975-7	2019	In contrast, MG132-mediated proteasome inhibition, which induces rigorous autophagy, promotes p62 degradation but accumulation of the DNA repair proteins CHK1 and RAD51.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	nucleoporin 62	Homo sapiens	94-97
31017975-7	2019	In contrast, MG132-mediated proteasome inhibition, which induces rigorous autophagy, promotes p62 degradation but accumulation of the DNA repair proteins CHK1 and RAD51.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	checkpoint kinase 1	Homo sapiens	154-158
31017975-7	2019	In contrast, MG132-mediated proteasome inhibition, which induces rigorous autophagy, promotes p62 degradation but accumulation of the DNA repair proteins CHK1 and RAD51.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	RAD51 recombinase	Homo sapiens	163-168
31017975-8	2019	However, pretreatment with an autophagy inhibitor offsets the effects of MG132 on CHK1 and RAD51 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	checkpoint kinase 1	Homo sapiens	82-86
31017975-8	2019	However, pretreatment with an autophagy inhibitor offsets the effects of MG132 on CHK1 and RAD51 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	RAD51 recombinase	Homo sapiens	91-96
30689267-6	2019	In contrast, knockdown of USP9X in breast cancer cells by siRNAs reduced RNF115 protein abundance, which was partially restored following treatment with proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-180	ubiquitin specific peptidase 9 X-linked	Homo sapiens	26-31
30782845-6	2019	The proteasome inhibitor MG132 abrogated GADD34 depletion-induced MCL-1 down-regulation, suggesting that GADD34 inhibits the proteasomal degradation of MCL-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	41-47
30782845-6	2019	The proteasome inhibitor MG132 abrogated GADD34 depletion-induced MCL-1 down-regulation, suggesting that GADD34 inhibits the proteasomal degradation of MCL-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	105-111
30992691-7	2019	Flow cytometry and Wright-Giemsa staining were used to study the effect of MG132 and ATRA on the GTF2I-RARA-transfected HL60 cell model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	general transcription factor IIi	Homo sapiens	97-102
30992691-7	2019	Flow cytometry and Wright-Giemsa staining were used to study the effect of MG132 and ATRA on the GTF2I-RARA-transfected HL60 cell model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	retinoic acid receptor alpha	Homo sapiens	103-107
30992691-14	2019	Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	general transcription factor IIi	Homo sapiens	49-54
30992691-14	2019	Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	retinoic acid receptor alpha	Homo sapiens	55-59
30992691-14	2019	Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	general transcription factor IIi	Homo sapiens	104-109
30992691-14	2019	Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	retinoic acid receptor alpha	Homo sapiens	110-114
30789754-5	2019	Incubation with the proteasome inhibitors MG-132 and lactacystin (10 muM, 24 h) significantly increased NPC1L1 protein levels in IECs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	NPC1 like intracellular cholesterol transporter 1	Homo sapiens	104-110
30689267-6	2019	In contrast, knockdown of USP9X in breast cancer cells by siRNAs reduced RNF115 protein abundance, which was partially restored following treatment with proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-180	ring finger protein 115	Homo sapiens	73-79
30772377-7	2019	Overexpression of UBC9 increased ubiquitination of Nav1.5, and proteasome inhibitor MG132 blocked the effect of UBC9 overexpression on Nav1.5 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	ubiquitin conjugating enzyme E2 I	Homo sapiens	112-116
30936965-2	2019	The aim of the current study was to investigate the effect of the proteasome inhibitor, MG132, on transforming growth factor (TGF)-beta1-induced expression of extracellular matrix proteins in rat renal interstitial fibroblasts (NRK-49F cells) and to better elucidate the mechanism by which MG132 functions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	transforming growth factor, beta 1	Rattus norvegicus	98-136
30936965-2	2019	The aim of the current study was to investigate the effect of the proteasome inhibitor, MG132, on transforming growth factor (TGF)-beta1-induced expression of extracellular matrix proteins in rat renal interstitial fibroblasts (NRK-49F cells) and to better elucidate the mechanism by which MG132 functions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	290-295	transforming growth factor, beta 1	Rattus norvegicus	98-136
30936965-3	2019	The level of connective tissue growth factor (CTGF), alpha-smooth muscle actin (SMA), fibronectin (FN) and collagen type III (Col III) in the MG132-pretreated groups was significantly decreased compared with groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	cellular communication network factor 2	Rattus norvegicus	13-44
30936965-3	2019	The level of connective tissue growth factor (CTGF), alpha-smooth muscle actin (SMA), fibronectin (FN) and collagen type III (Col III) in the MG132-pretreated groups was significantly decreased compared with groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	cellular communication network factor 2	Rattus norvegicus	46-50
30936965-3	2019	The level of connective tissue growth factor (CTGF), alpha-smooth muscle actin (SMA), fibronectin (FN) and collagen type III (Col III) in the MG132-pretreated groups was significantly decreased compared with groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	actin gamma 2, smooth muscle	Rattus norvegicus	53-78
30936965-3	2019	The level of connective tissue growth factor (CTGF), alpha-smooth muscle actin (SMA), fibronectin (FN) and collagen type III (Col III) in the MG132-pretreated groups was significantly decreased compared with groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	fibronectin 1	Rattus norvegicus	86-97
30936965-3	2019	The level of connective tissue growth factor (CTGF), alpha-smooth muscle actin (SMA), fibronectin (FN) and collagen type III (Col III) in the MG132-pretreated groups was significantly decreased compared with groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	transforming growth factor, beta 1	Rattus norvegicus	228-237
30936965-4	2019	MG132 significantly decreased mRNA and the protein levels of fibrosis-associated factors induced by TGF-beta1 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor, beta 1	Rattus norvegicus	100-109
30936965-5	2019	The MG132-pretreated groups exhibited lower phosphorylated-mothers against decapentaplegic homolog (p-Smad)2, p-Smad3 and FN protein expression compared with the groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	SMAD family member 2	Rattus norvegicus	102-108
30936965-5	2019	The MG132-pretreated groups exhibited lower phosphorylated-mothers against decapentaplegic homolog (p-Smad)2, p-Smad3 and FN protein expression compared with the groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	fibronectin 1	Rattus norvegicus	122-124
30936965-5	2019	The MG132-pretreated groups exhibited lower phosphorylated-mothers against decapentaplegic homolog (p-Smad)2, p-Smad3 and FN protein expression compared with the groups treated with TGF-beta1 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	transforming growth factor, beta 1	Rattus norvegicus	182-191
30772377-7	2019	Overexpression of UBC9 increased ubiquitination of Nav1.5, and proteasome inhibitor MG132 blocked the effect of UBC9 overexpression on Nav1.5 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	sodium voltage-gated channel alpha subunit 5	Homo sapiens	135-141
30881494-9	2019	The BAG3 protein was markedly induced upon exposure to bortezomib and MG132 in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	BAG cochaperone 3	Homo sapiens	4-8
30935019-5	2019	ZNF143 knockdown affected the stability of p53, which showed a dependence on MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	zinc finger protein 143	Homo sapiens	0-6
30998141-2	2019	METHODS: Western blot was used to detect the expression of BCL6 in K562/G01 cells before and after treatment with protease inhibitor MG-132.The RT-PCR and Western blot respectively were used to detect the mRNA and protein expression levels of BCL6 and USP2 in K562/G01 cells treated with or without ML364 (a ubiquitin-specific protease USP2 inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-139	BCL6 transcription repressor	Homo sapiens	59-63
30998141-4	2019	RESULTS: After treatment with protease inhibitor MG132, the BCL6 protein level of K562/G01 significantly increased (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	BCL6 transcription repressor	Homo sapiens	60-64
30935019-5	2019	ZNF143 knockdown affected the stability of p53, which showed a dependence on MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	tumor protein p53	Homo sapiens	43-46
30837587-9	2019	Further experiments involving immunoprecipitation and treatment with MG132, a proteasome inhibitor, showed that the KBTBD11-Cullin3 promotes ubiquitination and degradation of NFATc1 by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	kelch repeat and BTB domain containing 11	Homo sapiens	116-123
30837587-9	2019	Further experiments involving immunoprecipitation and treatment with MG132, a proteasome inhibitor, showed that the KBTBD11-Cullin3 promotes ubiquitination and degradation of NFATc1 by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	cullin 3	Homo sapiens	124-131
30837587-9	2019	Further experiments involving immunoprecipitation and treatment with MG132, a proteasome inhibitor, showed that the KBTBD11-Cullin3 promotes ubiquitination and degradation of NFATc1 by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	nuclear factor of activated T cells 1	Homo sapiens	175-181
30203323-8	2019	The proteasome inhibitor MG132 treatment resulted in more TTC3 aggregates in a short period of time.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tetratricopeptide repeat domain 3	Homo sapiens	58-62
30586628-6	2019	SIK2 protein levels were analyzed in primary adipocytes treated with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	salt inducible kinase 2	Homo sapiens	0-4
30488656-11	2019	Treatment of patient cells with MG-132 or staurosporine to induce activation of the intrinsic apoptosis pathway revealed significantly decreased cell viability with increased caspase-3 and caspase-7 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-38	caspase 3	Homo sapiens	175-184
30488656-11	2019	Treatment of patient cells with MG-132 or staurosporine to induce activation of the intrinsic apoptosis pathway revealed significantly decreased cell viability with increased caspase-3 and caspase-7 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-38	caspase 7	Homo sapiens	189-198
30695709-12	2019	Compared to DM 24 h group, MG-132 pretreatment significantly down-regulated ubiquitinated proteins, lowered the DNA damage and apoptosis by decreasing Caspase-3 and increasing Bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	caspase 3	Rattus norvegicus	151-160
30695709-12	2019	Compared to DM 24 h group, MG-132 pretreatment significantly down-regulated ubiquitinated proteins, lowered the DNA damage and apoptosis by decreasing Caspase-3 and increasing Bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	BCL2, apoptosis regulator	Rattus norvegicus	176-181
30765727-0	2019	MG132 protects against renal dysfunction by regulating Akt-mediated inflammation in diabetic nephropathy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	AKT serine/threonine kinase 1	Homo sapiens	55-58
30781396-8	2019	When blocking Nrf2 degradation with proteasome inhibitor MG132, ubiquitinated proteins were enhanced, and fisetin reduced ubiquitination of Nrf2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
30448557-8	2019	Experiments for treatment with 5-AzaC (DNMTs inhibitor), TSA (HDACs inhibitor), DOX (to activate PARP-1) or MG132 (proteasome inhibitor) revealed that the MBDs and PARP-1 was positively associated with miR-155 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	poly(ADP-ribose) polymerase 1	Homo sapiens	164-170
30448557-8	2019	Experiments for treatment with 5-AzaC (DNMTs inhibitor), TSA (HDACs inhibitor), DOX (to activate PARP-1) or MG132 (proteasome inhibitor) revealed that the MBDs and PARP-1 was positively associated with miR-155 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	microRNA 155	Homo sapiens	202-209
30765727-4	2019	Therefore, we hypothesized that MG132, specific proteasome inhibitor, could provide renoprotection by suppressing Akt-mediated inflammation in DN.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	AKT serine/threonine kinase 1	Homo sapiens	114-117
30765727-10	2019	In conclusion, MG132 significantly inhibits the development of DN by regulating Akt phosphorylation-mediated inflammatory activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	AKT serine/threonine kinase 1	Homo sapiens	80-83
30391277-7	2019	Using this biosensor we also show that selective proteasome inhibitors, such as lactacystin and MG132, inhibit degradation and affect the kinetics of IkappaBalpha in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	NFKB inhibitor alpha	Homo sapiens	150-162
30736789-8	2019	MG132 blocked downregulation of cyclin D1 protein by STL or STB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin D1	Homo sapiens	32-41
30736789-8	2019	MG132 blocked downregulation of cyclin D1 protein by STL or STB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	RNF217 antisense RNA 1 (head to head)	Homo sapiens	53-56
30716099-10	2019	Using knockdown (siRNA BIRC2), knockout (CRIPSR NIK) and proteasome machinery neutralization (MG132) approaches, we found that Debio 1143-mediated HIV latency reversal is BIRC2 degradation- and NIK stabilization-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	baculoviral IAP repeat containing 2	Homo sapiens	171-176
30418193-7	2019	Ubiquitin-proteasome pathway was observed to play a crucial role in the downregulation of XIAP and FLIP, as proteasomal inhibitor MG132 significantly reversed the downregulation of XIAP and FLIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	X-linked inhibitor of apoptosis	Homo sapiens	90-94
30418193-7	2019	Ubiquitin-proteasome pathway was observed to play a crucial role in the downregulation of XIAP and FLIP, as proteasomal inhibitor MG132 significantly reversed the downregulation of XIAP and FLIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	X-linked inhibitor of apoptosis	Homo sapiens	181-185
30675298-4	2019	The results revealed that the OVCA1 protein was unstable by MG132 inhibiting proteasome mediated degradation, co-immunoprecipitation and half-life measurement experiments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	diphthamide biosynthesis 1	Homo sapiens	30-35
30483783-0	2019	MG132 selectively upregulates MICB through the DNA damage response pathway in A549 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	MHC class I polypeptide-related sequence B	Homo sapiens	30-34
30760976-8	2019	Pretreatment with MG132, the decreased IRP2 levels caused by H2O2 treatment could be antagonized.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	iron responsive element binding protein 2	Homo sapiens	39-43
30974966-13	2019	Interestingly, treatment with the proteasome inhibitor MG132 (carbobenzoxy-Leu-Leu-leucinal) significantly negated the curcumin-induced Cx43 degradation, which suggests that curcumin-induced Cx43 degradation occurs through the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	gap junction protein alpha 1	Homo sapiens	136-140
30974966-13	2019	Interestingly, treatment with the proteasome inhibitor MG132 (carbobenzoxy-Leu-Leu-leucinal) significantly negated the curcumin-induced Cx43 degradation, which suggests that curcumin-induced Cx43 degradation occurs through the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	gap junction protein alpha 1	Homo sapiens	191-195
30552955-11	2019	MG-132, another proteasome inhibitor, also increased Cav3.2 protein levels in the cultured cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	53-59
30466837-5	2019	Here, we examined repair of PARP-1 DPCs in mouse fibroblasts and found that a proteasome inhibitor, MG-132, reduces repair resulting in accumulation of PARP-1 DPCs and increased alkylating agent cytotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-106	poly (ADP-ribose) polymerase family, member 1	Mus musculus	28-34
30466837-5	2019	Here, we examined repair of PARP-1 DPCs in mouse fibroblasts and found that a proteasome inhibitor, MG-132, reduces repair resulting in accumulation of PARP-1 DPCs and increased alkylating agent cytotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-106	poly (ADP-ribose) polymerase family, member 1	Mus musculus	152-158
30417443-6	2019	MG132 inhibited the degradation of Mlph, but E64D and Pepstatin A had no effect on Mlph.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	melanophilin	Homo sapiens	35-39
30483783-4	2019	The mechanism underlying the regulatory effect of a cancer treatment agent on the expression of NKG2D ligands was investigated using the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	killer cell lectin like receptor K1	Homo sapiens	96-101
30483783-5	2019	Following treatment for 8 h with MG132, the transcription levels of MICB and ULBP1 were upregulated 10.62- and 11.09-fold, respectively, and the expression levels of MICB and ULBP1 were increased by 68.18 and 23.65%, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	MHC class I polypeptide-related sequence B	Homo sapiens	68-72
30483783-5	2019	Following treatment for 8 h with MG132, the transcription levels of MICB and ULBP1 were upregulated 10.62- and 11.09-fold, respectively, and the expression levels of MICB and ULBP1 were increased by 68.18 and 23.65%, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	UL16 binding protein 1	Homo sapiens	77-82
30483783-5	2019	Following treatment for 8 h with MG132, the transcription levels of MICB and ULBP1 were upregulated 10.62- and 11.09-fold, respectively, and the expression levels of MICB and ULBP1 were increased by 68.18 and 23.65%, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	MHC class I polypeptide-related sequence B	Homo sapiens	166-170
30483783-5	2019	Following treatment for 8 h with MG132, the transcription levels of MICB and ULBP1 were upregulated 10.62- and 11.09-fold, respectively, and the expression levels of MICB and ULBP1 were increased by 68.18 and 23.65%, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	UL16 binding protein 1	Homo sapiens	175-180
30483783-7	2019	MG132 increased the transcription of MICB by acting at a site in the 480-bp MICB upstream promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	MHC class I polypeptide-related sequence B	Homo sapiens	37-41
30483783-7	2019	MG132 increased the transcription of MICB by acting at a site in the 480-bp MICB upstream promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	MHC class I polypeptide-related sequence B	Homo sapiens	76-80
30483783-8	2019	The activity of the MICB promoter was upregulated 1.77-fold following treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	MHC class I polypeptide-related sequence B	Homo sapiens	20-24
30483783-9	2019	MG132 treatment improved the cytotoxicity of NK cells, which was partially blocked by an antibody targeting NKG2D, and more specifically the MICB molecule.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	killer cell lectin like receptor K1	Homo sapiens	108-113
30483783-9	2019	MG132 treatment improved the cytotoxicity of NK cells, which was partially blocked by an antibody targeting NKG2D, and more specifically the MICB molecule.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	MHC class I polypeptide-related sequence B	Homo sapiens	141-145
30483783-10	2019	The expression of MICB induced by MG132 was inhibited by KU-55933 [ataxia telangiectasia mutated (ATM) kinase inhibitor], wortmannin (phosphoinositide 3 kinase inhibitor) and caffeine (ATM/ATM-Rad3-related inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	MHC class I polypeptide-related sequence B	Homo sapiens	18-22
30483783-11	2019	The phosphorylation of checkpoint kinase 2 (Chk2), an event associated with DNA damage, was observed following treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	checkpoint kinase 2	Homo sapiens	23-42
30483783-11	2019	The phosphorylation of checkpoint kinase 2 (Chk2), an event associated with DNA damage, was observed following treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	checkpoint kinase 2	Homo sapiens	44-48
30483783-12	2019	These results indicated that MG132 selectively upregulates the expression of MICB in A549 cells, and increases the NKG2D-mediated cytotoxicity of NK cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	MHC class I polypeptide-related sequence B	Homo sapiens	77-81
30483783-12	2019	These results indicated that MG132 selectively upregulates the expression of MICB in A549 cells, and increases the NKG2D-mediated cytotoxicity of NK cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	killer cell lectin like receptor K1	Homo sapiens	115-120
30483783-13	2019	The regulatory effect of MG132 may be associated with the activation of Chk2, an event associated with DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	checkpoint kinase 2	Homo sapiens	72-76
30396235-2	2018	However, we recently found that long-term incubation with proteasome inhibitors (PIs) such as PS-341 or MG132 induces IkappaBalpha degradation via an alternative pathway, lysosome, which results in NF-kappaB activation and confers resistance to PI-induced lung cancer cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	NFKB inhibitor alpha	Homo sapiens	118-130
32123827-7	2019	The proteasome inhibitor MG132 stabilized p53(DeltaCp44), particularly in mock-infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	42-45
30333866-4	2018	Subsequently, it was reported that MG-132, a specific proteasome inhibitor, may attenuate pVHL overexpression-induced reductions in NEK8 protein expression levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	von Hippel-Lindau tumor suppressor	Homo sapiens	90-94
30533198-8	2018	Inhibitor of Keap1-P-S349 p62 interaction, K67, had synergistic effect with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	sequestosome 1	Homo sapiens	26-29
30335496-7	2018	Apoptosis induced by seawater stimulation and MG132 were inhibited by ANGII receptor blocker and abrogated by the addition of ANG1-7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	angiotensinogen	Rattus norvegicus	70-75
30335496-7	2018	Apoptosis induced by seawater stimulation and MG132 were inhibited by ANGII receptor blocker and abrogated by the addition of ANG1-7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	angiogenin	Rattus norvegicus	126-130
30442180-14	2018	By challenging MNs with a proteasome inhibitor, we found that MNs were more vulnerable to MG132, with some accompanying phenotype changes, such as TDP43 translocation, NF inclusion, mitochondria distribution impairment, and activation of caspase3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	caspase 3	Homo sapiens	238-246
30191639-8	2018	Involvement of GSK3beta was also confirmed by treatment with lithium chloride, the inducer of GSK3beta phosphorylation, or MG132, the 26S proteasomal inhibitor, which also stabilized Snail1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	glycogen synthase kinase 3 beta	Homo sapiens	15-23
30333866-4	2018	Subsequently, it was reported that MG-132, a specific proteasome inhibitor, may attenuate pVHL overexpression-induced reductions in NEK8 protein expression levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	NIMA related kinase 8	Homo sapiens	132-136
30009504-8	2018	ELL2 protein has a short half-life and was stabilized by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	elongation factor for RNA polymerase II 2	Homo sapiens	0-4
30293573-5	2018	Interestingly, increased levels of aggregated mutant SP-A2, resulting from MG-132-mediated proteasome inhibition, could also be alleviated by 4-PBA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	surfactant protein A2	Homo sapiens	53-58
30241937-4	2018	Knockdown of OTUB2 decreased Gli2 protein level while the proteasome inhibitor MG-132 treatment restored Gli2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	GLI family zinc finger 2	Homo sapiens	105-109
30364320-7	2018	Overexpression of TANK-binding kinase 1 (TBK1) increased ABCA1 degradation, which was reversed by the proteasome inhibitor carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	TANK-binding kinase 1	Mus musculus	18-39
30364320-7	2018	Overexpression of TANK-binding kinase 1 (TBK1) increased ABCA1 degradation, which was reversed by the proteasome inhibitor carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	TANK-binding kinase 1	Mus musculus	41-45
30364320-7	2018	Overexpression of TANK-binding kinase 1 (TBK1) increased ABCA1 degradation, which was reversed by the proteasome inhibitor carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	57-62
29886078-6	2018	Then, we treated the stable 293FT cell lines with various small-molecule inhibitors and demonstrated that treatment with MG-132 and bortezomib, which target the proteasome and disrupt its function, could prevent TMEM8B-a degradation and induce protein expression in 293FT cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	transmembrane protein 8B	Homo sapiens	212-218
30347865-7	2018	In this study, we demonstrated that cell-based high-content measurements of EGFP-UL76 aggresomes responded to bortezomib and MG132 treatment in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	nuclear protein UL24	Human betaherpesvirus 5	81-85
30459603-8	2018	In addition, MG132 supplementation markedly abrogated the impacts of icariin on ER stress and TXNIP-mediated downstream events such as inflammation and STAT3 phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	thioredoxin interacting protein	Mus musculus	94-99
30459603-8	2018	In addition, MG132 supplementation markedly abrogated the impacts of icariin on ER stress and TXNIP-mediated downstream events such as inflammation and STAT3 phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	signal transducer and activator of transcription 3	Mus musculus	152-157
30180991-8	2018	Furthermore, pre-treatment of cells with MG-132 also abolished PDGF-induced beta-TrCP reduction, Cdc25A elevation and cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	76-85
30180991-8	2018	Furthermore, pre-treatment of cells with MG-132 also abolished PDGF-induced beta-TrCP reduction, Cdc25A elevation and cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	cell division cycle 25A	Homo sapiens	97-103
30046896-9	2018	Finally, the decreased levels of CREB and MITF proteins induced by 72 h pretreatment with GlcN were abrogated by the co-addition of the proteosomal degradation inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	cAMP responsive element binding protein 1	Homo sapiens	33-37
30046896-9	2018	Finally, the decreased levels of CREB and MITF proteins induced by 72 h pretreatment with GlcN were abrogated by the co-addition of the proteosomal degradation inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	melanocyte inducing transcription factor	Homo sapiens	42-46
29654697-5	2018	Consistently, melatonin reduced the expression of c-Myc at mRNA and protein levels, which was blocked by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	50-55
30274821-0	2018	Synergistic effect of Nutlin-3 combined with MG-132 on schwannoma cells through restoration of merlin and p53 tumour suppressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	95-101
30274821-0	2018	Synergistic effect of Nutlin-3 combined with MG-132 on schwannoma cells through restoration of merlin and p53 tumour suppressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	tumor protein p53	Homo sapiens	106-109
30274821-11	2018	Nutlin-3 combined with MG-132 narrowed this between-group difference and triggered stronger inhibitory effects on the growth of schwannomas through coordinated reactivation of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-29	tumor protein p53	Homo sapiens	176-179
30224716-10	2018	Moreover, selective inhibitors of ERK1/2, JNK, and p38 attenuated NNFE inhibitory effects on melanogenesis, and MG-132 (a proteasome inhibitor) prevented the NNFE-induced decline in tyrosinase protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	tyrosinase	Mus musculus	182-192
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	cell division cycle 25C	Homo sapiens	211-217
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	inhibitor of growth family member 5	Homo sapiens	256-260
30091530-10	2018	In summary, SAHA and/or MG132 can synergistically suppress the malignant phenotypes of neuroblastoma cells through the miRNA-ING5-histone acetylation axis and via proteasomal degradation, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	inhibitor of growth family member 5	Homo sapiens	125-129
30368781-5	2018	We show that Blimp-1 degradation is inhibited by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	PR/SET domain 1	Homo sapiens	13-20
30176247-0	2018	MG-132 treatment promotes TRAIL-mediated apoptosis in SEB-1 sebocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	TNF superfamily member 10	Homo sapiens	26-31
30176247-7	2018	Meanwhile, TRAIL concentrations in SEB-1 sebocytes treated with MG-132 were markedly elevated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	TNF superfamily member 10	Homo sapiens	11-16
30176247-9	2018	Silencing of TRAIL restored the cell viability of SEB-1 cells to a normal level after MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-92	TNF superfamily member 10	Homo sapiens	13-18
30176247-10	2018	Combined treatment of SEB-1 sebocytes with TRAIL and MG-132 synergistically triggered cell death, suppressed cell proliferation and survival, and promoted BIK expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	BCL2 interacting killer	Homo sapiens	155-158
30176247-11	2018	Furthermore, BCL2 Interacting Killer (BIK) knockdown via RNA interference participated in the recovery of cell survival reduced by treatment with TRAIL and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-162	BCL2 interacting killer	Homo sapiens	13-36
30176247-11	2018	Furthermore, BCL2 Interacting Killer (BIK) knockdown via RNA interference participated in the recovery of cell survival reduced by treatment with TRAIL and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-162	BCL2 interacting killer	Homo sapiens	38-41
30176247-12	2018	SIGNIFICANCE: These findings suggest that treatment with the selective proteasome suppressor MG-132 and TRAIL induces cell death in sebocytes through upregulation of BIK, a member of the Bcl-2 family.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	BCL2 interacting killer	Homo sapiens	166-169
30176247-12	2018	SIGNIFICANCE: These findings suggest that treatment with the selective proteasome suppressor MG-132 and TRAIL induces cell death in sebocytes through upregulation of BIK, a member of the Bcl-2 family.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	BCL2 apoptosis regulator	Homo sapiens	187-192
30190126-3	2018	We also found that ubiquitin ligase SPOP (speckle-type POZ protein) binds to FADD and mediates its degradation, which can be blocked by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	speckle type BTB/POZ protein	Homo sapiens	36-40
30190126-3	2018	We also found that ubiquitin ligase SPOP (speckle-type POZ protein) binds to FADD and mediates its degradation, which can be blocked by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	speckle type BTB/POZ protein	Homo sapiens	42-66
30190126-3	2018	We also found that ubiquitin ligase SPOP (speckle-type POZ protein) binds to FADD and mediates its degradation, which can be blocked by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	Fas associated via death domain	Homo sapiens	77-81
30333907-7	2018	We recognized a mismatch in TGIF2 protein and mRNA expression in EMT induced HSC-4 and SAS cells and found that TGIF2 protein was post-translationally degraded through a ubiquitin proteasome system by an MG132 proteasome inhibition assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	204-209	TGFB induced factor homeobox 2	Homo sapiens	112-117
29767559-8	2018	Pretreatments of Cos-7 cells with either the lysosomal inhibitor bafilomycin A1 or the proteasomal inhibitor MG132 partially reversed the inhibitory effects of GPS2 siRNA on BK protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	G protein pathway suppressor 2	Mus musculus	160-164
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	inhibitor of growth family member 5	Homo sapiens	60-64
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	phosphatase and tensin homolog	Homo sapiens	66-70
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	tumor protein p53	Homo sapiens	72-75
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	caspase 3	Homo sapiens	77-86
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	BCL2 associated X, apoptosis regulator	Homo sapiens	88-91
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	H3 histone pseudogene 16	Homo sapiens	93-96
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	interferon alpha inducible protein 27	Homo sapiens	102-105
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	matrix metallopeptidase 2	Homo sapiens	153-158
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	matrix metallopeptidase 9	Homo sapiens	160-165
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	perilipin 2	Homo sapiens	167-171
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	Nanog homeobox	Homo sapiens	173-178
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	180-185
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	cyclin D1	Homo sapiens	187-195
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	cyclin B1	Homo sapiens	197-205
30066887-9	2018	Secretion was further enhanced following pre-treatment with the JNK protein kinase inhibitor AEG3482 prior to MSU crystal stimulation (P&lt;0.05) and was abrogated when cells were preincubated with actinomycin D or the proteasome inhibitor MG132 (50, 100 and 200 microM).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-245	mitogen-activated protein kinase 8	Homo sapiens	64-67
30135544-8	2018	Furthermore, glycosylation deficiency enhances human PrP cytotoxicity induced by MG132 or the toxic prion peptide PrP 106-126.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	prion protein	Homo sapiens	53-56
30075033-8	2018	Our study indicated that activation of nuclear factor-kappa B (NF-kappaB) occurred in the cells immediately after EGFR-TKI treatment and also by gene silencing against oncogenic EGFR; and, MG132 treatment for inhibiting NF-kappaB activation affected cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	nuclear factor kappa B subunit 1	Homo sapiens	39-61
29991511-5	2018	Overexpression of GRWD1 decreased RPL23 protein levels and stability; this effect was restored upon treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	glutamate rich WD repeat containing 1	Homo sapiens	18-23
30075033-8	2018	Our study indicated that activation of nuclear factor-kappa B (NF-kappaB) occurred in the cells immediately after EGFR-TKI treatment and also by gene silencing against oncogenic EGFR; and, MG132 treatment for inhibiting NF-kappaB activation affected cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	nuclear factor kappa B subunit 1	Homo sapiens	63-72
29991511-5	2018	Overexpression of GRWD1 decreased RPL23 protein levels and stability; this effect was restored upon treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	ribosomal protein L23	Homo sapiens	34-39
30075033-8	2018	Our study indicated that activation of nuclear factor-kappa B (NF-kappaB) occurred in the cells immediately after EGFR-TKI treatment and also by gene silencing against oncogenic EGFR; and, MG132 treatment for inhibiting NF-kappaB activation affected cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	nuclear factor kappa B subunit 1	Homo sapiens	220-229
29968965-6	2018	Furthermore, IQUB overexpression or knockdown combined with treatment of Licl or MG-132 showed that IQUB activated Akt to promote GSK3beta phosphorylation, which in turn activated Wnt/beta-catenin signaling pathway in breast cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	IQ motif and ubiquitin domain containing	Homo sapiens	100-104
30167083-5	2018	Treatment with MG132 demonstrated an accumulation of MST2 in 25% of sarcoma cell lines, indicating that proteosomal degradation regulates MST2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	serine/threonine kinase 3	Homo sapiens	53-57
30167083-5	2018	Treatment with MG132 demonstrated an accumulation of MST2 in 25% of sarcoma cell lines, indicating that proteosomal degradation regulates MST2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	serine/threonine kinase 3	Homo sapiens	138-142
29968965-6	2018	Furthermore, IQUB overexpression or knockdown combined with treatment of Licl or MG-132 showed that IQUB activated Akt to promote GSK3beta phosphorylation, which in turn activated Wnt/beta-catenin signaling pathway in breast cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	AKT serine/threonine kinase 1	Homo sapiens	115-118
29968965-6	2018	Furthermore, IQUB overexpression or knockdown combined with treatment of Licl or MG-132 showed that IQUB activated Akt to promote GSK3beta phosphorylation, which in turn activated Wnt/beta-catenin signaling pathway in breast cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	glycogen synthase kinase 3 beta	Homo sapiens	130-138
29968965-6	2018	Furthermore, IQUB overexpression or knockdown combined with treatment of Licl or MG-132 showed that IQUB activated Akt to promote GSK3beta phosphorylation, which in turn activated Wnt/beta-catenin signaling pathway in breast cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	catenin beta 1	Homo sapiens	184-196
30186748-5	2018	Nuclear accumulation of HSF1 and Nrf2 transcription factors was detected upon both arsenite and MG132 treatment, while HSF2 nuclear levels increased in MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	heat shock transcription factor 1	Homo sapiens	24-28
29522376-4	2018	FBXL19 is an unstable protein with a half-life of ~3 h. FBXL19 can be polyubiquitinated, and the proteasome inhibitor MG-132 prolongs FBXL19 half-life, suggesting that FBXL19 degradation is mediated in the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-124	F-box and leucine rich repeat protein 19	Homo sapiens	0-6
30112065-0	2018	Impact of proteasome inhibitor MG-132 on expression of NF-kappaB, IL-1beta and histological remodeling after myocardial infarction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	interleukin 1 beta	Rattus norvegicus	66-74
30112065-6	2018	In conclusion, MG-132 was demonstrated to improve post-MI tissue remodeling, and the mechanism may be associated with the inhibition of NF-kappaB activation and the downregulation of inflammatory cytokines, such as IL-1beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	interleukin 1 beta	Rattus norvegicus	215-223
29901180-0	2018	MG-132 reverses multidrug resistance by activating the JNK signaling pathway in FaDu/T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	mitogen-activated protein kinase 8	Homo sapiens	55-58
29901180-9	2018	These results indicated that MG-132 reversed the MDR of hypopharyngeal carcinoma by downregulating P-gp/P-gp, and the underlying mechanism may be associated with the activation the of the JNK signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	phosphoglycolate phosphatase	Homo sapiens	99-103
29901180-9	2018	These results indicated that MG-132 reversed the MDR of hypopharyngeal carcinoma by downregulating P-gp/P-gp, and the underlying mechanism may be associated with the activation the of the JNK signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	phosphoglycolate phosphatase	Homo sapiens	104-108
29901180-9	2018	These results indicated that MG-132 reversed the MDR of hypopharyngeal carcinoma by downregulating P-gp/P-gp, and the underlying mechanism may be associated with the activation the of the JNK signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	mitogen-activated protein kinase 8	Homo sapiens	188-191
29748146-3	2018	The inhibition of HIF-1alpha accumulation induced by compound 4b was attenuated by treating the cells with MG132, a proteasome inhibitor, in a concentration-dependent manner, indicating that the compound 4b induces oxygen-independent proteasomal degradation of HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	hypoxia inducible factor 1 subunit alpha	Homo sapiens	18-28
29748146-3	2018	The inhibition of HIF-1alpha accumulation induced by compound 4b was attenuated by treating the cells with MG132, a proteasome inhibitor, in a concentration-dependent manner, indicating that the compound 4b induces oxygen-independent proteasomal degradation of HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	hypoxia inducible factor 1 subunit alpha	Homo sapiens	261-271
29852167-5	2018	Pretreatment of meniscus cells with 4-phenyl butyric acid, a small molecule chemical chaperone that alleviates ER stress, or with MG-132, a proteasome inhibitor, restored normal levels of ATG5 and autophagosome formation, and decreased expression of cleaved caspase 3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-136	autophagy related 5	Homo sapiens	188-192
30186748-5	2018	Nuclear accumulation of HSF1 and Nrf2 transcription factors was detected upon both arsenite and MG132 treatment, while HSF2 nuclear levels increased in MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	NFE2 like bZIP transcription factor 2	Homo sapiens	33-37
30186748-5	2018	Nuclear accumulation of HSF1 and Nrf2 transcription factors was detected upon both arsenite and MG132 treatment, while HSF2 nuclear levels increased in MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	heat shock transcription factor 2	Homo sapiens	119-123
29733818-6	2018	AMPD3 was comparably ubiquitinated in OLETF and LETO, and its degradation ex vivo was more sensitive to MG-132, a proteasome inhibitor, in OLETF than in LETO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-110	adenosine monophosphate deaminase 3	Rattus norvegicus	0-5
30116631-7	2018	Then we tested which of cell signal pathways regulating the production of IL-6 were activated when we added MG132 into the medium by Western blot and electrophoretic mobility shift assays (EMSA).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	interleukin 6	Homo sapiens	74-78
30116631-9	2018	Results: MG132 decreased the secretion of MCP-1 in the culture medium of RPE, but it increased the expression of IL-6 mRNA in RPE and IL-6 protein level in the culture medium of RPE.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	C-C motif chemokine ligand 2	Homo sapiens	42-47
30116631-9	2018	Results: MG132 decreased the secretion of MCP-1 in the culture medium of RPE, but it increased the expression of IL-6 mRNA in RPE and IL-6 protein level in the culture medium of RPE.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	interleukin 6	Homo sapiens	113-117
30116631-9	2018	Results: MG132 decreased the secretion of MCP-1 in the culture medium of RPE, but it increased the expression of IL-6 mRNA in RPE and IL-6 protein level in the culture medium of RPE.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	interleukin 6	Homo sapiens	134-138
30116631-10	2018	MG132 treatment was also found to enhance the level of phosphorylated p38 mitogen-activated protein kinases (MAPKs) and c-Jun N-terminal Kinase (JNK) by Western blotting.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 8	Homo sapiens	120-143
30116631-10	2018	MG132 treatment was also found to enhance the level of phosphorylated p38 mitogen-activated protein kinases (MAPKs) and c-Jun N-terminal Kinase (JNK) by Western blotting.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 8	Homo sapiens	145-148
30116631-11	2018	More importantly, the effect of MG132 on upregulating the levels of IL-6 was inhibited by SB203580, an inhibitor of P38 MAP kinases.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	interleukin 6	Homo sapiens	68-72
30116631-12	2018	But the JNK inhibitor, SP600125, cannot prevent the effect of upregulating the levels of IL-6 by MG132 in the RPE culture medium.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	interleukin 6	Homo sapiens	89-93
30116631-13	2018	Conclusions: We concluded that the proteasome inhibitor, MG132, upregulates IL-6 production in RPE cells through the activation of P38 MAPKs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	interleukin 6	Homo sapiens	76-80
29979702-9	2018	Treatment with the proteasome inhibitor MG-132 prevents such loss in proliferating NIH3T3 cells, suggesting the proteasomal degradation of the ALDH1L1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	aldehyde dehydrogenase 1 family, member L1	Mus musculus	143-150
29628506-6	2018	Also, c-Myc degradation by ZNF746 depletion was blocked by knockdown of F-box/WD repeat-containing protein 7 (FBW7) ubiquitin ligase or proteosomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	6-11
29628506-6	2018	Also, c-Myc degradation by ZNF746 depletion was blocked by knockdown of F-box/WD repeat-containing protein 7 (FBW7) ubiquitin ligase or proteosomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	zinc finger protein 746	Homo sapiens	27-33
29686000-7	2018	Proteasome inhibition with MG132 prevented Ang II-induced decrease of Kv7.4 levels and counteracted the functional impairment of ML213-induced relaxation in myography experiments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	angiotensinogen	Rattus norvegicus	43-49
29625985-7	2018	In the cells with a laboratory strain background, treatment with the proteasome inhibitor MG132 or the deletion of each transcriptional activator gene for the proteasome genes (RPN4, PDR1, or PDR3) led to marked impairment of model dough fermentation using the frozen cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	stress-regulated transcription factor RPN4	Saccharomyces cerevisiae S288C	177-181
29650159-5	2018	The rapid disappearance of intact CLV3-GFP requires the signal peptide and is inhibited by the proteasome inhibitor MG132 or coexpression with a mutated CDC48 that inhibits endoplasmic reticulum-associated protein degradation (ERAD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	CLAVATA3	Arabidopsis thaliana	34-38
29658600-0	2018	PDK1 inhibitor GSK2334470 synergizes with proteasome inhibitor MG-132 in multiple myeloma cells by inhibiting full AKT activity and increasing nuclear accumulation of the PTEN protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-69	pyruvate dehydrogenase kinase 1	Homo sapiens	0-4
29658600-0	2018	PDK1 inhibitor GSK2334470 synergizes with proteasome inhibitor MG-132 in multiple myeloma cells by inhibiting full AKT activity and increasing nuclear accumulation of the PTEN protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-69	AKT serine/threonine kinase 1	Homo sapiens	115-118
29658600-0	2018	PDK1 inhibitor GSK2334470 synergizes with proteasome inhibitor MG-132 in multiple myeloma cells by inhibiting full AKT activity and increasing nuclear accumulation of the PTEN protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-69	phosphatase and tensin homolog	Homo sapiens	171-175
29855346-4	2018	RESULTS: We found evidence that the ubiquitin-proteasome pathway can efficiently degrade STAT1 in ESCC cells, as MG132 treatment rapidly and dramatically increased STAT1 expression in these cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	signal transducer and activator of transcription 1	Homo sapiens	89-94
29668859-5	2018	In addition, the levels of OCT4 were decreased by exposing NCCIT cells to KRIBB53, and pretreating the cells with the proteasomal inhibitor MG132 reversed the KRIBB53-induced OCT4 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	POU class 5 homeobox 1	Homo sapiens	27-31
29855346-4	2018	RESULTS: We found evidence that the ubiquitin-proteasome pathway can efficiently degrade STAT1 in ESCC cells, as MG132 treatment rapidly and dramatically increased STAT1 expression in these cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	signal transducer and activator of transcription 1	Homo sapiens	164-169
29668859-5	2018	In addition, the levels of OCT4 were decreased by exposing NCCIT cells to KRIBB53, and pretreating the cells with the proteasomal inhibitor MG132 reversed the KRIBB53-induced OCT4 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	POU class 5 homeobox 1	Homo sapiens	175-179
29875689-9	2018	Incubating cells in MG132 minimally impacted G601S-Kv11.1 immunostaining, but it dramatically increased the diffuse immunostaining of F805C-Kv11.1 protein in the transitional ER.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	potassium voltage-gated channel subfamily H member 2	Homo sapiens	51-57
29899847-7	2018	HSP90 inhibitors suppressed ubiquitination processes which were involved in p53 degradation, but a proteasome inhibitor, MG-132, prevented the HSP90 inhibitors-induced p53 down-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	heat shock protein 90 alpha family class A member 1	Homo sapiens	143-148
29899847-7	2018	HSP90 inhibitors suppressed ubiquitination processes which were involved in p53 degradation, but a proteasome inhibitor, MG-132, prevented the HSP90 inhibitors-induced p53 down-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	tumor protein p53	Homo sapiens	168-171
29875689-9	2018	Incubating cells in MG132 minimally impacted G601S-Kv11.1 immunostaining, but it dramatically increased the diffuse immunostaining of F805C-Kv11.1 protein in the transitional ER.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	potassium voltage-gated channel subfamily H member 2	Homo sapiens	140-146
29805737-5	2018	In addition, following to the treatment of PTPRJ-transduced cells with MG132, a proteasome inhibitor, CD98hc levels did not decrease compared to controls, indicating that PTPRJ is involved in the regulation of CD98hc proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	protein tyrosine phosphatase receptor type J	Homo sapiens	43-48
29191257-8	2018	Mechanistically, MG132 arrested cells in the G2/M phase in association with increased p21waf1 and induced cell apoptosis, which was accompanied by cleaved PARP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	poly(ADP-ribose) polymerase 1	Homo sapiens	155-159
29522752-8	2018	Through the use of a dual luciferase reporter assay system and incubation with cycloheximide (CHX) MG132 and actidione (ActD), we found that DDX5 promoted MSR1 protein expression by stabilizing MSR1 mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	DEAD-box helicase 5	Homo sapiens	141-145
29805737-5	2018	In addition, following to the treatment of PTPRJ-transduced cells with MG132, a proteasome inhibitor, CD98hc levels did not decrease compared to controls, indicating that PTPRJ is involved in the regulation of CD98hc proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	solute carrier family 3 member 2	Homo sapiens	102-108
29805737-5	2018	In addition, following to the treatment of PTPRJ-transduced cells with MG132, a proteasome inhibitor, CD98hc levels did not decrease compared to controls, indicating that PTPRJ is involved in the regulation of CD98hc proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	protein tyrosine phosphatase receptor type J	Homo sapiens	171-176
29805737-5	2018	In addition, following to the treatment of PTPRJ-transduced cells with MG132, a proteasome inhibitor, CD98hc levels did not decrease compared to controls, indicating that PTPRJ is involved in the regulation of CD98hc proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	solute carrier family 3 member 2	Homo sapiens	102-106
29363325-6	2018	However, the HG effect on Orai1 protein was significantly attenuated by MG132 (a ubiquitin-proteasome inhibitor) and NH4Cl (a lysosomal pathway inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	ORAI calcium release-activated calcium modulator 1	Rattus norvegicus	26-31
29565467-6	2018	Using western blot analysis, this regulation appears to occur via protein synthesis but not protein stability as blockade of HIF-1alpha protein degradation by hypoxia mimic desferrioxamine (DFX) or proteasome inhibitor MG132 did not affect berberine"s effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	219-224	hypoxia inducible factor 1 subunit alpha	Homo sapiens	125-135
29748581-10	2018	Pretreatment of cells with an inhibitor of the proteasome (MG132), prevented leptin-induced OMA1 degradation, implicating the ubiquitination/proteasome system as a part of the protective leptin pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	leptin	Homo sapiens	77-83
29748581-10	2018	Pretreatment of cells with an inhibitor of the proteasome (MG132), prevented leptin-induced OMA1 degradation, implicating the ubiquitination/proteasome system as a part of the protective leptin pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	OMA1 zinc metallopeptidase	Homo sapiens	92-96
29748581-10	2018	Pretreatment of cells with an inhibitor of the proteasome (MG132), prevented leptin-induced OMA1 degradation, implicating the ubiquitination/proteasome system as a part of the protective leptin pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	leptin	Homo sapiens	187-193
29524884-11	2018	Moreover, a proteasome inhibitor, MG-132, and the lysosomotropic agent, hydroxychloroquine (HCQ) were found to abolish the inhibitory effect of steviol in Pkd1-/- cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	polycystin 1, transient receptor potential channel interacting	Canis lupus familiaris	155-159
29735364-9	2018	Treatment of MG132 (a proteasomal degradation inhibitor) almost abolished the decrease of MITF protein levels by MAHDP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	melanocyte inducing transcription factor	Homo sapiens	90-94
29712950-6	2018	IL-1alpha-primed ARPE-19 cells, human embryonal stem cell (hESC)-derived RPE cells, and primary human RPE cells were exposed to MG-132 and bafilomycin A to activate NLRP3 via the inhibition of proteasomes and autophagy, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-134	interleukin 1 alpha	Homo sapiens	0-9
29774099-5	2018	Additionally, the proteasome inhibitor, MG132, restored the decrease in Cdc25C levels in response to CPT, and significantly downregulated CPT-induced G2/M phase arrest, suggesting that CPT enhances G2/M phase arrest through proteasome-mediated Cdc25C degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	cell division cycle 25C	Homo sapiens	72-78
29774099-5	2018	Additionally, the proteasome inhibitor, MG132, restored the decrease in Cdc25C levels in response to CPT, and significantly downregulated CPT-induced G2/M phase arrest, suggesting that CPT enhances G2/M phase arrest through proteasome-mediated Cdc25C degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	cell division cycle 25C	Homo sapiens	244-250
29755465-5	2018	IRF3 can promote the degradation of TRIF protein in mammal and fish cells, but this effect could be inhibited by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	interferon regulatory factor 3	Homo sapiens	0-4
29755465-5	2018	IRF3 can promote the degradation of TRIF protein in mammal and fish cells, but this effect could be inhibited by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	TIR domain containing adaptor molecule 1	Homo sapiens	36-40
29246658-6	2018	While dispersed p62 puncti were found in STHdhQ7 cells, p62 bodies were initially present in the lysosomes and accumulated to the juxtanuclear regions of STHdhQ111 cells as MG132 incubation continued.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-178	sequestosome 1	Mus musculus	56-59
29580840-9	2018	When analysing the mechanism by which Vif might target the JAK/STAT pathway, we found Vif interacts with both STAT1 and STAT3, (but not STAT2), and its expression promotes ubiquitination and MG132-sensitive, proteosomal degradation of both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	Vif	Human immunodeficiency virus 1	38-41
29580840-9	2018	When analysing the mechanism by which Vif might target the JAK/STAT pathway, we found Vif interacts with both STAT1 and STAT3, (but not STAT2), and its expression promotes ubiquitination and MG132-sensitive, proteosomal degradation of both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	Vif	Human immunodeficiency virus 1	86-89
29580840-9	2018	When analysing the mechanism by which Vif might target the JAK/STAT pathway, we found Vif interacts with both STAT1 and STAT3, (but not STAT2), and its expression promotes ubiquitination and MG132-sensitive, proteosomal degradation of both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	signal transducer and activator of transcription 1	Homo sapiens	110-115
29580840-9	2018	When analysing the mechanism by which Vif might target the JAK/STAT pathway, we found Vif interacts with both STAT1 and STAT3, (but not STAT2), and its expression promotes ubiquitination and MG132-sensitive, proteosomal degradation of both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	signal transducer and activator of transcription 3	Homo sapiens	120-125
29330041-5	2018	Western blot analysis showed a significant decrease of total KCa2.2 protein content in GZ-treated slices which could be rescued by concomitant incubation with MG132 and CQ.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	potassium calcium-activated channel subfamily N member 2	Homo sapiens	61-67
29330041-7	2018	We then recorded epileptiform afterdischarges at hippocampal Schaffer collateral-CA1 synapses and confirmed that the GZ-induced increase was significantly attenuated by both MG132 and CQ, with MG132 being significantly more effective than CQ.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	carbonic anhydrase 1	Homo sapiens	81-84
28438434-10	2018	MG132, an inhibitor of proteasomal degradation, reversed the effect of CTGF on mtTFA protein expression in SAS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cellular communication network factor 2	Homo sapiens	71-75
28771721-6	2018	Treatment with the proteasomal inhibitor MG-132 revealed that vimentin is actively degraded by the proteasome in Moody cells and stabilized in the SKOV-3 cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	vimentin	Homo sapiens	62-70
28438434-10	2018	MG132, an inhibitor of proteasomal degradation, reversed the effect of CTGF on mtTFA protein expression in SAS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transcription factor A, mitochondrial	Homo sapiens	79-84
28438434-10	2018	MG132, an inhibitor of proteasomal degradation, reversed the effect of CTGF on mtTFA protein expression in SAS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tetraspanin 31	Homo sapiens	107-110
29407584-0	2018	The combination of TRAIL and MG-132 induces apoptosis in both TRAIL-sensitive and TRAIL-resistant human follicular lymphoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	TNF superfamily member 10	Homo sapiens	62-67
29407584-0	2018	The combination of TRAIL and MG-132 induces apoptosis in both TRAIL-sensitive and TRAIL-resistant human follicular lymphoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	TNF superfamily member 10	Homo sapiens	62-67
29407584-4	2018	In the present study, we examined the effects of MG-132 (a proteasome inhibitor), LiCl (a glycogen synthase kinase-3 inhibitor) and/or TRAIL on pro-apoptotic Bcl-2 family proteins such as Bim and Bid.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	BCL2 apoptosis regulator	Homo sapiens	158-163
29164633-12	2018	Pretreatment of MG132, a proteasome inhibitor, attenuated effect of Cap on AR degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	androgen receptor	Homo sapiens	75-77
29576851-3	2018	In ARPE-19 cells exposed to the proteasomal inhibitor MG132, HuR positively affects at posttranscriptional level p62 expression, a stress response gene involved in protein aggregate clearance with a role in AMD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	ELAV like RNA binding protein 1	Homo sapiens	61-64
29407955-7	2018	The application of Keap1 siRNA silencing and the proteasome inhibitor MG132 confirmed that peptide 1 could promote the Keap1-dependent poly-ubiquitination and proteasome-dependent degradation of Tau.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	kelch like ECH associated protein 1	Homo sapiens	119-124
29476063-4	2018	Site-directed mutagenesis V2S71A had the similar subcellular localization, but V2S71A formed fewer large aggregates in the cytoplasm compared to wild-type V2, whereas the level of aggregates came to a similar after treatment with MG132, which indicates that the S71A mutation might affect 26S proteasome-mediated degradation of V2 aggregates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	230-235	T cell receptor gamma variable 9	Homo sapiens	79-85
29576851-3	2018	In ARPE-19 cells exposed to the proteasomal inhibitor MG132, HuR positively affects at posttranscriptional level p62 expression, a stress response gene involved in protein aggregate clearance with a role in AMD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	sequestosome 1	Homo sapiens	113-116
29576851-4	2018	Here, we studied the early effects of the proautophagy AICAR + MG132 cotreatment on the HuR-p62 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	ELAV like RNA binding protein 1	Homo sapiens	88-91
29576851-4	2018	Here, we studied the early effects of the proautophagy AICAR + MG132 cotreatment on the HuR-p62 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	sequestosome 1	Homo sapiens	92-95
29576851-6	2018	Two-hour AICAR + MG132 induces both HuR cytoplasmic translocation and threonine phosphorylation via the Erk1/2 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	ELAV like RNA binding protein 1	Homo sapiens	36-39
29576851-6	2018	Two-hour AICAR + MG132 induces both HuR cytoplasmic translocation and threonine phosphorylation via the Erk1/2 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	mitogen-activated protein kinase 3	Homo sapiens	104-110
29196261-5	2018	Experiments using cycloheximide, MG132 and bafilomycin A1 have revealed that Sox9 is degraded through the ubiquitin-proteasome pathway and that A-674563 inhibits this degradation, resulting in larger amount of Sox9 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	SRY (sex determining region Y)-box 9	Mus musculus	77-81
29531806-7	2018	This hypothesis was confirmed by treating the cells with MG132 (a proteasome inhibitor), which provided almost identical endogenous peptide pattern as of the TGF-beta1-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	transforming growth factor beta 1	Homo sapiens	158-167
28861610-8	2018	Both, MG132 and aldosterone, significantly increased the abundance of beta-ENaC at the cell surface.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	sodium channel, nonvoltage-gated 1 beta	Mus musculus	70-79
28861610-9	2018	SGK1 activity was assessed by monitoring the phosphorylation of a downstream target, NDRG1, and was found to be increased by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	serum/glucocorticoid regulated kinase 1	Mus musculus	0-4
28861610-9	2018	SGK1 activity was assessed by monitoring the phosphorylation of a downstream target, NDRG1, and was found to be increased by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	N-myc downstream regulated gene 1	Mus musculus	85-90
29339435-8	2018	The ubiquitin E1 inhibitor UBEI-41 or the proteasome inhibitor MG132 prevented IRF5 degradation, supporting that its stability is regulated by the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	interferon regulatory factor 5	Homo sapiens	79-83
29332931-0	2018	Proteasome Inhibitor Carbobenzoxy-L-Leucyl-L-Leucyl-L-Leucinal (MG132) Enhances Therapeutic Effect of Paclitaxel on Breast Cancer by Inhibiting Nuclear Factor (NF)-kappaB Signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	144-170
29332931-1	2018	BACKGROUND Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132), a peptide aldehyde proteasome inhibitor, can inhibit tumor progression by inactivating nuclear factor (NF)-kappaB signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	149-175
30138927-1	2018	BACKGROUND/AIMS: Previously, we demonstrated that blockade of the intracellular clearance systems in human retinal pigment epithelial (RPE) cells by MG-132 and bafilomycin A1 (BafA) induces NLRP3 inflammasome signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-155	NLR family pyrin domain containing 3	Homo sapiens	190-195
29491214-5	2018	BPA degraded HIF-1alpha even in the presence of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	hypoxia inducible factor 1 subunit alpha	Homo sapiens	13-23
29911914-9	2018	However, MG132, an inhibitor of anaphase-promoting complex/cyclosome (APC/C), could rescue the prolonged time of GVBD and increase the expression level of CCNB1 of oocytes from the CRS mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	cyclin B1	Mus musculus	155-160
29911927-8	2018	Finally, N-terminal truncated ADNP mutants are routed towards cytosolic proteasomal degradation and rescued with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	activity dependent neuroprotector homeobox	Homo sapiens	30-34
30114705-11	2018	MG 132 induced the decrease in RARalpha in both cell lines, and hampered the differentiation of NB4 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	retinoic acid receptor alpha	Homo sapiens	31-39
28749203-8	2018	R175H p53 expression was rescued by addition of proteasome inhibitor MG132 to CB002, suggesting a role for ubiquitin-mediated degradation of the mutant protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	tumor protein p53	Homo sapiens	6-9
30138927-6	2018	METHODS: NLRP3 inflammasomes were activated in human RPE cells by blocking proteasomes and autophagy using MG-132 and bafilomycin A1 (BafA), respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-113	NLR family pyrin domain containing 3	Homo sapiens	9-14
30138927-11	2018	It also prevented IL-1beta release after exposure of primed cells to MG-132 and BafA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	interleukin 1 beta	Homo sapiens	18-26
30138927-13	2018	The activity of the lysosomal enzyme, cathepsin B, was reduced by MG-132 and BafA, suggesting that cathepsin B was not playing any role in this phenomenon.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	cathepsin B	Homo sapiens	38-49
29807365-6	2018	Inhibition of the proteasome with MG-132 or induction of oxidative stress with tert-butylhydroquinone (tBHQ) extended the half-life of Dendra2-Nrf2 by 6- and 28-fold, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	NFE2 like bZIP transcription factor 2	Homo sapiens	143-147
30485834-10	2018	We also checked if NF-kappaB inhibitor MG132 causes any change at the level of apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nuclear factor kappa B subunit 1	Homo sapiens	19-28
28681940-5	2018	Furthermore, we provided evidence that Runx2 was transcriptionally regulated by HSP90 when using MG132 and CHX chase assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	RUNX family transcription factor 2	Homo sapiens	39-44
29074603-7	2018	Decrease in Mcl-1 protein expression was abrogated by treatment with the proteasome inhibitor MG132, and was preceded by downregulation of the Mcl-1 deubiquitinase USP9X, a novel mechanism of Mcl-1 regulation in AML.Conclusions: The data support clinical testing of Pim and FLT3 inhibitor combination therapy for FLT3-ITD AML.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	12-17
29669333-9	2018	In vivo MG132 administration to NC/Nga mice with DNFB-induced dermatitis reduced Th17 cells but maintained the level of Th1 cells, resulting in the alleviation of dermatitis lesions by decreasing both serum IgE hyperproduction and mast cell migration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-13	negative elongation factor complex member C/D, Th1l	Mus musculus	81-84
29669333-12	2018	In vitro MG132 administration partially increased D/Ldm7 expression in a dose-dependent manner during DC maturation, and induced IFN-gamma production from autoreactive CD8+ T cells but not from CD4+ T cells following coculturing with D/Ldm7-upregulated DCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	interferon gamma	Mus musculus	129-138
29669333-13	2018	CONCLUSION: Although MG132 administration temporarily alleviated AD pathogenesis in NC/Nga mice, prolonged MG132 treatment may result in immunopathogenesis leading to chronic AD due to its side effect of maintaining Th1 levels via autoreactive CD8+ T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	negative elongation factor complex member C/D, Th1l	Mus musculus	216-219
30412487-3	2018	To advance knowledge of the little studied HSPA6, differentiated human neuronal SH-SY5Y cells were treated with the proteotoxic stress-inducing agent MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	heat shock protein family A (Hsp70) member 6	Homo sapiens	43-48
30412487-4	2018	A robust induction of HSPA6 was apparent which localized to the periphery of MG132-induced protein aggregates in the neuronal cytoplasm.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	heat shock protein family A (Hsp70) member 6	Homo sapiens	22-27
30412487-7	2018	Constitutively expressed HSPA8 (Hsc70) also localized tothe periphery of cytoplasmic protein aggregates following the treatment of differentiated human neuronal cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	heat shock protein family A (Hsp70) member 8	Homo sapiens	25-30
30412487-7	2018	Constitutively expressed HSPA8 (Hsc70) also localized tothe periphery of cytoplasmic protein aggregates following the treatment of differentiated human neuronal cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	heat shock protein family A (Hsp70) member 8	Homo sapiens	32-37
28681940-5	2018	Furthermore, we provided evidence that Runx2 was transcriptionally regulated by HSP90 when using MG132 and CHX chase assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	heat shock protein 90 alpha family class A member 1	Homo sapiens	80-85
29024409-5	2018	The proteasome inhibitor MG132 blunts the downregulation of beta-catenin by rhein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	catenin beta 1	Homo sapiens	60-72
28322449-5	2018	Western blotting analysis indicated that TGF-beta induced protein expression of E3 ubiquitin-protein ligase SMURF1, which contributed to the degradation of RUNX2 and SMAD1 as evidenced by SMURF1 inhibition using RNA interference and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	254-259	transforming growth factor, beta 1	Mus musculus	41-49
28322449-5	2018	Western blotting analysis indicated that TGF-beta induced protein expression of E3 ubiquitin-protein ligase SMURF1, which contributed to the degradation of RUNX2 and SMAD1 as evidenced by SMURF1 inhibition using RNA interference and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	254-259	SMAD specific E3 ubiquitin protein ligase 1	Mus musculus	108-114
28322449-5	2018	Western blotting analysis indicated that TGF-beta induced protein expression of E3 ubiquitin-protein ligase SMURF1, which contributed to the degradation of RUNX2 and SMAD1 as evidenced by SMURF1 inhibition using RNA interference and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	254-259	runt related transcription factor 2	Mus musculus	156-161
28322449-5	2018	Western blotting analysis indicated that TGF-beta induced protein expression of E3 ubiquitin-protein ligase SMURF1, which contributed to the degradation of RUNX2 and SMAD1 as evidenced by SMURF1 inhibition using RNA interference and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	254-259	SMAD family member 1	Mus musculus	166-171
29097054-3	2018	METHODS: The ABCA1 decay rate was evaluated in macrophages after treatment with LXR agonist and by incubation with control (C) or AGE-albumin concomitant or not with cycloheximide, MG-132, ammonium chloride and calpain inhibitors were utilized to inhibit, respectively, proteasome, lysosome and ABCA1 proteolysis at cell surface.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	181-187	ATP binding cassette subfamily A member 1	Homo sapiens	13-18
29155477-6	2017	Significantly, the proteasome inhibitor MG-132 prevented this oxLDL-attenuation differentiation phenotype by blocking HIF1alpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	hypoxia inducible factor 1 subunit alpha	Homo sapiens	118-127
29096318-9	2018	Histological examination showed deleterious effects of MG132 on pyramidal neurons and granule cell neurons in DG and CA3 sub-regions respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	carbonic anhydrase 3	Mus musculus	117-120
29533961-4	2018	Results suggest that the multivalent Cu-conjugated dendrimer 1G3-Cu (activator of Bax translocation) plays an important role in boosting the clinical impact of Bax accumulation stimulated by the proteasome inhibitor MG132, antimitotic taxanes, and the topo II inhibitor doxorubicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-221	BCL2 associated X, apoptosis regulator	Homo sapiens	82-85
29533961-4	2018	Results suggest that the multivalent Cu-conjugated dendrimer 1G3-Cu (activator of Bax translocation) plays an important role in boosting the clinical impact of Bax accumulation stimulated by the proteasome inhibitor MG132, antimitotic taxanes, and the topo II inhibitor doxorubicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-221	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163
29102663-11	2017	Pharmacological blockade of the proteasome with MG132 led to a further increase in NGF-induced TRPM8 expression, indicating that the proteasome system played a pivotal role in the degradation of TRPM8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	nerve growth factor	Homo sapiens	83-86
29102663-11	2017	Pharmacological blockade of the proteasome with MG132 led to a further increase in NGF-induced TRPM8 expression, indicating that the proteasome system played a pivotal role in the degradation of TRPM8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	transient receptor potential cation channel subfamily M member 8	Homo sapiens	95-100
29102663-11	2017	Pharmacological blockade of the proteasome with MG132 led to a further increase in NGF-induced TRPM8 expression, indicating that the proteasome system played a pivotal role in the degradation of TRPM8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	transient receptor potential cation channel subfamily M member 8	Homo sapiens	195-200
28939105-5	2017	PKCeta depletion had no effect on MCL1 mRNA but the decrease in Mcl-1 by PKCeta knockdown was blocked by proteasomal inhibitors, such as MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	64-69
29102179-5	2017	Importantly, fluorescent and immunofluorescent analyses of cells treated with the proteasome inhibitor MG132 demonstrates that 6b can selectively target and image HDAC6 within the inclusion body, the aggresome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	histone deacetylase 6	Homo sapiens	163-168
29039450-8	2017	Importantly, the PA-induced decrease in UCP3 was blocked by the proteasome inhibitor MG132, and insulin reduced UCP3 ubiquitination, thereby prohibiting its degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	uncoupling protein 3 (mitochondrial, proton carrier)	Mus musculus	40-44
29080716-6	2017	Hematoxylin and eosin as well as Cresyl Violet staining revealed substantial loss of cellular connections, distorted architecture and increased pyknosis in hippocampal CA1 and CA3 regions of MG132 mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	carbonic anhydrase 1	Mus musculus	168-171
29080716-6	2017	Hematoxylin and eosin as well as Cresyl Violet staining revealed substantial loss of cellular connections, distorted architecture and increased pyknosis in hippocampal CA1 and CA3 regions of MG132 mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	carbonic anhydrase 3	Mus musculus	176-179
29285074-8	2017	Furthermore, p38 MAPK and NF-kappaB inhibitors (SB203580 and MG-132, respectively) prevented PAE-induced proliferative inhibition in RL95-2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	mitogen-activated protein kinase 14	Homo sapiens	13-16
28150141-11	2017	Validating the in vivo studies, we demonstrate that treatment of human bronchial epithelial cells (Beas2b cells) with the proteasome inhibitor (MG-132) induces HIF-1alpha expression that is controlled by co-treatment with autophagy-inducing drug, cysteamine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-150	hypoxia inducible factor 1 subunit alpha	Homo sapiens	160-170
29070514-7	2017	MKP1 also can be stabilized by the proteasome inhibitor MG132, suggesting that MKP1 is constitutively degraded through the proteasome in the resting state.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	mitogen-activated protein kinase phosphatase 1	Arabidopsis thaliana	0-4
28941726-3	2017	In this study, we demonstrated the increases of BAG3 expression in the ventral midbrain of SNCAA53T transgenic mice and also in MG132-treated PC12 cells overexpressing wild-type SNCA (SNCAWT-PC12).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	BCL2-associated athanogene 3	Mus musculus	48-52
29070514-7	2017	MKP1 also can be stabilized by the proteasome inhibitor MG132, suggesting that MKP1 is constitutively degraded through the proteasome in the resting state.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	mitogen-activated protein kinase phosphatase 1	Arabidopsis thaliana	79-83
28963376-3	2017	Mass spectrometric analysis of PCBP1 immunoprecipitates from MG-132 treated TPC1 cells revealed a list of ubiquitin ligases associated with PCBP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	poly(rC) binding protein 1	Homo sapiens	31-36
28942144-7	2017	Pax7 expression also decreased in the presence of the proteasome inhibitor MG132, indicating that the proteasomal degradation of Pax7 protein is not critical for its reduced expression in microgravity culture.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	paired box 7	Homo sapiens	0-4
28942144-7	2017	Pax7 expression also decreased in the presence of the proteasome inhibitor MG132, indicating that the proteasomal degradation of Pax7 protein is not critical for its reduced expression in microgravity culture.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	paired box 7	Homo sapiens	129-133
29184507-14	2017	Importantly, the Kir2.1-Nav1.5 complexes were degraded following this route as demonstrated by the overexpression of Nedd4-2 and the inhibition of the proteasome with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	167-172	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	17-23
29184507-14	2017	Importantly, the Kir2.1-Nav1.5 complexes were degraded following this route as demonstrated by the overexpression of Nedd4-2 and the inhibition of the proteasome with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	167-172	sodium voltage-gated channel alpha subunit 5	Homo sapiens	24-30
29107984-10	2017	Treatment with other proteasome inhibitors MG132, epoxomicin, and carfilzomib also significantly decreased OATP1B3-mediated [3H]CCK-8 transport.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	solute carrier organic anion transporter family member 1B3	Homo sapiens	107-114
28844948-7	2017	Sort1 protein downregulation upon PI3K inhibition was blocked by pretreatment of MG132 but not Bafilomycin A1, suggesting that PI3K inhibition caused Sort1 degradation via the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	sortilin 1	Mus musculus	0-5
28844948-7	2017	Sort1 protein downregulation upon PI3K inhibition was blocked by pretreatment of MG132 but not Bafilomycin A1, suggesting that PI3K inhibition caused Sort1 degradation via the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	sortilin 1	Mus musculus	150-155
28880013-7	2017	Pretreatment with the proteasome inhibitors (MG-132 or bortezomib) blocked the osimertinib-induced degradation of PD-L1, but an inhibitor of autophagy (chloroquine) did not.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	CD274 molecule	Homo sapiens	114-119
29029378-4	2017	After inhibiting the proteasome with MG132, Gpn3-Flag was polyubiquitinated on K216, but not K189, in HEK293T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	GPN-loop GTPase 3	Homo sapiens	44-48
28814529-9	2017	VSMC treatment with MG132, a proteasome inhibitor, indicated that PD184161 influenced HIF-1alpha protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	hypoxia inducible factor 1 subunit alpha	Homo sapiens	86-96
28830914-5	2017	Although NAC is thought to be a glutathione precursor, NAC protected primary astrocytes from the toxicity of the proteasome inhibitor MG132 without eliciting any increase in glutathione.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	134-139	X-linked Kx blood group	Homo sapiens	55-58
28830914-7	2017	MG132 elicited a robust increase in the folding chaperone heat shock protein 70 (Hsp70), and NAC mitigated this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein family A (Hsp70) member 4	Homo sapiens	58-79
28830914-7	2017	MG132 elicited a robust increase in the folding chaperone heat shock protein 70 (Hsp70), and NAC mitigated this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein family A (Hsp70) member 4	Homo sapiens	81-86
28830914-9	2017	Consistent with this view, NAC abolished an increase in ubiquitinated proteins in MG132-treated astrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	X-linked Kx blood group	Homo sapiens	27-30
28963376-3	2017	Mass spectrometric analysis of PCBP1 immunoprecipitates from MG-132 treated TPC1 cells revealed a list of ubiquitin ligases associated with PCBP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	two pore segment channel 1	Homo sapiens	76-80
28963376-3	2017	Mass spectrometric analysis of PCBP1 immunoprecipitates from MG-132 treated TPC1 cells revealed a list of ubiquitin ligases associated with PCBP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	poly(rC) binding protein 1	Homo sapiens	140-145
28580641-6	2017	Notably, the reduction in BiP and IRE1alpha by melatonin was suppressed by the ubiquitin-proteasome inhibitor, MG132, but not by the autophagy inhibitor, bafilomycin A1, indicating involvement of the ER-associated protein degradation (ERAD) system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	heat shock protein family A (Hsp70) member 5	Homo sapiens	26-29
28807830-8	2017	Knockdown of USP5 in PANC-1 cells decreased FoxM1 protein level while the proteasome inhibitor MG-132 treatment restored FoxM1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-101	forkhead box M1	Homo sapiens	121-126
29042667-6	2017	Protein expression of viral infected cell protein 0 (bICP0), which is constitutively expressed during infection and is able to stimulate Nuclear factor kappa B (NF-kappaB), was completely inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	nuclear factor kappa B subunit 1	Homo sapiens	137-159
29042667-6	2017	Protein expression of viral infected cell protein 0 (bICP0), which is constitutively expressed during infection and is able to stimulate Nuclear factor kappa B (NF-kappaB), was completely inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	nuclear factor kappa B subunit 1	Homo sapiens	161-170
28861931-6	2017	MTA1 protein level was stabilized in THLE-2 cells after treatment with MG-132 to levels similar to those observed in HuH6 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-77	metastasis associated 1	Homo sapiens	0-4
28861931-7	2017	Mass spectrometric analysis of FLAG immunoprecipitates of FLAG-MTA1 transfected THLE-2 cells after MG-132 treated revealed candidate ubiquitin ligases that were interacting with MTA1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	metastasis associated 1	Homo sapiens	58-67
28861931-7	2017	Mass spectrometric analysis of FLAG immunoprecipitates of FLAG-MTA1 transfected THLE-2 cells after MG-132 treated revealed candidate ubiquitin ligases that were interacting with MTA1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	metastasis associated 1	Homo sapiens	63-67
28861931-9	2017	Coimmunoprecipitation of FLAG-tagged MTA1, but not IgG, in MG-132 treated and untreated THLE-2 cells cotransfected with either FLAG-MTA1 or Myc-TRIM25 revealed robust polyubiquitinated MTA1, confirming that the TRIM25 is the ubiquitin ligase for MTA1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	metastasis associated 1	Homo sapiens	37-41
28580641-6	2017	Notably, the reduction in BiP and IRE1alpha by melatonin was suppressed by the ubiquitin-proteasome inhibitor, MG132, but not by the autophagy inhibitor, bafilomycin A1, indicating involvement of the ER-associated protein degradation (ERAD) system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	34-43
28580641-7	2017	Melatonin treatment reduced the levels of transforming growth factor-beta-induced protein (TGFBIp) significantly, and this reduction was suppressed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	transforming growth factor beta induced	Homo sapiens	91-97
28715732-3	2017	In this study, we found that HSP90 was cleaved to a 55kDa protein after treatment with proteasome inhibitors including MG132 in leukemia cells but was not cleaved in other tissue-derived cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	heat shock protein 90 alpha family class A member 1	Homo sapiens	29-34
28765903-11	2017	TPA-induced FN expression was decreased by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	fibronectin 1	Homo sapiens	12-14
28765903-12	2017	Under the same condition, p53 protein expression, but not mRNA expression, was reversed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	tumor protein p53	Homo sapiens	26-29
28715732-4	2017	HSP90 has two major isoforms (HSP90alpha and HSP90beta), and both were cleaved by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
28715732-4	2017	HSP90 has two major isoforms (HSP90alpha and HSP90beta), and both were cleaved by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	heat shock protein 90 alpha family class A member 1	Homo sapiens	30-40
28715732-4	2017	HSP90 has two major isoforms (HSP90alpha and HSP90beta), and both were cleaved by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	heat shock protein 90 alpha family class B member 1	Homo sapiens	45-54
28715732-5	2017	MG132 treatment also induced a decrease in HSP90 client proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein 90 alpha family class A member 1	Homo sapiens	43-48
28715732-6	2017	MG132 treatment generated ROS, and the cleavage of HSP90 was blocked by a ROS scavenger, N-acetylcysteine (NAC).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein 90 alpha family class A member 1	Homo sapiens	51-56
28715732-7	2017	MG132 activated several caspases, and the activation was reduced by pretreatment with NAC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 10	Homo sapiens	24-32
28715732-8	2017	Based on an inhibitor study, the cleavage of HSP90 induced by MG132 was dependent on caspase 10 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	heat shock protein 90 alpha family class A member 1	Homo sapiens	45-50
28715732-8	2017	Based on an inhibitor study, the cleavage of HSP90 induced by MG132 was dependent on caspase 10 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	caspase 10	Homo sapiens	85-95
28715732-10	2017	MG132 upregulated VDUP-1 expression and reduced the GSH levels implying that the regulation of redox-related proteins is involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	thioredoxin interacting protein	Homo sapiens	18-24
28715732-11	2017	Taken all together, our results suggest that the cleavage of HSP90 by MG132 treatment is mediated by ROS generation and caspase 10 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	heat shock protein 90 alpha family class A member 1	Homo sapiens	61-66
28715732-11	2017	Taken all together, our results suggest that the cleavage of HSP90 by MG132 treatment is mediated by ROS generation and caspase 10 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	caspase 10	Homo sapiens	120-130
28669733-5	2017	The proteasomal inhibitor MG132 increased BCL11B expression in HTLV-1-infected cell lines, and colocalization of Tax with BCL11B was detected in the cytoplasm of HTLV-1-infected T-cells following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BAF chromatin remodeling complex subunit BCL11B	Homo sapiens	42-48
28946669-3	2017	Here, we observed that proteasome inhibitors, such as MG132 and bortezomib, in osteoclasts accelerated the degradation of c-Fms, a cognate receptor of macrophage colony-stimulating factor (M-CSF), and did not affect the amount of receptor activator of nuclear factor kappa-B (RANK), a receptor of receptor activator of nuclear factor kappa-B ligand (RANKL).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	colony stimulating factor 1 receptor	Mus musculus	122-127
28946669-3	2017	Here, we observed that proteasome inhibitors, such as MG132 and bortezomib, in osteoclasts accelerated the degradation of c-Fms, a cognate receptor of macrophage colony-stimulating factor (M-CSF), and did not affect the amount of receptor activator of nuclear factor kappa-B (RANK), a receptor of receptor activator of nuclear factor kappa-B ligand (RANKL).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	colony stimulating factor 1 (macrophage)	Mus musculus	189-194
28946669-3	2017	Here, we observed that proteasome inhibitors, such as MG132 and bortezomib, in osteoclasts accelerated the degradation of c-Fms, a cognate receptor of macrophage colony-stimulating factor (M-CSF), and did not affect the amount of receptor activator of nuclear factor kappa-B (RANK), a receptor of receptor activator of nuclear factor kappa-B ligand (RANKL).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	350-355
28870200-8	2017	In cyclin D1 degradation, we found that cyclin D1 downregulation by DKC-E70 was attenuated in presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	cyclin D1	Homo sapiens	3-12
28870200-8	2017	In cyclin D1 degradation, we found that cyclin D1 downregulation by DKC-E70 was attenuated in presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	cyclin D1	Homo sapiens	40-49
28870200-8	2017	In cyclin D1 degradation, we found that cyclin D1 downregulation by DKC-E70 was attenuated in presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	dyskerin pseudouridine synthase 1	Homo sapiens	68-71
28674081-5	2017	We found that the proteasome inhibitor MG132 induces progerin degradation through macroautophagy and strongly reduces progerin production through downregulation of SRSF-1 and SRSF-5 accumulation, controlling prelamin A mRNA aberrant splicing.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	serine and arginine rich splicing factor 1	Homo sapiens	164-170
28674081-5	2017	We found that the proteasome inhibitor MG132 induces progerin degradation through macroautophagy and strongly reduces progerin production through downregulation of SRSF-1 and SRSF-5 accumulation, controlling prelamin A mRNA aberrant splicing.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	serine and arginine rich splicing factor 5	Homo sapiens	175-181
28674081-7	2017	MG132 injection in skeletal muscle of LmnaG609G/G609G mice locally reduces SRSF-1 expression and progerin levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	serine and arginine-rich splicing factor 1	Mus musculus	75-81
28766684-3	2017	Tumor suppressor phosphatase and tensin homolog (PTEN) was found downregulated in NB4 cells and rescued by proteases inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	phosphatase and tensin homolog	Homo sapiens	49-53
28669733-5	2017	The proteasomal inhibitor MG132 increased BCL11B expression in HTLV-1-infected cell lines, and colocalization of Tax with BCL11B was detected in the cytoplasm of HTLV-1-infected T-cells following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BAF chromatin remodeling complex subunit BCL11B	Homo sapiens	122-128
28669733-5	2017	The proteasomal inhibitor MG132 increased BCL11B expression in HTLV-1-infected cell lines, and colocalization of Tax with BCL11B was detected in the cytoplasm of HTLV-1-infected T-cells following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	BAF chromatin remodeling complex subunit BCL11B	Homo sapiens	122-128
28613983-9	2017	AZM-mediated NOX4 reduction was restored by treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	NADPH oxidase 4	Homo sapiens	13-17
28955790-4	2017	According to the regulation of intrinsic ATF4 protein, stabilization of HiBiT-tagged ATF4 with a proteasome inhibitor, MG132, was observed by detecting luciferase activity in cell lysate and after SDS-PAGE and transfer onto a PVDF membrane.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	activating transcription factor 4	Mus musculus	41-45
28955790-4	2017	According to the regulation of intrinsic ATF4 protein, stabilization of HiBiT-tagged ATF4 with a proteasome inhibitor, MG132, was observed by detecting luciferase activity in cell lysate and after SDS-PAGE and transfer onto a PVDF membrane.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	activating transcription factor 4	Mus musculus	85-89
28806787-5	2017	Administration of MG132, a peptide aldehyde proteasome inhibitor, significantly increased the expression of heme oxygenase-1 (HO-1) in rat dopaminergic neurons in the substantia nigra and in the SH-SY5Y neuronal cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	heme oxygenase 1	Rattus norvegicus	108-124
28806787-5	2017	Administration of MG132, a peptide aldehyde proteasome inhibitor, significantly increased the expression of heme oxygenase-1 (HO-1) in rat dopaminergic neurons in the substantia nigra and in the SH-SY5Y neuronal cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	heme oxygenase 1	Rattus norvegicus	126-130
28806787-7	2017	MG132 increased the levels of HO-1 through the Akt, p38, and Nrf2 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heme oxygenase 1	Homo sapiens	30-34
28806787-7	2017	MG132 increased the levels of HO-1 through the Akt, p38, and Nrf2 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 14	Homo sapiens	52-55
28806787-7	2017	MG132 increased the levels of HO-1 through the Akt, p38, and Nrf2 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	NFE2 like bZIP transcription factor 2	Homo sapiens	61-65
28806787-9	2017	Furthermore, MG132-induced neuronal death was enhanced by the PINK1 G309D mutation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	PTEN induced kinase 1	Homo sapiens	62-67
28651835-6	2017	Further results showed that Andro induced the polyubiquitination of HIF-1alpha protein, and proteasome inhibitor MG132 reversed Andro-induced decrease in the expression of HIF-1alpha protein and VEGFA mRNA and protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	vascular endothelial growth factor A	Homo sapiens	195-200
28626006-9	2017	Subcellular localization and bimolecular fluorescence complementation experiments in the presence of MG132, a 26S proteasome inhibitor, showed that AtAIRP2 and ATP1/SDIRIP1 were colocalized to the cytosolic spherical body, which lies in close proximity to the nucleus, in tobacco (Nicotiana benthamiana) leaf cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	RING/U-box superfamily protein	Arabidopsis thaliana	148-155
28392346-7	2017	Inhibition of de novo protein synthesis and treatment of normal human primary epidermal melanocytes with proteasome inhibitor MG132 revealed that UCHL1 negatively regulates the stability of MITF by binding to the ubiquitinated protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	ubiquitin C-terminal hydrolase L1	Homo sapiens	146-151
28392346-7	2017	Inhibition of de novo protein synthesis and treatment of normal human primary epidermal melanocytes with proteasome inhibitor MG132 revealed that UCHL1 negatively regulates the stability of MITF by binding to the ubiquitinated protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	melanocyte inducing transcription factor	Homo sapiens	190-194
28626006-9	2017	Subcellular localization and bimolecular fluorescence complementation experiments in the presence of MG132, a 26S proteasome inhibitor, showed that AtAIRP2 and ATP1/SDIRIP1 were colocalized to the cytosolic spherical body, which lies in close proximity to the nucleus, in tobacco (Nicotiana benthamiana) leaf cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	ATPase subunit 1	Arabidopsis thaliana	160-164
28751541-5	2017	In cultured vascular smooth muscle cells (VSMCs), Cavin-1 was downregulated after inhibition of protein synthesis by cycloheximide, which was distinctly prevented by pretreatment with proteasome inhibitor MG132 but not by lysosomal inhibitor chloroquine, suggesting that proteasomal degradation resulted in Cavin-1 downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	205-210	caveolae associated protein 1	Homo sapiens	50-57
28369484-10	2017	These evidences suggest that NBS1 is regulated by two kind of mechanisms: complex formation dependent on ATM, and protein degradation mediated by an unknown MG132-resistant pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	157-162	nibrin	Homo sapiens	29-33
28738064-7	2017	Treatment with the proteasome inhibitor MG132 revealed that stable NSP3 dimers and monomers/dimerization intermediates are susceptible to proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	SH2 domain containing 3C	Homo sapiens	67-71
28769891-6	2017	We found that IAV downregulated the HDAC2 polypeptide level in A549 cells in an H1N1 strain-independent manner by up to 47%, which was recovered to almost 100% level in the presence of proteasome-inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	histone deacetylase 2	Homo sapiens	36-41
28676568-4	2017	Treatment with MG132, a proteasome inhibitor, also led to the accumulation of TRY, indicating that TRY proteolysis is mediated by the proteasome-dependent pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	Homeodomain-like superfamily protein	Arabidopsis thaliana	78-81
28676568-4	2017	Treatment with MG132, a proteasome inhibitor, also led to the accumulation of TRY, indicating that TRY proteolysis is mediated by the proteasome-dependent pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	Homeodomain-like superfamily protein	Arabidopsis thaliana	99-102
28485891-7	2017	Of interest was the finding that the degradation of catalase was rescued by MG132, a proteasome inhibitor, in the SNKD cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	catalase	Homo sapiens	52-60
28727885-9	2017	MG132-mediated aggresome formation upregulated ER stress sensors, the mitochondrial membrane potential drop, cytochrome c release to the cytoplasm, and activation of caspase-9 and -3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cytochrome c, somatic	Homo sapiens	109-121
28727885-9	2017	MG132-mediated aggresome formation upregulated ER stress sensors, the mitochondrial membrane potential drop, cytochrome c release to the cytoplasm, and activation of caspase-9 and -3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 9	Homo sapiens	166-182
28446729-7	2017	The administration of MG132, a proteasome inhibitor, or knockdown of ubiquitin-specific peptidase 9, X-linked (USP9X) both eliminated the effect of WP1130 in decreasing p53 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	tumor protein p53	Homo sapiens	169-172
28599312-5	2017	We found that the proteasome inhibitor MG132, or the Cullin-based E3 ligases inhibitor MLN4924, but not the autophagosome-lysosome inhibitor bafilomycin A1, stabilized endogenous HDAC6 protein in multiple cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	histone deacetylase 6	Homo sapiens	179-184
28363601-6	2017	Proteasome inhibition by MG132 exacerbated the effect of MGO on Trx1 and Glo2 degradation (18h), further suggesting a role for autophagy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	thioredoxin 1	Mus musculus	64-68
28363601-6	2017	Proteasome inhibition by MG132 exacerbated the effect of MGO on Trx1 and Glo2 degradation (18h), further suggesting a role for autophagy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	hydroxyacyl glutathione hydrolase	Mus musculus	73-77
28418925-9	2017	Treatment with MG132, a proteasome inhibitor, rescued the downregulation of ephrin-B2 and VEGFR2 signaling induced by syntenin knockdown.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	ephrin B2	Homo sapiens	76-85
28852398-4	2017	Our results showed that (1) conserved dopamine neurotrophic factor enhanced lactacystin/MG132-induced cell viability and morphology, and attenuated alpha-synuclein accumulation in differentiated PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	cerebral dopamine neurotrophic factor	Rattus norvegicus	28-66
28852398-5	2017	(2) Enzyme linked immunosorbent assay showed up-regulated 26S proteasomal activity in MG132-induced PC12 cells after pre- and posttreatment with conserved dopamine neurotrophic factor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	cerebral dopamine neurotrophic factor	Rattus norvegicus	145-183
28852398-7	2017	(3) With regard proteolytic enzymes (specifically, glutamyl peptide hydrolase, chymotrypsin, and trypsin), glutamyl peptide hydrolase activity was up-regulated in lactacystin/MG132-administered PC12 cells after pre- and posttreatment with conserved dopamine neurotrophic factor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-180	cerebral dopamine neurotrophic factor	Rattus norvegicus	239-277
28852398-8	2017	However, upregulation of chymotrypsin activity was only observed in MG132-administered PC12 cells pretreated with conserved dopamine neurotrophic factor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	cerebral dopamine neurotrophic factor	Rattus norvegicus	114-152
28652654-10	2017	Moreover, PLK inhibition decreases protein levels of Bcl-2; an effect that can be reversed by the proteasomal degradation inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-138	polo like kinase 1	Homo sapiens	10-13
28652654-10	2017	Moreover, PLK inhibition decreases protein levels of Bcl-2; an effect that can be reversed by the proteasomal degradation inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-138	BCL2 apoptosis regulator	Homo sapiens	53-58
28418925-9	2017	Treatment with MG132, a proteasome inhibitor, rescued the downregulation of ephrin-B2 and VEGFR2 signaling induced by syntenin knockdown.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	kinase insert domain receptor	Homo sapiens	90-96
28418925-9	2017	Treatment with MG132, a proteasome inhibitor, rescued the downregulation of ephrin-B2 and VEGFR2 signaling induced by syntenin knockdown.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	syndecan binding protein	Homo sapiens	118-126
28424976-0	2017	The Involvement of NR2B and tau Protein in MG132-Induced CREB Dephosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	19-23
28315668-6	2017	In addition, homocysteine (Hcy, a risk factor of CHD) treatment caused a decrease in cMyBP-C and an increase in KLHL3 expression, and the proteasome inhibitor MG132 reversed the Hcy-induced reduction of cMyBP-C expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	kelch like family member 3	Homo sapiens	112-117
28424976-0	2017	The Involvement of NR2B and tau Protein in MG132-Induced CREB Dephosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	cAMP responsive element binding protein 1	Homo sapiens	57-61
28424976-4	2017	The current study demonstrated that MG132-inhibited proteasome activity resulted in a dose dependence of CREB dephosphorylation at Ser133 as well as decreased phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunit NR2B (Tyr1472) and its tyrosine protein kinase Fyn (Tyr416).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	cAMP responsive element binding protein 1	Homo sapiens	105-109
28424976-4	2017	The current study demonstrated that MG132-inhibited proteasome activity resulted in a dose dependence of CREB dephosphorylation at Ser133 as well as decreased phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunit NR2B (Tyr1472) and its tyrosine protein kinase Fyn (Tyr416).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	223-227
28424976-4	2017	The current study demonstrated that MG132-inhibited proteasome activity resulted in a dose dependence of CREB dephosphorylation at Ser133 as well as decreased phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunit NR2B (Tyr1472) and its tyrosine protein kinase Fyn (Tyr416).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	270-273
29442024-5	2017	Inhibition of proteasomal degradation by MG132 blocked EA-AK0-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with MRB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cyclin D1	Homo sapiens	71-80
28593149-9	2017	Less expression of AR, but not NF-kappaB, was found in the TAC-MG132 group than in the TAC-cont group (p&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	androgen receptor	Rattus norvegicus	19-21
28593149-10	2017	CONCLUSION: MG-132 was found to suppress AR in the TAC-CMP model by blocking the UPS, which reduced fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-18	androgen receptor	Rattus norvegicus	41-43
28235656-4	2017	And treatment with CFTRinh-172, a CFTR inhibitor, reduced the expression of HDAC2 protein in K562 and SUP-B15 cells, which could be partially recovered by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	CF transmembrane conductance regulator	Homo sapiens	19-23
28235656-4	2017	And treatment with CFTRinh-172, a CFTR inhibitor, reduced the expression of HDAC2 protein in K562 and SUP-B15 cells, which could be partially recovered by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	histone deacetylase 2	Homo sapiens	76-81
28588709-10	2017	Importantly, MG132-induced proteasome blockade prevented degradation of RGS4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	regulator of G protein signaling 4	Homo sapiens	72-76
28915612-2	2017	It was found that ING5 overexpression suppressed proliferation, energy metabolism, migration, invasion, and induced G2/M arrest, apoptosis, dedifferentiation, senescence, mesenchymal- epithelial transition and chemoresistance to cisplatin, MG132, paclitaxel and SAHA in U87 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-245	inhibitor of growth family, member 5	Mus musculus	18-22
28881798-7	2017	AKAP4 knockdown lead to degradation of protien kinase A (PKA) which was rescued by proteosome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-110	LOC102642117	Mus musculus	0-5
27752740-7	2017	A 6-h incubation with the proteasome inhibitor MG-132 fully rescued vimentin from AHR-mediated proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	vimentin	Homo sapiens	68-76
27752740-7	2017	A 6-h incubation with the proteasome inhibitor MG-132 fully rescued vimentin from AHR-mediated proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	aryl hydrocarbon receptor	Homo sapiens	82-85
28186089-10	2017	Importantly, glycogen synthase kinase-3beta (GSK-3beta) inhibitor VIII and 26S proteasome inhibitor MG132 assays revealed that TIPE2 downregulated Snail1 and Snail2/Slug in a GSK-3beta- and proteasome-dependent manner possibly by impairing AKT signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	TNF alpha induced protein 8 like 2	Homo sapiens	127-132
28407860-3	2017	The ZGA of SCNT embryos at 2- and 4-cell stages was also enhanced by MG132 treatment through altering the RNA pol II status and increasing the expression of eIF3A and TFIIA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	eukaryotic translation initiation factor 3 subunit A	Homo sapiens	157-162
28407860-3	2017	The ZGA of SCNT embryos at 2- and 4-cell stages was also enhanced by MG132 treatment through altering the RNA pol II status and increasing the expression of eIF3A and TFIIA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	general transcription factor IIA subunit 1	Homo sapiens	167-172
28407860-5	2017	Expression of BCL-2, OCT4, NANOG and CDX2 in SCNT blastocysts developed from SCNT embryos and oocytes treated with MG132 was increased significantly (P &lt; 0.01), while the expression of pro-apoptotic BAX gene was suppressed significantly (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	BCL2 apoptosis regulator	Homo sapiens	14-19
28407860-5	2017	Expression of BCL-2, OCT4, NANOG and CDX2 in SCNT blastocysts developed from SCNT embryos and oocytes treated with MG132 was increased significantly (P &lt; 0.01), while the expression of pro-apoptotic BAX gene was suppressed significantly (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	POU class 5 homeobox 1	Homo sapiens	21-25
28407860-5	2017	Expression of BCL-2, OCT4, NANOG and CDX2 in SCNT blastocysts developed from SCNT embryos and oocytes treated with MG132 was increased significantly (P &lt; 0.01), while the expression of pro-apoptotic BAX gene was suppressed significantly (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	Nanog homeobox	Homo sapiens	27-32
28407860-5	2017	Expression of BCL-2, OCT4, NANOG and CDX2 in SCNT blastocysts developed from SCNT embryos and oocytes treated with MG132 was increased significantly (P &lt; 0.01), while the expression of pro-apoptotic BAX gene was suppressed significantly (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	caudal type homeobox 2	Homo sapiens	37-41
28407860-5	2017	Expression of BCL-2, OCT4, NANOG and CDX2 in SCNT blastocysts developed from SCNT embryos and oocytes treated with MG132 was increased significantly (P &lt; 0.01), while the expression of pro-apoptotic BAX gene was suppressed significantly (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	BCL2 associated X, apoptosis regulator	Homo sapiens	202-205
28407860-6	2017	In addition, MG132 treatment not only affected the expression patterns of H3K9 acetylation, H3K4 and H3K9 trimethylation, but also regulated the relative expression of SMYD3, ASH2L, KDM5B, HAT1, HDAC1 and HDAC2 of Debao porcine SCNT embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	SET and MYND domain containing 3	Homo sapiens	168-173
28407860-6	2017	In addition, MG132 treatment not only affected the expression patterns of H3K9 acetylation, H3K4 and H3K9 trimethylation, but also regulated the relative expression of SMYD3, ASH2L, KDM5B, HAT1, HDAC1 and HDAC2 of Debao porcine SCNT embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	ASH2 like, histone lysine methyltransferase complex subunit	Homo sapiens	175-180
28407860-6	2017	In addition, MG132 treatment not only affected the expression patterns of H3K9 acetylation, H3K4 and H3K9 trimethylation, but also regulated the relative expression of SMYD3, ASH2L, KDM5B, HAT1, HDAC1 and HDAC2 of Debao porcine SCNT embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	lysine demethylase 5B	Homo sapiens	182-187
28407860-6	2017	In addition, MG132 treatment not only affected the expression patterns of H3K9 acetylation, H3K4 and H3K9 trimethylation, but also regulated the relative expression of SMYD3, ASH2L, KDM5B, HAT1, HDAC1 and HDAC2 of Debao porcine SCNT embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	histone acetyltransferase 1	Homo sapiens	189-193
28407860-6	2017	In addition, MG132 treatment not only affected the expression patterns of H3K9 acetylation, H3K4 and H3K9 trimethylation, but also regulated the relative expression of SMYD3, ASH2L, KDM5B, HAT1, HDAC1 and HDAC2 of Debao porcine SCNT embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	histone deacetylase 1	Homo sapiens	195-200
28407860-6	2017	In addition, MG132 treatment not only affected the expression patterns of H3K9 acetylation, H3K4 and H3K9 trimethylation, but also regulated the relative expression of SMYD3, ASH2L, KDM5B, HAT1, HDAC1 and HDAC2 of Debao porcine SCNT embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	histone deacetylase 2	Homo sapiens	205-210
28404547-5	2017	Furthermore, cells were co-transfected with miR-320a and PBX3 expressing vector, or cells were transfected with miR-320a and treated with a nuclear factor kappa B (NF-kappaB) antagonist MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	186-191	nuclear factor kappa B subunit 1	Homo sapiens	140-162
28404547-5	2017	Furthermore, cells were co-transfected with miR-320a and PBX3 expressing vector, or cells were transfected with miR-320a and treated with a nuclear factor kappa B (NF-kappaB) antagonist MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	186-191	nuclear factor kappa B subunit 1	Homo sapiens	164-173
28404547-11	2017	PBX3 and MG132 co-transfection attenuated the effects of miR-320a on the expression of Col2alpha1, ACAN, sGAG and MMP-13(p &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	microRNA 320a	Homo sapiens	57-65
28404547-11	2017	PBX3 and MG132 co-transfection attenuated the effects of miR-320a on the expression of Col2alpha1, ACAN, sGAG and MMP-13(p &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	aggrecan	Homo sapiens	99-103
28404547-11	2017	PBX3 and MG132 co-transfection attenuated the effects of miR-320a on the expression of Col2alpha1, ACAN, sGAG and MMP-13(p &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	matrix metallopeptidase 13	Homo sapiens	114-120
28142215-7	2017	In particular, although STAT-1-dependent IDO expression is transcriptionally induced at a similar level in senescent and nonsenescent MSCs, IDO protein is specifically degraded by the proteasome in senescent ASCs and BM-MSCs, a process that could be reversed by the MG132 proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	266-271	indoleamine 2,3-dioxygenase 1	Homo sapiens	140-143
28052875-8	2017	Moreover, LXR activation-induced AQP2 protein expression was abolished by the protease inhibitor MG132 and the ubiquitination-deficient AQP2 (K270R).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	nuclear receptor subfamily 1, group H, member 2	Mus musculus	10-13
28052875-8	2017	Moreover, LXR activation-induced AQP2 protein expression was abolished by the protease inhibitor MG132 and the ubiquitination-deficient AQP2 (K270R).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	aquaporin 2	Mus musculus	33-37
28220348-0	2017	Proteasome inhibitor MG132 induces thyroid cancer cell apoptosis by modulating the activity of transcription factor FOXO3a.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	forkhead box O3	Homo sapiens	116-122
28220348-6	2017	Using flow cytometry, western blot, immunofluorescence staining and quantitative RT-PCR assays, we assessed proteasome inhibitor MG132-induced apoptosis in thyroid cancer cells and its effect on the expression and activity of forkhead Box O3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	forkhead box O3	Homo sapiens	226-241
28237621-10	2017	Finally, treatment of IMR-90 cells with MG-132 abrogated the reduction in XPC protein, suggesting an involvement of the proteasome in the reduction of XPC protein produced by treatment of cells with arsenic.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	74-77
28237621-10	2017	Finally, treatment of IMR-90 cells with MG-132 abrogated the reduction in XPC protein, suggesting an involvement of the proteasome in the reduction of XPC protein produced by treatment of cells with arsenic.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	151-154
28323983-8	2017	Mechanistic studies revealed that the reduction in COL1A1 but not COL1A2 protein by cortisol was blocked by lysosome inhibitor chloroquine or small interfering RNA (siRNA)-mediated knockdown of autophagy-related protein 7, an essential protein for autophagy, whereas the proteasome inhibitors MG132 and bortezomib were ineffective.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	293-298	collagen type I alpha 1 chain	Homo sapiens	51-57
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	93-96
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	113-116
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	113-116
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	113-116
28220348-8	2017	Strikingly, upon MG132 administration, the accumulation and nuclear translocation of transcription factor forkhead Box O3 as well as transcriptional upregulation of its proapoptotic target genes were found in thyroid cancer cells regardless of p53 status.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	forkhead box O3	Homo sapiens	106-121
28220348-10	2017	Altogether, we demonstrated that proteasome inhibitor MG132 induces thyroid cancer cell apoptosis at least partially through modulating forkhead Box O3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	forkhead box O3	Homo sapiens	136-151
27813153-8	2017	Crucially, ICT promoted proteasomal degradation of TRAF6, the critical adaptor protein that transduces RANKL/RANK signaling, and the inhibitory effect of ICT on osteoclastogenesis was reversed by the proteasomal inhibitor MG 132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-228	TNF receptor associated factor 6	Rattus norvegicus	51-56
28359145-6	2017	Moreover, we found that MG132-induced toxicity involving proteasome inhibition was also ameliorated by PTP1B inhibition in a human neuroblastoma cell line and mouse primary cortical neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	103-108
28359145-7	2017	Consistently, downregulation of the PTP1B homologue gene in Drosophila mitigated rotenone- and MG132-induced toxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	Protein tyrosine phosphatase 61F	Drosophila melanogaster	36-41
28301598-8	2017	Downregulation of Mcl-1 by S6K2 knockdown was partly restored by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	18-23
27993609-8	2017	The downregulation of p53 levels induced by CPF was partially blocked when cells were exposed to CPF in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	tumor protein p53	Homo sapiens	22-25
28189672-9	2017	Accordingly, MG132, an inhibitor of proteasomal degradation, reversed the effect of VA on HO-1 suggesting that decrease in HO-1 expression by VA is through protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	heme oxygenase 1	Mus musculus	90-94
28189672-9	2017	Accordingly, MG132, an inhibitor of proteasomal degradation, reversed the effect of VA on HO-1 suggesting that decrease in HO-1 expression by VA is through protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	heme oxygenase 1	Mus musculus	123-127
28322298-5	2017	Moreover, H2S and miR-455-3p could no longer increase the protein level of eNOS in the presence of proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	nitric oxide synthase 3	Homo sapiens	75-79
28301598-8	2017	Downregulation of Mcl-1 by S6K2 knockdown was partly restored by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	ribosomal protein S6 kinase B2	Homo sapiens	27-31
28407690-2	2017	After treated with cisplatin, MG132, paclitaxel and SAHA, BTG3 transfectants exhibited lower viability and higher apoptosis than the control in both time- and dose-dependent manners.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	BTG anti-proliferation factor 3	Homo sapiens	58-62
28212825-11	2017	Treatment of PAH model with MG-132 or bortezomib increased PTEN expression and accumulation of ubiquitinated-PTEN protein and decreased Akt phosphorylation, while didn"t change NEDD4 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	phosphatase and tensin homolog	Rattus norvegicus	59-63
28212825-11	2017	Treatment of PAH model with MG-132 or bortezomib increased PTEN expression and accumulation of ubiquitinated-PTEN protein and decreased Akt phosphorylation, while didn"t change NEDD4 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	phosphatase and tensin homolog	Rattus norvegicus	109-113
28212825-11	2017	Treatment of PAH model with MG-132 or bortezomib increased PTEN expression and accumulation of ubiquitinated-PTEN protein and decreased Akt phosphorylation, while didn"t change NEDD4 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	AKT serine/threonine kinase 1	Rattus norvegicus	136-139
28283022-12	2017	Co-expression of GFP-WR with TWIST1 and RELA led to proteasomal degradation of TWIST1, which could be inhibited by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	twist family bHLH transcription factor 1	Homo sapiens	29-35
28283022-12	2017	Co-expression of GFP-WR with TWIST1 and RELA led to proteasomal degradation of TWIST1, which could be inhibited by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	RELA proto-oncogene, NF-kB subunit	Homo sapiens	40-44
28283022-12	2017	Co-expression of GFP-WR with TWIST1 and RELA led to proteasomal degradation of TWIST1, which could be inhibited by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	twist family bHLH transcription factor 1	Homo sapiens	79-85
28087276-6	2017	Finally, AGO2 protein levels increase after treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	Argonaute 2	Drosophila melanogaster	9-13
27813087-7	2017	As expected the block of EGFR degradation, by exposure to the proteasome inhibitor MG132, significantly reduced iPA-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	epidermal growth factor receptor	Homo sapiens	25-29
27932549-16	2017	Inhibition of the proteasome with MG132 prevented HSPA2 degradation after 4HNE treatment indicating that the degradation of HSPA2 is likely to occur via a proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	heat shock protein 2	Mus musculus	50-55
27932549-16	2017	Inhibition of the proteasome with MG132 prevented HSPA2 degradation after 4HNE treatment indicating that the degradation of HSPA2 is likely to occur via a proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	heat shock protein 2	Mus musculus	124-129
28073696-2	2017	Here we report that SPOP binds to SIRT2 and mediates its degradation by the 26S proteasome, which can be blocked by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	speckle type BTB/POZ protein	Homo sapiens	20-24
28073696-2	2017	Here we report that SPOP binds to SIRT2 and mediates its degradation by the 26S proteasome, which can be blocked by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	sirtuin 2	Homo sapiens	34-39
28009721-8	2017	In contrast, MG132, a proteasome inhibitor, could significantly restore SI/R-induced Cav-3 decrease.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	caveolin 3	Rattus norvegicus	85-90
28196083-7	2017	The gastrin induced reduction in p27kip1 was prevented when cells were treated with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	gastrin	Homo sapiens	4-11
28196083-7	2017	The gastrin induced reduction in p27kip1 was prevented when cells were treated with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	cyclin dependent kinase inhibitor 1B	Homo sapiens	33-40
28196122-8	2017	Conversely, stabilization of ELAVL-1/HuR with the proteasome inhibitor MG-132 resulted in induction of GSK3beta at mRNA and protein level and attenuated FITC-albumin clearance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-77	ELAV like RNA binding protein 1	Homo sapiens	29-36
28196122-8	2017	Conversely, stabilization of ELAVL-1/HuR with the proteasome inhibitor MG-132 resulted in induction of GSK3beta at mRNA and protein level and attenuated FITC-albumin clearance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-77	ELAV like RNA binding protein 1	Homo sapiens	37-40
28196122-8	2017	Conversely, stabilization of ELAVL-1/HuR with the proteasome inhibitor MG-132 resulted in induction of GSK3beta at mRNA and protein level and attenuated FITC-albumin clearance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-77	glycogen synthase kinase 3 beta	Homo sapiens	103-111
28143565-15	2017	CMY-BR and CMK-BR cells were cross-resistant to CFZ and MG-132 but sensitive to DSF/Cu2+.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-62	C-X-C motif chemokine ligand 9	Homo sapiens	11-14
27447746-7	2017	The chemosensitivity of BTG1 transfectants to paclitaxel, cisplatin, MG132 or SAHA was positively correlated with its apoptotic induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	BTG anti-proliferation factor 1	Mus musculus	24-28
28035387-9	2017	When siSTAT3 and MG132 treatment was combined, levels of collagen I, MMP-1 and MMP-13 were reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	matrix metallopeptidase 1	Homo sapiens	69-74
28035387-9	2017	When siSTAT3 and MG132 treatment was combined, levels of collagen I, MMP-1 and MMP-13 were reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	matrix metallopeptidase 13	Homo sapiens	79-85
28456147-12	2017	Intriguingly, simultaneous treatment with MG-132, a 26S proteasomal inhibitor, recovered the ethanol-induced increase of TH protein expression and dopamine biosynthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	tyrosine hydroxylase	Homo sapiens	121-123
28122580-5	2017	However, addition of the proteasome inhibitor MG132 did result in significant restoration of Tat expression, indicating that the compounds are affecting Tat synthesis and/or degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	tyrosine aminotransferase	Homo sapiens	93-96
28122580-5	2017	However, addition of the proteasome inhibitor MG132 did result in significant restoration of Tat expression, indicating that the compounds are affecting Tat synthesis and/or degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	tyrosine aminotransferase	Homo sapiens	153-156
28114332-6	2017	The levels of TC-CPE were significantly increased after the N2A cells were treated with MG132 (a proteasome inhibitor), suggesting that TC-CPE was targeted to proteasomes for degradation in N2A cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	carboxypeptidase E	Homo sapiens	17-20
28114332-6	2017	The levels of TC-CPE were significantly increased after the N2A cells were treated with MG132 (a proteasome inhibitor), suggesting that TC-CPE was targeted to proteasomes for degradation in N2A cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	carboxypeptidase E	Homo sapiens	139-142
28114332-8	2017	Double labeling of CPE and calnexin (and ER marker) suggested the accumulation of TC-CPE in the ER, and the accumulation appears to be enhanced by the treatment of MG132 in the cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	carboxypeptidase E	Homo sapiens	19-22
28114332-8	2017	Double labeling of CPE and calnexin (and ER marker) suggested the accumulation of TC-CPE in the ER, and the accumulation appears to be enhanced by the treatment of MG132 in the cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	calnexin	Homo sapiens	27-35
28114332-8	2017	Double labeling of CPE and calnexin (and ER marker) suggested the accumulation of TC-CPE in the ER, and the accumulation appears to be enhanced by the treatment of MG132 in the cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	carboxypeptidase E	Homo sapiens	85-88
28086832-9	2017	Moreover, EGFR expression could be mostly restored by co-treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	epidermal growth factor receptor	Homo sapiens	10-14
28079886-6	2017	Interestingly, HIV-1 Nef release in EVs was enriched significantly when the cells were treated with autophagy activators perifosine, tomaxifen, MG-132, and autophagy inhibitors LY294002 and wortmannin suggesting a novel role of autophagy signaling in HIV-1 Nef release from astrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-150	Nef	Human immunodeficiency virus 1	21-24
27901482-7	2017	HG-triggered HIPK2 protein downregulation was rescued by both proteasome inhibitor MG132 and by protein phosphatase inhibitors Calyculin A (CL-A) and Okadaic Acid (OA).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	homeodomain interacting protein kinase 2	Homo sapiens	13-18
27888613-7	2017	Similarly, pharmaceutical inhibition of proteasome with MG132 would mimic the PSMC2 depletion induced defects in cell cycle arrest, apoptosis and colonies formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	proteasome 26S subunit, ATPase 2	Homo sapiens	78-83
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	tumor protein p53	Homo sapiens	92-95
27766434-0	2017	MG132 plus apoptosis antigen-1 (APO-1) antibody cooperate to restore p53 activity inducing autophagy and p53-dependent apoptosis in HPV16 E6-expressing keratinocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	69-72
27766434-0	2017	MG132 plus apoptosis antigen-1 (APO-1) antibody cooperate to restore p53 activity inducing autophagy and p53-dependent apoptosis in HPV16 E6-expressing keratinocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	105-108
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	tumor protein p53	Homo sapiens	92-95
27766434-3	2017	We investigated whether in HPV16 E6-expressing keratinocytes (KE6 cells), the restoration of p53 levels mediated by MG132 and/or activation of the CD95 pathway through apoptosis antigen-1 (APO-1) antibody are responsible for the induction of apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	tumor protein p53	Homo sapiens	93-96
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	tumor protein p53	Homo sapiens	26-29
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	26-29
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	tumor protein p53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	Fas cell surface death receptor	Homo sapiens	233-238
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	tumor protein p53	Homo sapiens	26-29
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	tumor protein p53	Homo sapiens	92-95
28278502-14	2017	By blocking proteasome with MG132, we observed that Kae induced an increased ubiquitination of DNMT3B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	DNA methyltransferase 3B	Mus musculus	95-101
28381809-8	2017	This coumestrol-induced reduction in tyrosinase protein levels was prevented by pretreatment with the proteasome inhibitor MG-132 or the lysosomal proteolysis inhibitor chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	tyrosinase	Mus musculus	37-47
27550925-6	2017	The addition of MG-132, a proteasome inhibitor, shows increased ubiquitination of Int3 in the presence of Gleevec.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	notch 4	Mus musculus	82-86
28419994-13	2017	Proteasome inhibitor MG132 markedly prevented the degradation of Mcl-1 and blocked bufalin-induced Mcl-1 reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	65-70
28419994-13	2017	Proteasome inhibitor MG132 markedly prevented the degradation of Mcl-1 and blocked bufalin-induced Mcl-1 reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	99-104
28625142-11	2017	MG132 significantly suppressed TGFbeta-induced upregulation of alpha-SMA, fibronectin, and vimentin, as well as TGFbeta-induced cell migration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor beta 1	Homo sapiens	31-38
28625142-11	2017	MG132 significantly suppressed TGFbeta-induced upregulation of alpha-SMA, fibronectin, and vimentin, as well as TGFbeta-induced cell migration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	fibronectin 1	Homo sapiens	74-85
28625142-11	2017	MG132 significantly suppressed TGFbeta-induced upregulation of alpha-SMA, fibronectin, and vimentin, as well as TGFbeta-induced cell migration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	vimentin	Homo sapiens	91-99
28625142-11	2017	MG132 significantly suppressed TGFbeta-induced upregulation of alpha-SMA, fibronectin, and vimentin, as well as TGFbeta-induced cell migration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor beta 1	Homo sapiens	112-119
28625142-12	2017	The phosphorylation levels of Smad2, ERK1/2, and FAK were also suppressed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	SMAD family member 2	Homo sapiens	30-35
28625142-12	2017	The phosphorylation levels of Smad2, ERK1/2, and FAK were also suppressed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	mitogen-activated protein kinase 3	Homo sapiens	37-43
28625142-12	2017	The phosphorylation levels of Smad2, ERK1/2, and FAK were also suppressed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	protein tyrosine kinase 2	Homo sapiens	49-52
28625142-13	2017	Additionally, the mRNA level and protein level of TGFbetaR-II decreased upon MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	transforming growth factor beta receptor 2	Homo sapiens	50-61
27862841-5	2017	Treatment with MG-132 resulted in robust detection of ILEI in the PCS-440-010, PC3 and DU145 cell lines, suggesting that at least in these cell lines, ILEI is actively degraded by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	FAM3 metabolism regulating signaling molecule C	Homo sapiens	54-58
29225318-7	2017	We observed that a proteasome inhibitor, MG132, inhibited CCM-caused down-expression of C/EBPbeta and C/EBPdelta proteins, and that CCM promoted the ubiquitination level of C/EBPbeta and C/EBPdelta proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	CCAAT enhancer binding protein beta	Homo sapiens	88-97
29225318-7	2017	We observed that a proteasome inhibitor, MG132, inhibited CCM-caused down-expression of C/EBPbeta and C/EBPdelta proteins, and that CCM promoted the ubiquitination level of C/EBPbeta and C/EBPdelta proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	CCAAT enhancer binding protein delta	Homo sapiens	102-112
29225318-7	2017	We observed that a proteasome inhibitor, MG132, inhibited CCM-caused down-expression of C/EBPbeta and C/EBPdelta proteins, and that CCM promoted the ubiquitination level of C/EBPbeta and C/EBPdelta proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	CCAAT enhancer binding protein beta	Homo sapiens	173-182
29225318-7	2017	We observed that a proteasome inhibitor, MG132, inhibited CCM-caused down-expression of C/EBPbeta and C/EBPdelta proteins, and that CCM promoted the ubiquitination level of C/EBPbeta and C/EBPdelta proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	CCAAT enhancer binding protein delta	Homo sapiens	187-197
27035356-0	2017	MG132 Induces Expression of Monocyte Chemotactic Protein-Induced Protein 1 in Vascular Smooth Muscle Cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	zinc finger CCCH-type containing 12A	Homo sapiens	28-74
27035356-2	2017	Therefore, we predict that in vascular smooth muscle (VSMCs), MCPIP1 may be induced by MCP-1 and undergo degradation, which can be inhibited by the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	zinc finger CCCH-type containing 12A	Homo sapiens	62-68
27035356-2	2017	Therefore, we predict that in vascular smooth muscle (VSMCs), MCPIP1 may be induced by MCP-1 and undergo degradation, which can be inhibited by the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	C-C motif chemokine ligand 2	Homo sapiens	87-92
27035356-4	2017	Treatment with MG132, however, elevated MCPIP1 protein levels through stimulation of the gene transcription, but not through increasing protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	zinc finger CCCH-type containing 12A	Homo sapiens	40-46
27035356-5	2017	MCPIP1 expression induced by MG132 was inhibited by alpha-amanitin inhibition of gene transcription or cycloheximide inhibition of protein synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	zinc finger CCCH-type containing 12A	Homo sapiens	0-6
27035356-6	2017	Our further studies showed that MCPIP1 expression induced by MG132 was inhibited by the inhibitors of AKT and p38 kinase, suggesting a role of the AKT-p38 pathway in MG132 effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	zinc finger CCCH-type containing 12A	Homo sapiens	32-38
27035356-6	2017	Our further studies showed that MCPIP1 expression induced by MG132 was inhibited by the inhibitors of AKT and p38 kinase, suggesting a role of the AKT-p38 pathway in MG132 effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	zinc finger CCCH-type containing 12A	Homo sapiens	32-38
27035356-8	2017	In summary, MCPIP1 expression is induced by MG132 likely through activation of the AKT-p38 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	zinc finger CCCH-type containing 12A	Homo sapiens	12-18
27862841-5	2017	Treatment with MG-132 resulted in robust detection of ILEI in the PCS-440-010, PC3 and DU145 cell lines, suggesting that at least in these cell lines, ILEI is actively degraded by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	proprotein convertase subtilisin/kexin type 1	Homo sapiens	79-82
27862841-5	2017	Treatment with MG-132 resulted in robust detection of ILEI in the PCS-440-010, PC3 and DU145 cell lines, suggesting that at least in these cell lines, ILEI is actively degraded by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	FAM3 metabolism regulating signaling molecule C	Homo sapiens	151-155
27862841-6	2017	Mass spectrometric analysis of FLAG immunoprecipitates of untreated and MG-132 treated FLAG-ILEI transfected cells indicated that UBE4A and UBE3C ubiquitin ligases were interacting with ILEI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	FAM3 metabolism regulating signaling molecule C	Homo sapiens	92-96
27862841-6	2017	Mass spectrometric analysis of FLAG immunoprecipitates of untreated and MG-132 treated FLAG-ILEI transfected cells indicated that UBE4A and UBE3C ubiquitin ligases were interacting with ILEI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	ubiquitination factor E4A	Homo sapiens	130-135
27862841-6	2017	Mass spectrometric analysis of FLAG immunoprecipitates of untreated and MG-132 treated FLAG-ILEI transfected cells indicated that UBE4A and UBE3C ubiquitin ligases were interacting with ILEI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	ubiquitin protein ligase E3C	Homo sapiens	140-145
27862841-6	2017	Mass spectrometric analysis of FLAG immunoprecipitates of untreated and MG-132 treated FLAG-ILEI transfected cells indicated that UBE4A and UBE3C ubiquitin ligases were interacting with ILEI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	FAM3 metabolism regulating signaling molecule C	Homo sapiens	186-190
27821720-7	2017	Treatment of the glk1glk2 mutant expressing functional GFP-GLK1 with a proteasome inhibitor, MG-132, induced the accumulation of polyubiquitinated GFP-GLK1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	GBF's pro-rich region-interacting factor 1	Arabidopsis thaliana	17-25
28373900-1	2017	Our previous study showed that proteasomal inhibitor MG132 can prevent diabetic nephropathy (DN) along with upregulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	nuclear factor, erythroid derived 2, like 2	Mus musculus	169-173
28373900-2	2017	The present study was to investigate whether MG132 can prevent DN in wild-type and Nrf2-KO mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	nuclear factor, erythroid derived 2, like 2	Mus musculus	83-87
28373900-9	2017	Deletion of Nrf2 gene resulted in a partial, but significant attenuation of MG132 renal protection in Nrf2-KO mice compared with wild-type mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	nuclear factor, erythroid derived 2, like 2	Mus musculus	12-16
28373900-9	2017	Deletion of Nrf2 gene resulted in a partial, but significant attenuation of MG132 renal protection in Nrf2-KO mice compared with wild-type mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	nuclear factor, erythroid derived 2, like 2	Mus musculus	102-106
28373900-11	2017	This work indicates that MG132 inhibits diabetes-increased proteasomal activity, resulting in Nrf2 and IkappaB upregulation and renal protection, which could be used as a strategy to prevent diabetic nephropathy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	nuclear factor, erythroid derived 2, like 2	Mus musculus	94-98
27659495-9	2017	In addition, the proteasome inhibitor MG132 treatment could actually increase the accumulation levels of CAT3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	solute carrier family 7 member 3	Homo sapiens	105-109
27821720-8	2017	Furthermore, the level of endogenous GLK1 in plants with damaged plastids was partially restored when those plants were treated with MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-139	GBF's pro-rich region-interacting factor 1	Arabidopsis thaliana	37-41
27821720-7	2017	Treatment of the glk1glk2 mutant expressing functional GFP-GLK1 with a proteasome inhibitor, MG-132, induced the accumulation of polyubiquitinated GFP-GLK1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	GBF's pro-rich region-interacting factor 1	Arabidopsis thaliana	55-63
27821720-7	2017	Treatment of the glk1glk2 mutant expressing functional GFP-GLK1 with a proteasome inhibitor, MG-132, induced the accumulation of polyubiquitinated GFP-GLK1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	GBF's pro-rich region-interacting factor 1	Arabidopsis thaliana	59-63
27852045-8	2016	The proteasome inhibitor MG132 or the pan-caspase inhibitor z-VAD-fmk extended BCR/Abl expression under oxygen/glucose shortage in K562 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
28035994-7	2016	Mechanistically, pre-treatment with the proteasome inhibitor MG-132 restored cyclin D1 levels in all obatoclax-treated cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	cyclin D1	Homo sapiens	77-86
27973439-6	2016	The specific proteasome inhibitor MG132 suppressed VDR agonist-induced decreases in KCa1.1 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	vitamin D receptor	Homo sapiens	51-54
27973439-6	2016	The specific proteasome inhibitor MG132 suppressed VDR agonist-induced decreases in KCa1.1 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	potassium calcium-activated channel subfamily M alpha 1	Homo sapiens	84-90
27521959-9	2016	In IS adipocyte, chemical activation of PP2A through MG132 and FTY720 showed decreased insulin sensitivity corroborated with decreased Akt phosphorylation and glucose uptake.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	40-44
27983599-8	2016	The half-life of administrated rhalpha-GLA was around 24 h in GLA-null cells; co-administration of proteasome inhibitor MG132 and rhalpha-GLA significantly restored the GLA enzyme activity by two-fold compared with rhalpha-GLA alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	galactosidase alpha	Homo sapiens	39-42
27983599-8	2016	The half-life of administrated rhalpha-GLA was around 24 h in GLA-null cells; co-administration of proteasome inhibitor MG132 and rhalpha-GLA significantly restored the GLA enzyme activity by two-fold compared with rhalpha-GLA alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	galactosidase alpha	Homo sapiens	62-65
27983599-8	2016	The half-life of administrated rhalpha-GLA was around 24 h in GLA-null cells; co-administration of proteasome inhibitor MG132 and rhalpha-GLA significantly restored the GLA enzyme activity by two-fold compared with rhalpha-GLA alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	galactosidase alpha	Homo sapiens	62-65
27983599-8	2016	The half-life of administrated rhalpha-GLA was around 24 h in GLA-null cells; co-administration of proteasome inhibitor MG132 and rhalpha-GLA significantly restored the GLA enzyme activity by two-fold compared with rhalpha-GLA alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	galactosidase alpha	Homo sapiens	62-65
27983599-8	2016	The half-life of administrated rhalpha-GLA was around 24 h in GLA-null cells; co-administration of proteasome inhibitor MG132 and rhalpha-GLA significantly restored the GLA enzyme activity by two-fold compared with rhalpha-GLA alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	galactosidase alpha	Homo sapiens	62-65
27983599-9	2016	Furthermore, co-treatment of rhalpha-GLA/MG132 in patient-derived fibroblasts increased Gb3 clearance by 30%, compared with rhalpha-GLA treatment alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	88-91
27983599-11	2016	Using this model, we demonstrated that MG132 prolongs rhalpha-GLA half-life and enhanced Gb3 clearance, shedding light on the direction of enhancing ERT efficacy in FD treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	galactosidase alpha	Homo sapiens	62-65
27983599-11	2016	Using this model, we demonstrated that MG132 prolongs rhalpha-GLA half-life and enhanced Gb3 clearance, shedding light on the direction of enhancing ERT efficacy in FD treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	89-92
27521959-9	2016	In IS adipocyte, chemical activation of PP2A through MG132 and FTY720 showed decreased insulin sensitivity corroborated with decreased Akt phosphorylation and glucose uptake.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	thymoma viral proto-oncogene 1	Mus musculus	135-138
26756900-6	2016	Nutlin-3alpha or MG132 abolished the suppressive effect of a COX-2 inhibitor on DOX-induced p53 increase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	prostaglandin-endoperoxide synthase 2	Homo sapiens	61-66
27611480-11	2016	The proteasomal inhibitor MG-132 caused p53 protein to increase, but it had no effect on cyclin E2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	tumor protein p53	Homo sapiens	40-43
26756900-6	2016	Nutlin-3alpha or MG132 abolished the suppressive effect of a COX-2 inhibitor on DOX-induced p53 increase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	tumor protein p53	Homo sapiens	92-95
27638906-2	2016	The proteasome inhibitor MG132 or surfactant protein C (SP-C) BRICHOS domain mutation G100S induced apoptosis in human AECs by activating the proapoptotic cathepsin D and reducing antiapoptotic angiotensin converting enzyme-2 (ACE-2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cathepsin D	Homo sapiens	155-166
27568838-4	2016	MG-132 pretreatment led to the increased expression of autophagy-related genes, ER stress-associated genes and IkappaB but decreased the expression levels of NF-kappaB and caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 3	Rattus norvegicus	172-181
27875574-6	2016	Treatment with MG132, a proteasome inhibitor reduced Mcl-1 degradation stimulated by chidamide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	53-58
27638906-5	2016	The results showed that either MG132 or G100S SP-C mutation activated all three canonical pathways of the UPR (IRE1/XBP1, ATF6, and PERK/eIF2alpha), which led to a significant increase in cathepsin D or in TACE (an ACE-2 ectodomain shedding enzyme) and eventually caused AEC apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	111-115
27638906-5	2016	The results showed that either MG132 or G100S SP-C mutation activated all three canonical pathways of the UPR (IRE1/XBP1, ATF6, and PERK/eIF2alpha), which led to a significant increase in cathepsin D or in TACE (an ACE-2 ectodomain shedding enzyme) and eventually caused AEC apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	activating transcription factor 6	Homo sapiens	122-126
27638906-5	2016	The results showed that either MG132 or G100S SP-C mutation activated all three canonical pathways of the UPR (IRE1/XBP1, ATF6, and PERK/eIF2alpha), which led to a significant increase in cathepsin D or in TACE (an ACE-2 ectodomain shedding enzyme) and eventually caused AEC apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	cathepsin D	Homo sapiens	188-199
27638906-5	2016	The results showed that either MG132 or G100S SP-C mutation activated all three canonical pathways of the UPR (IRE1/XBP1, ATF6, and PERK/eIF2alpha), which led to a significant increase in cathepsin D or in TACE (an ACE-2 ectodomain shedding enzyme) and eventually caused AEC apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	angiotensin converting enzyme 2	Homo sapiens	215-220
27696626-6	2016	The half-life of TLP was shown to be less than a few hours, and the proteasome inhibitor MG132 specifically suppressed TLP degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	TATA-box binding protein like 1	Homo sapiens	119-122
27354198-9	2016	While treatment with the proteasomal inhibitor, MG132, resulted in a 2-fold increase in HSPB6 levels, exposure to cadmium chloride produced a slight increase in HSPB6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	heat shock protein family B (small) member 6 L homeolog	Xenopus laevis	88-93
27794399-13	2016	MG-132 partially reversed the degradation of Akt, Src, c-Raf and Erk induced by ATO/PD, suggestive of ubiquitin-independent proteasome-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	thymoma viral proto-oncogene 1	Mus musculus	45-48
27655758-12	2016	Hepcidin significantly reduced biotinylated cell surface ZnT1 compared with control cells (P &lt; 0.05); chloroquine inhibited hepcidin-mediated degradation of ZnT1 (P &gt;= 0.05), whereas MG132 had no effect (P &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	hepcidin antimicrobial peptide	Homo sapiens	127-135
27655758-12	2016	Hepcidin significantly reduced biotinylated cell surface ZnT1 compared with control cells (P &lt; 0.05); chloroquine inhibited hepcidin-mediated degradation of ZnT1 (P &gt;= 0.05), whereas MG132 had no effect (P &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	solute carrier family 30 member 1	Homo sapiens	160-164
27794399-13	2016	MG-132 partially reversed the degradation of Akt, Src, c-Raf and Erk induced by ATO/PD, suggestive of ubiquitin-independent proteasome-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	Rous sarcoma oncogene	Mus musculus	50-53
27794399-13	2016	MG-132 partially reversed the degradation of Akt, Src, c-Raf and Erk induced by ATO/PD, suggestive of ubiquitin-independent proteasome-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	v-raf-leukemia viral oncogene 1	Mus musculus	55-60
27794399-13	2016	MG-132 partially reversed the degradation of Akt, Src, c-Raf and Erk induced by ATO/PD, suggestive of ubiquitin-independent proteasome-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	mitogen-activated protein kinase 1	Mus musculus	65-68
27091487-6	2016	In cells pretreated with the proteasome inhibitor MG132, CA no longer reversed the 6-OHDA-mediated induction of cleavage of caspase 3 and poly(ADP)-ribose polymerase and no longer reversed the suppression of proteasome activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	caspase 3	Homo sapiens	124-165
26526841-5	2016	In particular, recombinant sAPPalpha significantly suppressed MG132-triggered expression of the co-chaperone BAG3 and aggresome formation, and it partially rescued proteasomal activity in a dose-dependent manner in SH-SY5Y neuroblastoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	BAG cochaperone 3	Homo sapiens	109-113
26526841-6	2016	In analogy, sAPPalpha was able to inhibit MG132-induced BAG3 expression in primary hippocampal neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	BAG cochaperone 3	Homo sapiens	56-60
27521566-6	2016	Furthermore, inhibition of phosphatase activity by okadaic acid reduced MTCL1, which was restored by the addition of the protease inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	microtubule crosslinking factor 1	Homo sapiens	72-77
27701455-8	2016	RESULTS: Protein turnover studies, using 10 mug/ml cyclohexamide, 1 mug/ml lactocystin, or 100 mug/ml MG132, demonstrated faster HBEGF degradation at 20% O2 than 2% O2, mediated by the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-107	heparin binding EGF like growth factor	Homo sapiens	129-134
27421828-9	2016	Furthermore, clitocine regulates Mcl-1 expression at the posttranslational level as no obvious change is observed on mRNA level and proteasome inhibitor MG132 almost blocks the Mcl-1 suppression by clitocine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	177-182
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	BH3 interacting domain death agonist	Homo sapiens	98-101
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	BCL2 apoptosis regulator	Homo sapiens	106-111
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	BCL2 associated X, apoptosis regulator	Homo sapiens	139-142
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	tumor protein p53	Homo sapiens	147-150
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	cytochrome c, somatic	Homo sapiens	214-226
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	caspase 8	Homo sapiens	242-265
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	poly(ADP-ribose) polymerase 1	Homo sapiens	280-286
27455449-11	2016	Proteasome inhibitors, bortezomib and MG132, enhanced IL-8 production in both sides, apical and basolateral.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	C-X-C motif chemokine ligand 8	Homo sapiens	54-58
27230883-5	2016	The proteasome inhibitors MG132 and MG115 induced a decrease in the levels of Bid and Bcl-2 proteins, an increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, cytochrome c release and activation of caspases (-8, -9 and -3).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BH3 interacting domain death agonist	Rattus norvegicus	78-81
27761169-9	2016	The proteasome inhibitor MG132 increased the expression of immature A78T-HERG and increased both the immature and mature forms of WT-HERG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	potassium voltage-gated channel subfamily H member 2	Homo sapiens	73-77
27761169-9	2016	The proteasome inhibitor MG132 increased the expression of immature A78T-HERG and increased both the immature and mature forms of WT-HERG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	potassium voltage-gated channel subfamily H member 2	Homo sapiens	133-137
27480844-5	2016	Moreover, HIF1alpha siRNA and/or MG132 (a proteasome inhibitor) pretreatment significantly inhibited CSE-induced TRPA1 expression and HIF1alpha nuclear translocation in A549 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	transient receptor potential cation channel subfamily A member 1	Cavia porcellus	113-118
27480844-5	2016	Moreover, HIF1alpha siRNA and/or MG132 (a proteasome inhibitor) pretreatment significantly inhibited CSE-induced TRPA1 expression and HIF1alpha nuclear translocation in A549 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	hypoxia-inducible factor 1-alpha	Cavia porcellus	134-143
27480844-10	2016	In addition, treatment cells with HDAC2 siRNA plus 2%CSE resulted in increased HIF1alpha nuclear translocation and TRPA1 expression, which was significantly inhibited by MG132 and HIF1alpha siRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	histone deacetylase 2	Cavia porcellus	34-39
27480844-10	2016	In addition, treatment cells with HDAC2 siRNA plus 2%CSE resulted in increased HIF1alpha nuclear translocation and TRPA1 expression, which was significantly inhibited by MG132 and HIF1alpha siRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	hypoxia-inducible factor 1-alpha	Cavia porcellus	79-88
27480844-10	2016	In addition, treatment cells with HDAC2 siRNA plus 2%CSE resulted in increased HIF1alpha nuclear translocation and TRPA1 expression, which was significantly inhibited by MG132 and HIF1alpha siRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	transient receptor potential cation channel subfamily A member 1	Cavia porcellus	115-120
27230883-5	2016	The proteasome inhibitors MG132 and MG115 induced a decrease in the levels of Bid and Bcl-2 proteins, an increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, cytochrome c release and activation of caspases (-8, -9 and -3).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2, apoptosis regulator	Rattus norvegicus	86-91
27230883-5	2016	The proteasome inhibitors MG132 and MG115 induced a decrease in the levels of Bid and Bcl-2 proteins, an increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, cytochrome c release and activation of caspases (-8, -9 and -3).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2 associated X, apoptosis regulator	Rattus norvegicus	131-134
27230883-5	2016	The proteasome inhibitors MG132 and MG115 induced a decrease in the levels of Bid and Bcl-2 proteins, an increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, cytochrome c release and activation of caspases (-8, -9 and -3).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	139-142
27230883-5	2016	The proteasome inhibitors MG132 and MG115 induced a decrease in the levels of Bid and Bcl-2 proteins, an increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, cytochrome c release and activation of caspases (-8, -9 and -3).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	caspase 8	Rattus norvegicus	234-257
27473774-13	2016	Degradation, but not ubiquitination, of Smad3 was inhibited by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	SMAD family member 3	Homo sapiens	40-45
27588407-7	2016	Treatment with proteasome inhibitor MG132 completely reverses the reduced expression of beta-catenin in Caco-2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	catenin beta 1	Homo sapiens	88-100
27373828-9	2016	In addition, TGFBIp levels were significantly reduced under ER stress and this reduction was considerably suppressed by the ubiquitin proteasome inhibitor MG132, indicating TGFBIp degradation via the ER-associated degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	transforming growth factor beta induced	Homo sapiens	13-19
27551072-6	2016	The accumulation of GABARAP-containing protein aggregates was observed in the vicinity of sperm mitochondrial sheaths in the zygotes and increased in the embryos treated with proteasomal inhibitor MG132, in which intact sperm mitochondrial sheaths were observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	197-202	GABA type A receptor-associated protein	Homo sapiens	20-27
27373828-9	2016	In addition, TGFBIp levels were significantly reduced under ER stress and this reduction was considerably suppressed by the ubiquitin proteasome inhibitor MG132, indicating TGFBIp degradation via the ER-associated degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	transforming growth factor beta induced	Homo sapiens	173-179
27373828-10	2016	Treatment with 4-PBA not only protected against the GCD2 cell death induced by ER stress but also significantly suppressed the MG132-mediated increase in TGFBIp levels under ER stress.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	transforming growth factor beta induced	Homo sapiens	154-160
27424123-7	2016	MG132 treatment attenuated kahweol-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in kahweol-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin D1	Homo sapiens	44-53
27447743-5	2016	SAHA and MG132 exposure suppressed tumor growth by inhibiting proliferation and inducing apoptosis in nude mice, increased serum ALT and AST levels and decreased hemaglobin level, white blood cell and neutrophil numbers.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	solute carrier family 17 member 5	Homo sapiens	137-140
27462866-5	2016	Further mechanistic investigation demonstrated that overexpression of PDIA6 resulted in decreased phosphorylation of beta-catenin at Ser45 and Ser33/Ser37/Thr41, while increased beta-catenin nuclear accumulation, and upregulation of Wnt/ beta-catenin signaling target genes cyclinD1 and c-myc, which was abolished by ubiquitin-proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	348-353	protein disulfide isomerase family A member 6	Homo sapiens	70-75
27409347-4	2016	ING5 transfection desensitized cells to the chemotherapy of MG132, paclitaxel, and SAHA, which paralleled with apoptotic alteration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	inhibitor of growth family member 5	Homo sapiens	0-4
27339895-6	2016	Three hours later, IkappaBalpha starts to degrade, and ERK returns to basal or non-phosphorylation, and this lasts for the next 12 h. Finally, expression of CD3 and CD8 occurs in MOLT-4 along with reappearance of the IkappaBalpha ERK WWOX complex near 24 h. Inhibition of ERK phosphorylation by U0126 or IkappaBalpha degradation by MG132 prevents MOLT-4 maturation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	332-337	CD8a molecule	Homo sapiens	165-168
27181354-1	2016	We have previously reported the co-localization of O-propargyl-puromycin (OP-Puro) with SUMO-2/3 and ubiquitin at promyelocytic leukemia-nuclear bodies (PML-NBs) in the presence of the proteasome inhibitor MG132, implying a role for the ubiquitin family in sequestering OP-puromycylated immature polypeptides to the nucleus during impaired proteasome activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	small ubiquitin like modifier 2	Homo sapiens	88-96
27482906-6	2016	The proteasome inhibitor MG132 counteracted TNKSi-induced degradasome formation and AXIN2 stabilization, and this was accompanied by reduced transcription of AXIN2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	axin 2	Homo sapiens	158-163
27482906-9	2016	This can explain the decreased protein levels of AXIN2 after MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	axin 2	Homo sapiens	49-54
27267997-8	2016	Furthermore, cotreating cells individually with carnosic acid and proteasome inhibitor (MG-132) and carnosic acid and an ER stress modulator (salubrinal) restored protein levels of AR, suggesting that AR degradation is mediated by ER stress-dependent proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	androgen receptor	Homo sapiens	181-183
27267997-8	2016	Furthermore, cotreating cells individually with carnosic acid and proteasome inhibitor (MG-132) and carnosic acid and an ER stress modulator (salubrinal) restored protein levels of AR, suggesting that AR degradation is mediated by ER stress-dependent proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	androgen receptor	Homo sapiens	201-203
27146988-5	2016	Incorporation of adaptor protein Grb10 relieved Nedd4-2-induced current suppression as did application of the proteasome inhibitor Mg-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-137	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	48-55
27373420-6	2016	Moreover, we modified CAR expression in the two cell lines with proteasome inhibitor MG-132 and histone deacetylase inhibitor trichostatin A (TSA), and analyzed the adenovirus infection rates after modifying agent treatments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-91	CXADR Ig-like cell adhesion molecule	Homo sapiens	22-25
27373420-7	2016	Both TSA and MG-132 pretreatments could increase the CAR expression in the two cell lines, but the drug pretreatments could only make A549 cells more susceptible to adenovirus infectivity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	CXADR Ig-like cell adhesion molecule	Homo sapiens	53-56
27482906-6	2016	The proteasome inhibitor MG132 counteracted TNKSi-induced degradasome formation and AXIN2 stabilization, and this was accompanied by reduced transcription of AXIN2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	axin 2	Homo sapiens	84-89
27044261-6	2016	AZD9291-induced depletion of EGFR(L858R/T790M) protein was abrogated through inhibition of the proteasome with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	epidermal growth factor receptor	Homo sapiens	29-33
27277541-0	2016	Proteasome inhibitor MG132 potentiates TRAIL-induced apoptosis in gallbladder carcinoma GBC-SD cells via DR5-dependent pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF superfamily member 10	Homo sapiens	39-44
27277541-0	2016	Proteasome inhibitor MG132 potentiates TRAIL-induced apoptosis in gallbladder carcinoma GBC-SD cells via DR5-dependent pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF receptor superfamily member 10b	Homo sapiens	105-108
27277541-4	2016	In this study, we demonstrated that proteasome inhibitor MG132 in vitro and in vivo potentiates TRAIL-induced apoptosis in gallbladder carcinoma GBC-SD cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	TNF superfamily member 10	Homo sapiens	96-101
27277541-6	2016	The induction of apoptosis by proteasome inhibitor MG132 was mainly through the extrinsic apoptotic pathways of caspase activation such as caspase-8, caspase-3 and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	caspase 8	Homo sapiens	139-148
27277541-6	2016	The induction of apoptosis by proteasome inhibitor MG132 was mainly through the extrinsic apoptotic pathways of caspase activation such as caspase-8, caspase-3 and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	caspase 3	Homo sapiens	150-159
27277541-6	2016	The induction of apoptosis by proteasome inhibitor MG132 was mainly through the extrinsic apoptotic pathways of caspase activation such as caspase-8, caspase-3 and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	poly(ADP-ribose) polymerase 1	Homo sapiens	164-168
27277541-8	2016	Taken together, these findings indicate that MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway, and suggest that MG132 may be a promising agent for sensitizing GBC-SD cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	TNF receptor superfamily member 10b	Homo sapiens	129-132
27277541-8	2016	Taken together, these findings indicate that MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway, and suggest that MG132 may be a promising agent for sensitizing GBC-SD cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	TNF superfamily member 10	Homo sapiens	232-237
27277541-8	2016	Taken together, these findings indicate that MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway, and suggest that MG132 may be a promising agent for sensitizing GBC-SD cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	TNF receptor superfamily member 10b	Homo sapiens	129-132
27277541-8	2016	Taken together, these findings indicate that MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway, and suggest that MG132 may be a promising agent for sensitizing GBC-SD cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	TNF superfamily member 10	Homo sapiens	232-237
27181354-3	2016	Co-administration of puromycin and MG132 also facilitated redistribution of PML and the SUMO-targeted ubiquitin ligase RNF4 concurrently with SUMO-2/3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	PML nuclear body scaffold	Homo sapiens	76-79
27181354-3	2016	Co-administration of puromycin and MG132 also facilitated redistribution of PML and the SUMO-targeted ubiquitin ligase RNF4 concurrently with SUMO-2/3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	ring finger protein 4	Homo sapiens	119-123
27181354-2	2016	Here, we found that as expected puromycin induced SUMO-1/2/3 accumulation with ubiquitin at multiple nuclear foci in HeLa cells when co-exposed to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	small ubiquitin like modifier 1	Homo sapiens	50-60
27181354-3	2016	Co-administration of puromycin and MG132 also facilitated redistribution of PML and the SUMO-targeted ubiquitin ligase RNF4 concurrently with SUMO-2/3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	small ubiquitin like modifier 2	Homo sapiens	142-150
27233602-10	2016	The LCN-2 protein degradation was significantly attenuated by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	lipocalin 2	Rattus norvegicus	4-9
27441650-5	2016	SIK2 is mobilized to promote autophagy and protect the cells from apoptosis under PD solution or MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	salt inducible kinase 2	Homo sapiens	0-4
27486435-9	2016	The amount of MRAP was increased by the proteasome inhibitor MG132 and MRAP underwent ubiquitylation on lysine and other amino acids.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	melanocortin-2 receptor accessory protein	Cricetulus griseus	14-18
27486435-10	2016	Nonetheless, when protein synthesis was blocked with cycloheximide, MRAP was rapidly degraded even when MG132 was included and all lysines were replaced by arginines, implicating non-proteasomal degradation pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	melanocortin-2 receptor accessory protein	Cricetulus griseus	68-72
26592933-6	2016	In addition, activated AKT and ERK were significantly attenuated by MG132 and Bortezomib in cholesterol- induced cardiac hypertrophy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	AKT serine/threonine kinase 1	Rattus norvegicus	23-26
27245334-8	2016	Thus, 3-day subcutaneous hepcidin injection and acute direct hepcidin exposure in the Ussing chamber were capable of restoring the thalassemia-associated impairment of calcium transport; however, the positive effect of hepcidin on calcium transport was completely blocked by proteasome inhibitors MG132 and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	297-302	hepcidin antimicrobial peptide	Mus musculus	25-33
27245334-8	2016	Thus, 3-day subcutaneous hepcidin injection and acute direct hepcidin exposure in the Ussing chamber were capable of restoring the thalassemia-associated impairment of calcium transport; however, the positive effect of hepcidin on calcium transport was completely blocked by proteasome inhibitors MG132 and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	297-302	hepcidin antimicrobial peptide	Mus musculus	61-69
27245334-8	2016	Thus, 3-day subcutaneous hepcidin injection and acute direct hepcidin exposure in the Ussing chamber were capable of restoring the thalassemia-associated impairment of calcium transport; however, the positive effect of hepcidin on calcium transport was completely blocked by proteasome inhibitors MG132 and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	297-302	hepcidin antimicrobial peptide	Mus musculus	61-69
27033325-6	2016	Co-treatment with the proteasome inhibitor, MG132, abrogated the decrease in ERalpha levels caused by treatment with the ligands only.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	estrogen receptor 1	Homo sapiens	77-84
27281343-8	2016	Further biochemical studies with the Q838/844 mutant showed that this glycosylation-deficient ABCC11 was degraded faster than wild-type probably due to the enhancement of the MG132-sensitive protein degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-180	ATP binding cassette subfamily C member 11	Homo sapiens	94-100
26987571-6	2016	Moreover, the tumors treated with MG132/m showed higher levels of tumor suppressing proteins, hScrib and p53, as well as apoptotic degree, than tumors treated with free MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	tumor protein p53	Homo sapiens	105-108
27177927-5	2016	Furthermore, mutant CALR protein stability and secretion were examined using brefeldin A, MG132, spautin-1, and tunicamycin treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	calreticulin	Mus musculus	20-24
27283735-9	2016	Degradation of the Tat protein is accomplished through proteasomal pathway as proteasomal inhibitor MG132 blocked Tat degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	tyrosine aminotransferase	Homo sapiens	19-22
27283735-9	2016	Degradation of the Tat protein is accomplished through proteasomal pathway as proteasomal inhibitor MG132 blocked Tat degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	tyrosine aminotransferase	Homo sapiens	114-117
27051056-6	2016	The expression of Caspase3 and Beclin1 was detected by Western blot analysis and reverse transcription-polymerase chain reaction after treatment with 3.0 mug/mL of the cisplatin group and combined treatment with 1.5 mug/mL of MG132 group for 24 hours, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-231	caspase 3	Homo sapiens	18-26
27051056-6	2016	The expression of Caspase3 and Beclin1 was detected by Western blot analysis and reverse transcription-polymerase chain reaction after treatment with 3.0 mug/mL of the cisplatin group and combined treatment with 1.5 mug/mL of MG132 group for 24 hours, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-231	beclin 1	Homo sapiens	31-38
27105523-7	2016	Compared with untreated cells, the treatment of UBE2D3 overexpressing cells with the specific proteasome inhibitor (MG132) could up-regulate hTERT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	ubiquitin-conjugating enzyme E2D 3	Mus musculus	48-54
27105523-7	2016	Compared with untreated cells, the treatment of UBE2D3 overexpressing cells with the specific proteasome inhibitor (MG132) could up-regulate hTERT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	telomerase reverse transcriptase	Homo sapiens	141-146
27105523-8	2016	MG132 treatment of UBE2D3 overexpressed cells caused a clear and dramatic increase in the amount of ubiquitinated hTERT species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	ubiquitin-conjugating enzyme E2D 3	Mus musculus	19-25
27105523-8	2016	MG132 treatment of UBE2D3 overexpressed cells caused a clear and dramatic increase in the amount of ubiquitinated hTERT species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	telomerase reverse transcriptase	Homo sapiens	114-119
26592933-6	2016	In addition, activated AKT and ERK were significantly attenuated by MG132 and Bortezomib in cholesterol- induced cardiac hypertrophy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	Eph receptor B1	Rattus norvegicus	31-34
26969276-4	2016	The inhibition of proteasomes by MG-132 increased the percentage of TH molecules phosphorylated at their Ser19, Ser31 and/or Ser40 among the total TH proteins to about 70% in PC12D cells over a 24-hr period; although the percentage of phosphorylated TH molecules was about 20% under basal conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	tyrosine hydroxylase	Rattus norvegicus	68-70
27099442-10	2016	Upon inhibition of CacyBP/SIP nuclear translocation, there were no changes in protein levels of p27Kip1 and Cyclin E, while p27Kip1 decrease could be prevented by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	188-193	calcyclin binding protein	Homo sapiens	19-25
27099442-10	2016	Upon inhibition of CacyBP/SIP nuclear translocation, there were no changes in protein levels of p27Kip1 and Cyclin E, while p27Kip1 decrease could be prevented by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	188-193	cyclin dependent kinase inhibitor 1B	Homo sapiens	124-131
26969276-4	2016	The inhibition of proteasomes by MG-132 increased the percentage of TH molecules phosphorylated at their Ser19, Ser31 and/or Ser40 among the total TH proteins to about 70% in PC12D cells over a 24-hr period; although the percentage of phosphorylated TH molecules was about 20% under basal conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	tyrosine hydroxylase	Rattus norvegicus	147-149
26969276-4	2016	The inhibition of proteasomes by MG-132 increased the percentage of TH molecules phosphorylated at their Ser19, Ser31 and/or Ser40 among the total TH proteins to about 70% in PC12D cells over a 24-hr period; although the percentage of phosphorylated TH molecules was about 20% under basal conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	tyrosine hydroxylase	Rattus norvegicus	147-149
26714749-6	2016	Furthermore, proteosomal inhibitor MG132 treatment rescued the downregulation of CDK2 in SATB2-silenced SKOV3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	cyclin dependent kinase 2	Homo sapiens	81-85
27069137-7	2016	Degradation of p53 protein by silencing PANDA was prevented by treatment of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	tumor protein p53	Homo sapiens	15-18
27069137-7	2016	Degradation of p53 protein by silencing PANDA was prevented by treatment of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	promoter of CDKN1A antisense DNA damage activated RNA	Homo sapiens	40-45
26966065-10	2016	In another heart failure model, MG132 treatment reversed PLN degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	phospholamban	Mus musculus	57-60
26825690-7	2016	Treatment with the proteasomal inhibitor MG132 markedly attenuated the turnover of cell-associated mutant apoB-48, whereas treatment with inhibitors of autophagosomal/lysosomal function (e.g. 3-MA or ammonium chloride) had no effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	apolipoprotein B	Homo sapiens	106-113
26714749-6	2016	Furthermore, proteosomal inhibitor MG132 treatment rescued the downregulation of CDK2 in SATB2-silenced SKOV3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	SATB homeobox 2	Homo sapiens	89-94
26635026-8	2016	Interestingly, proteasome inhibition by MG132, had no effect on autophagy, but did reduce tau levels, indicating that NPAS4 may also degrade tau proteins through an unknown proteasome-mediated mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	neuronal PAS domain protein 4	Rattus norvegicus	118-123
26935904-14	2016	Decreased VEGFR-2 caused by ROS was ameliorated by beta-TrCP siRNA, proteasome inhibitor MG132 and GSK-3beta activity inhibitor (lithium chloride and SB216763).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	kinase insert domain receptor	Homo sapiens	10-17
27073579-8	2016	The EGFR protein expression and VM formation capability of hinokitiol-treated BCSCs were restored by co-treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	epidermal growth factor receptor	Homo sapiens	4-8
27113178-7	2016	The cells treated with obatoclax or MG-132 alone showed increased expression of ubiquitin and cleavage of PARP and caspase-9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	poly(ADP-ribose) polymerase 1	Homo sapiens	106-110
27113178-7	2016	The cells treated with obatoclax or MG-132 alone showed increased expression of ubiquitin and cleavage of PARP and caspase-9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	caspase 9	Homo sapiens	115-124
27113178-8	2016	Compared with the cells treated with obatoclax or MG-132 alone, the cells with a combined treatment exhibited significantly increased expression of ubiquitin, cleavage of PARP and caspase-9, and expression of phospho-Histone H3 (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	poly(ADP-ribose) polymerase 1	Homo sapiens	171-175
27113178-8	2016	Compared with the cells treated with obatoclax or MG-132 alone, the cells with a combined treatment exhibited significantly increased expression of ubiquitin, cleavage of PARP and caspase-9, and expression of phospho-Histone H3 (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	caspase 9	Homo sapiens	180-189
26786097-7	2016	Here we show that the proteasome inhibitors MG132 and bortezomib activate the RIPK3-MLKL necroptotic pathway in mouse fibroblasts as well as human leukemia cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	receptor-interacting serine-threonine kinase 3	Mus musculus	78-83
27016777-10	2016	In vitro, overexpression of SUMO2/3 de-stabilized HIF1A in hypoxia, and abrogated HIF1A expression following Mg132 treatment in normoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	small ubiquitin like modifier 2	Homo sapiens	28-33
27016777-10	2016	In vitro, overexpression of SUMO2/3 de-stabilized HIF1A in hypoxia, and abrogated HIF1A expression following Mg132 treatment in normoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	hypoxia inducible factor 1 subunit alpha	Homo sapiens	82-87
26786097-7	2016	Here we show that the proteasome inhibitors MG132 and bortezomib activate the RIPK3-MLKL necroptotic pathway in mouse fibroblasts as well as human leukemia cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	mixed lineage kinase domain-like	Mus musculus	84-88
26998273-4	2016	The POLD4 protein levels in the A549 cells decreased following treatment with 4NQO; however, MG132 could reverse this phenotype.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	DNA polymerase delta 4, accessory subunit	Homo sapiens	4-9
25263748-8	2016	Moreover, the addition of the proteasome inhibitor, MG132, strongly reversed the p,p"-DDE-reduced Nrf2 expression and gamma-GCS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
25263748-8	2016	Moreover, the addition of the proteasome inhibitor, MG132, strongly reversed the p,p"-DDE-reduced Nrf2 expression and gamma-GCS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	glutamate-cysteine ligase catalytic subunit	Homo sapiens	118-127
26743567-10	2016	Moreover, MG132 partially inhibited SnoN degradation in the hRPTECs under high-glucose conditions and SB-431542 decreased the phosphorylation of Smad2 and the expression of Smurf2 induced under high-glucose conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	SKI like proto-oncogene	Homo sapiens	36-40
26797017-11	2016	Liver injury induced by APAP was aggravated by MG132, possibly via elevation of connexin 32 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	gap junction protein beta 1	Homo sapiens	80-91
26577496-5	2016	Pretreatment with either the lysosomal inhibitor chloroquine, or the proteasomal inhibitor MG132 blocks HT-induced EGFR downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	epidermal growth factor receptor	Homo sapiens	115-119
26926171-11	2016	Inhibition of proteasomal degradation by MG132 attenuated MRB-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with MRB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cyclin D1	Homo sapiens	71-80
26721884-8	2016	In cells overexpressing OS9, total cellular NKCC2 protein levels were markedly decreased, an effect blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	OS9 endoplasmic reticulum lectin	Homo sapiens	24-27
26721884-8	2016	In cells overexpressing OS9, total cellular NKCC2 protein levels were markedly decreased, an effect blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	solute carrier family 12 member 1	Homo sapiens	44-49
26796273-5	2016	The effect of XBP-1 gene silencing on IRE1alpha-TRAF2-ASK1-JNK pathway under MG132 induced endoplasmic reticulum stress in Tca-8113 were investigated by real-time RT-PCR or western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	X-box binding protein 1	Homo sapiens	14-19
26796273-5	2016	The effect of XBP-1 gene silencing on IRE1alpha-TRAF2-ASK1-JNK pathway under MG132 induced endoplasmic reticulum stress in Tca-8113 were investigated by real-time RT-PCR or western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	38-47
26796273-5	2016	The effect of XBP-1 gene silencing on IRE1alpha-TRAF2-ASK1-JNK pathway under MG132 induced endoplasmic reticulum stress in Tca-8113 were investigated by real-time RT-PCR or western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	TNF receptor associated factor 2	Homo sapiens	48-53
26796273-5	2016	The effect of XBP-1 gene silencing on IRE1alpha-TRAF2-ASK1-JNK pathway under MG132 induced endoplasmic reticulum stress in Tca-8113 were investigated by real-time RT-PCR or western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	54-58
26796273-5	2016	The effect of XBP-1 gene silencing on IRE1alpha-TRAF2-ASK1-JNK pathway under MG132 induced endoplasmic reticulum stress in Tca-8113 were investigated by real-time RT-PCR or western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	mitogen-activated protein kinase 8	Homo sapiens	59-62
26796273-7	2016	RESULTS: XBP1 expression was reduced in transfected groups and MG132 groups.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	X-box binding protein 1	Homo sapiens	9-13
26796273-9	2016	Moreover, combined shRNA-XBP1 with MG132 further enhanced downregulated XBP1 expression and upregulated activation of ASK1-JNK signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	X-box binding protein 1	Homo sapiens	72-76
26796273-9	2016	Moreover, combined shRNA-XBP1 with MG132 further enhanced downregulated XBP1 expression and upregulated activation of ASK1-JNK signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	118-122
26796273-9	2016	Moreover, combined shRNA-XBP1 with MG132 further enhanced downregulated XBP1 expression and upregulated activation of ASK1-JNK signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	mitogen-activated protein kinase 8	Homo sapiens	123-126
26796273-10	2016	CONCLUSIONS: Silencing XBP1 expression under MG132 induced ER stress block the XBP1 survival pathway and synergism with MG132 to promote Tca8113 cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	X-box binding protein 1	Homo sapiens	23-27
26796273-10	2016	CONCLUSIONS: Silencing XBP1 expression under MG132 induced ER stress block the XBP1 survival pathway and synergism with MG132 to promote Tca8113 cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	X-box binding protein 1	Homo sapiens	79-83
26796273-10	2016	CONCLUSIONS: Silencing XBP1 expression under MG132 induced ER stress block the XBP1 survival pathway and synergism with MG132 to promote Tca8113 cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	X-box binding protein 1	Homo sapiens	23-27
26700459-4	2016	In the current study, we found that -421/-307 and -243/+53 regions at the ORP150 gene were responsible for its transactivation by MG132 in thyroid cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	hypoxia up-regulated 1	Homo sapiens	74-80
26212375-9	2016	Both chloroquine and MG132 increased mTOR and p-mTOR protein levels in +/+ osteoclasts, suggesting that mTOR undergoes both lysosomal and proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mechanistic target of rapamycin kinase	Homo sapiens	37-41
26212375-9	2016	Both chloroquine and MG132 increased mTOR and p-mTOR protein levels in +/+ osteoclasts, suggesting that mTOR undergoes both lysosomal and proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mechanistic target of rapamycin kinase	Homo sapiens	48-52
26212375-9	2016	Both chloroquine and MG132 increased mTOR and p-mTOR protein levels in +/+ osteoclasts, suggesting that mTOR undergoes both lysosomal and proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mechanistic target of rapamycin kinase	Homo sapiens	48-52
26731332-6	2016	RESULTS: In LX-2 cells, MG132 treatment was associated with the phosphorylation of c-Jun, activation of AP-1 and apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	83-88
26697750-6	2016	In addition, PIAS3 knockdown induced the destabilization of HIF-1alpha protein, and the destabilization was reversed by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	protein inhibitor of activated STAT 3	Homo sapiens	13-18
26697750-6	2016	In addition, PIAS3 knockdown induced the destabilization of HIF-1alpha protein, and the destabilization was reversed by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	hypoxia inducible factor 1 subunit alpha	Homo sapiens	60-70
26657849-6	2016	Treatment with the proteasome inhibitor MG132 resulted in accumulation of Ras2, indicating that Rck1 is involved in Ras2 degradation in a proteasome-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	Ras family GTPase RAS2	Saccharomyces cerevisiae S288C	74-78
26657849-6	2016	Treatment with the proteasome inhibitor MG132 resulted in accumulation of Ras2, indicating that Rck1 is involved in Ras2 degradation in a proteasome-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	putative serine/threonine protein kinase RCK1	Saccharomyces cerevisiae S288C	96-100
26657849-6	2016	Treatment with the proteasome inhibitor MG132 resulted in accumulation of Ras2, indicating that Rck1 is involved in Ras2 degradation in a proteasome-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	Ras family GTPase RAS2	Saccharomyces cerevisiae S288C	116-120
26625202-4	2016	This suppression of Notch1 in response to HDAC8 inhibition was abrogated by the proteasome inhibitor MG132 and siRNA-induced silencing of Fbwx7, indicating Notch1 suppression occurred through proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	notch receptor 1	Homo sapiens	20-26
26625202-4	2016	This suppression of Notch1 in response to HDAC8 inhibition was abrogated by the proteasome inhibitor MG132 and siRNA-induced silencing of Fbwx7, indicating Notch1 suppression occurred through proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	histone deacetylase 8	Homo sapiens	42-47
26625202-4	2016	This suppression of Notch1 in response to HDAC8 inhibition was abrogated by the proteasome inhibitor MG132 and siRNA-induced silencing of Fbwx7, indicating Notch1 suppression occurred through proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	notch receptor 1	Homo sapiens	156-162
26534988-4	2016	Proteasome inhibitors (calpain inhibitor I and MG132) and Hsp90 inhibitor geldanamycin, but not Hsp70 inhibitor pifithrin-mu, increased wild-type (WT) hPXR in the nucleus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	nuclear receptor subfamily 1 group I member 2	Homo sapiens	151-155
27132793-8	2016	The levels of LC3-I, LC3-II and LAMP1 increased in MG132 treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	lysosomal associated membrane protein 1	Homo sapiens	32-37
27132793-9	2016	The levels of gamma-tubulin and p62 also increased in MG132 treated cells, suggesting that inhibition of the UPP up-regulates autophagy-lysosome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	nucleoporin 62	Homo sapiens	32-35
26727015-9	2016	Treatment of controls with the proteosomal inhibitor MG132, which prevented CD36 downregulation, resulted in blunted lipid-induction of MTP, L-FABP and ApoC2 gene expression, as in MetS mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	microsomal triglyceride transfer protein	Mus musculus	136-139
26727015-9	2016	Treatment of controls with the proteosomal inhibitor MG132, which prevented CD36 downregulation, resulted in blunted lipid-induction of MTP, L-FABP and ApoC2 gene expression, as in MetS mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	fatty acid binding protein 1, liver	Mus musculus	141-147
26727015-9	2016	Treatment of controls with the proteosomal inhibitor MG132, which prevented CD36 downregulation, resulted in blunted lipid-induction of MTP, L-FABP and ApoC2 gene expression, as in MetS mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	apolipoprotein C2	Mus musculus	152-157
26410677-5	2016	The analysis on Tctex-1 protein was performed in the absence and presence of the ligands JWH 133, 2-AG, and AM 630, the protein biosynthesis inhibitor cycloheximide or the protein degradation blockers MG132, NH4Cl/leupeptin or bafilomycin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-206	dynein light chain Tctex-type 1	Homo sapiens	16-23
26062786-6	2016	Reduction of BACE1 protein levels by overexpression of DISC1 was accompanied by an accelerating decline rate of BACE1, and was blocked by the lysosomal inhibitor chloroquine, rather than proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	208-214	disrupted in schizophrenia 1	Mus musculus	55-60
26648402-8	2016	In addition, MG-132 inhibited the protein expression of the anti-apoptotic protein, B-cell lymphoma (Bcl)-2, whereas the expression levels of Bcl-2-associated X protein and caspase-3 were upregulated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	BCL2 apoptosis regulator	Homo sapiens	84-107
26648402-8	2016	In addition, MG-132 inhibited the protein expression of the anti-apoptotic protein, B-cell lymphoma (Bcl)-2, whereas the expression levels of Bcl-2-associated X protein and caspase-3 were upregulated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	caspase 3	Homo sapiens	173-182
26551455-12	2015	Moreover, the data of RNA pull-down and RIP showed that MIAT controlled Nrf2 cellular through enhancing Nrf2 stability, which was confirmed by CHX and MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	receptor interacting serine/threonine kinase 1	Rattus norvegicus	40-43
27774335-5	2016	Our results demonstrate that the proteasome inhibitor, MG132, initiates poly(ADP-ribose) polymerase (PARP) cleavage, caspase 3 activation, and nuclear condensation and fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	poly(ADP-ribose) polymerase 1	Homo sapiens	72-99
27774335-5	2016	Our results demonstrate that the proteasome inhibitor, MG132, initiates poly(ADP-ribose) polymerase (PARP) cleavage, caspase 3 activation, and nuclear condensation and fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	poly(ADP-ribose) polymerase 1	Homo sapiens	101-105
27774335-5	2016	Our results demonstrate that the proteasome inhibitor, MG132, initiates poly(ADP-ribose) polymerase (PARP) cleavage, caspase 3 activation, and nuclear condensation and fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	caspase 3	Homo sapiens	117-126
27774335-7	2016	All of these events can be attenuated without obvious reduction of MG132 induced protein ubiquitination by first treating the cells with NAC and IGF-1 separately or simultaneously prior to exposure to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-206	insulin like growth factor 1	Homo sapiens	145-150
26551455-12	2015	Moreover, the data of RNA pull-down and RIP showed that MIAT controlled Nrf2 cellular through enhancing Nrf2 stability, which was confirmed by CHX and MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	myocardial infarction associated transcript	Rattus norvegicus	56-60
26551455-12	2015	Moreover, the data of RNA pull-down and RIP showed that MIAT controlled Nrf2 cellular through enhancing Nrf2 stability, which was confirmed by CHX and MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	NFE2 like bZIP transcription factor 2	Rattus norvegicus	72-76
26551455-12	2015	Moreover, the data of RNA pull-down and RIP showed that MIAT controlled Nrf2 cellular through enhancing Nrf2 stability, which was confirmed by CHX and MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	NFE2 like bZIP transcription factor 2	Rattus norvegicus	104-108
26781795-4	2015	Treatment of HL-1 cells with either cycloheximide or MG132 caused an appreciable increase in the amount of AMPKalpha2 protein in ARID5B knockdown cells, which suggests that knockdown of ARID5B mRNA extends the half-life of AMPKalpha2 protein in HL-1 cells via yet unidentified mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	107-117
26781795-4	2015	Treatment of HL-1 cells with either cycloheximide or MG132 caused an appreciable increase in the amount of AMPKalpha2 protein in ARID5B knockdown cells, which suggests that knockdown of ARID5B mRNA extends the half-life of AMPKalpha2 protein in HL-1 cells via yet unidentified mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	AT rich interactive domain 5B (MRF1-like)	Mus musculus	186-192
26710253-8	2015	Surprisingly, we also found that DUSP4-deficient T but not B cells exhibited elevated STAT5 protein levels, and over-expressed DUSP4 destabilized STAT5 in vitro; moreover, this destabilization required the phosphatase activity of DUSP4, and was insensitive to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	260-265	signal transducer and activator of transcription 5A	Mus musculus	86-91
26710253-8	2015	Surprisingly, we also found that DUSP4-deficient T but not B cells exhibited elevated STAT5 protein levels, and over-expressed DUSP4 destabilized STAT5 in vitro; moreover, this destabilization required the phosphatase activity of DUSP4, and was insensitive to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	260-265	dual specificity phosphatase 4	Mus musculus	33-38
26710253-8	2015	Surprisingly, we also found that DUSP4-deficient T but not B cells exhibited elevated STAT5 protein levels, and over-expressed DUSP4 destabilized STAT5 in vitro; moreover, this destabilization required the phosphatase activity of DUSP4, and was insensitive to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	260-265	signal transducer and activator of transcription 5A	Mus musculus	146-151
26710253-8	2015	Surprisingly, we also found that DUSP4-deficient T but not B cells exhibited elevated STAT5 protein levels, and over-expressed DUSP4 destabilized STAT5 in vitro; moreover, this destabilization required the phosphatase activity of DUSP4, and was insensitive to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	260-265	dual specificity phosphatase 4	Mus musculus	127-132
25866162-8	2015	Treatment with the proteasome inhibitor MG132 showed significantly increased IGF1R protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	insulin like growth factor 1 receptor	Homo sapiens	77-82
26781795-4	2015	Treatment of HL-1 cells with either cycloheximide or MG132 caused an appreciable increase in the amount of AMPKalpha2 protein in ARID5B knockdown cells, which suggests that knockdown of ARID5B mRNA extends the half-life of AMPKalpha2 protein in HL-1 cells via yet unidentified mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	223-233
26781795-4	2015	Treatment of HL-1 cells with either cycloheximide or MG132 caused an appreciable increase in the amount of AMPKalpha2 protein in ARID5B knockdown cells, which suggests that knockdown of ARID5B mRNA extends the half-life of AMPKalpha2 protein in HL-1 cells via yet unidentified mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	AT rich interactive domain 5B (MRF1-like)	Mus musculus	129-135
26544511-8	2015	This likely occurs through the canonical polyubiquitination mechanism as APOBEC3B protein levels are restored by MG132 treatment and by altering a conserved E3 ligase-binding motif.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	apolipoprotein B mRNA editing enzyme catalytic subunit 3B	Homo sapiens	73-81
26313562-9	2015	Pretreatment with the proteasome inhibitor MG-132 restored the expression of PC2 in cells treated with cytokines but not in cells treated with nitric oxide donors or with endoplasmic reticulum stressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	polycystin 2, transient receptor potential cation channel	Mus musculus	77-80
26165741-0	2015	Dissociation of E-cadherin/beta-catenin complex by MG132 and bortezomib enhances CDDP induced cell death in oral cancer SCC-25 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	cadherin 1	Homo sapiens	16-26
26165741-0	2015	Dissociation of E-cadherin/beta-catenin complex by MG132 and bortezomib enhances CDDP induced cell death in oral cancer SCC-25 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	catenin beta 1	Homo sapiens	27-39
26165741-6	2015	Western blot results showed that MG132 or bortezomib induced high accumulation of ubiquitinated proteins and activation of apoptosis related protein caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	caspase 3	Homo sapiens	149-158
26165741-8	2015	However, knockdown of beta-catenin could decrease MG132 or bortezomib induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	catenin beta 1	Homo sapiens	22-34
26508620-8	2015	Also, the proteasome inhibitor MG132 prevented the brefeldin A (blocker of protein transport through Golgi)-reduced Cx43-P2 level and membrane Cx43 gap junction plaque.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	gap junction protein, alpha 1	Rattus norvegicus	116-123
26508620-8	2015	Also, the proteasome inhibitor MG132 prevented the brefeldin A (blocker of protein transport through Golgi)-reduced Cx43-P2 level and membrane Cx43 gap junction plaque.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	gap junction protein, alpha 1	Rattus norvegicus	116-120
26517515-9	2015	Furthermore, blocking proteasome activity by MG132 prevented the downregulation of cyclin A2, dephosphorylation of Akt and FOXO3a, and induction of apoptosis in cells co-treated with GOS and VPA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	cyclin A2	Homo sapiens	83-92
26517515-9	2015	Furthermore, blocking proteasome activity by MG132 prevented the downregulation of cyclin A2, dephosphorylation of Akt and FOXO3a, and induction of apoptosis in cells co-treated with GOS and VPA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	AKT serine/threonine kinase 1	Homo sapiens	115-118
26517515-9	2015	Furthermore, blocking proteasome activity by MG132 prevented the downregulation of cyclin A2, dephosphorylation of Akt and FOXO3a, and induction of apoptosis in cells co-treated with GOS and VPA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	forkhead box O3	Homo sapiens	123-129
26187567-7	2015	CFA-evoked pain was blocked in rats receiving a pre-emptive systemic dose of the NF-kappaB inhibitor MG132 and exacerbated in IKKca mice with constitutive NF-kappaB activity in astrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	81-90
25728680-8	2015	Moreover, the proteasome inhibitor MG-132, but not the inhibitors of lysosomal degradation bafilomycin and chloroquine, reversed the SOCS1-mediated reduction in MET expression, indicating that this process is distinct from Cbl-mediated downmodulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	suppressor of cytokine signaling 1	Homo sapiens	133-138
26381869-7	2015	Supplementation of S-nitroso-l-glutathione (GSNO), a NO donor, or MG132, a potent inhibitor of the 26S proteasome, prevented eNOS silencing and PTIO-induced DHFR reduction in human umbilical vein endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	dihydrofolate reductase	Homo sapiens	157-161
26381869-11	2015	Experiments performed in aortas confirmed that PTIO or eNOS deficiency reduces endothelial DHFR, which can be abolished by MG132 supplementation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	dihydrofolate reductase	Homo sapiens	91-95
26187567-7	2015	CFA-evoked pain was blocked in rats receiving a pre-emptive systemic dose of the NF-kappaB inhibitor MG132 and exacerbated in IKKca mice with constitutive NF-kappaB activity in astrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	155-164
26260897-1	2015	In the present study, treatment of Xenopus laevis A6 kidney epithelial cells with the proteasomal inhibitor, MG132, or the environmental toxicants, sodium arsenite or cadmium chloride, induced the accumulation of the small heat shock protein, HSP30, in total and in both soluble and insoluble protein fractions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	heat shock 70kDa protein L homeolog	Xenopus laevis	223-241
26260897-1	2015	In the present study, treatment of Xenopus laevis A6 kidney epithelial cells with the proteasomal inhibitor, MG132, or the environmental toxicants, sodium arsenite or cadmium chloride, induced the accumulation of the small heat shock protein, HSP30, in total and in both soluble and insoluble protein fractions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	heat shock protein 30E L homeolog	Xenopus laevis	243-248
26458400-16	2015	The increase of p65 protein by SUMO2/3 was abolished by MG132 treatment, a reversible inhibitor of proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	RELA proto-oncogene, NF-kB subunit	Homo sapiens	16-19
26398314-5	2015	The present study aimed to investigate the effect of the MG132 proteasome inhibitor on the expression levels of Cx43, ZO-1, 20S proteasome and ubiquitin in a rat model of HF, induced by adriamycin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	gap junction protein, alpha 1	Rattus norvegicus	112-116
26398314-5	2015	The present study aimed to investigate the effect of the MG132 proteasome inhibitor on the expression levels of Cx43, ZO-1, 20S proteasome and ubiquitin in a rat model of HF, induced by adriamycin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tight junction protein 1	Rattus norvegicus	118-122
26722330-5	2015	MG132 and anti-TNF-alpha antibody were used to inhibit the expression of p65 and TNF-alpha in the AML cell line, HL-60.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	RELA proto-oncogene, NF-kB subunit	Homo sapiens	73-76
26722330-5	2015	MG132 and anti-TNF-alpha antibody were used to inhibit the expression of p65 and TNF-alpha in the AML cell line, HL-60.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Homo sapiens	81-90
26415225-8	2015	Inhibition of proteasome with MG132 prevented JQ1-induced c-FLIP reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	CASP8 and FADD like apoptosis regulator	Homo sapiens	58-64
26398314-7	2015	In addition, MG132 inhibited the expression of 20S proteasome and ubiquitin, accompanied by an upregulation in the expression of Cx43 and ZO-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	gap junction protein, alpha 1	Rattus norvegicus	129-133
26398314-7	2015	In addition, MG132 inhibited the expression of 20S proteasome and ubiquitin, accompanied by an upregulation in the expression of Cx43 and ZO-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	tight junction protein 1	Rattus norvegicus	138-142
26722260-0	2015	Proteasome inhibitor MG-132 enhances histone deacetylase inhibitor SAHA-induced cell death of chronic myeloid leukemia cells by an ROS-mediated mechanism and downregulation of the Bcr-Abl fusion protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
26722260-9	2015	Notably, the ROS scavenger, N-acetyl-L-cysteine, almost fully reversed the cell death and Bcr-Abl downregulation that was induced by the combination of SAHA and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-167	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
26378039-5	2015	The essential role of SIP1 in GADD45G activities is further validated in the model of the proteasome inhibitor MG132-induced cell senescence.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	zinc finger E-box binding homeobox 2	Homo sapiens	22-26
26378039-5	2015	The essential role of SIP1 in GADD45G activities is further validated in the model of the proteasome inhibitor MG132-induced cell senescence.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	growth arrest and DNA damage inducible gamma	Homo sapiens	30-37
26958616-3	2015	The highlights include: (1) Denature-immunoprecipitation assay revealed ubiquitination of OCT4 in pluripotent H9 cells, which was enhancedby MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	POU class 5 homeobox 1	Homo sapiens	90-94
26958616-4	2015	(2) Well colocalization of ectopic OCT4 and FLAG-Ub was found in HeLa cells, which was also increased by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	POU class 5 homeobox 1	Homo sapiens	35-39
26958616-5	2015	(3) MG132 treatment decreased DPF2 cytoplasmic expression in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	double PHD fingers 2	Homo sapiens	30-34
26458400-16	2015	The increase of p65 protein by SUMO2/3 was abolished by MG132 treatment, a reversible inhibitor of proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	small ubiquitin like modifier 2	Homo sapiens	31-36
26377801-14	2015	In contrast, MG132 treatment increased PEX5 levels, implicating the proteasome in degrading PEX5, especially at high temperature.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	peroxin 5	Arabidopsis thaliana	39-43
26296461-6	2015	Combined treatment with the nuclear export inhibitor leptomycin B and the proteasome inhibitor MG132 led to the accumulation of hSETDB1 in the nucleus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	SET domain bifurcated histone lysine methyltransferase 1	Homo sapiens	128-135
26408692-4	2015	RESULTS: Expression of GADD34 dramatically enhanced MG132-induced cell death via protein synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	23-29
26408692-6	2015	Importantly, we found that accumulation of autophagy following MG132-treatment facilitated cell death in MEF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	E74 like ETS transcription factor 4	Homo sapiens	105-108
26057472-6	2015	Treatment of cells with Bafilomycin A1 (BafA1) a vacuolar H+ ATPase inhibitor increased the half-life of P-gp at the cell surface to 36.1+-0.5 h. Interestingly, treatment with the proteasomal inhibitors MG132, MG115 or lactacystin alone did not alter the half-life of the protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	203-208	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
26057472-7	2015	When cells were treated with both lysosomal and proteasomal inhibitors (BafA1 and MG132), the half-life was further prolonged to 39-50 h. Functional assays done with rhodamine 123 or calcein-AM, fluorescent substrates of P-gp, indicated that the transport function of P-gp was not affected by either biotinylation or treatment with BafA1 or proteasomal inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	ATP binding cassette subfamily B member 1	Homo sapiens	221-225
26057472-7	2015	When cells were treated with both lysosomal and proteasomal inhibitors (BafA1 and MG132), the half-life was further prolonged to 39-50 h. Functional assays done with rhodamine 123 or calcein-AM, fluorescent substrates of P-gp, indicated that the transport function of P-gp was not affected by either biotinylation or treatment with BafA1 or proteasomal inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	ATP binding cassette subfamily B member 1	Homo sapiens	268-272
26163823-8	2015	However, the feedback MEK2 downregulation was only observed at protein levels, which was blocked by the proteasome inhibitors, MG132 and bortezomib, suggesting that the MEK2 regulation is mediated at a post-translational level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	mitogen-activated protein kinase kinase 2	Homo sapiens	22-26
26163823-8	2015	However, the feedback MEK2 downregulation was only observed at protein levels, which was blocked by the proteasome inhibitors, MG132 and bortezomib, suggesting that the MEK2 regulation is mediated at a post-translational level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	mitogen-activated protein kinase kinase 2	Homo sapiens	169-173
26264759-6	2015	Consistent with a post-translational mechanism, we did not observe a reduction in Cx43 mRNA in electrically stimulated cells, while the proteasomal inhibitor MG132 maintained Cx43 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	gap junction protein alpha 1	Canis lupus familiaris	175-179
26269600-5	2015	Frequent loss of MOAP-1 expression, in at least some cancers, appears to be attributed to mRNA down-regulation and the rapid proteasomal degradation of MOAP-1 that could be reversed utilizing the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	217-222	modulator of apoptosis 1	Homo sapiens	17-23
26269600-5	2015	Frequent loss of MOAP-1 expression, in at least some cancers, appears to be attributed to mRNA down-regulation and the rapid proteasomal degradation of MOAP-1 that could be reversed utilizing the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	217-222	modulator of apoptosis 1	Homo sapiens	152-158
25888580-8	2015	MG132, a proteasome inhibitor, prevented the decrease of ACDase protein when cultured in CS-FCS, suggesting the involvement of ubiquitin/proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	N-acylsphingosine amidohydrolase 1	Homo sapiens	57-63
26238156-7	2015	Radiation-induced NF-kappaB expression and IkappaBalpha phosphorylation was attenuated in MG132 plus irradiation-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	NFKB inhibitor alpha	Homo sapiens	43-55
26418009-6	2015	MG-132, a proteasomal inhibitor also prevented the rosiglitazone-induced degradation of Runx2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	RUNX family transcription factor 2	Homo sapiens	88-93
25605253-3	2015	SAHA and/or HDAC2 siRNA increased Mdm2 ubiquitination, and MG132, an inhibitor of proteosome function, prevented HDAC2 inhibition-induced degradation of Mdm2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	histone deacetylase 2	Homo sapiens	113-118
25605253-3	2015	SAHA and/or HDAC2 siRNA increased Mdm2 ubiquitination, and MG132, an inhibitor of proteosome function, prevented HDAC2 inhibition-induced degradation of Mdm2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	MDM2 proto-oncogene	Homo sapiens	153-157
26377801-14	2015	In contrast, MG132 treatment increased PEX5 levels, implicating the proteasome in degrading PEX5, especially at high temperature.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	peroxin 5	Arabidopsis thaliana	92-96
26225746-7	2015	Notably, this reduction in the total-TH protein level was sensitive not only to a 26S proteasomal inhibitor, MG-132, but also to a PKA inhibitor, H-89.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-115	tyrosine hydroxylase	Rattus norvegicus	37-39
26179602-8	2015	MG132 and bafilomycin A, proteasomal and lysosomal inhibitors, respectively, also inhibited the ANG II-induced reduction in surface and total BKalpha, resulting in intracellular BKalpha accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	angiotensinogen	Homo sapiens	96-102
26179602-8	2015	MG132 and bafilomycin A, proteasomal and lysosomal inhibitors, respectively, also inhibited the ANG II-induced reduction in surface and total BKalpha, resulting in intracellular BKalpha accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	FCF1 rRNA-processing protein	Homo sapiens	142-149
26179602-8	2015	MG132 and bafilomycin A, proteasomal and lysosomal inhibitors, respectively, also inhibited the ANG II-induced reduction in surface and total BKalpha, resulting in intracellular BKalpha accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	FCF1 rRNA-processing protein	Homo sapiens	178-185
26052093-9	2015	In an orthotopic xenograft model of SCID mice, combination MG132 and IR therapy resulted in a significant increase in the tumor growth delay time and a decreased tumor tissue expression of TRAF6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	TNF receptor-associated factor 6	Mus musculus	189-194
26353013-14	2015	When proteasomal degradation of proteins was blocked by MG132 co-treatment, EBR treatment further induced PARP cleavage relative to drug treatment alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	collagen type XI alpha 2 chain	Homo sapiens	106-110
26212436-7	2015	The reduction of both Cx43 expression and GJIC induced by a mixture of TNF-alpha and IFN-gamma were blocked by pretreatment with proteasome inhibitors MG132 (0.5 muM) and epoxomicin (25 nM), a mixture of TNF-alpha and IFN-gamma significantly increased proteasome activity and Cx43 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	gap junction protein, alpha 1	Rattus norvegicus	22-26
26212436-7	2015	The reduction of both Cx43 expression and GJIC induced by a mixture of TNF-alpha and IFN-gamma were blocked by pretreatment with proteasome inhibitors MG132 (0.5 muM) and epoxomicin (25 nM), a mixture of TNF-alpha and IFN-gamma significantly increased proteasome activity and Cx43 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	tumor necrosis factor	Rattus norvegicus	71-80
26212436-7	2015	The reduction of both Cx43 expression and GJIC induced by a mixture of TNF-alpha and IFN-gamma were blocked by pretreatment with proteasome inhibitors MG132 (0.5 muM) and epoxomicin (25 nM), a mixture of TNF-alpha and IFN-gamma significantly increased proteasome activity and Cx43 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	interferon gamma	Rattus norvegicus	85-94
26212436-7	2015	The reduction of both Cx43 expression and GJIC induced by a mixture of TNF-alpha and IFN-gamma were blocked by pretreatment with proteasome inhibitors MG132 (0.5 muM) and epoxomicin (25 nM), a mixture of TNF-alpha and IFN-gamma significantly increased proteasome activity and Cx43 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	tumor necrosis factor	Rattus norvegicus	204-213
26212436-7	2015	The reduction of both Cx43 expression and GJIC induced by a mixture of TNF-alpha and IFN-gamma were blocked by pretreatment with proteasome inhibitors MG132 (0.5 muM) and epoxomicin (25 nM), a mixture of TNF-alpha and IFN-gamma significantly increased proteasome activity and Cx43 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	interferon gamma	Rattus norvegicus	218-227
26212436-7	2015	The reduction of both Cx43 expression and GJIC induced by a mixture of TNF-alpha and IFN-gamma were blocked by pretreatment with proteasome inhibitors MG132 (0.5 muM) and epoxomicin (25 nM), a mixture of TNF-alpha and IFN-gamma significantly increased proteasome activity and Cx43 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	gap junction protein, alpha 1	Rattus norvegicus	276-280
26317694-4	2015	The information derived from this analysis was used to study the functional role and the interplay of the identified HSEs in mediating the transcriptional activation of the UBC gene under conditions of proteotoxic stress, induced by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	258-263	ubiquitin C	Homo sapiens	173-176
26033448-5	2015	In a cell-based IkappaBalpha degradation assay, Thsp is a slow inhibitor and 4 hrs of treatment achieves the same effects as MG-132 at 30 min.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-131	NFKB inhibitor alpha	Homo sapiens	16-28
26102006-13	2015	The proteasome inhibitor MG-132 was able to increase YB-1 protein levels in control and LPS-treated cultures.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	Y box protein 1	Mus musculus	53-57
26036313-5	2015	In cIAP2 overexpressing cells a decreased sensitivity to the proteasome inhibitors bortezomib, MG132 and carfilzomib was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	baculoviral IAP repeat containing 3	Homo sapiens	3-8
25904053-5	2015	After treated with cisplatin, MG132, paclitaxel and SAHA, both BTG3 transfectants showed lower viability and higher apoptosis than the control in both time- and dose-dependent manners (p &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	BTG anti-proliferation factor 3	Homo sapiens	63-67
25904053-6	2015	BTG3 expression was restored after 5-aza-2"-deoxycytidine or MG132 treatment in gastric cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	BTG anti-proliferation factor 3	Homo sapiens	0-4
25872876-8	2015	In contrast, troglitazone caused a decrease in c-Myc levels, while the proteasomal inhibitor, MG132, rescued c-Myc, ASCT2 and GLS1 expression, as well as glutamine uptake and cell number.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	109-114
25980581-6	2015	Compared with the control, ING5 transfectants displayed drug resistance to triciribine, paclitaxel, cisplatin, SAHA, MG132 and parthenolide, which was positively related to their apoptotic induction and the overexpression of chemoresistance-related genes (MDR1, GRP78, GRP94, IRE, CD147, FBXW7, TOP1, TOP2, MLH1, MRP1, BRCP1 and GST-pi).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	inhibitor of growth family member 5	Homo sapiens	27-31
26050197-3	2015	After treated with cisplatin, MG132, paclitaxel and SAHA, both BTG1 transfectants showed lower mRNA viability and higher apoptosis than the control in both time- and dose-dependent manners (p &lt; 0.05) with the hypoexpression of chemoresistance-related genes (slug, CD147, GRP78, GRP94, FBXW7 TOP1, TOP2 and GST-pi).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	BTG anti-proliferation factor 1	Homo sapiens	63-67
26079886-4	2015	Following treatment with camptothecin, endogenous or overexpressed PPARgamma becomes destabilized; this was prevented in the presence of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	peroxisome proliferator activated receptor gamma	Mus musculus	67-76
25872876-8	2015	In contrast, troglitazone caused a decrease in c-Myc levels, while the proteasomal inhibitor, MG132, rescued c-Myc, ASCT2 and GLS1 expression, as well as glutamine uptake and cell number.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	solute carrier family 1 member 5	Homo sapiens	116-121
25872876-8	2015	In contrast, troglitazone caused a decrease in c-Myc levels, while the proteasomal inhibitor, MG132, rescued c-Myc, ASCT2 and GLS1 expression, as well as glutamine uptake and cell number.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	glutaminase	Homo sapiens	126-130
25877955-8	2015	The effects of SUMO overexpression, SUMO E3 overexpression, and Proteasome inhibitor MG132 respectively on the stability and transcriptional activity of HIF-1alpha were analyzed by immunoblot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	hypoxia inducible factor 1 subunit alpha	Homo sapiens	153-163
26096843-11	2015	Combined treatment with GSK3alpha/beta inhibitor LiCl or proteasome inhibitor MG132 blocked gamma-tocotrienol-induced reductions in c-Myc.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	132-137
25877955-13	2015	Proteasome inhibitor MG132 protected the stability and transcriptional activity of HIF-1alpha in the SRA01/04 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	hypoxia inducible factor 1 subunit alpha	Homo sapiens	83-93
26165647-5	2015	Since the expression levels of these CDK inhibitor proteins in FXR-knockdown Fa2N-4 cells were elevated in the presence of proteasomal inhibitor MG132, these CDK inhibitors may be subjected to the proteasomal degradation, thereby counteracting the increased expression of their cognate mRNAs, therefore similar levels of p16 and p21 proteins were observed in control and FXR-knockdown Fa2N-4 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	nuclear receptor subfamily 1 group H member 4	Homo sapiens	63-66
26165647-5	2015	Since the expression levels of these CDK inhibitor proteins in FXR-knockdown Fa2N-4 cells were elevated in the presence of proteasomal inhibitor MG132, these CDK inhibitors may be subjected to the proteasomal degradation, thereby counteracting the increased expression of their cognate mRNAs, therefore similar levels of p16 and p21 proteins were observed in control and FXR-knockdown Fa2N-4 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	cyclin dependent kinase inhibitor 2A	Homo sapiens	321-324
26165647-5	2015	Since the expression levels of these CDK inhibitor proteins in FXR-knockdown Fa2N-4 cells were elevated in the presence of proteasomal inhibitor MG132, these CDK inhibitors may be subjected to the proteasomal degradation, thereby counteracting the increased expression of their cognate mRNAs, therefore similar levels of p16 and p21 proteins were observed in control and FXR-knockdown Fa2N-4 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	cyclin dependent kinase inhibitor 1A	Homo sapiens	329-332
26165647-5	2015	Since the expression levels of these CDK inhibitor proteins in FXR-knockdown Fa2N-4 cells were elevated in the presence of proteasomal inhibitor MG132, these CDK inhibitors may be subjected to the proteasomal degradation, thereby counteracting the increased expression of their cognate mRNAs, therefore similar levels of p16 and p21 proteins were observed in control and FXR-knockdown Fa2N-4 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	nuclear receptor subfamily 1 group H member 4	Homo sapiens	371-374
25869056-8	2015	Results in experiments treated with MG-132 or cycloheximide (CHX) showed that andrographolide lowered the content of beta-catenin in cell nucleus resulting from accelerating the degradation of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	catenin (cadherin associated protein), beta 1	Mus musculus	117-129
26157550-5	2015	Inhibition of proteasomal degradation by MG132 blocked NAR-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with NAR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cyclin D1	Homo sapiens	68-77
26070564-8	2015	Co-administration of the inducible NOS inhibitor S-methylisothiourea or the proteasome inhibitor MG132 prevented LPS-induced LKB1 degradation and improved the survival rate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	toll-like receptor 4	Mus musculus	113-116
26070564-8	2015	Co-administration of the inducible NOS inhibitor S-methylisothiourea or the proteasome inhibitor MG132 prevented LPS-induced LKB1 degradation and improved the survival rate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	serine/threonine kinase 11	Mus musculus	125-129
26183326-6	2015	Finally, pretreatment of cells with the proteasome inhibitor MG132 markedly increases the level of aggresomes formed by Tks4(R43W).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	SH3 and PX domains 2B	Homo sapiens	120-124
26146544-8	2015	The dual specific proteasome/calpain inhibitor MG132 and the specific calpain inhibitor 1 rescued SMAD2 degradation, substantiating the ability of calpain to degrade SMAD2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	SMAD family member 2	Homo sapiens	98-103
26133378-0	2015	Hepatitis C Virus Nonstructural Protein 5A Inhibits MG132-Induced Apoptosis of Hepatocytes in Line with NF-kappaB-Nuclear Translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	nuclear factor kappa B subunit 1	Homo sapiens	104-113
26133378-7	2015	In agreement with this, after treatment with MG132, HCV NS5A could elevate the transcription of several NF-kappaB target genes such as BCL2 and BCLXL to inhibit MG132-induced apoptosis in hepatocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	nuclear factor kappa B subunit 1	Homo sapiens	104-113
26133378-7	2015	In agreement with this, after treatment with MG132, HCV NS5A could elevate the transcription of several NF-kappaB target genes such as BCL2 and BCLXL to inhibit MG132-induced apoptosis in hepatocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-166	nuclear factor kappa B subunit 1	Homo sapiens	104-113
26121043-6	2015	Since the down-regulation of cyclin D1 was completely blocked by a proteasome inhibitor MG132, the suppression of cyclin D1 expression by resibufogenin was considered to be in a proteasome-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	cyclin D1	Homo sapiens	29-38
26087957-10	2015	Furthermore, the effect of MK-2206 on Mcl-1 downregulation was abolished by GSK3beta inhibitor, lithium chloride and proteasome inhibitor, MG-132, suggesting that MK-2206 acted through a GSK3beta-mediated, proteasome-dependent protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-145	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	38-43
26087957-10	2015	Furthermore, the effect of MK-2206 on Mcl-1 downregulation was abolished by GSK3beta inhibitor, lithium chloride and proteasome inhibitor, MG-132, suggesting that MK-2206 acted through a GSK3beta-mediated, proteasome-dependent protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-145	glycogen synthase kinase 3 beta	Homo sapiens	187-195
25900982-3	2015	Combining 26S proteasome inhibitor (MG132) treatment with proximity-dependent biotin labeling (BioID) and semiquantitative mass spectrometry, here we identify SCF(beta-TrCP1/2) interacting partners.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	KIT ligand	Homo sapiens	159-162
25900982-3	2015	Combining 26S proteasome inhibitor (MG132) treatment with proximity-dependent biotin labeling (BioID) and semiquantitative mass spectrometry, here we identify SCF(beta-TrCP1/2) interacting partners.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	163-175
25900982-4	2015	Based on their enrichment in the presence of MG132, our data identify over 50 new putative SCF(beta-TrCP1/2) substrates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	KIT ligand	Homo sapiens	91-94
25900982-4	2015	Based on their enrichment in the presence of MG132, our data identify over 50 new putative SCF(beta-TrCP1/2) substrates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	beta-transducin repeat containing E3 ubiquitin protein ligase	Homo sapiens	95-107
25725482-3	2015	We report that an Fbxo25-mediated SCF ubiquitination pathway regulates the protein levels and activities of Tbx5 and Nkx2-5 based on our studies using MG132, proteasome inhibitor, and the temperature sensitive ubiquitin system in ts20 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	F-box protein 25	Mus musculus	18-24
25888683-8	2015	MG132, a proteasomal inhibitor, rescued PC-1 knockdown-dependent declines in alpha1C protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	polycystin 1, transient receptor potential channel interacting	Mus musculus	40-44
26098428-3	2015	By using a proteasome inhibitor MG132 and a translation inhibitor cyclohexamide, we showed that CDCA reduced HIF-1alpha protein by decreasing its translation but not by enhancing its degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	hypoxia inducible factor 1 subunit alpha	Homo sapiens	109-119
26098428-5	2015	Distinctly from CDCA, MG132 prevented SHP and an exogenous FXR agonist, GW4064 from reducing HIF-1alpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	nuclear receptor subfamily 0 group B member 2	Homo sapiens	38-41
26098428-5	2015	Distinctly from CDCA, MG132 prevented SHP and an exogenous FXR agonist, GW4064 from reducing HIF-1alpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	hypoxia inducible factor 1 subunit alpha	Homo sapiens	93-103
26087256-10	2015	RESULTS: Treatment with TSH/M22 induced TNFalpha protein and mRNA production by FCs, both of which were reduced when FCs were pretreated with MG132 and AKTi (p&lt;0.0001).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	tumor necrosis factor	Homo sapiens	40-48
25725482-3	2015	We report that an Fbxo25-mediated SCF ubiquitination pathway regulates the protein levels and activities of Tbx5 and Nkx2-5 based on our studies using MG132, proteasome inhibitor, and the temperature sensitive ubiquitin system in ts20 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	kit ligand	Mus musculus	34-37
25725482-3	2015	We report that an Fbxo25-mediated SCF ubiquitination pathway regulates the protein levels and activities of Tbx5 and Nkx2-5 based on our studies using MG132, proteasome inhibitor, and the temperature sensitive ubiquitin system in ts20 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	T-box 5	Mus musculus	108-112
25725482-3	2015	We report that an Fbxo25-mediated SCF ubiquitination pathway regulates the protein levels and activities of Tbx5 and Nkx2-5 based on our studies using MG132, proteasome inhibitor, and the temperature sensitive ubiquitin system in ts20 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	NK2 homeobox 5	Mus musculus	117-123
25821107-11	2015	Treatment of the cells with LY294002 resulted in a G1 cell cycle arrest, a nuclear expression of p27(Kip1), and a cytoplasmic p27(Kip1) accumulation after subsequent treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	181-186	zinc ribbon domain containing 2	Homo sapiens	97-100
25821107-11	2015	Treatment of the cells with LY294002 resulted in a G1 cell cycle arrest, a nuclear expression of p27(Kip1), and a cytoplasmic p27(Kip1) accumulation after subsequent treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	181-186	zinc ribbon domain containing 2	Homo sapiens	126-129
25821107-11	2015	Treatment of the cells with LY294002 resulted in a G1 cell cycle arrest, a nuclear expression of p27(Kip1), and a cytoplasmic p27(Kip1) accumulation after subsequent treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	181-186	cyclin dependent kinase inhibitor 1B	Homo sapiens	130-134
25821107-12	2015	Additionally, we found that the synergistic effect of MG132 and LY294002 resulted in a sub-G1 cell cycle arrest and apoptosis induction through poly (ADP-ribose) polymerase (PARP) cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	poly(ADP-ribose) polymerase 1	Homo sapiens	144-172
25821107-12	2015	Additionally, we found that the synergistic effect of MG132 and LY294002 resulted in a sub-G1 cell cycle arrest and apoptosis induction through poly (ADP-ribose) polymerase (PARP) cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	poly(ADP-ribose) polymerase 1	Homo sapiens	174-178
25733566-7	2015	The repression was abolished by the proteasome inhibitor MG132, suggesting that lamin B1 stabilizes RAD51 by preventing proteasome-mediated degradation in cells with IR-induced DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	lamin B1	Homo sapiens	80-88
25733566-7	2015	The repression was abolished by the proteasome inhibitor MG132, suggesting that lamin B1 stabilizes RAD51 by preventing proteasome-mediated degradation in cells with IR-induced DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	RAD51 recombinase	Homo sapiens	100-105
25475100-6	2015	MG132, a potent proteasome pathway inhibitor, abrogated TSA-induced protective effects, which was associated with the accumulation of ubiquitinated HDAC4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	histone deacetylase 4	Mus musculus	148-153
25640060-7	2015	The Hsp70 inhibitors greatly potentiated the toxicity of sublethal lactacystin or MG132 but not of paraquat.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	4-9
26056062-3	2015	Under isotonic conditions p53 expression increased after addition of the proteasome inhibitor MG132 indicating that cellular p53 levels in unperturbed cells is kept low by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	transformation related protein 53, pseudogene	Mus musculus	26-29
25997740-4	2015	MG132, an inhibitor of proteasomal degradation, induced the expression of HDAC3 in various anti-cancer drug-resistant cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	histone deacetylase 3	Mus musculus	74-79
26056062-3	2015	Under isotonic conditions p53 expression increased after addition of the proteasome inhibitor MG132 indicating that cellular p53 levels in unperturbed cells is kept low by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	transformation related protein 53, pseudogene	Mus musculus	125-128
25869100-6	2015	Pre-treatment of cells with MG-132 blocked capsaicin-mediated proteasomal degradation of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	catenin beta 1	Homo sapiens	89-101
25961950-9	2015	The inhibition of proteasomal degradation using MG132 (carbobenzoxy-Leu-Leu-leucinal) and lactacystin ameliorates resveratrol-stimulated down-regulation of TCF4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	transcription factor 7 like 2	Homo sapiens	156-160
25824035-8	2015	Moreover, in the presence of MG132, a decrease of HO-1 expression also occurred at 100 and 200 muM hemin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	heme oxygenase 1	Rattus norvegicus	50-54
25824035-9	2015	The effect of MG132 was mimicked by two additional mechanistically different approaches which also raised HO-1 content: a) co-incubations of hemin with ZnPP which increased HO-1 protein when used alone, and b) glomerular HO-1 over expression achieved by SB transposon mediated transgenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	heme oxygenase 1	Rattus norvegicus	106-110
25824035-9	2015	The effect of MG132 was mimicked by two additional mechanistically different approaches which also raised HO-1 content: a) co-incubations of hemin with ZnPP which increased HO-1 protein when used alone, and b) glomerular HO-1 over expression achieved by SB transposon mediated transgenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	heme oxygenase 1	Rattus norvegicus	173-177
25824035-9	2015	The effect of MG132 was mimicked by two additional mechanistically different approaches which also raised HO-1 content: a) co-incubations of hemin with ZnPP which increased HO-1 protein when used alone, and b) glomerular HO-1 over expression achieved by SB transposon mediated transgenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	heme oxygenase 1	Rattus norvegicus	173-177
25656993-7	2015	Furthermore, pretreatment with proteasome inhibitor MG132 completely blunted oxidant-induced p21 degradation, indicating a proteasome-dependent action.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	cyclin dependent kinase inhibitor 1A	Homo sapiens	93-96
25941117-6	2015	The effect of MG132 on MCF7 was reproduced on MCF10A cells in the presence of the glycogen synthase kinase 3beta (GSK-3beta) inhibitor VII.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	glycogen synthase kinase 3 beta	Homo sapiens	82-112
25941117-6	2015	The effect of MG132 on MCF7 was reproduced on MCF10A cells in the presence of the glycogen synthase kinase 3beta (GSK-3beta) inhibitor VII.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	glycogen synthase kinase 3 beta	Homo sapiens	114-123
25964540-9	2015	Molecular docking studies of kaempferol revealed comparable binding energies and similar docking poses on target proteins such as MG-132, a known NF-kappaB inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-136	nuclear factor kappa B subunit 1	Homo sapiens	146-155
25667221-9	2015	Consistent with a role for Cep55 in regulation of Akt stability, treatment with proteasome inhibitor, MG132, partially rescued the homozygous mutants.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-107	centrosomal protein 55 like	Danio rerio	27-32
25561363-5	2015	Treatment with the proteasome inhibitor MG132 increased protein levels of HDAC1 in cells transfected with HDAC1 but not in cells co-transfected with HDAC1 and c-Abl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	histone deacetylase 1	Homo sapiens	74-79
26137056-8	2015	MG-132-induced apoptosis was enhanced by the autophagy inhibitor 3-MA, which may be a result of caspase-3 activation in the EC9706 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 3	Homo sapiens	96-105
25713071-9	2015	Treatment with MG132 and inhibiting PKA with H89 or with a dominant-negative PKA abolished the cAMP-mediated reduction in SIRT6 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	sirtuin 6	Homo sapiens	122-127
25853243-7	2015	In addition, the proteasome inhibitor MG132 inhibits the endocytosis of TGFBIp.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	transforming growth factor beta induced	Homo sapiens	72-78
25596551-16	2015	Proteasome inhibitor MG132 reversed the decreased expression of cFos protein, and the decreased mRNA and protein expression of VEGFD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-68
25596551-16	2015	Proteasome inhibitor MG132 reversed the decreased expression of cFos protein, and the decreased mRNA and protein expression of VEGFD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	vascular endothelial growth factor D	Homo sapiens	127-132
25793965-4	2015	The pretreatment of AGS cells with a proteasome inhibitor, either MG132 or epoxomicin, protected against the degradation of beta-catenin induced by 1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	catenin beta 1	Homo sapiens	124-136
25561363-5	2015	Treatment with the proteasome inhibitor MG132 increased protein levels of HDAC1 in cells transfected with HDAC1 but not in cells co-transfected with HDAC1 and c-Abl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	histone deacetylase 1	Homo sapiens	106-111
25561363-5	2015	Treatment with the proteasome inhibitor MG132 increased protein levels of HDAC1 in cells transfected with HDAC1 but not in cells co-transfected with HDAC1 and c-Abl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	histone deacetylase 1	Homo sapiens	106-111
25637945-9	2015	Surprisingly, treatment with the proteasome inhibitor MG132, but not the lysosomal inhibitor chloroquine, caused Sesn2 to accumulate in the cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	sestrin 2	Mus musculus	113-118
25826722-4	2015	Herein, we demonstrate that acute combinatorial treatment with the proteasome inhibitors MG101 or MG132 and the histone deacetylase (HDAC) inhibitor valproic acid (VPA) increases gene expression of the pluripotency marker Oct3/4, and that MG101 alone is as effective as VPA in the induction of Oct3/4 mRNA expression in fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	POU class 5 homeobox 1	Homo sapiens	222-228
25826722-4	2015	Herein, we demonstrate that acute combinatorial treatment with the proteasome inhibitors MG101 or MG132 and the histone deacetylase (HDAC) inhibitor valproic acid (VPA) increases gene expression of the pluripotency marker Oct3/4, and that MG101 alone is as effective as VPA in the induction of Oct3/4 mRNA expression in fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	POU class 5 homeobox 1	Homo sapiens	294-300
25434725-11	2015	Pharmacological inhibition of HDAC6 by the selective inhibitor tubastatin A (TST) and its small hairpin RNA (shRNA)-mediated downregulation alters the assembly of MG-132-induced compact protein aggregates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-169	histone deacetylase 6	Rattus norvegicus	30-35
25434725-14	2015	Furthermore, the heat shock response is altered, and TST suppresses the MG-132-stimulated induction of HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	103-108
25637945-10	2015	In the presence of MG132, we observed that Sesn2 was ubiquitinated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	sestrin 2	Mus musculus	43-48
25637945-11	2015	However, LPS treatment attenuated Sesn2 ubiquitination induced by MG132, which resulted in Sesn2 accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	sestrin 2	Mus musculus	34-39
25637945-11	2015	However, LPS treatment attenuated Sesn2 ubiquitination induced by MG132, which resulted in Sesn2 accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	sestrin 2	Mus musculus	91-96
25322811-4	2015	We found that the proteasome inhibitor MG-132 specifically induces in NB4 cells an Nrf2-mediated antioxidant response which counteracts mitochondria-dependent apoptosis induced by the lipophilic cation dequalinium.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	NFE2 like bZIP transcription factor 2	Homo sapiens	83-87
25807533-10	2015	Pretreatment with protease inhibitor MG132, or selective knock-down of Siah2 (but not Keap1) significantly attenuated hypoglycemia-induced Nrf2 destabilization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	NFE2 like bZIP transcription factor 2	Homo sapiens	139-143
25815818-3	2015	A C-terminal cleaved product of Dicer protein was detected in the presence of MG132 during VV infection.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	dicer 1, ribonuclease III	Homo sapiens	32-37
25799543-8	2015	Proteasome inhibition (MG132) returned HIF-1alpha levels to control or wildtype levels respectively in these cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	hypoxia inducible factor 1 subunit alpha	Homo sapiens	39-49
24924397-4	2015	Treatment of cells with cycloheximide in the presence of proteasome inhibitor MG132 suggested that Mcl-1 protein levels were regulated at the post-translational step.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	99-104
25615907-8	2015	MG132 (a specific cell-permeable proteasome inhibitor) blocked mitotic entry and arrested cell cycle at G2 phase, preventing down-regulation of MMP-2 and -9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	matrix metallopeptidase 2	Homo sapiens	144-156
25601714-7	2015	Both lysosome inhibitors (chloroquine, pepstatin A plus E64d) and proteasome inhibitor MG132 can inhibit Hsf4-mediated Hsf1 protein degradation, but MG132 can induce Hsf1 activation as well.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	heat shock transcription factor 4	Homo sapiens	105-109
25601714-7	2015	Both lysosome inhibitors (chloroquine, pepstatin A plus E64d) and proteasome inhibitor MG132 can inhibit Hsf4-mediated Hsf1 protein degradation, but MG132 can induce Hsf1 activation as well.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	heat shock transcription factor 1	Homo sapiens	119-123
25601714-7	2015	Both lysosome inhibitors (chloroquine, pepstatin A plus E64d) and proteasome inhibitor MG132 can inhibit Hsf4-mediated Hsf1 protein degradation, but MG132 can induce Hsf1 activation as well.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	heat shock transcription factor 1	Homo sapiens	166-170
25601714-7	2015	Both lysosome inhibitors (chloroquine, pepstatin A plus E64d) and proteasome inhibitor MG132 can inhibit Hsf4-mediated Hsf1 protein degradation, but MG132 can induce Hsf1 activation as well.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-154	heat shock transcription factor 1	Homo sapiens	166-170
25615593-6	2015	Inhibition of proteasomal degradation by MG132 blocked TAN I-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with TAN I.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cyclin D1	Homo sapiens	70-79
25071087-7	2015	In vitro, overexpression of beta-catenin induced WT1 protein degradation through the ubiquitin proteasomal pathway, which was blocked by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-143	catenin (cadherin associated protein), beta 1	Mus musculus	28-40
25071087-7	2015	In vitro, overexpression of beta-catenin induced WT1 protein degradation through the ubiquitin proteasomal pathway, which was blocked by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-143	WT1 transcription factor	Mus musculus	49-52
25542213-8	2015	Furthermore, the inhibition of proteosomal degradation pathway using MG132 or LLNV drugs resulted in accumulation and co-localization of CUL4A with gamma-tubulin in the centrosome region.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	cullin 4A	Homo sapiens	137-142
25476842-5	2015	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases(-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BH3 interacting domain death agonist	Rattus norvegicus	64-67
25434876-6	2015	It was revealed that MG132 increased the expression of A53T alpha-syn and trehalose counteracted the increase of A53T alpha-syn induced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	synuclein alpha	Rattus norvegicus	60-69
25434876-6	2015	It was revealed that MG132 increased the expression of A53T alpha-syn and trehalose counteracted the increase of A53T alpha-syn induced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	synuclein alpha	Rattus norvegicus	118-127
25434876-6	2015	It was revealed that MG132 increased the expression of A53T alpha-syn and trehalose counteracted the increase of A53T alpha-syn induced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	synuclein alpha	Rattus norvegicus	118-127
25434876-9	2015	These results suggest that the PI, MG132, could induce autophagy in PC12 cells overexpressing A53T mutant alpha-syn and this autophagy could be completely inhibited by 3-MA, indicating that PI-induced autophagy is mediated by the upregulation of the macroautophagy class III PI3K pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	synuclein alpha	Rattus norvegicus	106-115
25476842-5	2015	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases(-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2, apoptosis regulator	Rattus norvegicus	69-74
25476842-5	2015	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases(-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2 associated X, apoptosis regulator	Rattus norvegicus	120-123
25476842-5	2015	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases(-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	caspase 8	Rattus norvegicus	212-234
25476842-5	2015	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases(-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	273-276
25476842-5	2015	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases(-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	poly (ADP-ribose) polymerase 1	Rattus norvegicus	300-306
25540198-6	2015	By applying inhibitors to selectively block the ubiquitin proteasome system (UPS) and autophagy-lysosomal pathway, we show that HNF1alpha protein content in HepG2 cells was not affected by bafilomycin A1 treatment, but it was dose-dependently increased by UPS inhibitors bortezomib and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	286-291	HNF1 homeobox A	Homo sapiens	128-137
25750920-8	2015	Finally, inhibition of the ubiquitin-proteasome system with MG132 produced TDP-43 aggregation similar to DUX4-FL expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	TAR DNA binding protein	Homo sapiens	75-81
25187114-8	2015	MG-132 treatment of MCF7 cells increased endogenous or exogenous RGS2 levels, suggesting a post-transcriptional regulatory mechanism that controls RGS2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	regulator of G protein signaling 2	Homo sapiens	65-69
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	77-80
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma	Homo sapiens	84-95
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	128-131
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma	Homo sapiens	143-154
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma	Homo sapiens	143-154
25187114-8	2015	MG-132 treatment of MCF7 cells increased endogenous or exogenous RGS2 levels, suggesting a post-transcriptional regulatory mechanism that controls RGS2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	regulator of G protein signaling 2	Homo sapiens	147-151
25629611-6	2015	Treatment of naive splenocytes with the proteasomal inhibitor, MG132, stabilized Ikaros expression and prevented Ikaros downregulation by Panc02 cells, in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	IKAROS family zinc finger 1	Mus musculus	81-87
25633295-7	2015	Additionally, LMP2 knockdown significantly reduced activated astrocytes and microglia, the expression nuclear factor kappa B (NF-kappaB) p65, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) and caused less accumulation of ischemia-induced protein ubiquitination compared with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	301-306	proteasome 20S subunit beta 9	Rattus norvegicus	14-18
25907486-3	2015	ABCA1 mRNA and protein expression in mature 3T3-L1 adipocytes post stimulation with various concentrations of insulin was detected by real-time fluorescence-based quantitative techniques and Western blot, respectively, in the absence and presence of CHX (cycloheximide, CHX), calpeptin (calpain pathway inhibitor) or MG-132 (proteasome pathway inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	317-323	ATP binding cassette subfamily A member 1	Homo sapiens	0-5
25907486-9	2015	Both calpeptin and MG-132 could partly reduce insulin-induced degradation of ABCA1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	insulin	Homo sapiens	46-53
25907486-9	2015	Both calpeptin and MG-132 could partly reduce insulin-induced degradation of ABCA1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	ATP binding cassette subfamily A member 1	Homo sapiens	77-82
25907486-10	2015	Compared with the negative control group, ABCA1 protein levels were significantly upregulated by cotreatment with calpeptin and MG-132, respectively (both P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-134	ATP binding cassette subfamily A member 1	Homo sapiens	42-47
25623232-10	2015	Furthermore, ZBP-89-mediated HDAC3 reduction was suppressed by IkappaB degradation inhibitors CAY10576 and MG132 but not by p65/p50 translocation inhibitor SN50, indicating that IkappaB decrease rather than the elevated activity of NF-kappaB contributed to HDAC3 reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	zinc finger protein 148	Mus musculus	13-19
25623232-10	2015	Furthermore, ZBP-89-mediated HDAC3 reduction was suppressed by IkappaB degradation inhibitors CAY10576 and MG132 but not by p65/p50 translocation inhibitor SN50, indicating that IkappaB decrease rather than the elevated activity of NF-kappaB contributed to HDAC3 reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	histone deacetylase 3	Mus musculus	29-34
25629611-6	2015	Treatment of naive splenocytes with the proteasomal inhibitor, MG132, stabilized Ikaros expression and prevented Ikaros downregulation by Panc02 cells, in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	IKAROS family zinc finger 1	Mus musculus	113-119
25629611-12	2015	MG132 treatment of naive CD3+ T cells stabilized Ikaros expression in the presence of Panc02 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	IKAROS family zinc finger 1	Mus musculus	49-55
25344893-7	2015	Mcl-1 expression was stabilized with MG-132, an inhibitor of proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5
25513960-5	2015	Proteasome inhibitors (MG132 and epoxomicin) suppressed TNF-alpha plus CHX-induced degradation of survivin, cIAP1, and XIAP as well as apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	tumor necrosis factor	Homo sapiens	56-65
25513960-5	2015	Proteasome inhibitors (MG132 and epoxomicin) suppressed TNF-alpha plus CHX-induced degradation of survivin, cIAP1, and XIAP as well as apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	baculoviral IAP repeat containing 2	Homo sapiens	108-113
25513960-5	2015	Proteasome inhibitors (MG132 and epoxomicin) suppressed TNF-alpha plus CHX-induced degradation of survivin, cIAP1, and XIAP as well as apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	X-linked inhibitor of apoptosis	Homo sapiens	119-123
25429107-8	2015	Both HDAC6 and p62 co-localized with ISG15 in an insoluble fraction of the cytosol, and this co-localization was magnified by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	histone deacetylase 6	Homo sapiens	5-10
25429107-8	2015	Both HDAC6 and p62 co-localized with ISG15 in an insoluble fraction of the cytosol, and this co-localization was magnified by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	sequestosome 1	Homo sapiens	15-18
25429107-8	2015	Both HDAC6 and p62 co-localized with ISG15 in an insoluble fraction of the cytosol, and this co-localization was magnified by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	ISG15 ubiquitin like modifier	Homo sapiens	37-42
25568123-5	2015	Downregulation of FMRP was dependent on group I mGluR activation and was blocked by a proteasome inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	fragile X messenger ribonucleoprotein 1	Mus musculus	18-22
25355627-6	2015	Proteotoxic stressors, such as celastrol and MG132, are known to activate HSF1, and are potent inducers of HSF1 binding and IER5 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	heat shock transcription factor 1	Homo sapiens	74-78
25774547-3	2015	We confirm that proteasome inhibitors MG-132 and bortezomib induce MKP-1 protein upregulation and we show that one of the ways in which bortezomib increases MKP-1 in breast cancer cells, in addition to inhibition of ubiquitin-proteasome system, is via upregulation of MKP-1 mRNA expression in p38 MAPK-mediated manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	dual specificity phosphatase 1	Homo sapiens	67-72
25774547-3	2015	We confirm that proteasome inhibitors MG-132 and bortezomib induce MKP-1 protein upregulation and we show that one of the ways in which bortezomib increases MKP-1 in breast cancer cells, in addition to inhibition of ubiquitin-proteasome system, is via upregulation of MKP-1 mRNA expression in p38 MAPK-mediated manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	dual specificity phosphatase 1	Homo sapiens	157-162
25774547-3	2015	We confirm that proteasome inhibitors MG-132 and bortezomib induce MKP-1 protein upregulation and we show that one of the ways in which bortezomib increases MKP-1 in breast cancer cells, in addition to inhibition of ubiquitin-proteasome system, is via upregulation of MKP-1 mRNA expression in p38 MAPK-mediated manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	dual specificity phosphatase 1	Homo sapiens	157-162
25774547-3	2015	We confirm that proteasome inhibitors MG-132 and bortezomib induce MKP-1 protein upregulation and we show that one of the ways in which bortezomib increases MKP-1 in breast cancer cells, in addition to inhibition of ubiquitin-proteasome system, is via upregulation of MKP-1 mRNA expression in p38 MAPK-mediated manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	mitogen-activated protein kinase 14	Homo sapiens	293-296
25590413-5	2015	We found that compared to the parental human uterus sarcoma cell line MES-SA cells, MES-SA/Dx5 cells highly expressed the ABCB1 was more resistant to MG132 and bortezomib, escaping the proteasome inhibitor-induced apoptosis pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	ATP binding cassette subfamily B member 1	Homo sapiens	122-127
25590413-7	2015	The data indicated that ABCB1 might play a role in the efflux of MG132 from the MES-SA/Dx5 cells to reduce MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	ATP binding cassette subfamily B member 1	Homo sapiens	24-29
25590413-7	2015	The data indicated that ABCB1 might play a role in the efflux of MG132 from the MES-SA/Dx5 cells to reduce MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	ATP binding cassette subfamily B member 1	Homo sapiens	24-29
26279425-9	2015	Moreover, MG132 exposed PTCs (L) demostrated blocked ubiquitinated Nox4 degradation and increased colocalization of Nox4/Ubiquitin by inmunofluorescence.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	NADPH oxidase 4	Homo sapiens	67-71
26279425-9	2015	Moreover, MG132 exposed PTCs (L) demostrated blocked ubiquitinated Nox4 degradation and increased colocalization of Nox4/Ubiquitin by inmunofluorescence.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	NADPH oxidase 4	Homo sapiens	116-120
25355627-6	2015	Proteotoxic stressors, such as celastrol and MG132, are known to activate HSF1, and are potent inducers of HSF1 binding and IER5 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	heat shock transcription factor 1	Homo sapiens	107-111
25355627-6	2015	Proteotoxic stressors, such as celastrol and MG132, are known to activate HSF1, and are potent inducers of HSF1 binding and IER5 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	immediate early response 5	Homo sapiens	124-128
25479723-7	2015	Inhibition of proteasomal degradation by MG132 attenuated silymarin-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with silymarin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cyclin D1	Homo sapiens	77-86
26620501-3	2015	The aim of this study is to determine the influence of intraventricular administration of MG-132, lactacystin and epoxomicin on the level in the rat striatum synapsin I - one of the most prominent neuron-specific phosphoproteins in the brain.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-96	synapsin I	Rattus norvegicus	158-168
25388970-5	2015	Blockage of UPS with MG-132 increased Cx31.1 level, but could not inhibit the degradation of Cx31.1 completely.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	gap junction protein beta 5	Homo sapiens	38-44
25792980-6	2015	Furthermore, the proteasomal inhibitor, MG132, dramatically increased SESN2 protein and its ubiquitination level while in the presence of MG132 insulin did not further increase SESN2 content, suggesting that insulin increases SESN2 content mainly via inhibiting its proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	sestrin 2	Homo sapiens	70-75
25792980-6	2015	Furthermore, the proteasomal inhibitor, MG132, dramatically increased SESN2 protein and its ubiquitination level while in the presence of MG132 insulin did not further increase SESN2 content, suggesting that insulin increases SESN2 content mainly via inhibiting its proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	insulin	Homo sapiens	208-215
25792980-6	2015	Furthermore, the proteasomal inhibitor, MG132, dramatically increased SESN2 protein and its ubiquitination level while in the presence of MG132 insulin did not further increase SESN2 content, suggesting that insulin increases SESN2 content mainly via inhibiting its proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	insulin	Homo sapiens	144-151
25069858-10	2015	Furthermore, rapamycin augmented MG-132-induced activation of extracellular signal-regulated kinases 1 and 2, which are involved in the regulation of cell death and survival.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	mitogen-activated protein kinase 3	Homo sapiens	62-108
26064977-5	2015	We found that palmitate and the proteasome inhibitor MG132 induced ER stress in beta-cells, resulting in decreased expression of the prosurvival proteins Bcl-2, Mcl-1, and Bcl-XL, and upregulation of the prodeath BH3-only protein PUMA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	BCL2 apoptosis regulator	Homo sapiens	154-159
25541949-12	2014	Treatment with MG132, a proteasome inhibitor, or siRNA of beta-TrCP1, an E3 ligase, prevented SIRT1 reduction induced by ULK1-siRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	sirtuin 1	Mus musculus	94-99
25723258-8	2015	Furthermore, treatment of cells with the proteasome inhibitor MG132 causes an enlargement of nucleolar SHIP1 containing structures.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	inositol polyphosphate-5-phosphatase D	Homo sapiens	103-108
25541949-12	2014	Treatment with MG132, a proteasome inhibitor, or siRNA of beta-TrCP1, an E3 ligase, prevented SIRT1 reduction induced by ULK1-siRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	unc-51 like kinase 1	Mus musculus	121-125
25084697-3	2014	We found that Src was degraded mainly by the proteasomal pathway because the proteasome inhibitor MG-132 but not the lysosome inhibitor NH4Cl suppressed the EPO-induced degradation of Src in F-36P cells and that knockdown of Cbl inhibited EPO-induced ubiquitination and degradation of Src in F-36P cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	14-17
25268952-3	2014	Here, we report that inhibition of proteasomal degradation with MG-132 and autophagy with bafilomycin A1 resulted in the release of IL-1beta but not that of IL-18 in human ARPE-19 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	interleukin 1 beta	Homo sapiens	132-140
25268952-6	2014	Along with IL-1beta, exposure to MG-132 and bafilomycin A1 resulted in the secretion of IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	interleukin 1 beta	Homo sapiens	11-19
25268952-6	2014	Along with IL-1beta, exposure to MG-132 and bafilomycin A1 resulted in the secretion of IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	C-X-C motif chemokine ligand 8	Homo sapiens	88-92
25501831-5	2014	In sharp contrast, TRAIL triggered full-blown cell death induction in HCT116 PIK3CA-mut cells treated with proteasome inhibitors such as bortezomib and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	TNF superfamily member 10	Homo sapiens	19-24
25501831-5	2014	In sharp contrast, TRAIL triggered full-blown cell death induction in HCT116 PIK3CA-mut cells treated with proteasome inhibitors such as bortezomib and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	77-83
25084697-3	2014	We found that Src was degraded mainly by the proteasomal pathway because the proteasome inhibitor MG-132 but not the lysosome inhibitor NH4Cl suppressed the EPO-induced degradation of Src in F-36P cells and that knockdown of Cbl inhibited EPO-induced ubiquitination and degradation of Src in F-36P cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	erythropoietin	Homo sapiens	157-160
25084697-3	2014	We found that Src was degraded mainly by the proteasomal pathway because the proteasome inhibitor MG-132 but not the lysosome inhibitor NH4Cl suppressed the EPO-induced degradation of Src in F-36P cells and that knockdown of Cbl inhibited EPO-induced ubiquitination and degradation of Src in F-36P cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	184-187
25084697-3	2014	We found that Src was degraded mainly by the proteasomal pathway because the proteasome inhibitor MG-132 but not the lysosome inhibitor NH4Cl suppressed the EPO-induced degradation of Src in F-36P cells and that knockdown of Cbl inhibited EPO-induced ubiquitination and degradation of Src in F-36P cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	Cbl proto-oncogene	Homo sapiens	225-228
25084697-3	2014	We found that Src was degraded mainly by the proteasomal pathway because the proteasome inhibitor MG-132 but not the lysosome inhibitor NH4Cl suppressed the EPO-induced degradation of Src in F-36P cells and that knockdown of Cbl inhibited EPO-induced ubiquitination and degradation of Src in F-36P cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	erythropoietin	Homo sapiens	239-242
25084697-3	2014	We found that Src was degraded mainly by the proteasomal pathway because the proteasome inhibitor MG-132 but not the lysosome inhibitor NH4Cl suppressed the EPO-induced degradation of Src in F-36P cells and that knockdown of Cbl inhibited EPO-induced ubiquitination and degradation of Src in F-36P cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	184-187
25446377-0	2014	Synergism of arsenic trioxide and MG132 in Raji cells attained by targeting BNIP3, autophagy, and mitochondria with low doses of valproic acid and vincristine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	BCL2 interacting protein 3	Homo sapiens	76-81
25446377-11	2014	We conclude that synergism between ATO and MG132 was attained in Raji cells by disruption of the perinuclear mitochondrial cluster, blockage of selective autophagy of mitochondria (mitophagy) by VCR, increased mitochondrial mass, and upregulation of BNIP3 by VPA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	BCL2 interacting protein 3	Homo sapiens	250-255
24752588-3	2014	In this study, proteasome inhibitor MG132 was used to treat hippocampal slices to explore the role and mechanism of Akt/glycogen synthase kinase-3beta (GSK-3beta) in proteasome inhibition-induced tau abnormality.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	AKT serine/threonine kinase 1	Homo sapiens	116-119
24752588-3	2014	In this study, proteasome inhibitor MG132 was used to treat hippocampal slices to explore the role and mechanism of Akt/glycogen synthase kinase-3beta (GSK-3beta) in proteasome inhibition-induced tau abnormality.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	glycogen synthase kinase 3 beta	Homo sapiens	152-161
24752588-7	2014	In addition, co-immunoprecipitation was used to investigate the interaction between Akt and Hsp90, Akt and protein phosphatase-2A (PP2A) in the MG132-treated organotypic hippocampal slices.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	AKT serine/threonine kinase 1	Homo sapiens	84-87
24752588-7	2014	In addition, co-immunoprecipitation was used to investigate the interaction between Akt and Hsp90, Akt and protein phosphatase-2A (PP2A) in the MG132-treated organotypic hippocampal slices.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	heat shock protein 90 alpha family class A member 1	Homo sapiens	92-97
24752588-7	2014	In addition, co-immunoprecipitation was used to investigate the interaction between Akt and Hsp90, Akt and protein phosphatase-2A (PP2A) in the MG132-treated organotypic hippocampal slices.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	AKT serine/threonine kinase 1	Homo sapiens	99-102
24752588-7	2014	In addition, co-immunoprecipitation was used to investigate the interaction between Akt and Hsp90, Akt and protein phosphatase-2A (PP2A) in the MG132-treated organotypic hippocampal slices.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	protein phosphatase 2 phosphatase activator	Homo sapiens	115-129
24752588-7	2014	In addition, co-immunoprecipitation was used to investigate the interaction between Akt and Hsp90, Akt and protein phosphatase-2A (PP2A) in the MG132-treated organotypic hippocampal slices.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	protein phosphatase 2 phosphatase activator	Homo sapiens	131-135
25192658-7	2014	MG132 was utilized to conform the effect of oroxylin A on degrading CHOP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA damage inducible transcript 3	Homo sapiens	68-72
25288803-4	2014	The treatment with MG132, an inhibitor of ubiquitin proteasome system, rescues the expression level and membrane localization of the SERCA1 mutant in a heterologous cellular model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Bos taurus	133-139
24805111-0	2014	p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	sequestosome 1	Homo sapiens	0-3
25169430-9	2014	A proteasome inhibitor, MG-132 (10muM), stabilized HO-1 protein in HEK 293T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	heme oxygenase 1	Homo sapiens	51-55
25244411-5	2014	In addition, there was a reduction in both the mRNA and protein expression of cyclin D1, while p21 protein expression was increased; the reduction in cyclin D1 expression was blocked by the proteasome inhibitor, MG132, or c-Jun N-terminal kinase (JNK) inhibitor; both beta-catenin and JNK were phosphorylated by activated PKG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	cyclin D1	Homo sapiens	78-87
25244411-5	2014	In addition, there was a reduction in both the mRNA and protein expression of cyclin D1, while p21 protein expression was increased; the reduction in cyclin D1 expression was blocked by the proteasome inhibitor, MG132, or c-Jun N-terminal kinase (JNK) inhibitor; both beta-catenin and JNK were phosphorylated by activated PKG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	cyclin dependent kinase inhibitor 1A	Homo sapiens	95-98
25244411-5	2014	In addition, there was a reduction in both the mRNA and protein expression of cyclin D1, while p21 protein expression was increased; the reduction in cyclin D1 expression was blocked by the proteasome inhibitor, MG132, or c-Jun N-terminal kinase (JNK) inhibitor; both beta-catenin and JNK were phosphorylated by activated PKG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	cyclin D1	Homo sapiens	150-159
25244411-5	2014	In addition, there was a reduction in both the mRNA and protein expression of cyclin D1, while p21 protein expression was increased; the reduction in cyclin D1 expression was blocked by the proteasome inhibitor, MG132, or c-Jun N-terminal kinase (JNK) inhibitor; both beta-catenin and JNK were phosphorylated by activated PKG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	catenin beta 1	Homo sapiens	268-280
25244411-5	2014	In addition, there was a reduction in both the mRNA and protein expression of cyclin D1, while p21 protein expression was increased; the reduction in cyclin D1 expression was blocked by the proteasome inhibitor, MG132, or c-Jun N-terminal kinase (JNK) inhibitor; both beta-catenin and JNK were phosphorylated by activated PKG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	mitogen-activated protein kinase 8	Homo sapiens	247-250
25244411-5	2014	In addition, there was a reduction in both the mRNA and protein expression of cyclin D1, while p21 protein expression was increased; the reduction in cyclin D1 expression was blocked by the proteasome inhibitor, MG132, or c-Jun N-terminal kinase (JNK) inhibitor; both beta-catenin and JNK were phosphorylated by activated PKG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	protein kinase cGMP-dependent 1	Homo sapiens	322-325
25323821-9	2014	Further studies showed that triptolide accelerates Tat protein degradation, which can be rescued by administration of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	tyrosine aminotransferase	Homo sapiens	51-54
25169430-10	2014	Co-treatment with sesamin decreased ubiquitinated HO-1 protein accumulation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	heme oxygenase 1	Homo sapiens	50-54
24805111-0	2014	p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	sequestosome 1	Homo sapiens	4-10
25025573-7	2014	The Pax7-induced reduction MyoD was attenuated by RFP siRNA and by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	paired box 7	Mus musculus	4-8
24805111-0	2014	p62/SQSTM1 is involved in caspase-8 associated cell death induced by proteasome inhibitor MG132 in U87MG cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	caspase 8	Homo sapiens	26-35
24805111-3	2014	We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132"s cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	caspase 8	Homo sapiens	101-110
24805111-3	2014	We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132"s cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	sequestosome 1	Homo sapiens	144-147
24805111-3	2014	We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132"s cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	sequestosome 1	Homo sapiens	148-154
24805111-3	2014	We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132"s cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	sequestosome 1	Homo sapiens	196-202
24805111-3	2014	We treated U87MG cells with the proteasome inhibitor MG132 and found that cell death correlated with caspase-8 activation and autophagy protein p62/SQSTM1.To explore the role of autophagy and p62/SQSTM1 in MG132-induced cancer cell death, we measured the alteration of MG132"s cytotoxicity by autophagy inhibition, autophagy induction or variation of p62/SQSTM1 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	sequestosome 1	Homo sapiens	196-202
24805111-5	2014	Moreover, U87MG cell death was dependent on p62/SQSTM1, and its function required its C-terminus UBA domain to attenuate the MG132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	sequestosome 1	Homo sapiens	44-47
24992982-0	2014	MCPIP1 contributes to the toxicity of proteasome inhibitor MG-132 in HeLa cells by the inhibition of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	zinc finger CCCH-type containing 12A	Homo sapiens	0-6
24993166-9	2014	Interestingly, TNF-alpha significantly decreased adiponectin and PPAR-gamma protein levels, while treatment with the proteasomal inhibitor MG-132 maintained PPAR-gamma levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-145	peroxisome proliferator activated receptor gamma	Homo sapiens	157-167
25175192-7	2014	The medium collected after incubation with drug-incorporated CPC with or without MWCNT inhibited TNFalpha-induced NF-kappaB activation indicating that the effective amount of MG132 was released.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-180	tumor necrosis factor	Mus musculus	97-105
24992982-0	2014	MCPIP1 contributes to the toxicity of proteasome inhibitor MG-132 in HeLa cells by the inhibition of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	nuclear factor kappa B subunit 1	Homo sapiens	101-110
24992982-1	2014	Recently, we have shown that the treatment of cells with proteasome inhibitor MG-132 results in the induction of expression of monocyte chemotactic protein-1 induced protein 1 (MCPIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	zinc finger CCCH-type containing 12A	Homo sapiens	127-175
24992982-1	2014	Recently, we have shown that the treatment of cells with proteasome inhibitor MG-132 results in the induction of expression of monocyte chemotactic protein-1 induced protein 1 (MCPIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	zinc finger CCCH-type containing 12A	Homo sapiens	177-183
24992982-5	2014	Using siRNA technology, we show here that MCPIP1 expression contributes to the toxic properties of MG-132 in HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	zinc finger CCCH-type containing 12A	Homo sapiens	42-48
24992982-6	2014	The inhibition of proteasome by MG-132 and epoxomicin markedly increased MCPIP1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-38	zinc finger CCCH-type containing 12A	Homo sapiens	73-79
24992982-7	2014	While MG-132 induces HeLa cell death, down-regulation of MCPIP1 expression by siRNA partially protects HeLa cells from MG-132 toxicity and restores Nuclear factor-kappaB (NF-kappaB) activity, inhibited by MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-125	zinc finger CCCH-type containing 12A	Homo sapiens	57-63
24992982-7	2014	While MG-132 induces HeLa cell death, down-regulation of MCPIP1 expression by siRNA partially protects HeLa cells from MG-132 toxicity and restores Nuclear factor-kappaB (NF-kappaB) activity, inhibited by MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-125	zinc finger CCCH-type containing 12A	Homo sapiens	57-63
25109327-11	2014	Moreover, after inhibition of Rac1 or GSK3 following proteasome inhibitor MG132 treatment, cyclin D1 expression at the protein level remained constant, indicating that Rac1 and GSK3 may regulate cyclin D1 turnover through phosphorylation and degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	Rac family small GTPase 1	Homo sapiens	30-34
25109327-11	2014	Moreover, after inhibition of Rac1 or GSK3 following proteasome inhibitor MG132 treatment, cyclin D1 expression at the protein level remained constant, indicating that Rac1 and GSK3 may regulate cyclin D1 turnover through phosphorylation and degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	cyclin D1	Homo sapiens	195-204
25338567-0	2014	Expression of costimulatory molecule CD86 in HL-60 cells induced by MG132 and its effect on allogeneic mixed lymphocyte reaction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	CD86 molecule	Homo sapiens	37-41
25338567-1	2014	This study was aimed to elucidate the expression of costimulatory molecule CD80 and CD86 in HL-60 cells induced by proteasome inhibitor MG132 and its effect on allogeneic mixed lymphocyte reaction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	CD80 molecule	Homo sapiens	75-79
25338567-1	2014	This study was aimed to elucidate the expression of costimulatory molecule CD80 and CD86 in HL-60 cells induced by proteasome inhibitor MG132 and its effect on allogeneic mixed lymphocyte reaction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	CD86 molecule	Homo sapiens	84-88
25338567-4	2014	Proteasome inhibitor MG132 at the concentrations of 2 or 3 micromol/L was used to stimulate the HL-60 cell cultured for 24 h and 48 h respectively, and the Annexin V/7-AAD staining and flow cytomotry were used to detect the apoptosis of the HL-60 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	annexin A5	Homo sapiens	156-165
25338567-6	2014	The mRNA expression of CD86 in the HL-60 cells treated with 1 micromol/L MG132 was detected by RT-PCR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	CD86 molecule	Homo sapiens	23-27
25338567-12	2014	Before MG132 treatment K562 cells did not express CD86, but the CD86 expression of the HL-60 cells was up-regulated time-dependently after MG132 treatment (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	7-12	CD86 molecule	Homo sapiens	64-68
25338567-12	2014	Before MG132 treatment K562 cells did not express CD86, but the CD86 expression of the HL-60 cells was up-regulated time-dependently after MG132 treatment (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	CD86 molecule	Homo sapiens	64-68
25338567-13	2014	The mRNA expression of CD86 in the HL-60 treated with MG132 was up-regulated time-dependently (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	CD86 molecule	Homo sapiens	23-27
25338567-16	2014	It is concluded that the high concentration of MG132 can directly kill HL-60 cells, low-concentration of MG132 can induce the expression of costimulatory molecule CD86 in HL-60 cells, also can improve the proliferation of PBMNC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	CD86 molecule	Homo sapiens	163-167
25170821-6	2014	With the treatment of MG132, the LRR domain may functions in preventing LRWD1 protein from proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	leucine rich repeats and WD repeat domain containing 1	Homo sapiens	72-77
24986862-8	2014	However, further depletion of ZO-2 in Eph4 ZO-1KO cells, which do not express ZO-3, caused decreased junctional localization and expression of DbpA, which were rescued by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	Y box protein 3	Mus musculus	143-147
25392730-10	2014	At the cellular level, treatment with proteasomal inhibitor, MG132, or lactacystin significantly increased GABAAalpha1 protein levels and Lys48-linked polyubiquitination of GABAAalpha1, but reduced proteasome activity in mouse primary cortical neurons (DIV 14 from E16 embryos).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	gamma-aminobutyric acid (GABA) A receptor, subunit alpha 1	Mus musculus	107-118
25392730-10	2014	At the cellular level, treatment with proteasomal inhibitor, MG132, or lactacystin significantly increased GABAAalpha1 protein levels and Lys48-linked polyubiquitination of GABAAalpha1, but reduced proteasome activity in mouse primary cortical neurons (DIV 14 from E16 embryos).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	gamma-aminobutyric acid (GABA) A receptor, subunit alpha 1	Mus musculus	173-184
25392730-13	2014	In addition, the inhibition of proteasomal activity by MG132 increased the expression of GABAAalpha1 in the ER.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	gamma-aminobutyric acid (GABA) A receptor, subunit alpha 1	Mus musculus	89-100
25246059-5	2014	Further, ERK inhibitor U0126 and NFkappaB inhibitor MG132 also inhibited A549 cell proliferation similar to 50 kappaM scutellarein treatment from 24 h to 48 h. The experimental results showed that scutellarein could inhibit proliferation of the human lung cancer cell line A549 through ERK and NFkappaB mediated by the EGFR pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	nuclear factor kappa B subunit 1	Homo sapiens	33-41
24986862-8	2014	However, further depletion of ZO-2 in Eph4 ZO-1KO cells, which do not express ZO-3, caused decreased junctional localization and expression of DbpA, which were rescued by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	tight junction protein 2	Mus musculus	30-34
24909615-0	2014	Inducible nitric oxide synthase mediates MG132 lethality in leukemic cells through mitochondrial depolarization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	nitric oxide synthase 2	Homo sapiens	0-31
24909615-6	2014	In MG132-treated cells, the increase in iNOS-derived oxidants was responsible for mitochondrial depolarization and caspase-dependent apoptosis, but was insignificant in G2/M arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	3-8	nitric oxide synthase 2	Homo sapiens	40-44
24909615-10	2014	In contrast to iNOS, endothelial NOS-driven cGMP-dependent signaling promoted mitochondrial function and survival of MG132-stressed cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	nitric oxide synthase 3	Homo sapiens	21-36
25042549-0	2014	MG132, a proteasome inhibitor, enhances LDL uptake in HepG2 cells in vitro by regulating LDLR and PCSK9 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	proprotein convertase subtilisin/kexin type 9	Homo sapiens	98-103
25044116-6	2014	Strikingly, treatment with MG132, a ubiquitin/proteasome system inhibitor, significantly increased the levels of both total and ubiquitinated raptor in GCD2 corneal fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	regulatory associated protein of MTOR complex 1	Homo sapiens	142-148
25044120-6	2014	Furthermore, suppression of Rbfox3-d31 protein degradation with the proteasome inhibitor MG132 attenuates the splicing activity of another Rbfox family member Rbfox2 by altering the subcellular localization of Rbfox2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	RNA binding fox-1 homolog 3	Gallus gallus	28-34
25044120-6	2014	Furthermore, suppression of Rbfox3-d31 protein degradation with the proteasome inhibitor MG132 attenuates the splicing activity of another Rbfox family member Rbfox2 by altering the subcellular localization of Rbfox2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	RNA binding fox-1 homolog 2	Gallus gallus	159-165
25042549-0	2014	MG132, a proteasome inhibitor, enhances LDL uptake in HepG2 cells in vitro by regulating LDLR and PCSK9 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	low density lipoprotein receptor	Homo sapiens	89-93
25044120-6	2014	Furthermore, suppression of Rbfox3-d31 protein degradation with the proteasome inhibitor MG132 attenuates the splicing activity of another Rbfox family member Rbfox2 by altering the subcellular localization of Rbfox2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	RNA binding fox-1 homolog 2	Gallus gallus	210-216
25042549-8	2014	RESULTS: Treatment of HepG2 cells with the specific proteasome inhibitor MG132 (0.03-3 mumol/L) dose-dependently increased LDLR mRNA and protein levels, as well as LDL uptake.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	low density lipoprotein receptor	Homo sapiens	123-127
25042549-9	2014	Short-term treatment with MG132 (0.3 mumol/L, up to 8 h) significantly increased both LDLR mRNA and protein levels in HepG2 cells, which was blocked by the specific PKC inhibitors GF 109203X, Go 6983 or staurosporine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	low density lipoprotein receptor	Homo sapiens	86-90
25042549-10	2014	In contrast, a longer treatment with MG132 (0.3 mumol/L, 24 h) did not change LDLR mRNA, but markedly increased LDLR protein by reducing PCSK9-mediated lysosome LDLR degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	low density lipoprotein receptor	Homo sapiens	112-116
25042549-10	2014	In contrast, a longer treatment with MG132 (0.3 mumol/L, 24 h) did not change LDLR mRNA, but markedly increased LDLR protein by reducing PCSK9-mediated lysosome LDLR degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	proprotein convertase subtilisin/kexin type 9	Homo sapiens	137-142
25042549-10	2014	In contrast, a longer treatment with MG132 (0.3 mumol/L, 24 h) did not change LDLR mRNA, but markedly increased LDLR protein by reducing PCSK9-mediated lysosome LDLR degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	low density lipoprotein receptor	Homo sapiens	112-116
25042549-11	2014	Furthermore, MG132 time-dependently suppressed PCSK9 expression in the HepG2 cells through a SREBP-1c related pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	proprotein convertase subtilisin/kexin type 9	Homo sapiens	47-52
25042549-11	2014	Furthermore, MG132 time-dependently suppressed PCSK9 expression in the HepG2 cells through a SREBP-1c related pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	sterol regulatory element binding transcription factor 1	Homo sapiens	93-101
25042549-12	2014	Combined treatment with MG132 (0.3 mumol/L) and pravastatin (5 mumol/L) strongly promoted LDLR expression and LDL uptake in HepG2 cells, and blocked the upregulation of PCSK9 caused by pravastatin alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	low density lipoprotein receptor	Homo sapiens	90-94
25042549-12	2014	Combined treatment with MG132 (0.3 mumol/L) and pravastatin (5 mumol/L) strongly promoted LDLR expression and LDL uptake in HepG2 cells, and blocked the upregulation of PCSK9 caused by pravastatin alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	proprotein convertase subtilisin/kexin type 9	Homo sapiens	169-174
25042549-13	2014	CONCLUSION: Inhibition of proteasome by MG132 in HepG2 cells plays dual roles in LDLR and PCSK9 expression, and exerts a beneficial effect on cholesterol homeostasis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	low density lipoprotein receptor	Homo sapiens	81-85
25042549-13	2014	CONCLUSION: Inhibition of proteasome by MG132 in HepG2 cells plays dual roles in LDLR and PCSK9 expression, and exerts a beneficial effect on cholesterol homeostasis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	proprotein convertase subtilisin/kexin type 9	Homo sapiens	90-95
24712725-8	2014	Inhibition of proteosomal degradation using MG-132 and Ada-(Ahx)3-(Leu)3-vinyl sulfone ameliorates PCA-induced downregulation of beta-catenin and cyclin D1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	catenin beta 1	Homo sapiens	129-141
24857540-5	2014	Treatment with trichostatin A, RNAlater, or MG-132 enhanced the expression of hepcidin in HepG2 cells, suggesting that histone deacetylation, instability of mRNA, or proteosomal degradation of the protein(s) that positively regulate hepcidin expression may be responsible for the decreased expression of hepcidin in HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	hepcidin antimicrobial peptide	Homo sapiens	78-86
24712725-8	2014	Inhibition of proteosomal degradation using MG-132 and Ada-(Ahx)3-(Leu)3-vinyl sulfone ameliorates PCA-induced downregulation of beta-catenin and cyclin D1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	cyclin D1	Homo sapiens	146-155
24825618-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BH3 interacting domain death agonist	Rattus norvegicus	64-67
24789436-8	2014	Moreover, pretreatment with 100 nM MG132 before IR-enhanced radiation induced cell cycle arrest by decreased CyclinD1 but increased Wee1 expression in A549 and H1299 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	cyclin D1	Homo sapiens	109-117
24825618-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2, apoptosis regulator	Rattus norvegicus	69-74
24825618-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2 associated X, apoptosis regulator	Rattus norvegicus	120-123
24825618-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	278-281
24613819-6	2014	Specific NF-kappaB inhibitors, pyrrolidine dithiocarbamate, MG132, and PS-1145, also attenuated TNF-alpha-mediated MMP-9 and VEGF expression as well as activity by suppressing their regulatory genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	nuclear factor kappa B subunit 1	Homo sapiens	9-18
24613819-6	2014	Specific NF-kappaB inhibitors, pyrrolidine dithiocarbamate, MG132, and PS-1145, also attenuated TNF-alpha-mediated MMP-9 and VEGF expression as well as activity by suppressing their regulatory genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	tumor necrosis factor	Homo sapiens	96-105
24613819-6	2014	Specific NF-kappaB inhibitors, pyrrolidine dithiocarbamate, MG132, and PS-1145, also attenuated TNF-alpha-mediated MMP-9 and VEGF expression as well as activity by suppressing their regulatory genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	matrix metallopeptidase 9	Homo sapiens	115-120
24613819-6	2014	Specific NF-kappaB inhibitors, pyrrolidine dithiocarbamate, MG132, and PS-1145, also attenuated TNF-alpha-mediated MMP-9 and VEGF expression as well as activity by suppressing their regulatory genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	vascular endothelial growth factor A	Homo sapiens	125-129
24860187-10	2014	The proteasome inhibitor MG132 suppressed degradation of full-length ACS7 in vivo, but had little effect on the N-terminal truncated form of ACS7, indicating that the N-terminus mediates the regulation of ACS7 stability through the ubiquitin-26S proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	1-amino-cyclopropane-1-carboxylate synthase 7	Arabidopsis thaliana	69-73
24789436-8	2014	Moreover, pretreatment with 100 nM MG132 before IR-enhanced radiation induced cell cycle arrest by decreased CyclinD1 but increased Wee1 expression in A549 and H1299 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	WEE1 G2 checkpoint kinase	Homo sapiens	132-136
24789436-9	2014	In addition, pretreatment of MG132 combined with IR significantly suppressed cell migration and invasion abilities in NSCLC cell lines, which was accompanied by decreased expression of matrix metalloproteinase (MMP)-2 and MMP-9 in NSCLC cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	matrix metallopeptidase 2	Homo sapiens	185-217
24789436-9	2014	In addition, pretreatment of MG132 combined with IR significantly suppressed cell migration and invasion abilities in NSCLC cell lines, which was accompanied by decreased expression of matrix metalloproteinase (MMP)-2 and MMP-9 in NSCLC cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	matrix metallopeptidase 9	Homo sapiens	222-227
24735796-5	2014	Cladosporol A-induced beta-catenin proteasomal degradation was examined in the presence of the specific inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	catenin beta 1	Homo sapiens	22-34
24891511-4	2014	A proteasome inhibitor MG132 prolonged the life span of the wild-type NPC1 expressed in COS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	NPC intracellular cholesterol transporter 1	Homo sapiens	70-74
24891511-6	2014	Accordingly, expression of an E3 ligase CHIP (carboxyl terminus of Hsp70-interacting protein) enhanced MG132-induced accumulation of ubiquitylated NPC1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	heat shock protein family A (Hsp70) member 4	Homo sapiens	67-72
24891511-6	2014	Accordingly, expression of an E3 ligase CHIP (carboxyl terminus of Hsp70-interacting protein) enhanced MG132-induced accumulation of ubiquitylated NPC1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	NPC intracellular cholesterol transporter 1	Homo sapiens	147-151
24895455-8	2014	However, the proteasome inhibitor MG132 rescued DeltaSIV INa, suggesting that the SIV motif is important for regulation of NaV1.5 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	sodium voltage-gated channel alpha subunit 5	Homo sapiens	123-129
24846764-5	2014	Furthermore, the degradation of both LTA2 and PDH E1alpha was inhibited by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	2-oxoacid dehydrogenases acyltransferase family protein	Arabidopsis thaliana	37-41
24846764-5	2014	Furthermore, the degradation of both LTA2 and PDH E1alpha was inhibited by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	pyruvate dehydrogenase E1 alpha	Arabidopsis thaliana	46-57
24923447-5	2014	The proteasome inhibitors MG132, lactacystin, and epoxomicin blocked PICT1 degradation, whereas the inhibition of E1 ubiquitin-activating enzyme by a specific inhibitor and genetic inactivation fail to repress PICT1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	NOP53 ribosome biogenesis factor	Homo sapiens	69-74
24939622-7	2014	Treatment with MG132, a proteasome inhibitor, suggested that the VPA-induced increase of GCPII protein level is dependent on the ubiquitin/proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	folate hydrolase 1	Homo sapiens	89-94
24811168-6	2014	Cdh1 interacted with PTEN via two separate domains, and their interaction was enhanced by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	cadherin 1	Homo sapiens	0-4
25092240-6	2014	The result indicated that ROS production, TRAF2, ASK1 and c-jun were elevated in MG-132 treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	TNF receptor associated factor 2	Homo sapiens	42-47
25092240-6	2014	The result indicated that ROS production, TRAF2, ASK1 and c-jun were elevated in MG-132 treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	49-53
25092240-6	2014	The result indicated that ROS production, TRAF2, ASK1 and c-jun were elevated in MG-132 treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-63
25092240-7	2014	Giving ROS scavenger N-acetyl-L-cysteine (NAC) largely prevented the effects of MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-86	X-linked Kx blood group	Homo sapiens	42-45
25092240-8	2014	Furthermore, treating with MG-132 lead to decreased XBP1 mRNA expression but could not completely block the expression of XBP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	X-box binding protein 1	Homo sapiens	52-56
25092240-9	2014	Taken together, these findings provide the evidence that MG-132 induced ER stress lead to Tca-8113 cells apoptosis through ROS generation and TRAF2-ASK1-JNK signal pathway activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-63	TNF receptor associated factor 2	Homo sapiens	142-147
25092240-9	2014	Taken together, these findings provide the evidence that MG-132 induced ER stress lead to Tca-8113 cells apoptosis through ROS generation and TRAF2-ASK1-JNK signal pathway activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-63	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	148-152
25092240-9	2014	Taken together, these findings provide the evidence that MG-132 induced ER stress lead to Tca-8113 cells apoptosis through ROS generation and TRAF2-ASK1-JNK signal pathway activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-63	mitogen-activated protein kinase 8	Homo sapiens	153-156
24499369-6	2014	KCNE1-D85N was highly ubiquitinated and rapidly degraded as compared to the wild-type; a proteasome inhibitor, MG132, inhibited its degradation and increased its steady-state level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	0-5
25092240-0	2014	Upregulated ROS production induced by the proteasome inhibitor MG-132 on XBP1 gene expression and cell apoptosis in Tca-8113 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-69	X-box binding protein 1	Homo sapiens	73-77
24811168-6	2014	Cdh1 interacted with PTEN via two separate domains, and their interaction was enhanced by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	phosphatase and tensin homolog	Homo sapiens	21-25
24967154-9	2014	Interestingly, the administration of the proteasome inhibitor MG132 caused differential effects on the three AZ-binding proteins, having no effect on ODC, preventing the degradation of AZIN1, but unexpectedly increasing the degradation of AZIN2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	antizyme inhibitor 1	Homo sapiens	185-190
24967154-9	2014	Interestingly, the administration of the proteasome inhibitor MG132 caused differential effects on the three AZ-binding proteins, having no effect on ODC, preventing the degradation of AZIN1, but unexpectedly increasing the degradation of AZIN2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	antizyme inhibitor 2	Homo sapiens	239-244
24967154-10	2014	Inhibitors of the lysosomal function partially prevented the effect of MG132 on AZIN2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	antizyme inhibitor 2	Homo sapiens	80-85
24595757-6	2014	However, the levels of phosphorylated LAT and PLCgamma1 in Dow2-induced anergic T cells could be rescued in the presence of the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-155	linker for activation of T cells	Mus musculus	38-41
24380877-11	2014	Moreover, we demonstrate that also the induction of autophagy by MG132 resulted in elevated Nrf2 binding to Pept1-ARE1 and increased PEPT1 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	NFE2 like bZIP transcription factor 2	Homo sapiens	92-96
24380877-11	2014	Moreover, we demonstrate that also the induction of autophagy by MG132 resulted in elevated Nrf2 binding to Pept1-ARE1 and increased PEPT1 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	solute carrier family 15 member 1	Homo sapiens	108-113
24380877-11	2014	Moreover, we demonstrate that also the induction of autophagy by MG132 resulted in elevated Nrf2 binding to Pept1-ARE1 and increased PEPT1 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	VPS52 subunit of GARP complex	Homo sapiens	114-118
24380877-11	2014	Moreover, we demonstrate that also the induction of autophagy by MG132 resulted in elevated Nrf2 binding to Pept1-ARE1 and increased PEPT1 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	solute carrier family 15 member 1	Homo sapiens	133-138
24595757-6	2014	However, the levels of phosphorylated LAT and PLCgamma1 in Dow2-induced anergic T cells could be rescued in the presence of the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-155	phospholipase C, gamma 1	Mus musculus	46-55
24985177-7	2014	Fludarabine (10 mumol/L), MG-132 (1 mumol/L) and PS-341 (1 mumol/L) could induce cell death of RelB+ and RelB- CLL cells co-cultured with hBMSCs in a time dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	RELB proto-oncogene, NF-kB subunit	Homo sapiens	95-99
24691740-9	2014	P-gp and NF-kappaB significantly decreased; however, p53 increased in FaDu/T + MG132 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	tumor protein p53	Homo sapiens	53-56
24691740-10	2014	These results suggested that the proteasome inhibitor MG132 reversed the malignant characteristics of FaDu/T by enhancing apoptosis and inhibiting P-gp.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	ATP binding cassette subfamily B member 1	Homo sapiens	147-151
24691740-11	2014	MG132 was also able to inhibit the nuclear translocation of NF-kappaB and increase the expression of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	101-104
24985177-7	2014	Fludarabine (10 mumol/L), MG-132 (1 mumol/L) and PS-341 (1 mumol/L) could induce cell death of RelB+ and RelB- CLL cells co-cultured with hBMSCs in a time dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	RELB proto-oncogene, NF-kB subunit	Homo sapiens	105-109
24985177-11	2014	Enhancement of RelB activity may increase CLL cells" sensitivity to proteasome inhibitor bortezomib and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-110	RELB proto-oncogene, NF-kB subunit	Homo sapiens	15-19
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BH3 interacting domain death agonist	Rattus norvegicus	64-67
25606422-11	2014	When cells were treated with MG132, KRT13 protein level was increased and kept almost the same in normal and patient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	keratin 13	Homo sapiens	36-41
24381309-6	2014	Although expression of mutant TDP-43 in glial cells via stereotaxic injection does not lead to robust neurological phenotypes, systemic inhibition of the proteasome activity via MG132 in postnatal mice could exacerbate glial TDP-43-mediated toxicity and cause mice to die earlier.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-183	TAR DNA binding protein	Mus musculus	225-231
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2, apoptosis regulator	Rattus norvegicus	69-74
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	Bcl2-like 1	Rattus norvegicus	76-82
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2 associated X, apoptosis regulator	Rattus norvegicus	127-130
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	caspase 8	Rattus norvegicus	229-252
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	291-294
24631255-5	2014	The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), an increase in the tumor suppressor p53 levels and cleavage of PARP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	poly (ADP-ribose) polymerase 1	Rattus norvegicus	318-324
24789201-5	2014	Treatment with the proteasome inhibitor MG132 (5 microM) causes CAR to accumulate in the cytoplasm of transfected HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	nuclear receptor subfamily 1 group I member 3	Homo sapiens	64-67
24795145-4	2014	RanBPM was also recruited to aggresomes following treatment with the proteasome inhibitor MG132 and the DNA-damaging agent etoposide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	RAN binding protein 9	Homo sapiens	0-6
24789201-6	2014	In the presence of MG132, TCPOBOP increases CCRP ubiquitination in HepG2 cells co-expressing CAR, while CAR ubiquitination was not detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	nuclear receptor subfamily 1 group I member 3	Homo sapiens	93-96
24789201-6	2014	In the presence of MG132, TCPOBOP increases CCRP ubiquitination in HepG2 cells co-expressing CAR, while CAR ubiquitination was not detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	nuclear receptor subfamily 1 group I member 3	Homo sapiens	104-107
24789201-7	2014	MG132 treatment of HepG2 also attenuated of TCPOBOP-induced CAR transcriptional activation on reporter constructs which contain CAR-binding DNA elements derived from the human CYP2B6 gene.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear receptor subfamily 1 group I member 3	Homo sapiens	60-63
24789201-7	2014	MG132 treatment of HepG2 also attenuated of TCPOBOP-induced CAR transcriptional activation on reporter constructs which contain CAR-binding DNA elements derived from the human CYP2B6 gene.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear receptor subfamily 1 group I member 3	Homo sapiens	128-131
24789201-7	2014	MG132 treatment of HepG2 also attenuated of TCPOBOP-induced CAR transcriptional activation on reporter constructs which contain CAR-binding DNA elements derived from the human CYP2B6 gene.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	176-182
24789201-8	2014	The elevation of cytoplasmic CAR protein with MG132 correlated with an increase of HSP70, and to a lesser extent HSP60.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	nuclear receptor subfamily 1 group I member 3	Homo sapiens	29-32
24789201-8	2014	The elevation of cytoplasmic CAR protein with MG132 correlated with an increase of HSP70, and to a lesser extent HSP60.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	heat shock protein family A (Hsp70) member 4	Homo sapiens	83-88
24789201-8	2014	The elevation of cytoplasmic CAR protein with MG132 correlated with an increase of HSP70, and to a lesser extent HSP60.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	heat shock protein family D (Hsp60) member 1	Homo sapiens	113-118
24631023-2	2014	We have recently demonstrated that proteasome activity is increased in laminin alpha2 chain-deficient muscle and that treatment with the nonpharmaceutical proteasome inhibitor MG-132 reduces muscle pathology in laminin alpha2 chain-deficient dy(3K)/dy(3K) mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	laminin, alpha 2	Mus musculus	71-91
24631023-2	2014	We have recently demonstrated that proteasome activity is increased in laminin alpha2 chain-deficient muscle and that treatment with the nonpharmaceutical proteasome inhibitor MG-132 reduces muscle pathology in laminin alpha2 chain-deficient dy(3K)/dy(3K) mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	laminin, alpha 2	Mus musculus	211-231
24584782-9	2014	MG132 significantly enhanced cisplatin-induced apoptosis in association with the activation of caspase-3 and -8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	95-111
24747689-7	2014	In addition, when resveratrol was added to the medium containing MG132, the Mt number increased significantly by 39%, this effect was diminished by the addition of the SIRT1 inhibitor EX527.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	sirtuin 1	Homo sapiens	168-173
24442344-7	2014	The treatment of activated blastocysts with the proteasome inhibitor MG132 demonstrated that proteolysis is associated with down-regulation of ERalpha expression in activated blastocysts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	estrogen receptor 1 (alpha)	Mus musculus	143-150
24732420-8	2014	Further signaling dissection revealed that PDGF-BB posttranscriptional upregulated p21WAF1/Cip1 protein expression, which was inhibited by rapamycin, an activator of autophagy via suppressing mammalian target of rapamycin (mTOR), rather than MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	242-247	cyclin dependent kinase inhibitor 1A	Homo sapiens	91-95
24732420-8	2014	Further signaling dissection revealed that PDGF-BB posttranscriptional upregulated p21WAF1/Cip1 protein expression, which was inhibited by rapamycin, an activator of autophagy via suppressing mammalian target of rapamycin (mTOR), rather than MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	242-247	mechanistic target of rapamycin kinase	Homo sapiens	192-221
24563465-6	2014	Endogenously expressed and plasmid-mediated overexpressed levels of Pah1p were more abundant in the stationary phase of cells treated with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	phosphatidate phosphatase PAH1	Saccharomyces cerevisiae S288C	68-73
24603988-7	2014	The downregulation of Bcl-2 by PM was not due to proteasomal or lysosomal proteolytic degradation of Bcl-2, since treatment with PM in the presence of proteasomal inhibitors MG132 or lactacystin (LAC) or calpain inhibitor MG101 failed to block the downregulation of Bcl-2 by PM.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	BCL2 apoptosis regulator	Homo sapiens	22-27
24855826-9	2014	We found that ML106-induced tyrosinase down-regulation was restored by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	tyrosinase	Mus musculus	28-38
24788149-4	2014	We therefore analyzed the L02 cells with MG132 and siRNA treatment for different expression of p21 related to lipid accumulation and lipotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	H3 histone pseudogene 16	Homo sapiens	95-98
24498857-7	2014	ASBT inhibition by RSV was reversed by proteasome inhibitors (MG-132 and lactacystin) and the ubiquitin inhibitor LDN57444, suggesting involvement of the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	solute carrier family 10 member 2	Homo sapiens	0-4
24736394-8	2014	And the degradation of beta-catenin mediated by KCTD1 was alleviated by the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	catenin beta 1	Homo sapiens	23-35
24736394-8	2014	And the degradation of beta-catenin mediated by KCTD1 was alleviated by the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	potassium channel tetramerization domain containing 1	Homo sapiens	48-53
24562306-8	2014	Pretreatment with the proteasome inhibitor MG132 (80 nmol/L) abolished DHA-induced tyrosinase reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	tyrosinase	Mus musculus	83-93
24535016-10	2014	Combined treatment of ZD55-TRAIL and MG132 (a proteasome inhibitor) robustly increased the expression of death receptor 5 (DR5), which enhanced the apoptosis response without significant toxicity to normal liver cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	TNF receptor superfamily member 10b	Homo sapiens	105-121
24535016-10	2014	Combined treatment of ZD55-TRAIL and MG132 (a proteasome inhibitor) robustly increased the expression of death receptor 5 (DR5), which enhanced the apoptosis response without significant toxicity to normal liver cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	TNF receptor superfamily member 10b	Homo sapiens	123-126
24691096-7	2014	The proteolysis of p12 could be efficiently blocked by both calpain inhibitor ALLN and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	DNA polymerase delta 4, accessory subunit	Homo sapiens	19-22
24663680-3	2014	Treatment with a proteasome inhibitor, MG132, significantly increased the immature, but not the mature, hKv1.5 protein at 37 C, however, there were no changes in either the immature or mature hKv1.5 proteins at low temperature following MG132 exposure.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	potassium voltage-gated channel subfamily A member 5	Homo sapiens	104-110
24449419-7	2014	MG132, a specific proteasome inhibitor, blocked Cd2+-induced reduction in PTEN protein as well as Akt phosphorylation, implicating the involvement of proteasome-mediated PTEN degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	CD2 antigen	Mus musculus	48-51
24449419-7	2014	MG132, a specific proteasome inhibitor, blocked Cd2+-induced reduction in PTEN protein as well as Akt phosphorylation, implicating the involvement of proteasome-mediated PTEN degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	phosphatase and tensin homolog	Mus musculus	74-78
24449419-7	2014	MG132, a specific proteasome inhibitor, blocked Cd2+-induced reduction in PTEN protein as well as Akt phosphorylation, implicating the involvement of proteasome-mediated PTEN degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	thymoma viral proto-oncogene 1	Mus musculus	98-101
24449419-7	2014	MG132, a specific proteasome inhibitor, blocked Cd2+-induced reduction in PTEN protein as well as Akt phosphorylation, implicating the involvement of proteasome-mediated PTEN degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	phosphatase and tensin homolog	Mus musculus	170-174
24721402-5	2014	Then, the expressions of GFP and PDIP1 were again detected in the cells which were treated by ammonium chloride or MG132, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	potassium channel tetramerization domain containing 13	Homo sapiens	33-38
23958055-9	2014	When we treated the MGMT-positive GSCs with TMZ plus MG-132 (an NF-kappaB inhibitor), the antitumor activity was significantly enhanced compared to that of GSCs treated with TMZ alone (P &lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	O-6-methylguanine-DNA methyltransferase	Homo sapiens	20-24
24658419-5	2014	Additionally, MG132 experiments indicate that other E3-ligases regulate p53 stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	transformation related protein 53, pseudogene	Mus musculus	72-75
24495648-9	2014	Therefore, MG132 decreases senescence, p65 phosphorylation, and the DOX-induced Bcl-2 antiapoptotic protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	RELA proto-oncogene, NF-kB subunit	Homo sapiens	39-42
24495648-9	2014	Therefore, MG132 decreases senescence, p65 phosphorylation, and the DOX-induced Bcl-2 antiapoptotic protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	BCL2 apoptosis regulator	Homo sapiens	80-85
24495648-10	2014	The MG132 + DOX treatment induced upregulation of proapoptotic genes BAX, DIABLO, NOXA, DR4, and FAS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	BCL2 associated X, apoptosis regulator	Homo sapiens	69-72
24495648-10	2014	The MG132 + DOX treatment induced upregulation of proapoptotic genes BAX, DIABLO, NOXA, DR4, and FAS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	diablo IAP-binding mitochondrial protein	Homo sapiens	74-80
24495648-10	2014	The MG132 + DOX treatment induced upregulation of proapoptotic genes BAX, DIABLO, NOXA, DR4, and FAS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	82-86
24495648-10	2014	The MG132 + DOX treatment induced upregulation of proapoptotic genes BAX, DIABLO, NOXA, DR4, and FAS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	major histocompatibility complex, class II, DR beta 4	Homo sapiens	88-91
23430344-8	2014	CAPE and both chemotherapeutic agents reduced Bcl-2, while only CAPE and MG132 significantly increased Bax level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	BCL2 associated X, apoptosis regulator	Homo sapiens	103-106
23430344-11	2014	However, only MG132 caused the translocation of Smac/DIABLO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	diablo IAP-binding mitochondrial protein	Homo sapiens	48-52
23430344-11	2014	However, only MG132 caused the translocation of Smac/DIABLO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	diablo IAP-binding mitochondrial protein	Homo sapiens	53-59
23430344-13	2014	All treatments induced activation of caspases 3/7, but only CAPE and MG132 led to the activation of caspase 9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	caspase 9	Homo sapiens	100-109
23435415-6	2014	The loss of p38beta protein in ILK-depleted cells is partially rescued by the 26S proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	mitogen-activated protein kinase 11	Homo sapiens	12-19
23435415-6	2014	The loss of p38beta protein in ILK-depleted cells is partially rescued by the 26S proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	integrin linked kinase	Homo sapiens	31-34
23958055-11	2014	Our results show that MG-132 may inhibit NF-kappaB expression and further decrease MGMT expression, resulting in a synergistic effect on MGMT-positive GSCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	O-6-methylguanine-DNA methyltransferase	Homo sapiens	83-87
23958055-11	2014	Our results show that MG-132 may inhibit NF-kappaB expression and further decrease MGMT expression, resulting in a synergistic effect on MGMT-positive GSCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	O-6-methylguanine-DNA methyltransferase	Homo sapiens	137-141
23958055-9	2014	When we treated the MGMT-positive GSCs with TMZ plus MG-132 (an NF-kappaB inhibitor), the antitumor activity was significantly enhanced compared to that of GSCs treated with TMZ alone (P &lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	nuclear factor kappa B subunit 1	Homo sapiens	64-73
23958055-10	2014	Furthermore, we found that MGMT expression decreased through the down-regulation of NF-kappaB expression by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	O-6-methylguanine-DNA methyltransferase	Homo sapiens	27-31
23958055-10	2014	Furthermore, we found that MGMT expression decreased through the down-regulation of NF-kappaB expression by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	nuclear factor kappa B subunit 1	Homo sapiens	84-93
23958055-11	2014	Our results show that MG-132 may inhibit NF-kappaB expression and further decrease MGMT expression, resulting in a synergistic effect on MGMT-positive GSCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	nuclear factor kappa B subunit 1	Homo sapiens	41-50
24438070-5	2014	The proteasome inhibitor MG-132 led to an increase in IRS-1 protein level that inhibited osteoblastic differentiation, suggesting a role for proteasomal regulation in maintaining the appropriate expression level of IRS-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	insulin receptor substrate 1	Mus musculus	54-59
24231468-7	2014	The cycloheximide-associated decline of HSP70 was blocked by the proteasomal inhibitor, MG132, but had little effect on the relative level of HSP30.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	heat shock 70kDa protein L homeolog	Xenopus laevis	40-45
24438070-5	2014	The proteasome inhibitor MG-132 led to an increase in IRS-1 protein level that inhibited osteoblastic differentiation, suggesting a role for proteasomal regulation in maintaining the appropriate expression level of IRS-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	insulin receptor substrate 1	Mus musculus	215-220
24173102-7	2014	Further experiments with cycloheximide (protein synthesis inhibitor) and MG132 (proteasome inhibitor) revealed that ALD can upregulate NKCC1 by increasing protein stability, i.e., reducing ubiquitination of NKCC1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	solute carrier family 12 member 2	Homo sapiens	135-140
24145130-6	2014	However, treatment with proteasomal inhibitor MG132 showed polyubiquitinated-PP2Ac molecules (~65-250kDa) abundantly in siNT controls but low in siEDD-transfectants, implicating PP2Ac as an EDD substrate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	77-82
24145130-6	2014	However, treatment with proteasomal inhibitor MG132 showed polyubiquitinated-PP2Ac molecules (~65-250kDa) abundantly in siNT controls but low in siEDD-transfectants, implicating PP2Ac as an EDD substrate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	178-183
24145130-6	2014	However, treatment with proteasomal inhibitor MG132 showed polyubiquitinated-PP2Ac molecules (~65-250kDa) abundantly in siNT controls but low in siEDD-transfectants, implicating PP2Ac as an EDD substrate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	ubiquitin protein ligase E3 component n-recognin 5	Homo sapiens	147-150
24497960-6	2014	OCT4 induced by cobalt and nickel was due primarily to protein stabilization because MG132 stabilized OCT4 in cells treated with either metals and because neither nickel nor cobalt significantly modulated its steady-state mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	POU class 5 homeobox 1	Homo sapiens	0-4
24497960-6	2014	OCT4 induced by cobalt and nickel was due primarily to protein stabilization because MG132 stabilized OCT4 in cells treated with either metals and because neither nickel nor cobalt significantly modulated its steady-state mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	POU class 5 homeobox 1	Homo sapiens	102-106
24913775-8	2014	Mechanistically, we show that auranofin-induced VEGFR3 downregulation is blocked by antioxidant N-acetyl-L-cysteine (NAC) and lysosome inhibitor chloroquine, but is promoted by proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	199-204	fms related receptor tyrosine kinase 4	Homo sapiens	48-54
24177323-11	2014	Mass spectrometry revealed a single MG132-sensitive tryptic cleavage after R1745 in an extended Filamin A loop, which would separate its actin-binding domain from its carboxy terminal glycoprotein Ibalpha-binding domain.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	filamin, alpha	Mus musculus	96-105
24991536-3	2014	MG132, as a ubiquitin proteasome, could improve renal injury by regulating several signaling pathways, such as NF- kappa B, TGF- beta , Nrf2-oxidative stress, and MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor beta 1	Homo sapiens	124-133
24991536-3	2014	MG132, as a ubiquitin proteasome, could improve renal injury by regulating several signaling pathways, such as NF- kappa B, TGF- beta , Nrf2-oxidative stress, and MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	NFE2 like bZIP transcription factor 2	Homo sapiens	136-140
24111984-5	2014	The protein-synthesis inhibitor cycloheximide also enhanced Scg2 activation, and the proteasome inhibitor ZLLLH diminished the KT5720-mediated augmentation of Scg2 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	secretogranin II	Mus musculus	159-163
24511554-0	2014	MG132 ameliorates kidney lesions by inhibiting the degradation of Smad7 in streptozotocin-induced diabetic nephropathy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	SMAD family member 7	Rattus norvegicus	66-71
24511554-9	2014	CONCLUSION: MG132 alleviates kidney damage by inhibiting Smad7 ubiquitin degradation and TGF-beta activation in DN.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	SMAD family member 7	Rattus norvegicus	57-62
24511554-9	2014	CONCLUSION: MG132 alleviates kidney damage by inhibiting Smad7 ubiquitin degradation and TGF-beta activation in DN.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	transforming growth factor, beta 1	Rattus norvegicus	89-97
25003128-11	2014	The present results support the hypothesis that MG132 may alleviate kidney damage by inhibiting SnoN degradation and TGF-beta activation, suggesting that the ubiquitin-proteasome pathway may become a new therapeutic target for DN.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	transforming growth factor, beta 1	Rattus norvegicus	117-125
24100623-4	2013	SIRT1 depletion via transfection of specific siRNA into HeLa cells resulted in a significant increase in ATF4 protein, which was observed specifically in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	195-200	sirtuin 1	Homo sapiens	0-5
24646621-7	2014	Interestingly, genipin markedly inhibited c-Fos protein expression in BMMs, which was reversed in the presence of the proteosome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-145	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	42-47
24349175-12	2013	Further investigation revealed that EGb-mediated c-Jun degradation was preceded by ubiquitination of c-Jun and could be prevented by the proteosome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-164	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-54
24349175-12	2013	Further investigation revealed that EGb-mediated c-Jun degradation was preceded by ubiquitination of c-Jun and could be prevented by the proteosome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-164	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	101-106
23973256-10	2013	Double labeling immunofluorescence showed that LPC increased the colocalization of Cx43 with ubiquitin, and pretreatment with MG132 effectively prevented LPC-induced gap junction disassembly.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	gap junction protein, alpha 1	Rattus norvegicus	83-87
24142515-9	2013	Diminished steady-state levels of glycan-deficient ABCA3 isoforms were rescued by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	ATP binding cassette subfamily A member 3	Homo sapiens	51-56
24100623-4	2013	SIRT1 depletion via transfection of specific siRNA into HeLa cells resulted in a significant increase in ATF4 protein, which was observed specifically in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	195-200	activating transcription factor 4	Homo sapiens	105-109
24100623-5	2013	Consistent with SIRT1 depletion data, transient transfection of cells with SIRT1-overexpressing plasmid induced a decrease in the ATF4 protein level in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	sirtuin 1	Homo sapiens	75-80
24100623-5	2013	Consistent with SIRT1 depletion data, transient transfection of cells with SIRT1-overexpressing plasmid induced a decrease in the ATF4 protein level in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	activating transcription factor 4	Homo sapiens	130-134
24100623-6	2013	Interestingly, however, ATF4 mRNA was not affected by SIRT1, even in the presence of MG132, indicating that SIRT1-induced suppression of ATF4 synthesis occurs under post-transcriptional control.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	sirtuin 1	Homo sapiens	108-113
24261825-5	2013	API-1 treatment decreased the half-life of Mcl-1, whereas inhibition of the proteasome with MG132 rescued Mcl-1 reduction induced by API-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	106-111
25006397-5	2013	NO donor stimulation of endothelial cells for &gt;72 hours, which was associated with sustained Src activation and Cav-1 phosphorylation, ubiquitination, and degradation, was blocked by NOS inhibitor L-NAME, Src inhibitor PP2, and proteosomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	253-258	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	208-211
24221993-14	2013	The proteosomal inhibitor MG132 partly restored HIF-1alpha level and (18)F-FDG uptake in resveratrol-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	hypoxia inducible factor 1 subunit alpha	Homo sapiens	48-58
24055520-8	2013	Moreover, we found that NF-kappaB inhibitors, such as MG-132, bortezomib, Bay 11-7082 or Nemo binding domain (NBD) binding peptide, also strongly prevented IGF-II from inducing STS gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-60	nuclear factor kappa B subunit 1	Homo sapiens	24-33
24055520-8	2013	Moreover, we found that NF-kappaB inhibitors, such as MG-132, bortezomib, Bay 11-7082 or Nemo binding domain (NBD) binding peptide, also strongly prevented IGF-II from inducing STS gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-60	insulin like growth factor 2	Homo sapiens	156-162
24261825-5	2013	API-1 treatment decreased the half-life of Mcl-1, whereas inhibition of the proteasome with MG132 rescued Mcl-1 reduction induced by API-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	baculoviral IAP repeat containing 2	Homo sapiens	133-138
24076371-6	2013	Notably, quercetin inhibited nuclear factor-kappaB (NF-kappaB) activation by inhibiting degradation of the inhibitor of kappa Balpha (IkappaBalpha) in LPS-stimulated BV2 microglial cells corresponding to the inhibitory effect of specific NF-kappaB inhibitors, namely proteasome inhibitor I (PSI) and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	300-305	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	134-146
24085292-4	2013	However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	nuclear factor kappa B subunit 1	Homo sapiens	81-90
24085292-4	2013	However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	125-130
24085292-4	2013	However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	baculoviral IAP repeat containing 3	Homo sapiens	132-137
24085292-4	2013	However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	X-linked inhibitor of apoptosis	Homo sapiens	139-143
24085292-4	2013	However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	C-X-C motif chemokine ligand 8	Homo sapiens	149-153
24085292-4	2013	However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	NFKB inhibitor alpha	Homo sapiens	233-245
23263852-6	2013	Proteasome inhibitor MG132 could increase c-Myc protein in abundance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	42-47
24191027-7	2013	Lastly, blocking the proteosomal degradation of MCPIP1 by MG132 abrogated HIV-1 production in phorbol 12-myristate 13-acetate/ionomycin-stimulated human CD4+ T cells isolated from healthy donors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	zinc finger CCCH-type containing 12A	Homo sapiens	48-54
24236122-6	2013	Moreover, the LPS-induced downregulation of Cx43 was blocked following inhibition of 26S proteasome activity using the reversible proteasome inhibitor MG132 or the irreversible proteasome inhibitor lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	gap junction protein, alpha 1	Rattus norvegicus	44-48
23992566-5	2013	A proteasome inhibitor MG132 and siRNA-mediated downregulation of cIAP1 abrogated the SNIPER(ER)-induced ERalpha degradation, suggesting that the ERalpha is degraded by proteasome subsequent to cIAP1-mediated ubiquitylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	estrogen receptor 1	Homo sapiens	146-153
24005240-5	2013	The reduction in MKP1 expression occurred at a posttranscriptional level and was blocked by the proteasome inhibitor MG132, whereas that CPT-induced downregulation of MKP1 was not due to proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	dual specificity phosphatase 1	Homo sapiens	17-21
23703673-10	2013	BI 6727 administration or PLK2 knockdown decreased cellular protein levels of antiapoptotic myeloid cell leukemia 1 (Mcl-1), an effect reversed by the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-179	polo like kinase 2	Homo sapiens	26-30
23911694-0	2013	The role of Src protein in the process formation of PC12 cells induced by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	12-15
23911694-7	2013	Using immunological methods we detected phosphorylation of TrkA, prolongedactivation of Src, and ERK1/2 with nuclear translocation of the latter during MG-132-induced process formation of PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	59-63
23911694-7	2013	Using immunological methods we detected phosphorylation of TrkA, prolongedactivation of Src, and ERK1/2 with nuclear translocation of the latter during MG-132-induced process formation of PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	88-91
23911694-7	2013	Using immunological methods we detected phosphorylation of TrkA, prolongedactivation of Src, and ERK1/2 with nuclear translocation of the latter during MG-132-induced process formation of PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	mitogen activated protein kinase 3	Rattus norvegicus	97-103
23911694-9	2013	MG-132-induced sustained ERK1/2 activation, nuclear translocation and neuritogenesis required the intact function of Src since these phenomena were markedly reduced or failed upon chemical inhibition of Src tyrosine protein kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	mitogen activated protein kinase 3	Rattus norvegicus	25-31
23911694-9	2013	MG-132-induced sustained ERK1/2 activation, nuclear translocation and neuritogenesis required the intact function of Src since these phenomena were markedly reduced or failed upon chemical inhibition of Src tyrosine protein kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	117-120
23911694-9	2013	MG-132-induced sustained ERK1/2 activation, nuclear translocation and neuritogenesis required the intact function of Src since these phenomena were markedly reduced or failed upon chemical inhibition of Src tyrosine protein kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	203-206
23952686-6	2013	AtMBP-1 has a short half-life in vivo and is stabilized by the proteasome inhibitor MG132, indicating that it is degraded via the ubiquitin-dependent proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	myrosinase-binding protein 1	Arabidopsis thaliana	0-7
23994832-4	2013	When cells were treated with a proteasome inhibitor (MG132) or an MDM2 antagonist (Nutlin-3), p53 expression was not reduced in N protein-overexpressed cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	tumor protein p53	Homo sapiens	94-97
23325562-7	2013	Furthermore, proteosomal inhibitor MG132 suppressed AMPK activation, GSK3beta phosphorylation, cleaved PARP and deceased AEG-1 induced by ursolic acid in HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	glycogen synthase kinase 3 beta	Homo sapiens	69-77
23325562-7	2013	Furthermore, proteosomal inhibitor MG132 suppressed AMPK activation, GSK3beta phosphorylation, cleaved PARP and deceased AEG-1 induced by ursolic acid in HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	poly(ADP-ribose) polymerase 1	Homo sapiens	103-107
23325562-7	2013	Furthermore, proteosomal inhibitor MG132 suppressed AMPK activation, GSK3beta phosphorylation, cleaved PARP and deceased AEG-1 induced by ursolic acid in HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	metadherin	Homo sapiens	121-126
23146908-6	2013	Dissociation of AR-transcription complexes was due to degradation because inhibition of the proteasome system by MG132 caused accumulation of AR at enhancer/promoter elements.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	androgen receptor	Homo sapiens	16-18
23146908-6	2013	Dissociation of AR-transcription complexes was due to degradation because inhibition of the proteasome system by MG132 caused accumulation of AR at enhancer/promoter elements.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	androgen receptor	Homo sapiens	142-144
23146908-8	2013	Interestingly, knockdown of ZIPK by siRNA had a similar effect as MG132, leading to reduced transcription but enhanced accumulation of AR at androgen-response elements.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	death associated protein kinase 3	Homo sapiens	28-32
23146908-8	2013	Interestingly, knockdown of ZIPK by siRNA had a similar effect as MG132, leading to reduced transcription but enhanced accumulation of AR at androgen-response elements.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	androgen receptor	Homo sapiens	135-137
23934994-10	2013	The rpn3-L140P allele restored Mec1-W2368A to nearly wild-type protein levels at 37 , an effect partially mimicked by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	protein kinase MEC1	Saccharomyces cerevisiae S288C	31-35
23873832-4	2013	Furthermore, PAK4-mediated down-regulation of p57(Kip2) was reversed by MG132, a specific proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	p21 (RAC1) activated kinase 4	Homo sapiens	13-17
23873832-4	2013	Furthermore, PAK4-mediated down-regulation of p57(Kip2) was reversed by MG132, a specific proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	cyclin dependent kinase inhibitor 1C	Homo sapiens	46-49
23873832-4	2013	Furthermore, PAK4-mediated down-regulation of p57(Kip2) was reversed by MG132, a specific proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	cyclin dependent kinase inhibitor 1C	Homo sapiens	50-54
23703673-10	2013	BI 6727 administration or PLK2 knockdown decreased cellular protein levels of antiapoptotic myeloid cell leukemia 1 (Mcl-1), an effect reversed by the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-179	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	92-115
23703673-10	2013	BI 6727 administration or PLK2 knockdown decreased cellular protein levels of antiapoptotic myeloid cell leukemia 1 (Mcl-1), an effect reversed by the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-179	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	117-122
23665451-9	2013	However, MG132 was toxic to human CD34+ cells at high concentrations, and both drugs had a small range of effective dosage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	CD34 molecule	Homo sapiens	34-38
24098681-6	2013	Intriguingly, the IMAGe-associated mutant CDKN1C proteins were fairly stable even in the presence of cycloheximide, whereas the wild-type protein was almost completely degraded via the proteasome pathway, as shown by the lack of degradation with addition of a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-287	cyclin dependent kinase inhibitor 1C	Homo sapiens	42-48
23994633-0	2013	Proteasome inhibitor MG132 enhances TRAIL-induced apoptosis and inhibits invasion of human osteosarcoma OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF superfamily member 10	Homo sapiens	36-41
23994633-2	2013	This study aimed to discuss the effect of proteasome inhibitor MG132 on the TRAIL-induced apoptosis of human osteosarcoma OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	TNF superfamily member 10	Homo sapiens	76-81
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	TNF receptor superfamily member 10b	Homo sapiens	104-107
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	caspase 3	Homo sapiens	109-118
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	caspase 8	Homo sapiens	120-129
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	interferon alpha inducible protein 27	Homo sapiens	134-137
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	cyclin dependent kinase inhibitor 1B	Homo sapiens	138-142
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	matrix metallopeptidase 9	Homo sapiens	175-180
23685957-9	2013	Furthermore, curcumin dose-dependently reduced the expression of AP transcription factor AP-2gamma in NTera-2 cells, whereas the pretreatment with the proteasome inhibitor MG132 blocked both the curcumin-induced reduction of AP-2gamma and antiproliferative effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	transcription factor AP-2 gamma	Homo sapiens	89-98
23685957-9	2013	Furthermore, curcumin dose-dependently reduced the expression of AP transcription factor AP-2gamma in NTera-2 cells, whereas the pretreatment with the proteasome inhibitor MG132 blocked both the curcumin-induced reduction of AP-2gamma and antiproliferative effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	transcription factor AP-2 gamma	Homo sapiens	225-234
23708311-7	2013	In addition, pretreatment with the NF-kappaB inhibitor MG132 blocked VA/TNF-alpha-induced apoptosis by suppression of NF-kappaB-dependent Fas expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	tumor necrosis factor	Homo sapiens	72-81
23850521-3	2013	Activation of TLR3 by polyinosinic-polycytidylic acid [poly (I:C)] was shown to trigger the decline of cyclin D1/2 protein levels in pancreatic beta-cell lines, which could be reversed by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	213-218	toll like receptor 3	Homo sapiens	14-18
23850521-3	2013	Activation of TLR3 by polyinosinic-polycytidylic acid [poly (I:C)] was shown to trigger the decline of cyclin D1/2 protein levels in pancreatic beta-cell lines, which could be reversed by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	213-218	cyclin D1	Homo sapiens	103-114
24027419-10	2013	In contrast to oxidative stress, MG132 and 17AAG treatments showed mitochondrial retention of Hsp60; however, MG132 combination either with hsp60 shRNA or 17AAG induced its translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	heat shock protein family D (Hsp60) member 1	Homo sapiens	94-99
24027419-10	2013	In contrast to oxidative stress, MG132 and 17AAG treatments showed mitochondrial retention of Hsp60; however, MG132 combination either with hsp60 shRNA or 17AAG induced its translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	heat shock protein family D (Hsp60) member 1	Homo sapiens	140-145
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	96-118
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	120-129
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	tumor necrosis factor	Mus musculus	160-169
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	tissue inhibitor of metalloproteinase 1	Mus musculus	192-197
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	jun proto-oncogene	Mus musculus	250-255
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	matrix metallopeptidase 9	Mus musculus	289-293
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	207-212	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	96-118
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	207-212	tumor necrosis factor	Mus musculus	160-169
24279124-5	2013	Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kappaB), significantly inhibited the TNF-alpha-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	207-212	tissue inhibitor of metalloproteinase 1	Mus musculus	192-197
23893020-5	2013	METHODS: Human colon cancer HCT116 Bax positive and negative cell lines were treated with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	BCL2 associated X, apoptosis regulator	Homo sapiens	35-38
23677714-8	2013	Moreover, inhibition of the proteaosome pathway by MG132 caused a significant recovery in the migration ability of U-87 MG cells and augmented the Cdc42 protein levels after luteolin treatment, suggesting that pharmacological inhibition of migration via luteolin treatment is likely to preferentially facilitate the protein degradation of Cdc42.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	cell division cycle 42	Homo sapiens	147-152
23677714-8	2013	Moreover, inhibition of the proteaosome pathway by MG132 caused a significant recovery in the migration ability of U-87 MG cells and augmented the Cdc42 protein levels after luteolin treatment, suggesting that pharmacological inhibition of migration via luteolin treatment is likely to preferentially facilitate the protein degradation of Cdc42.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	cell division cycle 42	Homo sapiens	339-344
23807085-6	2013	2-Deoxy-D-ribose also increased the amount of hydroxy-HIF-1alpha in the presence of the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-115	hypoxia inducible factor 1 subunit alpha	Homo sapiens	54-64
23911785-9	2013	The expression of IkappaBalpha was dose- and time-dependently decreased, and NF-kappaBp65 and MCP-1 were increased under high glucose conditions, which could be mostly reversed by adding MG132 (p&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	187-192	NFKB inhibitor alpha	Rattus norvegicus	18-30
23813634-0	2013	A novel hydroxysuberamide derivative potentiates MG132-mediated anticancer activity against human hormone refractory prostate cancers--the role of histone deacetylase and endoplasmic reticulum stress.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	histone deacetylase 9	Homo sapiens	147-166
23911785-9	2013	The expression of IkappaBalpha was dose- and time-dependently decreased, and NF-kappaBp65 and MCP-1 were increased under high glucose conditions, which could be mostly reversed by adding MG132 (p&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	187-192	C-C motif chemokine ligand 2	Rattus norvegicus	94-99
24009686-6	2013	Treatment of AGS and HEK293T cells with proteasome inhibitors MG132 or Omuralide increases Drosha protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	drosha ribonuclease III	Homo sapiens	91-97
24001151-5	2013	Furthermore, we show that mahanine treatment induces the degradation of DNMT1 and DNMT3B, but not DNMT3A, via the ubiquitin-proteasome pathway; an effect which is rescued in the presence of a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	DNA methyltransferase 1	Homo sapiens	72-77
23615711-8	2013	In addition to the transcriptional regulation, we found that Chac1 protein expression was only detected in the presence of MG132, a proteasome inhibitor, even though mouse Chac1 gene was transiently overexpressed in Neuro2a cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	ChaC, cation transport regulator 1	Mus musculus	61-66
23701246-6	2013	Mas degradation was robustly inhibited by the proteasome inhibitor MG132 in time- and dose-dependent manners, and the expression of PSD95 impaired Mas ubiquitination, indicating that the PSD95-Mas association inhibits Mas receptor degradation via the ubiquitin-proteasome proteolytic pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	discs large MAGUK scaffold protein 4	Homo sapiens	187-192
23664424-6	2013	Treatment with MG132, an indirect NF-kappaB inhibitor, effectively reduced p-IkappaBalpha, p-NF-kappaB, MMP-2 and MMP-9 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	34-43
23664424-6	2013	Treatment with MG132, an indirect NF-kappaB inhibitor, effectively reduced p-IkappaBalpha, p-NF-kappaB, MMP-2 and MMP-9 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	93-102
23904368-0	2013	Effect of the protease inhibitor MG132 on the transforming growth factor-beta/Smad signaling pathway in HSC-T6 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	SMAD family member 7	Rattus norvegicus	78-82
23904368-3	2013	This study aimed to examine the effect of the protease inhibitor MG132 on the signaling pathway of TGFbeta/Smad in HSC-T6 cells and seek a novel therapeutic approach for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	transforming growth factor, beta 1	Rattus norvegicus	99-106
23904368-3	2013	This study aimed to examine the effect of the protease inhibitor MG132 on the signaling pathway of TGFbeta/Smad in HSC-T6 cells and seek a novel therapeutic approach for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	SMAD family member 7	Rattus norvegicus	107-111
23904368-6	2013	The mRNA and protein expression levels of TGFbeta1, Smad3 and Smad7 were determined in HSC-T6 cells by real-time PCR and Western blotting, respectively, after treatment with MG132 at different concentrations (1, 2, 3 mumol/L) or RPMI1640 alone (serving as control).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	transforming growth factor, beta 1	Rattus norvegicus	42-50
23904368-8	2013	After treatment with MG132 at 1, 2 or 3 mumol/L for 24 h, the mRNA expression levels of TGF-beta1 and Smad3 were significantly decreased (P&lt;0.05), but the Smad7 mRNA expression had no significant change (P&gt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	transforming growth factor, beta 1	Rattus norvegicus	88-97
23904368-8	2013	After treatment with MG132 at 1, 2 or 3 mumol/L for 24 h, the mRNA expression levels of TGF-beta1 and Smad3 were significantly decreased (P&lt;0.05), but the Smad7 mRNA expression had no significant change (P&gt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	SMAD family member 3	Rattus norvegicus	102-107
23904368-8	2013	After treatment with MG132 at 1, 2 or 3 mumol/L for 24 h, the mRNA expression levels of TGF-beta1 and Smad3 were significantly decreased (P&lt;0.05), but the Smad7 mRNA expression had no significant change (P&gt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	SMAD family member 7	Rattus norvegicus	158-163
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	transforming growth factor, beta 1	Rattus norvegicus	40-47
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	SMAD family member 7	Rattus norvegicus	48-52
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	transforming growth factor, beta 1	Rattus norvegicus	136-144
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	SMAD family member 3	Rattus norvegicus	146-151
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	SMAD family member 7	Rattus norvegicus	205-210
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	229-234	transforming growth factor, beta 1	Rattus norvegicus	40-47
23904368-11	2013	It was concluded that the inhibition of TGFbeta/Smad pathway in HSC-T6 cells by MG132 can reduce the production of profibrosis factors (TGFbeta1, Smad3) and promote the expression of anti-fibrosis factor (Smad7), suggesting that MG132 may become a potential therapeutic alternative for liver fibrosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	229-234	SMAD family member 7	Rattus norvegicus	48-52
23872411-7	2013	Treatment of mice with the lysosome inhibitor, chloroquine, or the proteasome inhibitor, MG132, increased ileal ASBT protein levels in BBMVs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	solute carrier family 10, member 2	Mus musculus	112-116
23872411-8	2013	CA-mediated reduction of ASBT protein levels in the ABPC-pretreated mice was attenuated by co-treatment with chloroquine or MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	solute carrier family 10, member 2	Mus musculus	25-29
23720426-7	2013	Chromatin immunoprecipitation analysis showed that NFkappaB binding to the Cox-2 promoter increased at 12 hours after progesterone withdrawal in vivo, and real-time PCR analysis showed that the NFkappaB inhibitors pyrrolidine dithiocarbamate and MG-132 inhibited Cox-2 mRNA expression in vivo and in vitro, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	246-252	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	51-59
23720426-7	2013	Chromatin immunoprecipitation analysis showed that NFkappaB binding to the Cox-2 promoter increased at 12 hours after progesterone withdrawal in vivo, and real-time PCR analysis showed that the NFkappaB inhibitors pyrrolidine dithiocarbamate and MG-132 inhibited Cox-2 mRNA expression in vivo and in vitro, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	246-252	cytochrome c oxidase II, mitochondrial	Mus musculus	75-80
23720426-7	2013	Chromatin immunoprecipitation analysis showed that NFkappaB binding to the Cox-2 promoter increased at 12 hours after progesterone withdrawal in vivo, and real-time PCR analysis showed that the NFkappaB inhibitors pyrrolidine dithiocarbamate and MG-132 inhibited Cox-2 mRNA expression in vivo and in vitro, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	246-252	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	194-202
23644046-5	2013	As a consequence of p300"s physical absence, FOXP3 becomes less acetylated and eventually degraded, a process that cannot be rescued by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-166	E1A binding protein p300	Homo sapiens	20-24
23644046-5	2013	As a consequence of p300"s physical absence, FOXP3 becomes less acetylated and eventually degraded, a process that cannot be rescued by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	161-166	forkhead box P3	Homo sapiens	45-50
23490586-8	2013	Cycloheximide (CHX)-chase assay revealed that MEK/ERK1/2 inhibition accelerated adiponectin protein degradation, which was prevented by MG132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	midkine	Mus musculus	46-49
23490586-8	2013	Cycloheximide (CHX)-chase assay revealed that MEK/ERK1/2 inhibition accelerated adiponectin protein degradation, which was prevented by MG132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	mitogen-activated protein kinase 3	Mus musculus	50-56
23490586-8	2013	Cycloheximide (CHX)-chase assay revealed that MEK/ERK1/2 inhibition accelerated adiponectin protein degradation, which was prevented by MG132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	adiponectin, C1Q and collagen domain containing	Mus musculus	80-91
23894359-6	2013	The degradation of AKAP3 was significantly inhibited by MG-132, a proteasome inhibitor, indicating that AKAP3 degradation occurs via the proteasomal machinery.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-62	A-kinase anchoring protein 3	Bos taurus	19-24
23708668-6	2013	The stability of BLH at normal culture conditions was analyzed with the protein synthesis inhibitor cycloheximide and the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	bleomycin hydrolase	Homo sapiens	17-20
23998584-2	2013	Apoptosis of HL-60 cells was detected by flow cytometry, the expression of P21, P27 and P53 proteins in HL-60 cells treated with MG132 was assayed by Western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	H3 histone pseudogene 16	Homo sapiens	75-78
23998584-2	2013	Apoptosis of HL-60 cells was detected by flow cytometry, the expression of P21, P27 and P53 proteins in HL-60 cells treated with MG132 was assayed by Western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	interferon alpha inducible protein 27	Homo sapiens	80-83
23998584-2	2013	Apoptosis of HL-60 cells was detected by flow cytometry, the expression of P21, P27 and P53 proteins in HL-60 cells treated with MG132 was assayed by Western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	tumor protein p53	Homo sapiens	88-91
23998584-7	2013	The expression of P21 and P27 protein increased after treatment of HL-60 cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	H3 histone pseudogene 16	Homo sapiens	18-21
23998584-7	2013	The expression of P21 and P27 protein increased after treatment of HL-60 cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	interferon alpha inducible protein 27	Homo sapiens	26-29
23998584-9	2013	It is concluded that high dose of MG132 can induce the apoptosis of HL-60 cells, and has direct killing effect on HL-60 cells, but this inducing apoptotic effect on HL-60 cells can not be realized through caspase-8 and caspase-9 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	caspase 8	Homo sapiens	205-214
23998584-9	2013	It is concluded that high dose of MG132 can induce the apoptosis of HL-60 cells, and has direct killing effect on HL-60 cells, but this inducing apoptotic effect on HL-60 cells can not be realized through caspase-8 and caspase-9 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	caspase 9	Homo sapiens	219-228
23998584-10	2013	The P21 and P27 protein may be involved in MG132 induced HL-60 cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	H3 histone pseudogene 16	Homo sapiens	4-7
23998584-10	2013	The P21 and P27 protein may be involved in MG132 induced HL-60 cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	interferon alpha inducible protein 27	Homo sapiens	12-15
23922739-8	2013	We here show that, under proteasomal inhibitor MG-132, ELAVL1/HuR is up-regulated at both mRNA and protein levels, and that this protein binds and post-transcriptionally regulates SQSTM1/p62 mRNA in ARPE-19 cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	ELAV like RNA binding protein 1	Homo sapiens	55-61
23922739-8	2013	We here show that, under proteasomal inhibitor MG-132, ELAVL1/HuR is up-regulated at both mRNA and protein levels, and that this protein binds and post-transcriptionally regulates SQSTM1/p62 mRNA in ARPE-19 cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	ELAV like RNA binding protein 1	Homo sapiens	62-65
23922739-8	2013	We here show that, under proteasomal inhibitor MG-132, ELAVL1/HuR is up-regulated at both mRNA and protein levels, and that this protein binds and post-transcriptionally regulates SQSTM1/p62 mRNA in ARPE-19 cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	sequestosome 1	Homo sapiens	180-186
23922739-8	2013	We here show that, under proteasomal inhibitor MG-132, ELAVL1/HuR is up-regulated at both mRNA and protein levels, and that this protein binds and post-transcriptionally regulates SQSTM1/p62 mRNA in ARPE-19 cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	sequestosome 1	Homo sapiens	187-190
23901248-16	2013	Treatment of HTM cells with an autophagy activator (MG132) or inhibitors (wortmannin, bafilomycin A1) significantly increased and decreased the number of small ASB10-stained vesicles, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	ankyrin repeat and SOCS box containing 10	Homo sapiens	160-165
23894359-6	2013	The degradation of AKAP3 was significantly inhibited by MG-132, a proteasome inhibitor, indicating that AKAP3 degradation occurs via the proteasomal machinery.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-62	A-kinase anchoring protein 3	Bos taurus	104-109
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	eukaryotic translation initiation factor 2A	Homo sapiens	333-342
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	DNA damage inducible transcript 3	Homo sapiens	345-369
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	DNA damage inducible transcript 3	Homo sapiens	371-375
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	eukaryotic translation initiation factor 2A	Homo sapiens	283-331
23701727-6	2013	The proteasome inhibitor MG-132 can effectively counteract the geldanamycin-induced reduction of TrkA expression and it can render TrkA and ERK1/2 phosphorylation but not that of protein kinase B/Akt by nerve growth factor again inducible.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	97-101
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	DNA damage inducible transcript 3	Homo sapiens	377-384
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	464-467
23701727-6	2013	The proteasome inhibitor MG-132 can effectively counteract the geldanamycin-induced reduction of TrkA expression and it can render TrkA and ERK1/2 phosphorylation but not that of protein kinase B/Akt by nerve growth factor again inducible.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	131-135
23701727-6	2013	The proteasome inhibitor MG-132 can effectively counteract the geldanamycin-induced reduction of TrkA expression and it can render TrkA and ERK1/2 phosphorylation but not that of protein kinase B/Akt by nerve growth factor again inducible.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	mitogen activated protein kinase 3	Rattus norvegicus	140-146
23701727-6	2013	The proteasome inhibitor MG-132 can effectively counteract the geldanamycin-induced reduction of TrkA expression and it can render TrkA and ERK1/2 phosphorylation but not that of protein kinase B/Akt by nerve growth factor again inducible.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	AKT serine/threonine kinase 1	Rattus norvegicus	196-199
23701727-6	2013	The proteasome inhibitor MG-132 can effectively counteract the geldanamycin-induced reduction of TrkA expression and it can render TrkA and ERK1/2 phosphorylation but not that of protein kinase B/Akt by nerve growth factor again inducible.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	nerve growth factor	Rattus norvegicus	203-222
23642711-11	2013	Yet, despite the fact that the -210 bp NFkappaB site acts as a suppressor element, overall mRNA and protein expression were inhibited in monocytes treated with MG132 (NFkappaB/proteasome inhibitor) or SN50 (NFkappaB-p50 blocking peptide), suggesting that NFkappaB acts as both an activator and silencer of TL1A expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	160-165	nuclear factor kappa B subunit 1	Homo sapiens	39-47
23423712-7	2013	Pretreatment with MG132, an inhibitor of proteasome activity, and BAY11-7082, an inhibitor of IkappaBalpha phosphorylation, both inhibited NF-kappaB p65 translocation and significantly promoted apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	nuclear factor kappa B subunit 1	Homo sapiens	139-148
23423712-7	2013	Pretreatment with MG132, an inhibitor of proteasome activity, and BAY11-7082, an inhibitor of IkappaBalpha phosphorylation, both inhibited NF-kappaB p65 translocation and significantly promoted apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	RELA proto-oncogene, NF-kB subunit	Homo sapiens	149-152
23423712-11	2013	The detrimental role of MG132 and BAY11-7082 appears related to the exaggerated JNK phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	mitogen-activated protein kinase 8	Homo sapiens	80-83
23567159-11	2013	To determine if increased ubiquitination of SOCS2 by E2 led to degradation by proteasome, hOBs were pretreated with the proteasome inhibitor MG132 (5 muM) which blocked E2 reduction of SOCS2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	suppressor of cytokine signaling 2	Homo sapiens	44-49
23567159-11	2013	To determine if increased ubiquitination of SOCS2 by E2 led to degradation by proteasome, hOBs were pretreated with the proteasome inhibitor MG132 (5 muM) which blocked E2 reduction of SOCS2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	leptin	Homo sapiens	90-94
23567159-11	2013	To determine if increased ubiquitination of SOCS2 by E2 led to degradation by proteasome, hOBs were pretreated with the proteasome inhibitor MG132 (5 muM) which blocked E2 reduction of SOCS2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	suppressor of cytokine signaling 2	Homo sapiens	185-190
23642711-11	2013	Yet, despite the fact that the -210 bp NFkappaB site acts as a suppressor element, overall mRNA and protein expression were inhibited in monocytes treated with MG132 (NFkappaB/proteasome inhibitor) or SN50 (NFkappaB-p50 blocking peptide), suggesting that NFkappaB acts as both an activator and silencer of TL1A expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	160-165	nuclear factor kappa B subunit 1	Homo sapiens	167-175
23642711-11	2013	Yet, despite the fact that the -210 bp NFkappaB site acts as a suppressor element, overall mRNA and protein expression were inhibited in monocytes treated with MG132 (NFkappaB/proteasome inhibitor) or SN50 (NFkappaB-p50 blocking peptide), suggesting that NFkappaB acts as both an activator and silencer of TL1A expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	160-165	nuclear factor kappa B subunit 1	Homo sapiens	167-175
23642711-11	2013	Yet, despite the fact that the -210 bp NFkappaB site acts as a suppressor element, overall mRNA and protein expression were inhibited in monocytes treated with MG132 (NFkappaB/proteasome inhibitor) or SN50 (NFkappaB-p50 blocking peptide), suggesting that NFkappaB acts as both an activator and silencer of TL1A expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	160-165	nuclear factor kappa B subunit 1	Homo sapiens	167-175
23642711-11	2013	Yet, despite the fact that the -210 bp NFkappaB site acts as a suppressor element, overall mRNA and protein expression were inhibited in monocytes treated with MG132 (NFkappaB/proteasome inhibitor) or SN50 (NFkappaB-p50 blocking peptide), suggesting that NFkappaB acts as both an activator and silencer of TL1A expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	160-165	TNF superfamily member 15	Homo sapiens	306-310
23535871-7	2013	MG132 reduced tumor growth and the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Mus musculus	45-54
23485335-4	2013	RESULTS: MG132 and lactacystin induced an increase in the intracellular levels of Hsp70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	heat shock protein family A (Hsp70) member 4	Homo sapiens	82-87
23485335-5	2013	MnSOD was up-regulated by MG132 and celastrol, and GST-pi was up-regulated by MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	superoxide dismutase 2	Homo sapiens	0-5
23535871-7	2013	MG132 reduced tumor growth and the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interleukin 6	Mus musculus	59-63
23535871-8	2013	NF-kappaB, MuRF1 and MAFbx were also inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	0-9
23535871-8	2013	NF-kappaB, MuRF1 and MAFbx were also inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	tripartite motif-containing 63	Mus musculus	11-16
23535871-8	2013	NF-kappaB, MuRF1 and MAFbx were also inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	F-box protein 32	Mus musculus	21-26
23535871-11	2013	CONCLUSION: Our results demonstrate that MG132-induced inhibition of the ubiquitin-proteasome pathway in cancer cachexia decreased the activity of NF-kappaB and the degradation of IkappaBalpha, and reduced the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue, accompanied by downregulation of MuRF1 and MAFbx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	147-156
23535871-11	2013	CONCLUSION: Our results demonstrate that MG132-induced inhibition of the ubiquitin-proteasome pathway in cancer cachexia decreased the activity of NF-kappaB and the degradation of IkappaBalpha, and reduced the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue, accompanied by downregulation of MuRF1 and MAFbx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	180-192
23535871-11	2013	CONCLUSION: Our results demonstrate that MG132-induced inhibition of the ubiquitin-proteasome pathway in cancer cachexia decreased the activity of NF-kappaB and the degradation of IkappaBalpha, and reduced the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue, accompanied by downregulation of MuRF1 and MAFbx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	tumor necrosis factor	Mus musculus	220-229
23535871-11	2013	CONCLUSION: Our results demonstrate that MG132-induced inhibition of the ubiquitin-proteasome pathway in cancer cachexia decreased the activity of NF-kappaB and the degradation of IkappaBalpha, and reduced the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue, accompanied by downregulation of MuRF1 and MAFbx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	interleukin 6	Mus musculus	234-238
23535871-11	2013	CONCLUSION: Our results demonstrate that MG132-induced inhibition of the ubiquitin-proteasome pathway in cancer cachexia decreased the activity of NF-kappaB and the degradation of IkappaBalpha, and reduced the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue, accompanied by downregulation of MuRF1 and MAFbx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	tripartite motif-containing 63	Mus musculus	307-312
23535871-11	2013	CONCLUSION: Our results demonstrate that MG132-induced inhibition of the ubiquitin-proteasome pathway in cancer cachexia decreased the activity of NF-kappaB and the degradation of IkappaBalpha, and reduced the levels of TNF-alpha and IL-6 in serum and gastrocnemius tissue, accompanied by downregulation of MuRF1 and MAFbx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	F-box protein 32	Mus musculus	317-322
23651583-5	2013	Furthermore, resveratrol promoted Nanog suppression via proteasomal degradation, which was inhibited by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	Nanog homeobox	Homo sapiens	34-39
23600800-8	2013	The reduction in P2X3 expression levels was reversed by the proteasomal inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	purinergic receptor P2X 3	Homo sapiens	17-21
23840880-4	2013	Conversely, CDC25B depletion causes a loss of centrin 2 from the centrosome, which can be rescued by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	cell division cycle 25B	Homo sapiens	12-18
23840880-4	2013	Conversely, CDC25B depletion causes a loss of centrin 2 from the centrosome, which can be rescued by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	centrin 2	Homo sapiens	46-55
22890317-8	2013	AICAR-induced depletion of EGFR protein can be abrogated through inhibition of the proteasome with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	epidermal growth factor receptor	Homo sapiens	27-31
23470959-8	2013	In MCF-7 cells, depletion of DDX3 reduced by more than 50% camptothecin-induced p53 accumulation, and this effect was blocked by inhibition of the proteasome with MG132, indicating that DDX3 regulates p53 not at expression level but rather its stabilization after DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	DEAD-box helicase 3 X-linked	Homo sapiens	29-33
23640883-4	2013	Here, we show that both forskolin- and IGF-1-mediated reductions of EF2K activity in PC12 cells are due to decreased EF2K protein levels, and this is attenuated by application of the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	205-210	insulin-like growth factor 1	Rattus norvegicus	39-44
23524145-10	2013	This down-regulation is closely related to the inhibition effect of Celecoxib on the AKT/GSK-3beta pathway, and was blocked upon addition of GSK-3beta inhibitor LiCl or the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	194-199	AKT serine/threonine kinase 1	Homo sapiens	85-88
23524145-10	2013	This down-regulation is closely related to the inhibition effect of Celecoxib on the AKT/GSK-3beta pathway, and was blocked upon addition of GSK-3beta inhibitor LiCl or the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	194-199	glycogen synthase kinase 3 beta	Homo sapiens	89-98
23750283-7	2013	Additionally, tumor angiogenesis was inhibited, and p53 protein levels were augmented, by intratumoral injection of the ubiquitin-proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	tumor protein p53	Homo sapiens	52-55
23470959-8	2013	In MCF-7 cells, depletion of DDX3 reduced by more than 50% camptothecin-induced p53 accumulation, and this effect was blocked by inhibition of the proteasome with MG132, indicating that DDX3 regulates p53 not at expression level but rather its stabilization after DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	DEAD-box helicase 3 X-linked	Homo sapiens	186-190
23470959-8	2013	In MCF-7 cells, depletion of DDX3 reduced by more than 50% camptothecin-induced p53 accumulation, and this effect was blocked by inhibition of the proteasome with MG132, indicating that DDX3 regulates p53 not at expression level but rather its stabilization after DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	tumor protein p53	Homo sapiens	201-204
24103208-14	2013	CONCLUSIONS: The proteasome inhibitor MG-132 significantly inhibited IkappaB-alpha degradation thus preventing NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	NFKB inhibitor alpha	Rattus norvegicus	69-82
23465077-4	2013	The proteasome inhibitor MG132 increased the P-gp level, enhanced its ubiquitination, and delayed the disappearance of the ubiquitinated P-gp.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	ATP binding cassette subfamily B member 1	Homo sapiens	45-49
23465077-4	2013	The proteasome inhibitor MG132 increased the P-gp level, enhanced its ubiquitination, and delayed the disappearance of the ubiquitinated P-gp.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	ATP binding cassette subfamily B member 1	Homo sapiens	137-141
23416168-9	2013	Treatment of NRCM with proteasome inhibitor MG132 increased p53 and miR-34a levels and reduced BLC2/BAX ratio.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	tumor protein p53	Homo sapiens	60-63
23416168-9	2013	Treatment of NRCM with proteasome inhibitor MG132 increased p53 and miR-34a levels and reduced BLC2/BAX ratio.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	microRNA 34a	Homo sapiens	68-75
23416168-9	2013	Treatment of NRCM with proteasome inhibitor MG132 increased p53 and miR-34a levels and reduced BLC2/BAX ratio.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	BCL2 associated X, apoptosis regulator	Homo sapiens	100-103
23317035-9	2013	A PI3K specific inhibitor (LY294002), Akt inhibitor VIII (Akti) and NF-kappaB inhibitors (Bay-11-7082 and MG-132) attenuated the induction of ICAM-1 by PGE2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-77
23317035-9	2013	A PI3K specific inhibitor (LY294002), Akt inhibitor VIII (Akti) and NF-kappaB inhibitors (Bay-11-7082 and MG-132) attenuated the induction of ICAM-1 by PGE2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	intercellular adhesion molecule 1	Mus musculus	142-148
23551903-0	2013	Proteasome inhibitor MG-132 induces MCPIP1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	zinc finger CCCH-type containing 12A	Homo sapiens	36-42
23551903-4	2013	Treatment of HepG2 or HeLa cells with proteasome inhibitor MG-132 resulted in a significant increase of MCPIP1 expression, both at mRNA and protein level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	zinc finger CCCH-type containing 12A	Homo sapiens	104-110
23551903-6	2013	Instead, the observed protein increase was blocked by actinomycin D, suggesting the involvement of de novo mRNA synthesis in the increase of MCPIP1 protein following MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-172	zinc finger CCCH-type containing 12A	Homo sapiens	141-147
23551903-7	2013	Using several inhibitors we determined the participation of extracellular-signal-regulated kinase 1/2 and p38 kinases in MCPIP1 upregulation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-150	mitogen-activated protein kinase 3	Homo sapiens	60-101
23551903-7	2013	Using several inhibitors we determined the participation of extracellular-signal-regulated kinase 1/2 and p38 kinases in MCPIP1 upregulation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-150	mitogen-activated protein kinase 14	Homo sapiens	106-109
23551903-7	2013	Using several inhibitors we determined the participation of extracellular-signal-regulated kinase 1/2 and p38 kinases in MCPIP1 upregulation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-150	zinc finger CCCH-type containing 12A	Homo sapiens	121-127
23551903-9	2013	Overexpression of MCPIP1-myc protein decreased the viability of HeLa cells but not HepG2 cells, which correlates with the increased susceptibility of HeLa cells to MG-132 toxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-170	zinc finger CCCH-type containing 12A	Homo sapiens	18-24
22751120-10	2013	The downstream effects of JAM-A knockdown on HER2 and phospho-AKT were partially reversed upon treatment with the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	F11 receptor	Homo sapiens	26-31
22751120-10	2013	The downstream effects of JAM-A knockdown on HER2 and phospho-AKT were partially reversed upon treatment with the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	erb-b2 receptor tyrosine kinase 2	Homo sapiens	45-49
23587486-5	2013	Mechanistic analysis revealed that in the presence of HCV, STAT3 protein was preferentially ubiquitinated, and degradation was blocked by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	signal transducer and activator of transcription 3	Homo sapiens	59-64
23504328-2	2013	This study demonstrates that treating P3HR1 cells with a proteasome inhibitor, MG132, causes the accumulation of SUMO-Rta and promotes the expression of EA-D.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	RNA binding fox-1 homolog 2	Homo sapiens	118-121
23543742-8	2013	The proteasome inhibitor MG-132 interfered with this decrease, resulting in elevated levels of polysumoylated Nrf2 that was also ubiquitylated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	NFE2 like bZIP transcription factor 2	Homo sapiens	110-114
23475934-5	2013	Treatment with proteasome inhibitor MG-132 was able to restore both nonsense and missense mutant PTEN protein levels in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	phosphatase and tensin homolog	Homo sapiens	97-101
23501055-4	2013	We detected that GA had no effect on mRNA level of HIF-1alpha which targets VEGF gene, but the increase of HIF-1alpha protein expression in hypoxia was repressed by GA, which can be reversed by proteasomal inhibitor MG132 and siRNA of VHL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-221	hypoxia inducible factor 1, alpha subunit	Mus musculus	107-117
23504328-2	2013	This study demonstrates that treating P3HR1 cells with a proteasome inhibitor, MG132, causes the accumulation of SUMO-Rta and promotes the expression of EA-D.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	collagen like tail subunit of asymmetric acetylcholinesterase	Homo sapiens	153-157
23519470-5	2013	We show here that treatment of prostate cancer PPC-1 cells with the superoxide generators menadione, paraquat, or buthionine sulfoximine down-regulates c-FLIP long (c-FLIP(L)) protein levels, which is prevented by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	239-244	CASP8 and FADD like apoptosis regulator	Homo sapiens	152-158
23519470-5	2013	We show here that treatment of prostate cancer PPC-1 cells with the superoxide generators menadione, paraquat, or buthionine sulfoximine down-regulates c-FLIP long (c-FLIP(L)) protein levels, which is prevented by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	239-244	CASP8 and FADD like apoptosis regulator	Homo sapiens	165-174
23449802-5	2013	Overexpression of Nsp1beta resulted in a reduction of KPNA1 levels in a dose-dependent manner, and treatment of the cells with the proteasome inhibitor MG132 restored KPNA1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	karyopherin subunit alpha 1	Homo sapiens	167-172
23585478-6	2013	Furthermore, proteasome inhibition by MG-132 reversed the clearance of IF proteins in cells overexpressing gigaxonin, demonstrating the involvement of the proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	giant axonal neuropathy	Mus musculus	107-116
23589924-11	2013	MG132 treatment increased cyclin G1 protein expression in cyclin G1-GFP-transfected Ishikawa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin G1	Homo sapiens	26-35
23390006-7	2013	Ubiquitination of Nrf2 and Keap1 was detected using immunoprecipitation after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
23390006-7	2013	Ubiquitination of Nrf2 and Keap1 was detected using immunoprecipitation after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	kelch like ECH associated protein 1	Homo sapiens	27-32
23373825-5	2013	Cell-free degradation and in planta stabilization assays in the presence of MG132, an inhibitor of proteasome activity, demonstrated that the degradation of GL3 and EGL3 proteins is 26S UPS-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	basic helix-loop-helix (bHLH) DNA-binding superfamily protein	Arabidopsis thaliana	157-160
23373825-5	2013	Cell-free degradation and in planta stabilization assays in the presence of MG132, an inhibitor of proteasome activity, demonstrated that the degradation of GL3 and EGL3 proteins is 26S UPS-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	basic helix-loop-helix (bHLH) DNA-binding superfamily protein	Arabidopsis thaliana	165-169
23589924-11	2013	MG132 treatment increased cyclin G1 protein expression in cyclin G1-GFP-transfected Ishikawa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin G1	Homo sapiens	58-67
23611845-7	2013	The level of Tat in the presence of NC was increased by treating cells with a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	tyrosine aminotransferase	Homo sapiens	13-16
23593480-3	2013	Consistent with our finding that PI-induced apoptosis requires de novo protein synthesis, the proteasomal inhibitor MG-132 induced expression of the BH3-only protein Noxa at the transcriptional level in a JNK1-dependent, but JNK2-opposing manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-122	phorbol-12-myristate-13-acetate-induced protein 1	Mus musculus	166-170
22689054-4	2013	Many ER stress inducers, including thapsigargin, MG132 or paclitaxel, increased expression levels of GRP78 and CLU, as well as post-translationally modified hypoglycosylated CLU forms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	heat shock protein family A (Hsp70) member 5	Homo sapiens	101-106
22689054-4	2013	Many ER stress inducers, including thapsigargin, MG132 or paclitaxel, increased expression levels of GRP78 and CLU, as well as post-translationally modified hypoglycosylated CLU forms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	clusterin	Homo sapiens	111-114
22689054-4	2013	Many ER stress inducers, including thapsigargin, MG132 or paclitaxel, increased expression levels of GRP78 and CLU, as well as post-translationally modified hypoglycosylated CLU forms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	clusterin	Homo sapiens	174-177
23593480-3	2013	Consistent with our finding that PI-induced apoptosis requires de novo protein synthesis, the proteasomal inhibitor MG-132 induced expression of the BH3-only protein Noxa at the transcriptional level in a JNK1-dependent, but JNK2-opposing manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-122	mitogen-activated protein kinase 8	Mus musculus	205-209
23593480-3	2013	Consistent with our finding that PI-induced apoptosis requires de novo protein synthesis, the proteasomal inhibitor MG-132 induced expression of the BH3-only protein Noxa at the transcriptional level in a JNK1-dependent, but JNK2-opposing manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-122	mitogen-activated protein kinase 9	Mus musculus	225-229
23536609-6	2013	Furthermore, the AtWEE1-green fluorescent protein (GFP) signal in Arabidopsis primary roots treated with the proteasome inhibitor MG132 was significantly increased compared with mock-treated controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	WEE1-like kinase	Arabidopsis thaliana	17-23
23412907-5	2013	In an attempt to identify Sulf-2 specific inhibitor, we found that proteasomal inhibitors such as MG132, Lactacystin and Bortezomib treatment abolished Sulf-2 expression in multiple breast cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	sulfatase 2	Homo sapiens	26-32
23412907-5	2013	In an attempt to identify Sulf-2 specific inhibitor, we found that proteasomal inhibitors such as MG132, Lactacystin and Bortezomib treatment abolished Sulf-2 expression in multiple breast cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	sulfatase 2	Homo sapiens	152-158
23375957-7	2013	MG132 caused a large increase in steady-state levels of SUMO-1 and of sumoylated proteins, and this was especially true for detergent-insoluble proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	small ubiquitin like modifier 1	Homo sapiens	56-62
23559011-5	2013	Ubiquitination of c-FLIP(L) was increased by hyperthermia, and proteasome inhibitor MG132 prevented heat-induced downregulation of c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	CASP8 and FADD like apoptosis regulator	Homo sapiens	131-140
23333241-9	2013	Moreover, in the presence of proteasome inhibitor (MG-132) or ubiquitin E1 inhibitor (PYR-41), protective effect of Iduna was significantly weaken.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-57	ring finger protein 146	Mus musculus	116-121
22944069-5	2013	Furthermore treatment of the cells with MG132, an inhibitor of the 26S proteasome, prevented the destabilizing effect of lithium on AChE-S.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	acetylcholinesterase (Cartwright blood group)	Homo sapiens	132-138
23419712-10	2013	Co-treatment with a proteasome inhibitor, MG-132, eliminated peroxynitrite-induced MYPT1 downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	protein phosphatase 1, regulatory subunit 12A	Mus musculus	83-88
23352172-9	2013	Furthermore, E. muris-induced inhibition of BMDMs cell death was abolished in the presence of MG132, a proteasome inhibitor that blocks NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	nuclear factor kappa B subunit 1	Homo sapiens	136-145
23517112-5	2013	RESULTS: Treatment with 0.5-1 muM MG132 alone or 30 ng/mL Bortezomib alone induced a limited apoptosis in MPM cells associated with the elevated Mcl-1 protein level and hyperactive PI3K/Akt signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	145-150
23532763-0	2013	Proteasome inhibitor (MG132) rescues Nav1.5 protein content and the cardiac sodium current in dystrophin-deficient mdx (5cv) mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	sodium channel, voltage-gated, type V, alpha	Mus musculus	37-43
23532763-0	2013	Proteasome inhibitor (MG132) rescues Nav1.5 protein content and the cardiac sodium current in dystrophin-deficient mdx (5cv) mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	dystrophin, muscular dystrophy	Mus musculus	94-104
23532763-4	2013	MG132 rescued both the total amount of Nav1.5 protein and l Na but, unlike in previous studies, de novo expression of dystrophin was not observed in skeletal or cardiac muscle.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	sodium channel, voltage-gated, type V, alpha	Mus musculus	39-45
23532763-4	2013	MG132 rescued both the total amount of Nav1.5 protein and l Na but, unlike in previous studies, de novo expression of dystrophin was not observed in skeletal or cardiac muscle.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	dystrophin, muscular dystrophy	Mus musculus	118-128
23517112-5	2013	RESULTS: Treatment with 0.5-1 muM MG132 alone or 30 ng/mL Bortezomib alone induced a limited apoptosis in MPM cells associated with the elevated Mcl-1 protein level and hyperactive PI3K/Akt signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	AKT serine/threonine kinase 1	Homo sapiens	186-189
23262029-9	2013	Treatment with the proteasome inhibitor, MG132, blocked the MVNP-triggered decrease of FoxO3, and the treatment with the serine/threonine phosphatase inhibitor, calyculin A, revealed that MVNP increased phosphorylation of FoxO3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	forkhead box O3	Homo sapiens	87-92
23179179-7	2013	In addition, we report that Bax-deficient HCT116 cells exposed to TRAIL for a prolonged period lost their sensitivity to TRAIL as a result of downregulation of TRAIL receptor expression, and became resistant to combination of TRAIL and other drugs such as MG-132 and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	256-262	BCL2 associated X, apoptosis regulator	Homo sapiens	28-31
23179179-7	2013	In addition, we report that Bax-deficient HCT116 cells exposed to TRAIL for a prolonged period lost their sensitivity to TRAIL as a result of downregulation of TRAIL receptor expression, and became resistant to combination of TRAIL and other drugs such as MG-132 and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	256-262	TNF superfamily member 10	Homo sapiens	66-71
24009867-9	2013	Inhibitors of these signaling pathways reduced MG132-mediated upregulation of PAI-1 in varying degrees and most prominent effects were observed with SB203580, a p38 MAPK pathway inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	serpin family E member 1	Rattus norvegicus	78-83
24009867-10	2013	The regulation of tPA/PAI-1 activity by proteasome inhibitor in rat primary astrocytes may underlie the observed CNS effects of MG132 such as neuroprotection.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	serpin family E member 1	Rattus norvegicus	22-27
24009867-0	2013	Transcriptional Upregulation of Plasminogen Activator Inhibitor-1 in Rat Primary Astrocytes by a Proteasomal Inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	serpin family E member 1	Rattus norvegicus	32-65
24009867-4	2013	We found that submicromolar concentration of MG132, a cell permeable peptide-aldehyde inhibitor of ubiquitin proteasome pathway selectively upregulates PAI-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	serpin family E member 1	Rattus norvegicus	152-157
24009867-5	2013	Upregulation of PAI-1 mRNA as well as increased PAI-1 promoter reporter activity suggested that MG132 transcriptionally increased PAI-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	serpin family E member 1	Rattus norvegicus	16-21
24009867-5	2013	Upregulation of PAI-1 mRNA as well as increased PAI-1 promoter reporter activity suggested that MG132 transcriptionally increased PAI-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	serpin family E member 1	Rattus norvegicus	48-53
24009867-5	2013	Upregulation of PAI-1 mRNA as well as increased PAI-1 promoter reporter activity suggested that MG132 transcriptionally increased PAI-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	serpin family E member 1	Rattus norvegicus	48-53
23262029-9	2013	Treatment with the proteasome inhibitor, MG132, blocked the MVNP-triggered decrease of FoxO3, and the treatment with the serine/threonine phosphatase inhibitor, calyculin A, revealed that MVNP increased phosphorylation of FoxO3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	forkhead box O3	Homo sapiens	222-227
23444357-9	2013	The shby-1 root phenotype was partially phenocopied by treatment of wild-type roots with the proteosome inhibitor MG132 or the gibberellic acid (GA) synthesis inhibitor paclobutrazol (PAC).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	vacuolar protein sorting-associated protein, putative (DUF1162)	Arabidopsis thaliana	4-8
23525727-9	2013	In KYSE220 cells, pretreatment of MG-132 significantly abrogated upregulation of p65 and APE-1 levels induced by MCP-1, and treatment with 10 and 20 nM p65 siRNA significantly inhibited APE-1 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	RELA proto-oncogene, NF-kB subunit	Homo sapiens	81-84
23525727-9	2013	In KYSE220 cells, pretreatment of MG-132 significantly abrogated upregulation of p65 and APE-1 levels induced by MCP-1, and treatment with 10 and 20 nM p65 siRNA significantly inhibited APE-1 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	89-94
23525727-9	2013	In KYSE220 cells, pretreatment of MG-132 significantly abrogated upregulation of p65 and APE-1 levels induced by MCP-1, and treatment with 10 and 20 nM p65 siRNA significantly inhibited APE-1 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	C-C motif chemokine ligand 2	Homo sapiens	113-118
23525727-9	2013	In KYSE220 cells, pretreatment of MG-132 significantly abrogated upregulation of p65 and APE-1 levels induced by MCP-1, and treatment with 10 and 20 nM p65 siRNA significantly inhibited APE-1 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	RELA proto-oncogene, NF-kB subunit	Homo sapiens	152-155
23525727-9	2013	In KYSE220 cells, pretreatment of MG-132 significantly abrogated upregulation of p65 and APE-1 levels induced by MCP-1, and treatment with 10 and 20 nM p65 siRNA significantly inhibited APE-1 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	186-191
23203344-8	2013	MG132, a proteasomal inhibitor, completely abolished tyrosinase downregulation due to PC102 and partially reduced the downregulation of MITF and beta-catenin due to PC102.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tyrosinase	Homo sapiens	53-63
23203344-8	2013	MG132, a proteasomal inhibitor, completely abolished tyrosinase downregulation due to PC102 and partially reduced the downregulation of MITF and beta-catenin due to PC102.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	melanocyte inducing transcription factor	Homo sapiens	136-140
23203344-8	2013	MG132, a proteasomal inhibitor, completely abolished tyrosinase downregulation due to PC102 and partially reduced the downregulation of MITF and beta-catenin due to PC102.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	catenin beta 1	Homo sapiens	145-157
23275442-8	2013	The ubiquitin E1 inhibitor UBEI-41 or the proteasome inhibitor MG132 prevented IRF5 degradation, supporting the idea that its stability is regulated by the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	interferon regulatory factor 5	Homo sapiens	79-83
23403203-5	2013	Inhibition of lysosomes or proteasomes by co-treatment with antofine and their respective specific inhibitors, NH4Cl or MG132, partially inhibited the antofine-induced decrease in Cx43 protein levels, but did not inhibit the antofine-induced inhibition of GJIC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	gap junction protein, alpha 1	Rattus norvegicus	180-184
23288781-6	2013	KRAS expression was also evaluated in cells transfected with pRC-U and treated with MG-132 or cycloheximide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
23288781-11	2013	After pRC-U transfection, KRAS stability was increased in the presence of MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-80	KRAS proto-oncogene, GTPase	Homo sapiens	26-30
23278405-3	2013	The SlNAC1 protein was found to be stable in the presence of proteasome-specific inhibitor MG132 or MG115 and ubiquitinated in plant cells, suggesting that the SlNAC1 is subject to the ubiquitin-proteasome system-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	NAC domain protein	Solanum lycopersicum	4-10
23445492-0	2013	Pentoxifylline and the proteasome inhibitor MG132 induce apoptosis in human leukemia U937 cells through a decrease in the expression of Bcl-2 and Bcl-XL and phosphorylation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	BCL2 apoptosis regulator	Homo sapiens	136-141
23167462-9	2013	VOZ2 degradation during cold exposure was completely inhibited by the addition of the 26S proteasome inhibitor, MG132, a finding that suggested that VOZ2 degradation is dependent on the ubiquitin/26S proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	vascular plant one zinc finger protein 2	Arabidopsis thaliana	0-4
23167462-9	2013	VOZ2 degradation during cold exposure was completely inhibited by the addition of the 26S proteasome inhibitor, MG132, a finding that suggested that VOZ2 degradation is dependent on the ubiquitin/26S proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	vascular plant one zinc finger protein 2	Arabidopsis thaliana	149-153
21955141-8	2013	The high sensitivity of WERI-Rb to ABT-737 can be increased by downregulating Mcl-1 using the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-121	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	78-83
23445492-0	2013	Pentoxifylline and the proteasome inhibitor MG132 induce apoptosis in human leukemia U937 cells through a decrease in the expression of Bcl-2 and Bcl-XL and phosphorylation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	BCL2 like 1	Homo sapiens	146-152
23445492-0	2013	Pentoxifylline and the proteasome inhibitor MG132 induce apoptosis in human leukemia U937 cells through a decrease in the expression of Bcl-2 and Bcl-XL and phosphorylation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	RELA proto-oncogene, NF-kB subunit	Homo sapiens	176-179
23445492-6	2013	The greatest percentage of apoptosis was obtained with a combination of the drugs; likewise, PTX and MG132 induce G1 phase cell cycle arrest and cleavage of caspases -3,-8, -9 and cytochrome c release and mitochondrial membrane potential loss in U937 human leukemia cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	caspase 3	Homo sapiens	157-175
23445492-6	2013	The greatest percentage of apoptosis was obtained with a combination of the drugs; likewise, PTX and MG132 induce G1 phase cell cycle arrest and cleavage of caspases -3,-8, -9 and cytochrome c release and mitochondrial membrane potential loss in U937 human leukemia cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	cytochrome c, somatic	Homo sapiens	180-192
23293026-4	2013	Treatment of proteasome inhibitor, MG132, blocked high glucose-induced AMPKalpha2 down-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	71-81
23220333-0	2013	Therapeutic effect of MG-132 on diabetic cardiomyopathy is associated with its suppression of proteasomal activities: roles of Nrf2 and NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	127-131
23220333-0	2013	Therapeutic effect of MG-132 on diabetic cardiomyopathy is associated with its suppression of proteasomal activities: roles of Nrf2 and NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	136-145
23220333-1	2013	MG-132, a proteasome inhibitor, can upregulate nuclear factor (NF) erythroid 2-related factor 2 (Nrf2)-mediated antioxidative function and downregulate NF-kappaB-mediated inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor, erythroid derived 2, like 2	Mus musculus	47-95
23220333-1	2013	MG-132, a proteasome inhibitor, can upregulate nuclear factor (NF) erythroid 2-related factor 2 (Nrf2)-mediated antioxidative function and downregulate NF-kappaB-mediated inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor, erythroid derived 2, like 2	Mus musculus	97-101
23220333-1	2013	MG-132, a proteasome inhibitor, can upregulate nuclear factor (NF) erythroid 2-related factor 2 (Nrf2)-mediated antioxidative function and downregulate NF-kappaB-mediated inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	152-161
23220333-10	2013	MG-132 treatment significantly increased the cardiac expression of Nrf2 and its downstream antioxidant genes with a significant increase of total antioxidant capacity and also significantly decreased the expression of IkappaB and the nuclear accumulation and DNA-binding activity of NF-kappaB in the heart.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor, erythroid derived 2, like 2	Mus musculus	67-71
23220333-10	2013	MG-132 treatment significantly increased the cardiac expression of Nrf2 and its downstream antioxidant genes with a significant increase of total antioxidant capacity and also significantly decreased the expression of IkappaB and the nuclear accumulation and DNA-binding activity of NF-kappaB in the heart.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	283-292
23261467-0	2013	Proteasome inhibitor MG132 induces NAG-1/GDF15 expression through the p38 MAPK pathway in glioblastoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	growth differentiation factor 15	Homo sapiens	35-40
23220333-11	2013	These results suggest that MG-132 has a therapeutic effect on diabetic cardiomyopathy in OVE26 diabetic mice, possibly through the upregulation of Nrf2-dependent antioxidative function and downregulation of NF-kappaB-mediated inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	nuclear factor, erythroid derived 2, like 2	Mus musculus	147-151
23220333-11	2013	These results suggest that MG-132 has a therapeutic effect on diabetic cardiomyopathy in OVE26 diabetic mice, possibly through the upregulation of Nrf2-dependent antioxidative function and downregulation of NF-kappaB-mediated inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	207-216
23160820-6	2013	Simultaneous ectopic overexpression of RBCK1 and PXR decreased PXR levels in AD-293 cells, and this decrease was inhibited by the proteasomal inhibitor MG-132 (carbobenzoxy-Leu-Leu-leucinal).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	RANBP2-type and C3HC4-type zinc finger containing 1	Homo sapiens	39-44
23160820-6	2013	Simultaneous ectopic overexpression of RBCK1 and PXR decreased PXR levels in AD-293 cells, and this decrease was inhibited by the proteasomal inhibitor MG-132 (carbobenzoxy-Leu-Leu-leucinal).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	nuclear receptor subfamily 1 group I member 2	Homo sapiens	49-52
23160820-6	2013	Simultaneous ectopic overexpression of RBCK1 and PXR decreased PXR levels in AD-293 cells, and this decrease was inhibited by the proteasomal inhibitor MG-132 (carbobenzoxy-Leu-Leu-leucinal).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	nuclear receptor subfamily 1 group I member 2	Homo sapiens	63-66
23221556-11	2013	Inhibition of the ubiquitin-dependent pathway by the chemical proteasome inhibitor MG132 prevented HIF-1alpha degradation in the presence of ORF34.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	hypoxia inducible factor 1 subunit alpha	Homo sapiens	99-109
23221556-11	2013	Inhibition of the ubiquitin-dependent pathway by the chemical proteasome inhibitor MG132 prevented HIF-1alpha degradation in the presence of ORF34.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	family with sequence similarity 120C	Homo sapiens	141-146
23382546-5	2013	Ago2 was inducibly ubiquitinated in activated T cells and its down-regulation was inhibited by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	argonaute RISC catalytic component 2	Homo sapiens	0-4
23076972-5	2013	POU3F4 protein levels were low and could be restored by MG132, a proteasome inhibitor, in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	POU class 3 homeobox 4	Homo sapiens	0-6
23261467-10	2013	Consequently, inhibiting p38 phosphorylation blocked activation of the NAG-1 promoter and decreased mRNA stability, indicating that p38 MAPK activation mediates both MG132-dependent promoter activation and mRNA stabilization of NAG-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	mitogen-activated protein kinase 14	Homo sapiens	25-28
23261467-10	2013	Consequently, inhibiting p38 phosphorylation blocked activation of the NAG-1 promoter and decreased mRNA stability, indicating that p38 MAPK activation mediates both MG132-dependent promoter activation and mRNA stabilization of NAG-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	growth differentiation factor 15	Homo sapiens	71-76
23261467-10	2013	Consequently, inhibiting p38 phosphorylation blocked activation of the NAG-1 promoter and decreased mRNA stability, indicating that p38 MAPK activation mediates both MG132-dependent promoter activation and mRNA stabilization of NAG-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	mitogen-activated protein kinase 14	Homo sapiens	132-135
23261467-0	2013	Proteasome inhibitor MG132 induces NAG-1/GDF15 expression through the p38 MAPK pathway in glioblastoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	growth differentiation factor 15	Homo sapiens	41-46
23261467-10	2013	Consequently, inhibiting p38 phosphorylation blocked activation of the NAG-1 promoter and decreased mRNA stability, indicating that p38 MAPK activation mediates both MG132-dependent promoter activation and mRNA stabilization of NAG-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	growth differentiation factor 15	Homo sapiens	228-233
23261467-0	2013	Proteasome inhibitor MG132 induces NAG-1/GDF15 expression through the p38 MAPK pathway in glioblastoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mitogen-activated protein kinase 14	Homo sapiens	70-73
23261467-5	2013	Here, we show that the proteasome inhibitors MG132 and bortezomib induced NAG-1 expression and secretion in glioblastoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	growth differentiation factor 15	Homo sapiens	74-79
23261467-6	2013	MG132 increased NAG-1 expression through transcriptional and post-transcriptional mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	growth differentiation factor 15	Homo sapiens	16-21
23261467-8	2013	At post-transcriptional levels, MG132 stabilized NAG-1 mRNA by increasing the half-life from 1.5 h to &gt;8 h. Because of the dramatic increase in mRNA stability, this is likely the major contributor to MG132-mediated NAG-1 induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	growth differentiation factor 15	Homo sapiens	49-54
23261467-8	2013	At post-transcriptional levels, MG132 stabilized NAG-1 mRNA by increasing the half-life from 1.5 h to &gt;8 h. Because of the dramatic increase in mRNA stability, this is likely the major contributor to MG132-mediated NAG-1 induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	growth differentiation factor 15	Homo sapiens	218-223
23261467-8	2013	At post-transcriptional levels, MG132 stabilized NAG-1 mRNA by increasing the half-life from 1.5 h to &gt;8 h. Because of the dramatic increase in mRNA stability, this is likely the major contributor to MG132-mediated NAG-1 induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	203-208	growth differentiation factor 15	Homo sapiens	49-54
23261467-9	2013	Further probing into the mechanism revealed that MG132 increased phosphorylation of the p38 MAPK pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	mitogen-activated protein kinase 14	Homo sapiens	88-91
23201403-5	2013	When cells were exposed to a proteasome inhibitor, MG132, the MAPO1 level significantly increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	folliculin interacting protein 2	Homo sapiens	62-67
23142711-9	2013	We also found that Ang II activates UPS in the heart and MG132 attenuates Ang II-induced collagen synthesis via suppression of the NF-kappaB/TGF-beta/Smad2 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	angiogenin	Rattus norvegicus	74-77
23142711-9	2013	We also found that Ang II activates UPS in the heart and MG132 attenuates Ang II-induced collagen synthesis via suppression of the NF-kappaB/TGF-beta/Smad2 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	transforming growth factor, beta 1	Rattus norvegicus	141-149
23142711-9	2013	We also found that Ang II activates UPS in the heart and MG132 attenuates Ang II-induced collagen synthesis via suppression of the NF-kappaB/TGF-beta/Smad2 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	SMAD family member 2	Rattus norvegicus	150-155
23322017-5	2013	We found that a decrease of tyrosinase protein by kadsuralignan F was fully recovered by MG132, a proteasome inhibitor, but not by chloroquine, a lysosome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	tyrosinase	Homo sapiens	28-38
22759348-6	2013	Further study showed the proteasome inhibitor MG-132 reversed the GA-decreased ABCB1 level and prolonged half-life of ABCB1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-52	ATP binding cassette subfamily B member 1	Homo sapiens	79-84
23132297-0	2013	Potential role for Nrf2 activation in the therapeutic effect of MG132 on diabetic nephropathy in OVE26 diabetic mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	19-23
23132297-3	2013	The present study was designed to explore the therapeutic effect of Nrf2 induced by proteasomal inhibitor MG132 at a low dose (10 mug/kg) on diabetic nephropathy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	nuclear factor, erythroid derived 2, like 2	Mus musculus	68-72
23132297-8	2013	Mechanistic study using human renal tubular HK11 cells confirmed the role of Nrf2, as silencing the Nrf2 gene with its specific siRNA abolished MG132 prevention of high-glucose-induced profibrotic response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	NFE2 like bZIP transcription factor 2	Homo sapiens	77-81
23132297-8	2013	Mechanistic study using human renal tubular HK11 cells confirmed the role of Nrf2, as silencing the Nrf2 gene with its specific siRNA abolished MG132 prevention of high-glucose-induced profibrotic response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	NFE2 like bZIP transcription factor 2	Homo sapiens	100-104
23132297-10	2013	These results suggest that MG132 upregulates Nrf2 function via inhibition of diabetes-increased proteasomal activity, which can provide the basis for the therapeutic effect of MG132 on the kidney against diabetes-induced oxidative damage, inflammation, fibrosis, and eventual dysfunction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	nuclear factor, erythroid derived 2, like 2	Mus musculus	45-49
23132297-10	2013	These results suggest that MG132 upregulates Nrf2 function via inhibition of diabetes-increased proteasomal activity, which can provide the basis for the therapeutic effect of MG132 on the kidney against diabetes-induced oxidative damage, inflammation, fibrosis, and eventual dysfunction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	nuclear factor, erythroid derived 2, like 2	Mus musculus	45-49
23159618-5	2013	Intriguingly, proteasome inhibition by MG132 caused FLAG-mNip45, together with SUMOylated proteins, to localize in nuclear domains associated with promyelocytic leukemia protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	PML nuclear body scaffold	Homo sapiens	147-177
22759348-6	2013	Further study showed the proteasome inhibitor MG-132 reversed the GA-decreased ABCB1 level and prolonged half-life of ABCB1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-52	ATP binding cassette subfamily B member 1	Homo sapiens	118-123
23995664-8	2013	We found that MG132, a proteasome inhibitor, almost completely abolished both the downregulation of tyrosinase levels and the inhibition of melanin synthesis by okadaic acid.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	tyrosinase	Mus musculus	100-110
23069210-8	2013	Furthermore, we show that Msp58 is upregulated in multiple different cell lines upon the treatment with proteasome inhibitor MG132 and exogenously expressed Msp58 is ubiquitinated, suggesting that Msp58 is degraded by the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	microspherule protein 1	Homo sapiens	26-31
23700163-8	2013	Interestingly, pretreatment with a proteasome inhibitor (MG132) could restore RhoA to its basal level, most likely through ubiquitin-proteasome pathway (UPP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	ras homolog family member A	Canis lupus familiaris	78-82
23020756-7	2013	We also demonstrated that MG132 activated ASK1 and siASK1 compromised the MG132-induced apoptosis of glioma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	42-46
23719846-9	2013	MG132, a proteasome inhibitor abolished TNFalpha suppression of D2 activity whereas BAY11-7082 or 6-amino-4-(4-phenoxyphenylethylamino) quinazoline, inhibitors of nuclear factor-kappaB (NF-kappaB) failed to attenuate the effect of TNFalpha on D2 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Homo sapiens	40-48
23738337-0	2013	Impact of high glucose and proteasome inhibitor MG132 on histone H2A and H2B ubiquitination in rat glomerular mesangial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	histone cluster 1, H2bg	Rattus norvegicus	73-76
23690212-4	2013	Moreover, MG132 (26S proteasome inhibitor) partially inhibited TPA-induced degradation of PKB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	protein tyrosine kinase 2 beta	Homo sapiens	90-93
23357875-5	2013	Pretreatment with the proteasome inhibitor MG132 or glycogen synthase kinase-3beta (GSK-3beta) inhibitors (LiCl and SB216763) attenuated the effect of DIF-1, suggesting that DIF-1 induced c-Myc protein degradation through GSK-3beta activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	188-193
23357875-5	2013	Pretreatment with the proteasome inhibitor MG132 or glycogen synthase kinase-3beta (GSK-3beta) inhibitors (LiCl and SB216763) attenuated the effect of DIF-1, suggesting that DIF-1 induced c-Myc protein degradation through GSK-3beta activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	glycogen synthase kinase 3 beta	Homo sapiens	222-231
24096134-8	2013	Hsp70 levels were higher in MG132-treated cells when N-acetyl cysteine was applied.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	heat shock protein 1B	Mus musculus	0-5
23314608-6	2013	In addition, KRP3 protein was stabilized when treated with MG132, an inhibitor of the 26S proteasome, indicating that the protein may be regulated by 26S proteasome-mediated protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	inhibitor/interactor with cyclin-dependent kinase	Arabidopsis thaliana	13-17
23229893-13	2013	SUMO-1 labelling of lysosomes showed a major increase between 24 and 48 h post-incubation of 1321N1 cells with MG132 resulting in an increase in a 90 kDa SUMO-1-positive band that was immunopositive for Hsp90 and immunoprecipitated with an anti-SUMO-1 antibody.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	small ubiquitin like modifier 1	Homo sapiens	0-6
23589759-1	2013	The present study tested whether MG132 increases vascular nuclear factor E2-related factor-2 (Nrf2) expression and transcription to provide a therapeutic effect on diabetes-induced pathogenic changes in the aorta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	58-92
23229893-13	2013	SUMO-1 labelling of lysosomes showed a major increase between 24 and 48 h post-incubation of 1321N1 cells with MG132 resulting in an increase in a 90 kDa SUMO-1-positive band that was immunopositive for Hsp90 and immunoprecipitated with an anti-SUMO-1 antibody.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	small ubiquitin like modifier 1	Homo sapiens	154-160
23229893-13	2013	SUMO-1 labelling of lysosomes showed a major increase between 24 and 48 h post-incubation of 1321N1 cells with MG132 resulting in an increase in a 90 kDa SUMO-1-positive band that was immunopositive for Hsp90 and immunoprecipitated with an anti-SUMO-1 antibody.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	heat shock protein 90 alpha family class A member 1	Homo sapiens	203-208
23229893-13	2013	SUMO-1 labelling of lysosomes showed a major increase between 24 and 48 h post-incubation of 1321N1 cells with MG132 resulting in an increase in a 90 kDa SUMO-1-positive band that was immunopositive for Hsp90 and immunoprecipitated with an anti-SUMO-1 antibody.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	small ubiquitin like modifier 1	Homo sapiens	154-160
23533688-0	2013	Preventive and therapeutic effects of MG132 by activating Nrf2-ARE signaling pathway on oxidative stress-induced cardiovascular and renal injury.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	NFE2 like bZIP transcription factor 2	Homo sapiens	58-62
23533688-5	2013	As a proteasomal inhibitor, MG132 was reported to activate Nrf2 expression and function, which was accompanied with significant preventive and/or therapeutic effect on cardiovascular and renal diseases under most conditions; therefore, MG132 seems to be a potentially effective drug to be used in the prevention of oxidative damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	NFE2 like bZIP transcription factor 2	Homo sapiens	59-63
23533688-5	2013	As a proteasomal inhibitor, MG132 was reported to activate Nrf2 expression and function, which was accompanied with significant preventive and/or therapeutic effect on cardiovascular and renal diseases under most conditions; therefore, MG132 seems to be a potentially effective drug to be used in the prevention of oxidative damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	236-241	NFE2 like bZIP transcription factor 2	Homo sapiens	59-63
23533688-6	2013	In this paper, we will summarize the information available regarding the effect of MG132 on oxidative stress-induced cardiovascular and renal damage, especially through Nrf2-ARE signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	NFE2 like bZIP transcription factor 2	Homo sapiens	169-173
23589759-1	2013	The present study tested whether MG132 increases vascular nuclear factor E2-related factor-2 (Nrf2) expression and transcription to provide a therapeutic effect on diabetes-induced pathogenic changes in the aorta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	nuclear factor, erythroid derived 2, like 2	Mus musculus	94-98
23589759-5	2013	However, these pathological changes seen at the 6 months of diabetes were abolished in OVE26 mice treated with MG-132 for 3 months that were also associated with a significant increase in Nrf2 expression in the aorta as well as transcription of downstream genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-117	nuclear factor, erythroid derived 2, like 2	Mus musculus	188-192
23589759-6	2013	These results suggest that chronic treatment with low-dose MG132 can afford an effective therapy for diabetes-induced pathogenic changes in the aorta, which is associated with the increased Nrf2 expression and transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	190-194
24399732-8	2013	RESULTS: The results showed that TGF-beta1 (5 ng/ml) can stimulate the proliferation of NRK-49F cells.MG-132 (0.25-5 muM) inhibited TGF-beta1-induced proliferation in a dose-dependent manner through G1-arrest; TGF-beta1 alone did not induce apoptosis (3.8 +- 0.4% vs. 4.7 +- 1.6%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	transforming growth factor, beta 1	Rattus norvegicus	33-42
24399732-8	2013	RESULTS: The results showed that TGF-beta1 (5 ng/ml) can stimulate the proliferation of NRK-49F cells.MG-132 (0.25-5 muM) inhibited TGF-beta1-induced proliferation in a dose-dependent manner through G1-arrest; TGF-beta1 alone did not induce apoptosis (3.8 +- 0.4% vs. 4.7 +- 1.6%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	transforming growth factor, beta 1	Rattus norvegicus	132-141
24399732-8	2013	RESULTS: The results showed that TGF-beta1 (5 ng/ml) can stimulate the proliferation of NRK-49F cells.MG-132 (0.25-5 muM) inhibited TGF-beta1-induced proliferation in a dose-dependent manner through G1-arrest; TGF-beta1 alone did not induce apoptosis (3.8 +- 0.4% vs. 4.7 +- 1.6%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	transforming growth factor, beta 1	Rattus norvegicus	132-141
24399732-9	2013	However, pretreatment with MG-132 significantly induced apoptosis in TGF-b1-stimulated NRK-49F cells in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	transforming growth factor, beta 1	Rattus norvegicus	69-75
23536801-5	2013	Allocortex cultures were more vulnerable to MG132 despite greater MG132-induced rises in heat shock protein 70, heme oxygenase 1, and catalase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	89-110
23577147-6	2013	In human breast cancer cells, paclitaxel treatment resulted in MCL-1 degradation which was prevented by a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	63-68
23536801-5	2013	Allocortex cultures were more vulnerable to MG132 despite greater MG132-induced rises in heat shock protein 70, heme oxygenase 1, and catalase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	heme oxygenase 1	Rattus norvegicus	112-142
23505411-4	2013	Treatment with MG132 reduced the phosphorylation of NF-kappaB and the activity of MMP-9, indicating upregulation of MMP-9 through the NF-kappaB signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	52-61
23536832-8	2013	Interestingly, proteasome inhibitor, MG-132, abolished the effect of steviol on CFTR protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	CF transmembrane conductance regulator	Canis lupus familiaris	80-84
23505411-4	2013	Treatment with MG132 reduced the phosphorylation of NF-kappaB and the activity of MMP-9, indicating upregulation of MMP-9 through the NF-kappaB signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	134-143
23826657-1	2013	OBJECTIVES: To evaluate the effects of the proteasome inhibitor MG-132 on the expression of nuclear factor (NF)-kappaB p65, inhibitor (I)-kappaB, tumour necrosis factor (TNF)-alpha, and interleukin (IL)-1beta in the cartilage and synovial tissues of rats with osteoarthritis (OA), and to investigate the role that the ubiquitin/proteasome system (UPS) plays in the OA process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	synaptotagmin 1	Rattus norvegicus	119-122
23409140-6	2013	The expression of miR221/222 is sensitive to proteasome inhibition with MG132 suggesting a link between p27 regulation by miRs and the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	microRNA 221	Mus musculus	18-24
23409140-6	2013	The expression of miR221/222 is sensitive to proteasome inhibition with MG132 suggesting a link between p27 regulation by miRs and the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	cyclin-dependent kinase inhibitor 1B	Mus musculus	104-107
23457570-6	2013	In cells treated with the proteasome inhibitors MG-132 or lactacystin, both endogenous and exogenous Osx protein expression increased in a time-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	Sp7 transcription factor 7	Mus musculus	101-104
23418516-5	2013	We found that HSF1alpha is significantly more active than the beta isoform after exposure to the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	heat shock factor 1	Mus musculus	14-23
23301094-9	2013	In addition, co-treatment with AM114 or MG132 (proteosomal inhibitors) could partially restore DVL3 expression under the treatment of metformin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	dishevelled segment polarity protein 3	Homo sapiens	95-99
23078624-3	2012	Western blotting and coimmunoprecipitation analyses verified that the MDA-7/IL-24 protein was ubiquitinated and degraded by the 26S proteasome in Hela cells, which was confirmed by protein accumulation treated with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	236-241	interleukin 24	Homo sapiens	70-75
23739641-6	2013	Following serum stimulation, eGFP-c-Myc accumulated in the presence of the proteasome inhbitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	myelocytomatosis oncogene	Mus musculus	36-39
22902867-8	2012	This decrease was partially blocked by pretreatment with a proteasome inhibitor MG-132, indicating that proteasomal degradation contributed to the loss of hTERT protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-86	telomerase reverse transcriptase	Homo sapiens	155-160
22367315-0	2012	Proteasome inhibitor MG132 induces selective apoptosis in glioblastoma cells through inhibition of PI3K/Akt and NFkappaB pathways, mitochondrial dysfunction, and activation of p38-JNK1/2 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	AKT serine/threonine kinase 1	Homo sapiens	104-107
22367315-0	2012	Proteasome inhibitor MG132 induces selective apoptosis in glioblastoma cells through inhibition of PI3K/Akt and NFkappaB pathways, mitochondrial dysfunction, and activation of p38-JNK1/2 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	nuclear factor kappa B subunit 1	Homo sapiens	112-120
22367315-0	2012	Proteasome inhibitor MG132 induces selective apoptosis in glioblastoma cells through inhibition of PI3K/Akt and NFkappaB pathways, mitochondrial dysfunction, and activation of p38-JNK1/2 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mitogen-activated protein kinase 14	Homo sapiens	176-179
22367315-0	2012	Proteasome inhibitor MG132 induces selective apoptosis in glioblastoma cells through inhibition of PI3K/Akt and NFkappaB pathways, mitochondrial dysfunction, and activation of p38-JNK1/2 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mitogen-activated protein kinase 8	Homo sapiens	180-186
22367315-4	2012	Mechanistically, MG132 arrested cells in G2/M phase of the cell cycle and increased p21(WAF1) protein immunocontent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	84-87
22367315-4	2012	Mechanistically, MG132 arrested cells in G2/M phase of the cell cycle and increased p21(WAF1) protein immunocontent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	88-92
22367315-6	2012	MG132 promoted mitochondrial depolarization and decreased the mitochondrial antiapoptotic protein bcl-xL; it also induced activation of JNK and p38, and inhibition of NFkappaB and PI3K/Akt survival pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BCL2 like 1	Homo sapiens	98-104
22367315-6	2012	MG132 promoted mitochondrial depolarization and decreased the mitochondrial antiapoptotic protein bcl-xL; it also induced activation of JNK and p38, and inhibition of NFkappaB and PI3K/Akt survival pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 8	Homo sapiens	136-139
22367315-6	2012	MG132 promoted mitochondrial depolarization and decreased the mitochondrial antiapoptotic protein bcl-xL; it also induced activation of JNK and p38, and inhibition of NFkappaB and PI3K/Akt survival pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 14	Homo sapiens	144-147
22367315-6	2012	MG132 promoted mitochondrial depolarization and decreased the mitochondrial antiapoptotic protein bcl-xL; it also induced activation of JNK and p38, and inhibition of NFkappaB and PI3K/Akt survival pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	167-175
22367315-6	2012	MG132 promoted mitochondrial depolarization and decreased the mitochondrial antiapoptotic protein bcl-xL; it also induced activation of JNK and p38, and inhibition of NFkappaB and PI3K/Akt survival pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	AKT serine/threonine kinase 1	Homo sapiens	185-188
23256568-8	2012	RESULTS: c-FLIPL down-regulation induced by 17-AAG can be reversed with the proteasome inhibitor MG132, which suggested that c-FLIPL degradation is mediated by a ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	CASP8 and FADD like apoptosis regulator	Homo sapiens	9-16
23256568-8	2012	RESULTS: c-FLIPL down-regulation induced by 17-AAG can be reversed with the proteasome inhibitor MG132, which suggested that c-FLIPL degradation is mediated by a ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	CASP8 and FADD like apoptosis regulator	Homo sapiens	125-132
23041672-6	2012	Further analysis showed that NES(AR) can signal for polyubiquitination and that degradation of NES(AR)-containing fusion proteins can be blocked by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	androgen receptor	Homo sapiens	33-35
22367315-7	2012	Pre-treatment of GBMs with the mitochondrial permeability transition pore inhibitor, bongkrekic acid, or pharmacological inhibitors of JNK1/2 and p38, SP600125 and SB203580, attenuated MG132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	mitogen-activated protein kinase 8	Homo sapiens	135-141
22367315-7	2012	Pre-treatment of GBMs with the mitochondrial permeability transition pore inhibitor, bongkrekic acid, or pharmacological inhibitors of JNK1/2 and p38, SP600125 and SB203580, attenuated MG132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	mitogen-activated protein kinase 14	Homo sapiens	146-149
23078624-3	2012	Western blotting and coimmunoprecipitation analyses verified that the MDA-7/IL-24 protein was ubiquitinated and degraded by the 26S proteasome in Hela cells, which was confirmed by protein accumulation treated with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	236-241	interleukin 24	Homo sapiens	76-81
22819792-8	2012	Overexpression of SIRT2 inhibits lysosome-mediated autophagic turnover by interfering with aggresome formation and also makes cells more vulnerable to accumulated protein-mediated cytotoxicity by MG132 and amyloid beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	sirtuin 2	Homo sapiens	18-23
22819792-9	2012	Moreover, MG132-induced accumulation of ubiquitinated proteins and p62 as well as cytotoxicity are attenuated in siRNA-mediated SIRT2-silencing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	nucleoporin 62	Homo sapiens	67-70
22819792-9	2012	Moreover, MG132-induced accumulation of ubiquitinated proteins and p62 as well as cytotoxicity are attenuated in siRNA-mediated SIRT2-silencing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	sirtuin 2	Homo sapiens	128-133
22670665-5	2012	We found that HO-1 protein level is increased by about 70% in p53-wt B16F10 cells in response to proteasome inhibitor MG132 after 6 h. Likewise, a 6.8 fold increase in HO-1 level was observed after cell exposure to the highly specific proteasome inhibitor bortezomib after 6 h of treatment in B16F10 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	heme oxygenase 1	Mus musculus	14-18
22670665-5	2012	We found that HO-1 protein level is increased by about 70% in p53-wt B16F10 cells in response to proteasome inhibitor MG132 after 6 h. Likewise, a 6.8 fold increase in HO-1 level was observed after cell exposure to the highly specific proteasome inhibitor bortezomib after 6 h of treatment in B16F10 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	transformation related protein 53, pseudogene	Mus musculus	62-65
22670665-5	2012	We found that HO-1 protein level is increased by about 70% in p53-wt B16F10 cells in response to proteasome inhibitor MG132 after 6 h. Likewise, a 6.8 fold increase in HO-1 level was observed after cell exposure to the highly specific proteasome inhibitor bortezomib after 6 h of treatment in B16F10 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	heme oxygenase 1	Mus musculus	168-172
22923157-6	2012	Interestingly such pro-apoptosis effect in LNCaP cells was associated with reduced c-Flip levels through proteasomal degradation via increased reactive oxygen species production and p38 activation; such c-Flip reduction was reversed in the presence of either the proteasome inhibitor MG132 or the reactive oxygen species scavenger N-acetyl-cysteine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	284-289	CASP8 and FADD like apoptosis regulator	Homo sapiens	83-89
23011889-9	2012	SCP and PIs: MG132, PI-1, or epoxomicin interact synergistically to potently inhibit cancer cell growth, alter cell cycle, induce apoptosis, reduce NFkappaB activity, and increase ROS generation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	nuclear factor kappa B subunit 1	Homo sapiens	148-156
23152053-3	2012	We investigated here whether prevention of Bim degradation by a proteasomal inhibitor, MG132, would induce apoptosis in mast cells with the D816V mutation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	BCL2 like 11	Homo sapiens	43-46
23152053-5	2012	MG132 at 1 muM induced apoptosis in all cell types, an effect accompanied by increased BH3-only proapoptotic protein Bim.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BCL2 like 11	Homo sapiens	117-120
23152053-6	2012	The raise of Bim was accompanied by caspase-3 activation, and a caspase-3 inhibitor reduced MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	BCL2 like 11	Homo sapiens	13-16
23152053-6	2012	The raise of Bim was accompanied by caspase-3 activation, and a caspase-3 inhibitor reduced MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	caspase 3	Homo sapiens	64-73
23152053-7	2012	Further, MG132 caused a reduction of activated Erk, a negative regulator of Bim expression, and thus Bim upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	mitogen-activated protein kinase 1	Homo sapiens	47-50
23152053-7	2012	Further, MG132 caused a reduction of activated Erk, a negative regulator of Bim expression, and thus Bim upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	BCL2 like 11	Homo sapiens	76-79
23152053-7	2012	Further, MG132 caused a reduction of activated Erk, a negative regulator of Bim expression, and thus Bim upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	BCL2 like 11	Homo sapiens	101-104
22923157-6	2012	Interestingly such pro-apoptosis effect in LNCaP cells was associated with reduced c-Flip levels through proteasomal degradation via increased reactive oxygen species production and p38 activation; such c-Flip reduction was reversed in the presence of either the proteasome inhibitor MG132 or the reactive oxygen species scavenger N-acetyl-cysteine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	284-289	CASP8 and FADD like apoptosis regulator	Homo sapiens	203-209
23053665-7	2012	The decrease of ERalpha protein after bergapten treatment results from the ubiquitine-proteasome pathway as demonstrated by the use of MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	135-141	estrogen receptor 1	Homo sapiens	16-23
22932898-3	2012	In the present study, we observe a surprising outcome that Bmi-1 and Ezh2 levels are reduced by treatment with the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	59-64
22810651-7	2012	In addition, protein degradation and ubiquitin assays revealed TNFAIP1 overexpression resulted in ubiquitin-mediated degradation of KCTD10 proteins, which was significantly alleviated with the proteasome inhibitor MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	TNF alpha induced protein 1	Homo sapiens	63-70
22810651-7	2012	In addition, protein degradation and ubiquitin assays revealed TNFAIP1 overexpression resulted in ubiquitin-mediated degradation of KCTD10 proteins, which was significantly alleviated with the proteasome inhibitor MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	potassium channel tetramerization domain containing 10	Homo sapiens	132-138
22936401-6	2012	Proteasome inhibitor MG-132 significantly reduced expression of TGF-beta1 and vimentin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	transforming growth factor beta 1	Homo sapiens	64-73
22936401-6	2012	Proteasome inhibitor MG-132 significantly reduced expression of TGF-beta1 and vimentin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	vimentin	Homo sapiens	78-86
22932898-3	2012	In the present study, we observe a surprising outcome that Bmi-1 and Ezh2 levels are reduced by treatment with the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	69-73
22932898-6	2012	Moreover, knockdown of Nrf1 attenuates the MG132-dependent increase in proteasome subunit expression and restores Bmi-1 and Ezh2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	nuclear respiratory factor 1	Homo sapiens	23-27
22932898-7	2012	The MG132-dependent loss of Bmi-1 and Ezh2 is associated with reduced cell proliferation, accumulation of cells in G(2), and increased apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	28-33
22932898-7	2012	The MG132-dependent loss of Bmi-1 and Ezh2 is associated with reduced cell proliferation, accumulation of cells in G(2), and increased apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	38-42
22932898-8	2012	These effects are attenuated by forced expression of Bmi-1, suggesting that PcG proteins, consistent with a prosurvival action, may antagonize the action of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	157-162	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	53-58
22535637-11	2012	Accelerated KLF6 degradation in the presence of SV1 was abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	Kruppel-like factor 6	Mus musculus	12-16
22652456-3	2012	To investigate the function and regulation of PACRG, cells were treated with the proteasomal inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-110	parkin coregulated	Homo sapiens	46-51
22582971-9	2012	This decrease in MyoD protein involved ubiquitin-mediated proteasomal activity with proteasome inhibitor MG132 or autophagy-dependent lysosomal degradation with lysosomal inhibitor bafilomycin A1 (Baf-A1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	myogenic differentiation 1	Mus musculus	17-21
22531154-5	2012	In addition, we demonstrate that the cytoplasmic proteasome is required for UCP1 degradation from mitochondria that the process is inhibited by the proteasome inhibitor MG132 and that dissipation of the mitochondrial membrane potential inhibits degradation of UCP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	uncoupling protein 1	Homo sapiens	76-80
22531154-5	2012	In addition, we demonstrate that the cytoplasmic proteasome is required for UCP1 degradation from mitochondria that the process is inhibited by the proteasome inhibitor MG132 and that dissipation of the mitochondrial membrane potential inhibits degradation of UCP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	uncoupling protein 1	Homo sapiens	260-264
22767315-6	2012	Of note, when translation was blocked in the presence of cycloheximide (CHX), levels of both N-glycosylated and unglycosylated COX-2 proteins induced by cadmium rapidly declined but the decline was prevented by MG132, a 26S proteasomal inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-216	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	127-132
22920997-5	2012	On the other hand, the treatment with the proteasome inhibitor MG132 or the deletion of the F-box from AtFBS1 increases beta-glucuronidase (GUS) activity in plants containing a translational fusion of AtFBS1 with the GUS reporter gene, indicating that AtFBS1 is degraded by the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	F-box family protein	Arabidopsis thaliana	201-207
22920997-6	2012	MG132 treatment of seedlings containing a gene fusion between AtFBS1 and the TAP (Tandem Affinity Purification) cassette causes an increase in the half-life of the protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	F-box family protein	Arabidopsis thaliana	62-68
22920997-5	2012	On the other hand, the treatment with the proteasome inhibitor MG132 or the deletion of the F-box from AtFBS1 increases beta-glucuronidase (GUS) activity in plants containing a translational fusion of AtFBS1 with the GUS reporter gene, indicating that AtFBS1 is degraded by the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	F-box family protein	Arabidopsis thaliana	201-207
22787216-0	2012	Severe acute respiratory syndrome coronavirus replication is severely impaired by MG132 due to proteasome-independent inhibition of M-calpain.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	calpain 2	Homo sapiens	132-141
22807448-5	2012	Although Rnd3 turnover is blocked by treatment of cells with MG132, we provide evidence that such turnover is mediated indirectly by effects on the Rnd3 effectors, rather than on Rnd3 itself, which is not significantly ubiquitinated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	Rho family GTPase 3a	Danio rerio	9-13
22664331-0	2012	DJ-1 protein protects dopaminergic neurons against 6-OHDA/MG-132-induced neurotoxicity in rats.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-64	Parkinsonism associated deglycase	Rattus norvegicus	0-4
22664331-2	2012	In this study, DJ-1 protein was administrated into medial forebrain bundle of PD model rats those had been microinjected with 6-hydroxydopamine (6-OHDA) or MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-162	Parkinsonism associated deglycase	Rattus norvegicus	15-19
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	DNA damage inducible transcript 3	Homo sapiens	91-115
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	DNA damage inducible transcript 3	Homo sapiens	117-121
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	poly(ADP-ribose) polymerase 1	Homo sapiens	132-160
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	poly(ADP-ribose) polymerase 1	Homo sapiens	162-166
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	caspase 3	Homo sapiens	172-181
22787216-6	2012	Since MG132 also inhibits the cysteine protease m-calpain, we addressed the role of calpains in the early SARS-CoV life cycle using calpain inhibitors III (MDL28170) and VI (SJA6017).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	calpain 2	Homo sapiens	48-57
22707286-5	2012	In addition, degradation of A53T and WT alpha-Syn was blocked after Ubiquitin Proteasome System (UPS) inhibitor (MG132) was applied in those PC12 cells overexpressing A53T or WT alpha-Syn, suggesting that A53T alpha-Syn could be degraded by both UPS and macroautophagy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	synuclein alpha	Rattus norvegicus	40-49
22875985-5	2012	Moreover, MG132 treatment of proliferating fibroblasts led to increased superoxide anion levels, juxtanuclear accumulation of ubiquitin- and p62/SQSTM1-positive protein aggregates, and apoptotic cell death, whereas MG132-treated quiescent cells displayed fewer juxtanuclear protein aggregates, less apoptosis, and higher levels of mitochondrial superoxide dismutase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	sequestosome 1	Homo sapiens	141-144
22875985-5	2012	Moreover, MG132 treatment of proliferating fibroblasts led to increased superoxide anion levels, juxtanuclear accumulation of ubiquitin- and p62/SQSTM1-positive protein aggregates, and apoptotic cell death, whereas MG132-treated quiescent cells displayed fewer juxtanuclear protein aggregates, less apoptosis, and higher levels of mitochondrial superoxide dismutase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	sequestosome 1	Homo sapiens	145-151
22707286-5	2012	In addition, degradation of A53T and WT alpha-Syn was blocked after Ubiquitin Proteasome System (UPS) inhibitor (MG132) was applied in those PC12 cells overexpressing A53T or WT alpha-Syn, suggesting that A53T alpha-Syn could be degraded by both UPS and macroautophagy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	synuclein alpha	Rattus norvegicus	178-187
22707286-5	2012	In addition, degradation of A53T and WT alpha-Syn was blocked after Ubiquitin Proteasome System (UPS) inhibitor (MG132) was applied in those PC12 cells overexpressing A53T or WT alpha-Syn, suggesting that A53T alpha-Syn could be degraded by both UPS and macroautophagy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	synuclein alpha	Rattus norvegicus	178-187
22822047-10	2012	Activation of the GLP1 pathway induced proteasome-dependent C/EBPB degradation in beta cells as the proteasome inhibitor MG132 restored the downregulation of C/EBPB protein by exenatide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	glucagon	Mus musculus	18-22
22879419-7	2012	The protective effects of MG-132 pretreatment were partially reversed by the PPARalpha antagonist GW6471 but not by the PPARgamma antagonist GW9662; in contrast, neither agent reduced the protective effects of LA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	peroxisome proliferator activated receptor alpha	Homo sapiens	77-86
22879419-10	2012	CONCLUSIONS: Our data suggest that pretreatment with proteasome inhibitors reduces oxidative injury in ARPE-19 cells and that the underlying mechanisms are different for different proteasome inhibitors, with PPARalpha-dependent effects for MG-132 and PPAR-independent effects for LA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	peroxisome proliferator activated receptor alpha	Homo sapiens	208-217
22879419-10	2012	CONCLUSIONS: Our data suggest that pretreatment with proteasome inhibitors reduces oxidative injury in ARPE-19 cells and that the underlying mechanisms are different for different proteasome inhibitors, with PPARalpha-dependent effects for MG-132 and PPAR-independent effects for LA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	peroxisome proliferator activated receptor alpha	Homo sapiens	208-212
22822047-10	2012	Activation of the GLP1 pathway induced proteasome-dependent C/EBPB degradation in beta cells as the proteasome inhibitor MG132 restored the downregulation of C/EBPB protein by exenatide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	60-66
22822047-10	2012	Activation of the GLP1 pathway induced proteasome-dependent C/EBPB degradation in beta cells as the proteasome inhibitor MG132 restored the downregulation of C/EBPB protein by exenatide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	158-164
22513214-0	2012	The proteasome inhibitor MG132 potentiates TRAIL receptor agonist-induced apoptosis by stabilizing tBid and Bik in human head and neck squamous cell carcinoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	TNF superfamily member 10	Homo sapiens	43-48
22929228-5	2012	Proteasome inhibitor MG132, which causes polyQ proteins accumulation and aggregation, enhanced the sequestration of IRBIT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	adenosylhomocysteinase like 1	Homo sapiens	116-121
22513214-0	2012	The proteasome inhibitor MG132 potentiates TRAIL receptor agonist-induced apoptosis by stabilizing tBid and Bik in human head and neck squamous cell carcinoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	BCL2 interacting killer	Homo sapiens	108-111
22513214-4	2012	Generation and accumulation of tBid through the cooperative action of MG132 with TRAIL or AY4 and Bik accumulation through MG132-mediated proteasome inhibition are critical to the synergistic apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	BCL2 interacting killer	Homo sapiens	98-101
22513214-2	2012	Here, we investigated the effects of the proteasome inhibitor MG132 in combination with tumor necrosis factor-related apoptosis inducing ligand (TRAIL) or agonistic TRAIL receptor 1 (DR4)-specific monoclonal antibody, AY4, on sensitization of TRAIL- and AY4-resistant human HNSCC cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	TNF receptor superfamily member 10a	Homo sapiens	183-186
22549135-7	2012	Synergistically increased gene expression was significantly inhibited by MG132, an NF-kappaB inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	nuclear factor kappa B subunit 1	Homo sapiens	83-92
22314265-0	2012	Noxa/Mcl-1 balance influences the effect of the proteasome inhibitor MG-132 in combination with anticancer agents in pancreatic cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	0-4
22314265-0	2012	Noxa/Mcl-1 balance influences the effect of the proteasome inhibitor MG-132 in combination with anticancer agents in pancreatic cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	5-10
22314265-8	2012	The lack of an enhanced apoptosis induction could be correlated with high levels of Mcl-1 in response to the combined treatment with MG-132 and doxorubicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-139	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	84-89
22314265-9	2012	Thus, the results indicate that regulation of the antiapoptotic and proapoptotic Bcl-2 family members Noxa and Mcl-1 is predicative of the effectiveness of the combination of MG-132 with different anticancer agents on apoptosis induction in pancreatic cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-181	BCL2 apoptosis regulator	Homo sapiens	81-86
22314265-9	2012	Thus, the results indicate that regulation of the antiapoptotic and proapoptotic Bcl-2 family members Noxa and Mcl-1 is predicative of the effectiveness of the combination of MG-132 with different anticancer agents on apoptosis induction in pancreatic cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-181	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	102-106
22314265-9	2012	Thus, the results indicate that regulation of the antiapoptotic and proapoptotic Bcl-2 family members Noxa and Mcl-1 is predicative of the effectiveness of the combination of MG-132 with different anticancer agents on apoptosis induction in pancreatic cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-181	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	111-116
22543707-8	2012	Treatment with the autophagy inhibitor 3-MA or the proteasome inhibitors lactacystin and MG-132 increased Htt552 levels in PC12 cells infected with Ad-Htt-18Q-552 or Ad-Htt-100Q-552.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-95	huntingtin	Rattus norvegicus	106-109
22497927-7	2012	ABCA-1 content and cellular cholesterol efflux were reduced by 33% and 47%, respectively, in macrophages treated with AGE-alb, and both were restored by treatment with 4-phenyl butyric acid (a chemical chaperone that alleviates ER stress), but not MG132 (a proteasome inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	248-253	ATP binding cassette subfamily A member 1	Homo sapiens	0-6
22172403-11	2012	When the proteasome inhibitor MG132 was added to the ZOL-treated cells, we observed a partial restoration of the expression of cyclin A, cyclin B1, and p27(KIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	cyclin A2	Homo sapiens	127-135
22172403-11	2012	When the proteasome inhibitor MG132 was added to the ZOL-treated cells, we observed a partial restoration of the expression of cyclin A, cyclin B1, and p27(KIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	cyclin B1	Homo sapiens	137-146
22172403-11	2012	When the proteasome inhibitor MG132 was added to the ZOL-treated cells, we observed a partial restoration of the expression of cyclin A, cyclin B1, and p27(KIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	interferon alpha inducible protein 27	Homo sapiens	152-155
22172403-11	2012	When the proteasome inhibitor MG132 was added to the ZOL-treated cells, we observed a partial restoration of the expression of cyclin A, cyclin B1, and p27(KIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	cyclin dependent kinase inhibitor 1B	Homo sapiens	156-160
22430153-9	2012	Depletion of Nudel by RNAi reduced the dynein-associated mfGbeta, impaired the MG132-induced aggresome formation, and markedly prolonged the half-life of nascent Gbeta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	nudE neurodevelopment protein 1 like 1	Homo sapiens	13-18
22079846-0	2012	MG132 alleviates liver injury induced by intestinal ischemia/reperfusion in rats: involvement of the AhR and NFkappaB pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	aryl hydrocarbon receptor	Rattus norvegicus	101-104
22079846-3	2012	MG132 might function as an AhR agonist through proteasome inhibition, possibly through the inhibition of NFkappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	aryl hydrocarbon receptor	Rattus norvegicus	27-30
22079846-13	2012	CONCLUSIONS: This study demonstrated that MG132 has a significant effect in protection against liver injury induced by intestinal I/R, which may be due to modulation of the AhR and NFkappaB pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	aryl hydrocarbon receptor	Rattus norvegicus	173-176
22640743-7	2012	Treatment with MG132, a proteasomal inhibitor, restored beta-catenin protein levels, suggesting that SIRT1-mediated degradation of beta-catenin requires proteasomal activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	catenin beta 1	Homo sapiens	56-68
22640743-7	2012	Treatment with MG132, a proteasomal inhibitor, restored beta-catenin protein levels, suggesting that SIRT1-mediated degradation of beta-catenin requires proteasomal activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	sirtuin 1	Homo sapiens	101-106
22640743-7	2012	Treatment with MG132, a proteasomal inhibitor, restored beta-catenin protein levels, suggesting that SIRT1-mediated degradation of beta-catenin requires proteasomal activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	catenin beta 1	Homo sapiens	131-143
22543707-8	2012	Treatment with the autophagy inhibitor 3-MA or the proteasome inhibitors lactacystin and MG-132 increased Htt552 levels in PC12 cells infected with Ad-Htt-18Q-552 or Ad-Htt-100Q-552.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-95	huntingtin	Rattus norvegicus	151-154
22538490-5	2012	Moreover, when compared to wild-type DA neurons, LRRK2-G2019S iPSC-derived DA neurons were more sensitive to caspase-3 activation caused by exposure to hydrogen peroxide, MG-132, and 6-hydroxydopamine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	171-177	leucine rich repeat kinase 2	Homo sapiens	49-54
22360658-3	2012	The AR-NH1 of ~90 kDa was observed in an androgen-independent LNCaP subline and was further accumulated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	androgen receptor	Homo sapiens	4-6
22464285-5	2012	Pre-treatment with the proteasome inhibitor (MG132) prevented OxLA mediated loss of PPAR stability and transactivity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	peroxisome proliferator activated receptor alpha	Rattus norvegicus	84-88
22538490-5	2012	Moreover, when compared to wild-type DA neurons, LRRK2-G2019S iPSC-derived DA neurons were more sensitive to caspase-3 activation caused by exposure to hydrogen peroxide, MG-132, and 6-hydroxydopamine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	171-177	caspase 3	Homo sapiens	109-118
22532597-7	2012	Contrarily, forced expressed MGMT could be downregulated by STAT3 inhibitor which was partially rescued by the proteasome inhibitor, MG132, suggesting the STAT3-mediated posttranscriptional regulation of the protein levels of MGMT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	O-6-methylguanine-DNA methyltransferase	Homo sapiens	29-33
21882190-6	2012	Proteasome inhibitor MG132 blocked the inhibitory effect of HG on RARalpha and RXRalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	retinoic acid receptor alpha	Homo sapiens	66-74
21882190-6	2012	Proteasome inhibitor MG132 blocked the inhibitory effect of HG on RARalpha and RXRalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	retinoid X receptor alpha	Homo sapiens	79-87
22492229-6	2012	In addition, we also show that the glutamate-induced down-regulation of TSC2 protein is blocked by proteasome inhibitor MG132, indicating the involvement of proteasome-mediated protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	TSC complex subunit 2	Homo sapiens	72-76
22382637-4	2012	The degradation of ATR kinase in these cells was through the proteasomal pathway as it was reversed by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	ATR serine/threonine kinase	Homo sapiens	19-22
22382637-8	2012	Although degradation of ATR kinase was reversed by MG132, it was not affected by the nuclear export inhibitor, leptomycin B, suggesting that ATR kinase is degraded within the nucleus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	ATR serine/threonine kinase	Homo sapiens	24-27
22532597-7	2012	Contrarily, forced expressed MGMT could be downregulated by STAT3 inhibitor which was partially rescued by the proteasome inhibitor, MG132, suggesting the STAT3-mediated posttranscriptional regulation of the protein levels of MGMT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	signal transducer and activator of transcription 3	Homo sapiens	60-65
22532597-7	2012	Contrarily, forced expressed MGMT could be downregulated by STAT3 inhibitor which was partially rescued by the proteasome inhibitor, MG132, suggesting the STAT3-mediated posttranscriptional regulation of the protein levels of MGMT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	signal transducer and activator of transcription 3	Homo sapiens	155-160
22532597-7	2012	Contrarily, forced expressed MGMT could be downregulated by STAT3 inhibitor which was partially rescued by the proteasome inhibitor, MG132, suggesting the STAT3-mediated posttranscriptional regulation of the protein levels of MGMT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	O-6-methylguanine-DNA methyltransferase	Homo sapiens	226-230
21986941-4	2012	Here, we show that Sox4 protein is rapidly degraded by the proteasome as indicated by pharmacological inhibition with Mg132 and epoxymycin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	SRY-box transcription factor 4	Homo sapiens	19-23
22388098-7	2012	Western blotting and/or caspase activity data indicated that PAB downregulated anti-apoptotic Bcl-2 protein and activated caspase-9 and caspase-3, which were largely rescued by NAC or MG-132 (proteasome inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	BCL2 apoptosis regulator	Homo sapiens	94-99
22388098-7	2012	Western blotting and/or caspase activity data indicated that PAB downregulated anti-apoptotic Bcl-2 protein and activated caspase-9 and caspase-3, which were largely rescued by NAC or MG-132 (proteasome inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	caspase 9	Homo sapiens	122-131
22388098-7	2012	Western blotting and/or caspase activity data indicated that PAB downregulated anti-apoptotic Bcl-2 protein and activated caspase-9 and caspase-3, which were largely rescued by NAC or MG-132 (proteasome inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	caspase 3	Homo sapiens	136-145
22474335-6	2012	The ladders of polyubiquitinated p53 were not detectable in the presence of the proteasome inhibitor MG132 and were less sensitive to proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	tumor protein p53	Homo sapiens	33-36
22537555-7	2012	Further studies suggested that hBD-2 mRNA and protein expression in responsive to andro were attenuated by pretreatment with SB203580 (an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK)), MG-132 (an inhibitor of nuclear factor kappaB (NF-kappaB)), and an NF-kappaB activator inhibitor, but not by an inhibitor of ERK (PD98059) or by an inhibitor of JNK(SP600125).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	defensin beta 4A	Homo sapiens	31-36
22396550-8	2012	Hypercapnia-induced RelB processing was sensitive to proteasomal inhibition by MG-132 but was independent of the activity of glycogen synthase kinase 3beta or MALT-1, both of which have been previously shown to mediate RelB processing.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	RELB proto-oncogene, NF-kB subunit	Homo sapiens	20-24
22322648-10	2012	Hsp70 interacted with HIF-1alpha under hypoxic conditions and evidenced increased binding when treated with MG132, a proteasomal inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	0-5
22427561-10	2012	The proteasome inhibitor MG-132 suppressed the GlcN-induced reduction in the molecular mass of TNF-alpha-induced ICAM-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	tumor necrosis factor	Homo sapiens	95-104
22427561-10	2012	The proteasome inhibitor MG-132 suppressed the GlcN-induced reduction in the molecular mass of TNF-alpha-induced ICAM-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	intercellular adhesion molecule 1	Homo sapiens	113-119
22509835-5	2012	The decrease in the p53 protein by QUE/As(+3) was reversed by adding the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	tumor protein p53	Homo sapiens	20-23
22285817-7	2012	In addition, we showed that knockdown of NF-YA sensitized breast cancer cells to the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	nuclear transcription factor Y subunit alpha	Homo sapiens	41-46
22306003-0	2012	SUMO-2/3 conjugates accumulating under heat shock or MG132 treatment result largely from new protein synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	small ubiquitin like modifier 3	Homo sapiens	0-8
22306003-2	2012	Conjugates of SUMO-2 and SUMO-3 (SUMO-2/3) accumulate in cells exposed to various stress stimuli or to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	small ubiquitin like modifier 2	Homo sapiens	14-20
22230367-5	2012	To examine the BI-1-associated P450 2E1 degradation mechanism, cells were treated with the lysosome inhibitor, bafilomycin and the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	transmembrane BAX inhibitor motif containing 6	Mus musculus	15-19
22306003-2	2012	Conjugates of SUMO-2 and SUMO-3 (SUMO-2/3) accumulate in cells exposed to various stress stimuli or to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	small ubiquitin like modifier 3	Homo sapiens	25-31
22306003-2	2012	Conjugates of SUMO-2 and SUMO-3 (SUMO-2/3) accumulate in cells exposed to various stress stimuli or to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	small ubiquitin like modifier 3	Homo sapiens	33-41
22306003-3	2012	Although the proteins modified by SUMO-2/3 during heat shock or under MG132 treatment have been identified, the significance of this modification remains unclear.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	small ubiquitin like modifier 3	Homo sapiens	34-42
22306003-4	2012	Our data show that the inhibition of translation by puromycin or cycloheximide blocks both the heat shock and MG132 induced accumulation of SUMO-2/3 conjugates in HEK 293T and U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	small ubiquitin like modifier 3	Homo sapiens	140-148
22306003-7	2012	We suggest that the SUMO-2/3 conjugates accumulating under the heat shock or MG132 treatment result largely from new protein synthesis and that portion of them is incorrectly folded.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	small ubiquitin like modifier 3	Homo sapiens	20-28
22345097-8	2012	API-1-induced reduction of c-FLIP could be blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	baculoviral IAP repeat containing 2	Homo sapiens	0-5
22345097-8	2012	API-1-induced reduction of c-FLIP could be blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	CASP8 and FADD like apoptosis regulator	Homo sapiens	27-33
22310326-11	2012	Treatment of primary human hepatocytes with the proteasome inhibitor MG132 increased RXRalpha suggesting the involvement of the proteasome pathway in regulation of RXRalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	retinoid X receptor alpha	Homo sapiens	85-93
22310326-11	2012	Treatment of primary human hepatocytes with the proteasome inhibitor MG132 increased RXRalpha suggesting the involvement of the proteasome pathway in regulation of RXRalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	retinoid X receptor alpha	Homo sapiens	164-172
22383538-9	2012	The proteasome inhibitor MG132 reduces Borealin phosphorylation in mitosis and increases the steady-state level of Borealin, especially in mutants lacking the C-terminus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cell division cycle associated 8	Homo sapiens	39-47
22383538-9	2012	The proteasome inhibitor MG132 reduces Borealin phosphorylation in mitosis and increases the steady-state level of Borealin, especially in mutants lacking the C-terminus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cell division cycle associated 8	Homo sapiens	115-123
22383538-11	2012	These results suggest that the effect of MG132 on Borealin is due to the inhibition of an intracellular protease other than the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cell division cycle associated 8	Homo sapiens	50-58
22266922-9	2012	Furthermore, superoxide             dismutase (SOD) 2, catalase (CTX) and GSH peroxidase (GPX) siRNAs enhanced HPF             cell death by MG132, which was not correlated with ROS and GSH level changes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	superoxide dismutase 2	Homo sapiens	13-53
22369110-6	2012	This reduction was partially blocked by pretreatment with 26S proteasome inhibitor MG-132, indicating that proteasomal degradation was involved in GGA-induced disappearance of cyclin D1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-89	cyclin D1	Homo sapiens	176-185
22266922-9	2012	Furthermore, superoxide             dismutase (SOD) 2, catalase (CTX) and GSH peroxidase (GPX) siRNAs enhanced HPF             cell death by MG132, which was not correlated with ROS and GSH level changes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	65-68
22227409-7	2012	In addition, treatment with MG132 blocked MDM2-mediated p53 ubiquitination and degradation, and led to accumulation of p53 in Gli3 siRNA-overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	MDM2 proto-oncogene	Homo sapiens	42-46
22227409-7	2012	In addition, treatment with MG132 blocked MDM2-mediated p53 ubiquitination and degradation, and led to accumulation of p53 in Gli3 siRNA-overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	tumor protein p53	Homo sapiens	56-59
22227409-7	2012	In addition, treatment with MG132 blocked MDM2-mediated p53 ubiquitination and degradation, and led to accumulation of p53 in Gli3 siRNA-overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	tumor protein p53	Homo sapiens	119-122
22227409-7	2012	In addition, treatment with MG132 blocked MDM2-mediated p53 ubiquitination and degradation, and led to accumulation of p53 in Gli3 siRNA-overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	GLI family zinc finger 3	Homo sapiens	126-130
22120110-5	2012	Moreover, treatment of MCF-7 cells overexpressed FLAG-GABARAPL1-6HIS with the HSP90 inhibitor 17-AAG promotes the GABARAPL1 degradation, a process that is blocked by proteasome inhibitors such as MG132, bortezomib and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	GABA type A receptor associated protein like 1	Homo sapiens	54-63
22120110-5	2012	Moreover, treatment of MCF-7 cells overexpressed FLAG-GABARAPL1-6HIS with the HSP90 inhibitor 17-AAG promotes the GABARAPL1 degradation, a process that is blocked by proteasome inhibitors such as MG132, bortezomib and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	heat shock protein 90 alpha family class A member 1	Homo sapiens	78-83
22120110-5	2012	Moreover, treatment of MCF-7 cells overexpressed FLAG-GABARAPL1-6HIS with the HSP90 inhibitor 17-AAG promotes the GABARAPL1 degradation, a process that is blocked by proteasome inhibitors such as MG132, bortezomib and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	GABA type A receptor associated protein like 1	Homo sapiens	114-123
22246236-5	2012	Knockdown of migfilin by siRNA, transfection of a mutant beta-catenin at Ser37 which is a critical phosphorylation site of GSK-3beta, GSK-3beta inhibitor LiCl, or proteasome inhibitor MG132 reversed the migfilin-mediated beta-catenin degradation and transcription inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-189	filamin binding LIM protein 1	Homo sapiens	13-21
21567392-5	2012	Pretreatment of myotubes with proteasome inhibitors MG132 or lactacystin or knockdown of MuRF1 by RNAi blocked the TWEAK-induced degradation of MyHC and myotube atrophy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	TNF superfamily member 12	Homo sapiens	115-120
21567392-5	2012	Pretreatment of myotubes with proteasome inhibitors MG132 or lactacystin or knockdown of MuRF1 by RNAi blocked the TWEAK-induced degradation of MyHC and myotube atrophy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	myosin heavy chain 6	Homo sapiens	144-148
22246236-5	2012	Knockdown of migfilin by siRNA, transfection of a mutant beta-catenin at Ser37 which is a critical phosphorylation site of GSK-3beta, GSK-3beta inhibitor LiCl, or proteasome inhibitor MG132 reversed the migfilin-mediated beta-catenin degradation and transcription inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-189	catenin beta 1	Homo sapiens	57-69
22033459-4	2012	The decrease in TRAF6 was inhibited by proteasome inhibitors MG-132, lactacystin and N-acetyl-leucyl-leucyl-norleucinal.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	TNF receptor associated factor 6	Homo sapiens	16-21
22310719-4	2012	MG132 caused the phosphorylation of GSK3beta at Ser(9) and, to a lesser extent, Thr(390), the dephosphorylation of p70S6K at Thr(389), and the phosphorylation of p70S6K at Thr(421) and Ser(424).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	ribosomal protein S6 kinase B1	Homo sapiens	115-121
22310719-4	2012	MG132 caused the phosphorylation of GSK3beta at Ser(9) and, to a lesser extent, Thr(390), the dephosphorylation of p70S6K at Thr(389), and the phosphorylation of p70S6K at Thr(421) and Ser(424).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	ribosomal protein S6 kinase B1	Homo sapiens	162-168
22310719-5	2012	The specific p38 inhibitor SB203080 reduced the p-GSK3beta(Ser9) and autophagy through the phosphorylation of p70S6K(Thr389); however, it augmented the levels of p-ERK, p-GSK3beta(Thr390), and p-70S6K(Thr421/Ser424) induced by MG132, and increased apoptotic cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	mitogen-activated protein kinase 14	Homo sapiens	13-16
22310719-6	2012	The GSK inhibitor SB216763, but not lithium, inhibited the MG132-induced phosphorylation of p38, and the downstream signaling pathway was consistent with that in SB203580-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	mitogen-activated protein kinase 14	Homo sapiens	92-95
22315970-15	2012	On the other hand, phosphorylated BCA2 protein is stabilized by interaction with 14-3-3sigma both with and without proteasome inhibitor MG-132 suggesting that BCA2 is regulated by multiple degradation pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-142	ring finger protein 115	Homo sapiens	34-38
22085560-9	2012	Cycloheximide (CHX)-chase assay revealed that 4-HNE exposure accelerated adiponectin protein degradation, which was prevented by MG132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	adiponectin, C1Q and collagen domain containing	Homo sapiens	73-84
22310719-3	2012	The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	activating transcription factor 6	Homo sapiens	107-112
22310719-3	2012	The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	114-118
22310719-3	2012	The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	DNA damage inducible transcript 3	Homo sapiens	140-144
22310719-3	2012	The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	BCL2 associated X, apoptosis regulator	Homo sapiens	184-187
22310719-3	2012	The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	caspase 3	Homo sapiens	192-204
22310719-4	2012	MG132 caused the phosphorylation of GSK3beta at Ser(9) and, to a lesser extent, Thr(390), the dephosphorylation of p70S6K at Thr(389), and the phosphorylation of p70S6K at Thr(421) and Ser(424).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	glycogen synthase kinase 3 beta	Homo sapiens	36-44
22159221-8	2012	Omega-3 PUFA treatment appeared to accelerate AR protein degradation, which could be blocked by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	androgen receptor	Homo sapiens	46-48
22056306-7	2012	In contrast, ectopically expression of Mdm2 decreases PolH expression, which can be abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	MDM2 proto-oncogene	Homo sapiens	39-43
22262167-9	2012	Surprisingly, treatment of HAdV-infected cells with proteasome inhibitor MG132 only partially restored the protein levels of Mdm2 and Mdm4, suggesting that they may also be downregulated through an additional mechanism independent of proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	transformed mouse 3T3 cell double minute 2	Mus musculus	125-129
22262167-9	2012	Surprisingly, treatment of HAdV-infected cells with proteasome inhibitor MG132 only partially restored the protein levels of Mdm2 and Mdm4, suggesting that they may also be downregulated through an additional mechanism independent of proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	transformed mouse 3T3 cell double minute 4	Mus musculus	134-138
22024133-3	2012	Vinblastine treatment of KB-3 cells initially resulted in a phosphatase-sensitive mobility shift in Mcl-1 and then subsequent loss of Mcl-1 protein expression which was prevented by MG132, suggesting that phosphorylation triggered proteosome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	182-187	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	134-139
22076938-8	2012	AICAR induced Nanog degradation, an effect inhibited by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	0-5
22076938-8	2012	AICAR induced Nanog degradation, an effect inhibited by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	Nanog homeobox	Homo sapiens	14-19
22277058-12	2012	Co-treatment with the proteasome inhibitor MG132 enabled us to classify 64 kinases as true Hsp90 clients.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	heat shock protein 90 alpha family class A member 1	Homo sapiens	91-96
22628303-5	2012	The ubiquitin proteasome inhibitor MG132 also phosphorylates ATF2 and inhibits renin expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	activating transcription factor 2	Mus musculus	61-65
22179018-6	2012	Using RPTC, mitochondrial and cytosolic calpain 10 increased in the presence of MG132 (Lon/proteasome inhibitor) but only cytosolic calpain 10 increased in the presence of epoxomicin (proteasome inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	calpain 10	Homo sapiens	40-50
22179018-6	2012	Using RPTC, mitochondrial and cytosolic calpain 10 increased in the presence of MG132 (Lon/proteasome inhibitor) but only cytosolic calpain 10 increased in the presence of epoxomicin (proteasome inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	lon peptidase 1, mitochondrial	Homo sapiens	87-90
22179018-7	2012	Furthermore, TBHP and H(2)O(2) oxidized mitochondrial calpain 10, decreased mitochondrial, but not cytosolic calpain 10, and pretreatment with MG132 blocked TBHP-induced degradation of calpain 10.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	calpain 10	Homo sapiens	54-64
22179018-7	2012	Furthermore, TBHP and H(2)O(2) oxidized mitochondrial calpain 10, decreased mitochondrial, but not cytosolic calpain 10, and pretreatment with MG132 blocked TBHP-induced degradation of calpain 10.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	calpain 10	Homo sapiens	109-119
22179018-7	2012	Furthermore, TBHP and H(2)O(2) oxidized mitochondrial calpain 10, decreased mitochondrial, but not cytosolic calpain 10, and pretreatment with MG132 blocked TBHP-induced degradation of calpain 10.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	calpain 10	Homo sapiens	109-119
22100705-6	2012	Using MG-132, we found that the proteolytic processing changed the subcellular localization of zCaMKP-N from the nucleus to the cytosol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-12	protein phosphatase, Mg2+/Mn2+ dependent, 1E	Danio rerio	95-103
22791147-9	2012	Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	glycogen synthase kinase 3 beta	Homo sapiens	13-22
22791147-9	2012	Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	caspase 3	Homo sapiens	67-76
22791147-9	2012	Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	poly(ADP-ribose) polymerase 1	Homo sapiens	81-85
22791147-9	2012	Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	catenin beta 1	Homo sapiens	171-183
22791147-9	2012	Furthermore, GSK 3beta inhibitor SB216763 blocked the cleavages of caspase-3 and PARP induced by ursolic acid and proteosomal inhibitor MG132 disturbed down-regulation of beta-catenin, activation of caspase-3 and decreased mitochondrial membrane potential (MMP) induced by ursolic acid in SK-OV-3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	caspase 3	Homo sapiens	199-208
22628303-6	2012	Knockdown of ATF2 attenuated the suppression of renin gene expression by MG132, thus demonstrating that ATF2 mediates the inhibitory effect of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	activating transcription factor 2	Mus musculus	13-17
22628303-6	2012	Knockdown of ATF2 attenuated the suppression of renin gene expression by MG132, thus demonstrating that ATF2 mediates the inhibitory effect of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	activating transcription factor 2	Mus musculus	13-17
22628303-6	2012	Knockdown of ATF2 attenuated the suppression of renin gene expression by MG132, thus demonstrating that ATF2 mediates the inhibitory effect of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	activating transcription factor 2	Mus musculus	104-108
22628303-7	2012	In addition, MG132 increased the DNA-binding of ATF2 as well as the ratio of bound ATF2 to CREB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	activating transcription factor 2	Mus musculus	48-52
22628303-7	2012	In addition, MG132 increased the DNA-binding of ATF2 as well as the ratio of bound ATF2 to CREB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	activating transcription factor 2	Mus musculus	83-87
22628303-7	2012	In addition, MG132 increased the DNA-binding of ATF2 as well as the ratio of bound ATF2 to CREB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cAMP responsive element binding protein 1	Mus musculus	91-95
22072743-7	2012	BAG3 coimmunoprecipitates with BRAF protein, and its down-modulation results in a significant reduction of BRAF protein levels, which can be reverted by incubation with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	194-199	BAG cochaperone 3	Homo sapiens	0-4
23006579-4	2012	Moreover, the increase in HIF-1alpha induced by exposure to MG132 alone in normoxia was diminished by PMS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	hypoxia inducible factor 1 subunit alpha	Homo sapiens	26-36
23018488-9	2012	Furthermore, the DNAJB14-dependent degradation of CFTRDeltaF508 was compromised by MG132, a proteasome inhibitor, indicating that DNAJB14 can enhance the degradation of a misfolded membrane protein using the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	DnaJ heat shock protein family (Hsp40) member B14	Homo sapiens	17-24
23018488-9	2012	Furthermore, the DNAJB14-dependent degradation of CFTRDeltaF508 was compromised by MG132, a proteasome inhibitor, indicating that DNAJB14 can enhance the degradation of a misfolded membrane protein using the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	DnaJ heat shock protein family (Hsp40) member B14	Homo sapiens	130-137
22109885-7	2012	Pretreatment with 26S proteasome inhibitor, MG132, significantly restores COX-2 protein and PG synthesis, indicating that COX-2 undergoes proteasomal degradation in the presence of TGF-beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	74-79
22109885-7	2012	Pretreatment with 26S proteasome inhibitor, MG132, significantly restores COX-2 protein and PG synthesis, indicating that COX-2 undergoes proteasomal degradation in the presence of TGF-beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	122-127
22109885-7	2012	Pretreatment with 26S proteasome inhibitor, MG132, significantly restores COX-2 protein and PG synthesis, indicating that COX-2 undergoes proteasomal degradation in the presence of TGF-beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	transforming growth factor beta 1	Homo sapiens	181-189
22074660-3	2012	The repression of p300 expression by SMAR1 is relieved upon treatment with proteosomal inhibitors MG132 and Lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	E1A binding protein p300	Homo sapiens	18-22
22074660-3	2012	The repression of p300 expression by SMAR1 is relieved upon treatment with proteosomal inhibitors MG132 and Lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	BTG3 associated nuclear protein	Homo sapiens	37-42
22977658-5	2012	Moreover, we found that the proteasome inhibitor MG132 could inhibit IL-6/TGF-beta-mediated downregulation of FOXP3 protein, which reveals a potential pathway for modulating Treg activity by preventing FOXP3 degradation during inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	interleukin 6	Homo sapiens	69-73
22977658-5	2012	Moreover, we found that the proteasome inhibitor MG132 could inhibit IL-6/TGF-beta-mediated downregulation of FOXP3 protein, which reveals a potential pathway for modulating Treg activity by preventing FOXP3 degradation during inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	transforming growth factor beta 1	Homo sapiens	74-82
22977658-5	2012	Moreover, we found that the proteasome inhibitor MG132 could inhibit IL-6/TGF-beta-mediated downregulation of FOXP3 protein, which reveals a potential pathway for modulating Treg activity by preventing FOXP3 degradation during inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	forkhead box P3	Homo sapiens	110-115
22977658-5	2012	Moreover, we found that the proteasome inhibitor MG132 could inhibit IL-6/TGF-beta-mediated downregulation of FOXP3 protein, which reveals a potential pathway for modulating Treg activity by preventing FOXP3 degradation during inflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	forkhead box P3	Homo sapiens	202-207
21907792-11	2012	In contrast, using proteasome inhibitors MG132 and lactacystin, we demonstrated that JAK2 governs ERalpha protein stability via the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	Janus kinase 2	Homo sapiens	85-89
21907792-11	2012	In contrast, using proteasome inhibitors MG132 and lactacystin, we demonstrated that JAK2 governs ERalpha protein stability via the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	estrogen receptor 1	Homo sapiens	98-105
22032857-9	2012	In contrast, treatment with MG132 reduced the expression of TNFAIP6 and HAS2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	TNF alpha induced protein 6	Sus scrofa	60-67
22032857-9	2012	In contrast, treatment with MG132 reduced the expression of TNFAIP6 and HAS2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	hyaluronan synthase 2	Sus scrofa	72-76
22956975-7	2012	Both EA and MG132 blocked CFA-induced GLAST and GLT-1 downregulation within the spinal cord.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	solute carrier family 1 member 3	Rattus norvegicus	38-43
22956975-7	2012	Both EA and MG132 blocked CFA-induced GLAST and GLT-1 downregulation within the spinal cord.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	solute carrier family 1 member 2	Rattus norvegicus	48-53
22072743-7	2012	BAG3 coimmunoprecipitates with BRAF protein, and its down-modulation results in a significant reduction of BRAF protein levels, which can be reverted by incubation with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	194-199	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	31-35
22072743-7	2012	BAG3 coimmunoprecipitates with BRAF protein, and its down-modulation results in a significant reduction of BRAF protein levels, which can be reverted by incubation with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	194-199	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	107-111
22302044-6	2012	Further studies revealed that resveratrol inhibited c-Myc protein accumulation via up-regulation of SirT1 expression and deacetylase activity, and this loss of c-Myc protein was abolished by inhibiting its degradation in the presence of MG132, a potent inhibitor of proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	237-242	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	160-165
22007720-7	2012	CNTF stimulated the ubiquitination of TH in both neurons and neuroblastoma cells, and the proteasome inhibitors MG-132 and lactacystin prevented the CNTF-induced loss of TH protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	ciliary neurotrophic factor	Homo sapiens	149-153
22007720-7	2012	CNTF stimulated the ubiquitination of TH in both neurons and neuroblastoma cells, and the proteasome inhibitors MG-132 and lactacystin prevented the CNTF-induced loss of TH protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	tyrosine hydroxylase	Homo sapiens	170-172
22489690-8	2012	Expression of phospho-Akt and p53 showed no detectable change during the first 48 h. Pretreatment with the NF-kappaB inhibitor MG132 before exposure to isorhamnetin blocked the nuclear accumulation of p50 and p65, thereby inhibiting cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	AKT serine/threonine kinase 1	Homo sapiens	22-25
22736942-0	2012	M-opsin protein degradation is inhibited by MG-132 in Rpe65-/- retinal explant culture.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	retinal pigment epithelium 65	Mus musculus	54-59
22736942-7	2012	RESULTS: Degradation of the M-opsin protein in Rpe65(-/-) mouse retina was inhibited by the proteasome inhibitor MG-132 but not by the lysosomal inhibitor pepstatin A and E64d.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	retinal pigment epithelium 65	Mus musculus	47-52
23430855-0	2012	Treatment of Human Fibroblasts Carrying NPC1 Missense Mutations with MG132 Leads to an Improvement of Intracellular Cholesterol Trafficking.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	NPC intracellular cholesterol transporter 1	Homo sapiens	40-44
23430855-7	2012	Treatment of fibroblasts carrying NPC1 missense mutations in homo or hemizygosity, with the proteasome inhibitor MG132 or glycerol 10%, a chemical chaperone known to stabilize misfolded proteins, resulted in a significant increase of NPC1 protein levels in all cell lines, indicating that these mutants are subjected to proteasomal degradation due to protein misfolding The increment of NPC1 mutant protein induced by the proteasome inhibitor was associated with a localization of NPC1 protein within lysosomal/LE compartment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	NPC intracellular cholesterol transporter 1	Homo sapiens	234-238
23430855-7	2012	Treatment of fibroblasts carrying NPC1 missense mutations in homo or hemizygosity, with the proteasome inhibitor MG132 or glycerol 10%, a chemical chaperone known to stabilize misfolded proteins, resulted in a significant increase of NPC1 protein levels in all cell lines, indicating that these mutants are subjected to proteasomal degradation due to protein misfolding The increment of NPC1 mutant protein induced by the proteasome inhibitor was associated with a localization of NPC1 protein within lysosomal/LE compartment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	NPC intracellular cholesterol transporter 1	Homo sapiens	234-238
23430855-7	2012	Treatment of fibroblasts carrying NPC1 missense mutations in homo or hemizygosity, with the proteasome inhibitor MG132 or glycerol 10%, a chemical chaperone known to stabilize misfolded proteins, resulted in a significant increase of NPC1 protein levels in all cell lines, indicating that these mutants are subjected to proteasomal degradation due to protein misfolding The increment of NPC1 mutant protein induced by the proteasome inhibitor was associated with a localization of NPC1 protein within lysosomal/LE compartment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	NPC intracellular cholesterol transporter 1	Homo sapiens	234-238
22113267-5	2012	In this chapter, we describe a protocol that uses small inhibitory RNA (si RNA) interference followed by electrophoretic mobility shift assay (EMSA) to analyze the regulation of NFkappaB DNA binding by nuclear IkappaBalpha induced by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	259-264	nuclear factor kappa B subunit 1	Homo sapiens	178-186
22113267-5	2012	In this chapter, we describe a protocol that uses small inhibitory RNA (si RNA) interference followed by electrophoretic mobility shift assay (EMSA) to analyze the regulation of NFkappaB DNA binding by nuclear IkappaBalpha induced by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	259-264	NFKB inhibitor alpha	Homo sapiens	210-222
22113267-6	2012	Using this protocol, we show that in human leukemia Hut-78 cells that exhibit high levels of NFkappaB DNA binding activity, MG132 induces nuclear translocation and accumulation of IkappaBalpha, which then specifically inhibits NFkappaB DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	nuclear factor kappa B subunit 1	Homo sapiens	93-101
22113267-6	2012	Using this protocol, we show that in human leukemia Hut-78 cells that exhibit high levels of NFkappaB DNA binding activity, MG132 induces nuclear translocation and accumulation of IkappaBalpha, which then specifically inhibits NFkappaB DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	NFKB inhibitor alpha	Homo sapiens	180-192
22113267-6	2012	Using this protocol, we show that in human leukemia Hut-78 cells that exhibit high levels of NFkappaB DNA binding activity, MG132 induces nuclear translocation and accumulation of IkappaBalpha, which then specifically inhibits NFkappaB DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	nuclear factor kappa B subunit 1	Homo sapiens	227-235
22489690-8	2012	Expression of phospho-Akt and p53 showed no detectable change during the first 48 h. Pretreatment with the NF-kappaB inhibitor MG132 before exposure to isorhamnetin blocked the nuclear accumulation of p50 and p65, thereby inhibiting cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	tumor protein p53	Homo sapiens	30-33
22489690-8	2012	Expression of phospho-Akt and p53 showed no detectable change during the first 48 h. Pretreatment with the NF-kappaB inhibitor MG132 before exposure to isorhamnetin blocked the nuclear accumulation of p50 and p65, thereby inhibiting cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	nuclear factor kappa B subunit 1	Homo sapiens	201-204
22489690-8	2012	Expression of phospho-Akt and p53 showed no detectable change during the first 48 h. Pretreatment with the NF-kappaB inhibitor MG132 before exposure to isorhamnetin blocked the nuclear accumulation of p50 and p65, thereby inhibiting cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	RELA proto-oncogene, NF-kB subunit	Homo sapiens	209-212
21964832-8	2012	We observed that TPA-induced             down-regulation of p53 protein was prevented by ALLN and MG132, but not by chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	plasminogen activator, tissue type	Homo sapiens	17-20
21964832-7	2012	To verify the regulatory mechanism of p53 protein expression, we investigated             the effects of proteasomal inhibitors (ALLN and MG132) or a lysosomal inhibitor             (chloroquine) on TPA-induced down-regulation of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	plasminogen activator, tissue type	Homo sapiens	199-202
21964832-8	2012	We observed that TPA-induced             down-regulation of p53 protein was prevented by ALLN and MG132, but not by chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	tumor protein p53	Homo sapiens	60-63
23213349-3	2012	The increase in both Ha-Ras and Ki-Ras was insensitive to the protein synthesis inhibitor, cycloheximide, and was occluded by the proteasomal inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-159	KRAS proto-oncogene, GTPase	Homo sapiens	32-38
22018973-10	2012	Furthermore, the upregulated expression of MMP-3, SP, and CGRP in the arthritic rats was normalized by MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	matrix metallopeptidase 3	Rattus norvegicus	43-48
22018973-10	2012	Furthermore, the upregulated expression of MMP-3, SP, and CGRP in the arthritic rats was normalized by MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	calcitonin-related polypeptide alpha	Rattus norvegicus	58-62
22018973-11	2012	We conclude that the proteasome inhibitor MG132 reduces pain and joint destruction, probably by involving the peripheral nervous system, and that changes in SP and CGRP expression correlate with alterations in behavioural responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	calcitonin-related polypeptide alpha	Rattus norvegicus	164-168
23213349-5	2012	Indeed, the late reduction in Ha-Ras and Ki-Ras was due to a recovery of proteasomal degradation because it was sensitive to MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-131	KRAS proto-oncogene, GTPase	Homo sapiens	41-47
23284813-9	2012	The reduction in Drp1 and Mff protein levels was rescued following treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	mitochondrial fission factor	Homo sapiens	26-29
22479149-1	2012	The proteasome inhibitor MG132 had been shown to prevent galactose induction of the S. cerevisiae GAL1 gene, demonstrating that ubiquitin proteasome-dependent degradation of transcription factors plays an important role in the regulation of gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	galactokinase	Saccharomyces cerevisiae S288C	98-102
22844424-8	2012	Further, we found proteasomal inhibitor MG132, but not lysosomal inhibitors leupeptin and pepstatin A, could restore ABCG2 protein levels in LMWH-treated SP cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	117-122
23226437-0	2012	Systemic perturbation of the ERK signaling pathway by the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	mitogen-activated protein kinase 1	Homo sapiens	29-32
23226437-3	2012	It has been proposed that MG132 treatment reduces growth factor-stimulated phosphorylation of extracellular signal-regulated kinases (ERKs), at least in part through upregulation of dual specificity phosphatases (DUSPs).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	mitogen-activated protein kinase 1	Homo sapiens	134-138
23226437-4	2012	Here, we show that the effects of MG132 treatment on ERK signaling are more widespread, leading to a reduction in activation of the upstream kinase MEK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	mitogen-activated protein kinase 1	Homo sapiens	53-56
23226437-4	2012	Here, we show that the effects of MG132 treatment on ERK signaling are more widespread, leading to a reduction in activation of the upstream kinase MEK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	mitogen-activated protein kinase kinase 7	Homo sapiens	148-151
23226437-5	2012	This suggests that MG132 systemically perturbs the intracellular phosphoproteome, impacting ERK signaling by reducing phosphorylation status at multiple levels of the kinase cascade.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	mitogen-activated protein kinase 1	Homo sapiens	92-95
23284813-9	2012	The reduction in Drp1 and Mff protein levels was rescued following treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	dynamin 1 like	Homo sapiens	17-21
23029347-13	2012	Eventually AZA induced AQP1 ubiquitination, while proteasome inhibitor MG132 reversed AZA"s down-regulating effect upon AQP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	aquaporin 1	Mus musculus	120-124
22912784-7	2012	The CSE-induced GM-CSF expression was synergistically enhanced by the addition of the proteasome inhibitor MG-132, but inhibited by AG-1478, an inhibitor of the epidermal growth factor receptor (EGFR) kinase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-113	colony stimulating factor 2	Homo sapiens	16-22
22438966-8	2012	Down-regulation of GRP78 by siRNA, co-treatment with EGCG (a GRP78 inhibitor) or with MG132 (a proteasome inhibitor) could enhance celecoxib-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	heat shock protein family A (Hsp70) member 5	Homo sapiens	19-24
22570727-4	2012	We showed that the SAM domain mutations dramatically destabilized the EPHA2 protein in a proteasome-dependent pathway, as evidenced by the increase of EPHA2 receptor levels in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	217-222	EPH receptor A2	Homo sapiens	70-75
22570727-4	2012	We showed that the SAM domain mutations dramatically destabilized the EPHA2 protein in a proteasome-dependent pathway, as evidenced by the increase of EPHA2 receptor levels in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	217-222	EPH receptor A2	Homo sapiens	151-156
22586448-8	2012	Treatment of human kidney cells with nicotinic agonists, an NFkappaB inhibitor (Bay11), or a proteasome inhibitor (MG132) effectively inhibited their inflammatory responses following stimulation with LPS or TNFalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	tumor necrosis factor	Homo sapiens	207-215
22235305-4	2012	miR-122 up-regulation was not specific for GSI-1 but was also seen during apoptosis induced by chemotherapies including doxorubicin and proteasome blockers (bortezomib, MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	microRNA 122	Homo sapiens	0-7
22276183-7	2012	Prevention of HNF-4alpha degradation by treating with proteasome inhibitor MG132 also prevented the inhibitory effect of TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	hepatocyte nuclear factor 4 alpha	Homo sapiens	14-24
22276183-7	2012	Prevention of HNF-4alpha degradation by treating with proteasome inhibitor MG132 also prevented the inhibitory effect of TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	transforming growth factor beta 1	Homo sapiens	121-130
23139858-6	2012	This phenotypic change was completely reversed by p53 reactivation via treatment with proteasome inhibitor MG132 or co-knockdown of E3 ligase HDM2 and partially suppressed by ATP treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	tumor protein p53	Homo sapiens	50-53
21975282-13	2011	Treatment with inhibitors of NF-kappaB such as MG132, PDTC or expression of Ad-IkappaB-alphaM in VSMCs prevented VSMC proliferation and PAI-1 expression induced by high glucose.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	serpin family E member 1	Rattus norvegicus	136-141
22193447-0	2011	[MG-132 enhances MSCs survival and IL-10 secretion under hypoxia and serum deprivation condition].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	1-7	interleukin 10	Homo sapiens	35-40
22193447-11	2011	Furthermore, the induced IL-1beta and TNF-alpha transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-kappaBp65 nuclear translocation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	interleukin 1 beta	Homo sapiens	25-33
22193447-11	2011	Furthermore, the induced IL-1beta and TNF-alpha transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-kappaBp65 nuclear translocation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	tumor necrosis factor	Homo sapiens	38-47
22193447-11	2011	Furthermore, the induced IL-1beta and TNF-alpha transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-kappaBp65 nuclear translocation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	RELA proto-oncogene, NF-kB subunit	Homo sapiens	140-152
22193447-11	2011	Furthermore, the induced IL-1beta and TNF-alpha transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-kappaBp65 nuclear translocation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-184	interleukin 1 beta	Homo sapiens	25-33
22193447-11	2011	Furthermore, the induced IL-1beta and TNF-alpha transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-kappaBp65 nuclear translocation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-184	tumor necrosis factor	Homo sapiens	38-47
22193447-11	2011	Furthermore, the induced IL-1beta and TNF-alpha transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-kappaBp65 nuclear translocation by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-184	RELA proto-oncogene, NF-kB subunit	Homo sapiens	140-152
22193447-12	2011	Importantly, MG-132 effectively enhanced H/SD-induced transcription and secretion of IL-10, which is an important paracrine factor from MSCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	interleukin 10	Homo sapiens	85-90
22086178-9	2011	Furthermore, we discovered that the Cdc20 mediated degradation of Sp100 is diminished by the proteasome inhibitor MG132, which suggests that the ubiquitination pathway is involved in this process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	cell division cycle 20	Homo sapiens	36-41
22008847-7	2011	In contrast, MG-132 (blocking the activity of 26S proteasome and thereby preventing nuclear translocation of NF-kappaB) significantly inhibited activation of NF-kappaB and mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	nuclear factor kappa B subunit 1	Homo sapiens	109-118
22008847-7	2011	In contrast, MG-132 (blocking the activity of 26S proteasome and thereby preventing nuclear translocation of NF-kappaB) significantly inhibited activation of NF-kappaB and mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	nuclear factor kappa B subunit 1	Homo sapiens	158-167
21933686-4	2011	Treatment with MG132 (0.5 muM) retained its beneficial effect with 3 different LV of increasing size up to 10.9 Kb (p&lt;0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	latexin	Homo sapiens	26-29
22120628-7	2011	Unlike Doxorubicin, Etoposide, Actinomycin D and Wortmannin, a proteasome inhibitor MG132 significantly enhanced TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	TNF superfamily member 10	Homo sapiens	113-118
22120628-9	2011	Among these proteasome inhibitors, Velcade, the only approved drug, was as effective as MG132 in enhancing TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	TNF superfamily member 10	Homo sapiens	107-112
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	TNF receptor superfamily member 10b	Homo sapiens	55-58
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	TNF superfamily member 10	Homo sapiens	62-67
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	tumor protein p53	Homo sapiens	105-108
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	tumor protein p53	Homo sapiens	132-135
22074820-4	2011	The proteasome inhibitors MG132, lactacystin, and proteasome inhibitor I dramatically inhibited cell proliferation and induced apoptosis of PEL cells through the accumulation of p21 and p27.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	H3 histone pseudogene 16	Homo sapiens	178-181
22074820-4	2011	The proteasome inhibitors MG132, lactacystin, and proteasome inhibitor I dramatically inhibited cell proliferation and induced apoptosis of PEL cells through the accumulation of p21 and p27.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	interferon alpha inducible protein 27	Homo sapiens	186-189
22086178-9	2011	Furthermore, we discovered that the Cdc20 mediated degradation of Sp100 is diminished by the proteasome inhibitor MG132, which suggests that the ubiquitination pathway is involved in this process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	SP100 nuclear antigen	Homo sapiens	66-71
22001063-8	2011	Blocking Elongin C mediated degradation by MG132 indicates the potential for ubiquitin-mediated Elongin C regulation of Notch4(ICD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	elongin C	Homo sapiens	9-18
22001063-8	2011	Blocking Elongin C mediated degradation by MG132 indicates the potential for ubiquitin-mediated Elongin C regulation of Notch4(ICD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	elongin C	Homo sapiens	96-105
22001063-8	2011	Blocking Elongin C mediated degradation by MG132 indicates the potential for ubiquitin-mediated Elongin C regulation of Notch4(ICD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	notch receptor 4	Homo sapiens	120-126
22001063-8	2011	Blocking Elongin C mediated degradation by MG132 indicates the potential for ubiquitin-mediated Elongin C regulation of Notch4(ICD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	N-acetylglucosamine-1-phosphate transferase subunits alpha and beta	Homo sapiens	127-130
21901230-8	2011	Furthermore, both IRAK1/4 inhibitor and a specific proteasome inhibitor MG-132 could attenuate TRAFs expression as well as TF expression induced by anti-beta2GPI/beta2GPI complex.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	apolipoprotein H	Homo sapiens	153-161
21421692-6	2011	c-Jun N-terminal kinase (JNK) inhibitor attenuated the growth inhibition and death by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	mitogen-activated protein kinase 8	Homo sapiens	0-23
21421692-6	2011	c-Jun N-terminal kinase (JNK) inhibitor attenuated the growth inhibition and death by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	mitogen-activated protein kinase 8	Homo sapiens	25-28
21421692-8	2011	Although p38 inhibitor slightly enhanced HPF cell growth inhibition by MG132, this inhibitor and siRNA prevented HPF cell death induced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	mitogen-activated protein kinase 14	Homo sapiens	9-12
21421692-8	2011	Although p38 inhibitor slightly enhanced HPF cell growth inhibition by MG132, this inhibitor and siRNA prevented HPF cell death induced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	mitogen-activated protein kinase 14	Homo sapiens	9-12
21421692-11	2011	ERK and JNK siRNAs decreased anonymous ubiquitinated protein levels in MG132-treated HPF cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	mitogen-activated protein kinase 1	Homo sapiens	0-3
21421692-11	2011	ERK and JNK siRNAs decreased anonymous ubiquitinated protein levels in MG132-treated HPF cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	mitogen-activated protein kinase 8	Homo sapiens	8-11
21421692-13	2011	Especially, p38 inhibitor attenuated HPF cell death by MG132, which was in part related to changes in ROS and GSH levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	mitogen-activated protein kinase 14	Homo sapiens	12-15
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	50-53
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	54-58
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	160-163
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	164-168
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	160-163
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cyclin dependent kinase inhibitor 1A	Homo sapiens	164-168
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cyclin dependent kinase inhibitor 1A	Homo sapiens	50-53
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cyclin dependent kinase inhibitor 1A	Homo sapiens	54-58
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cyclin dependent kinase inhibitor 1A	Homo sapiens	160-163
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cyclin dependent kinase inhibitor 1A	Homo sapiens	164-168
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cyclin dependent kinase inhibitor 1A	Homo sapiens	160-163
21850573-5	2011	In addition, MG132 increased the protein level of p21(WAF1) in a dose-dependent manner in the presence of serotonin, 10 muM MG132 led to a 4.2-fold increase in p21(WAF1) protein level, and this effect was not mediated by increasing p21(WAF1) mRNA level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cyclin dependent kinase inhibitor 1A	Homo sapiens	164-168
21850573-6	2011	More importantly, cell lacking p21(WAF1) by siRNA transfection abolished the inhibitive effect of MG132 on cells proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	cyclin dependent kinase inhibitor 1A	Homo sapiens	31-34
21850573-6	2011	More importantly, cell lacking p21(WAF1) by siRNA transfection abolished the inhibitive effect of MG132 on cells proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	cyclin dependent kinase inhibitor 1A	Homo sapiens	35-39
21793045-9	2011	However, the level of TRAF2 was restored after treatment with a proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-92	TNF receptor associated factor 2	Homo sapiens	22-27
22111595-0	2011	Comparative study of the influence of proteasome inhibitor MG132 and ganciclovir on the cytomegalovirus-specific CD8(+) T-cell immune response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	CD8a molecule	Homo sapiens	113-116
21901230-8	2011	Furthermore, both IRAK1/4 inhibitor and a specific proteasome inhibitor MG-132 could attenuate TRAFs expression as well as TF expression induced by anti-beta2GPI/beta2GPI complex.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	apolipoprotein H	Homo sapiens	162-170
22111595-4	2011	In this study we investigated the influence of proteasome inhibitor MG132 and ganciclovir on the CMV-specific CD8(+) T-cell immune response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	CD8a molecule	Homo sapiens	110-113
21819973-0	2011	Proteasome inhibitor MG132-induced apoptosis via ER stress-mediated apoptotic pathway and its potentiation by protein tyrosine kinase p56lck in human Jurkat T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	134-140
22111595-5	2011	We found that interferon-gamma (IFN-gamma) production in response to CMV-infected fibroblasts was reduced under the influence of MG132 in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	interferon gamma	Homo sapiens	14-30
22111595-5	2011	We found that interferon-gamma (IFN-gamma) production in response to CMV-infected fibroblasts was reduced under the influence of MG132 in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	interferon gamma	Homo sapiens	32-41
22111595-7	2011	Likewise, CMV-specific cytotoxicity of CD8(+) T cells was decreased in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	CD8a molecule	Homo sapiens	39-42
22027144-3	2011	In this study, we characterized the effect of two proteasome inhibitors, bortezomib and MG132, on maturation, subcellular localization and residual activity of mutant GAA in the patient fibroblasts carrying c.546G&gt;T mutation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	alpha glucosidase	Homo sapiens	167-170
22071628-2	2011	Previously we have demonstrated that proteasome inhibitors thiostrepton, MG132 and bortezomib paradoxically inhibit transcriptional activity and mRNA/protein expression of FOXM1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	forkhead box M1	Homo sapiens	172-177
22509550-4	2011	Meanwhile, the impact of MG132 (a proteasome inhibitor) pretreatment on the expressions of beta-catenin and cyclin D1 was observed through Western blot analysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	catenin beta 1	Homo sapiens	91-103
22509550-4	2011	Meanwhile, the impact of MG132 (a proteasome inhibitor) pretreatment on the expressions of beta-catenin and cyclin D1 was observed through Western blot analysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cyclin D1	Homo sapiens	108-117
22509550-7	2011	MG132 pretreatment prevented the inhibition of beta-catenin signaling triggered by selenite in HCT 116 and SW480 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	catenin beta 1	Homo sapiens	47-59
22074827-3	2011	In this report, we show that PCSK9 treatment can lead to ubiquitination of LDLR, which was enhanced in the presence of proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	proprotein convertase subtilisin/kexin type 9	Homo sapiens	29-34
22074827-3	2011	In this report, we show that PCSK9 treatment can lead to ubiquitination of LDLR, which was enhanced in the presence of proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	low density lipoprotein receptor	Homo sapiens	75-79
21953463-7	2011	The degradation of KLF5 by SMURF2 was blocked by the proteasome inhibitor MG132, and SMURF2 efficiently ubiquitinated both overexpressed and endogenous KLF5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	Kruppel like factor 5	Homo sapiens	19-23
21953463-7	2011	The degradation of KLF5 by SMURF2 was blocked by the proteasome inhibitor MG132, and SMURF2 efficiently ubiquitinated both overexpressed and endogenous KLF5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	SMAD specific E3 ubiquitin protein ligase 2	Homo sapiens	27-33
22078414-9	2011	This dramatic Mcl-1 accumulation was also observed when cells were treated with other two proteasome inhibitors, MG132 and calpain inhibitor I (ALLN).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	heat shock protein family A (Hsp70) member 5	Homo sapiens	86-91
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	heat shock protein family A (Hsp70) member 5	Homo sapiens	92-95
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	DNA damage inducible transcript 3	Homo sapiens	100-104
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	DNA damage inducible transcript 3	Homo sapiens	105-112
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	mitogen-activated protein kinase 8	Homo sapiens	128-131
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	BCL2 antagonist/killer 1	Homo sapiens	159-162
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	cytochrome c, somatic	Homo sapiens	215-227
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	caspase 9	Homo sapiens	251-281
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	BH3 interacting domain death agonist	Homo sapiens	295-298
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	collagen type XI alpha 2 chain	Homo sapiens	303-307
21819973-5	2011	MG132-induced cytotoxicity, apoptotic sub-G(1) peak, Bak activation, and Deltapsim loss were markedly reduced by p38MAPK inhibitor, but not by JNK inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BCL2 antagonist/killer 1	Homo sapiens	53-56
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein family A (Hsp70) member 5	Homo sapiens	59-64
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein family A (Hsp70) member 5	Homo sapiens	65-68
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA damage inducible transcript 3	Homo sapiens	73-77
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA damage inducible transcript 3	Homo sapiens	78-85
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BCL2 antagonist/killer 1	Homo sapiens	132-135
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase like 2	Homo sapiens	219-222
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	223-226
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	256-259
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase like 2	Homo sapiens	268-271
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	256-259
21819973-7	2011	The cytotoxicity of MG132 toward p56(lck)-positive Jurkat T cell clone was not affected by the Src-like kinase inhibitor PP2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	cyclin dependent kinase like 2	Homo sapiens	33-36
21819973-7	2011	The cytotoxicity of MG132 toward p56(lck)-positive Jurkat T cell clone was not affected by the Src-like kinase inhibitor PP2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	37-40
21819973-8	2011	These results demonstrated that MG132-induced apoptosis was caused by ER stress and subsequent activation of mitochondria-dependent caspase cascade, and that the presence of p56(lck) enhances MG132-induced apoptosis by augmenting ER stress-mediated apoptotic events in Jurkat T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	cyclin dependent kinase like 2	Homo sapiens	174-177
21819973-8	2011	These results demonstrated that MG132-induced apoptosis was caused by ER stress and subsequent activation of mitochondria-dependent caspase cascade, and that the presence of p56(lck) enhances MG132-induced apoptosis by augmenting ER stress-mediated apoptotic events in Jurkat T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	178-181
21871886-3	2011	Downregulation of AR protein, but not mRNA, was blocked by proteasome inhibitors, MG132 and bortezomib, indicating that the pathway regulation is mediated at multiple points.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	androgen receptor	Homo sapiens	18-20
22340220-5	2011	MG132 was employed to block the endogenous IkappaBalpha degradation before PA administration, and then its effect on PA-inducing cell apoptosis and PGC-1alpha mRNA expression was analyzed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	43-55
22340220-5	2011	MG132 was employed to block the endogenous IkappaBalpha degradation before PA administration, and then its effect on PA-inducing cell apoptosis and PGC-1alpha mRNA expression was analyzed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	148-158
22340220-9	2011	Pretreatment with MG132 to inhibit the degradation of IkappaBalpha, partially prevented the down-regulation of PGC-1alpha mRNA expression after 12-hour PA treatment in accordance with the decrease of PA induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	54-66
22340220-9	2011	Pretreatment with MG132 to inhibit the degradation of IkappaBalpha, partially prevented the down-regulation of PGC-1alpha mRNA expression after 12-hour PA treatment in accordance with the decrease of PA induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	111-121
21751234-4	2011	HDAC inhibition reduced the cleaved caspases 3, 6, 9, PARP, and TUNEL positive ESCs, which were abrogated with MG132 (0.5  micromol/L), a specific proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	poly (ADP-ribose) polymerase family, member 1	Mus musculus	54-58
21877197-8	2011	Treatment with proteasome inhibitor MG132 prevented CK18 degradation and increased CK18 protein indicating translational regulation of CK18.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	keratin 18	Homo sapiens	52-56
21877197-8	2011	Treatment with proteasome inhibitor MG132 prevented CK18 degradation and increased CK18 protein indicating translational regulation of CK18.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	keratin 18	Homo sapiens	83-87
21877197-8	2011	Treatment with proteasome inhibitor MG132 prevented CK18 degradation and increased CK18 protein indicating translational regulation of CK18.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	keratin 18	Homo sapiens	83-87
21751234-6	2011	HDAC inhibition increases the up-regulation of GATA4, MEF2C, Nkx2.5, cardiac actin, and alpha-SMA mRNA and protein levels that were abrogated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	GATA binding protein 4	Mus musculus	47-52
21751234-6	2011	HDAC inhibition increases the up-regulation of GATA4, MEF2C, Nkx2.5, cardiac actin, and alpha-SMA mRNA and protein levels that were abrogated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	myocyte enhancer factor 2C	Mus musculus	54-59
21751234-6	2011	HDAC inhibition increases the up-regulation of GATA4, MEF2C, Nkx2.5, cardiac actin, and alpha-SMA mRNA and protein levels that were abrogated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	NK2 homeobox 5	Mus musculus	61-67
21751234-6	2011	HDAC inhibition increases the up-regulation of GATA4, MEF2C, Nkx2.5, cardiac actin, and alpha-SMA mRNA and protein levels that were abrogated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	actin alpha 2, smooth muscle, aorta	Mus musculus	88-97
21751234-8	2011	Notably, HDAC inhibitors led to noticeable HDAC4 degradation, which was effectively prevented by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	histone deacetylase 4	Mus musculus	43-48
21751234-9	2011	Luciferase assay demonstrates an activation of MEF2 cardiac transcriptional factor by HDAC inhibition, which was repressed by MG132, revealing that the degradation of HDAC4 allows for the activation of MEF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	myocyte enhancer factor 2C	Mus musculus	47-51
21751234-9	2011	Luciferase assay demonstrates an activation of MEF2 cardiac transcriptional factor by HDAC inhibition, which was repressed by MG132, revealing that the degradation of HDAC4 allows for the activation of MEF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	histone deacetylase 4	Mus musculus	167-172
21751234-9	2011	Luciferase assay demonstrates an activation of MEF2 cardiac transcriptional factor by HDAC inhibition, which was repressed by MG132, revealing that the degradation of HDAC4 allows for the activation of MEF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	myocyte enhancer factor 2C	Mus musculus	202-206
22031102-4	2011	Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	47-50
21835786-6	2011	Additionally, ORF61 was shown to be partially colocalized with activated IRF3 in the nucleus upon treatment with MG132, an inhibitor of proteasomes, and the direct interaction between ORF61 and activated IRF3 was confirmed by a coimmunoprecipitation assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	ubiquitin E3 ligase ICP0	Human alphaherpesvirus 3	14-19
21835786-6	2011	Additionally, ORF61 was shown to be partially colocalized with activated IRF3 in the nucleus upon treatment with MG132, an inhibitor of proteasomes, and the direct interaction between ORF61 and activated IRF3 was confirmed by a coimmunoprecipitation assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	interferon regulatory factor 3	Homo sapiens	73-77
21835786-6	2011	Additionally, ORF61 was shown to be partially colocalized with activated IRF3 in the nucleus upon treatment with MG132, an inhibitor of proteasomes, and the direct interaction between ORF61 and activated IRF3 was confirmed by a coimmunoprecipitation assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	ubiquitin E3 ligase ICP0	Human alphaherpesvirus 3	184-189
21835786-6	2011	Additionally, ORF61 was shown to be partially colocalized with activated IRF3 in the nucleus upon treatment with MG132, an inhibitor of proteasomes, and the direct interaction between ORF61 and activated IRF3 was confirmed by a coimmunoprecipitation assay.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	interferon regulatory factor 3	Homo sapiens	204-208
22034875-4	2011	RESULTS: We found that Cas-/- mouse embryonic fibroblasts (MEFs), as well as empty vector-transfected Cas-/- MEFs (Cas-/- (EV)) are significantly resistant to cell death induced by proteasome inhibitors, such as MG132 and Bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	breast cancer anti-estrogen resistance 1	Mus musculus	23-26
22034875-4	2011	RESULTS: We found that Cas-/- mouse embryonic fibroblasts (MEFs), as well as empty vector-transfected Cas-/- MEFs (Cas-/- (EV)) are significantly resistant to cell death induced by proteasome inhibitors, such as MG132 and Bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	breast cancer anti-estrogen resistance 1	Mus musculus	102-105
22034875-4	2011	RESULTS: We found that Cas-/- mouse embryonic fibroblasts (MEFs), as well as empty vector-transfected Cas-/- MEFs (Cas-/- (EV)) are significantly resistant to cell death induced by proteasome inhibitors, such as MG132 and Bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	breast cancer anti-estrogen resistance 1	Mus musculus	102-105
22034875-5	2011	As expected, wild-type MEFs (WT) and Cas-/- MEFs reconstituted with full-length Cas (Cas-FL) were sensitive to MG132- and Bortezomib-induced apoptosis that involved activation of a caspase-cascade, including Caspase-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	breast cancer anti-estrogen resistance 1	Mus musculus	37-40
22034875-5	2011	As expected, wild-type MEFs (WT) and Cas-/- MEFs reconstituted with full-length Cas (Cas-FL) were sensitive to MG132- and Bortezomib-induced apoptosis that involved activation of a caspase-cascade, including Caspase-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	breast cancer anti-estrogen resistance 1	Mus musculus	80-83
22034875-5	2011	As expected, wild-type MEFs (WT) and Cas-/- MEFs reconstituted with full-length Cas (Cas-FL) were sensitive to MG132- and Bortezomib-induced apoptosis that involved activation of a caspase-cascade, including Caspase-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	breast cancer anti-estrogen resistance 1	Mus musculus	85-91
22034875-6	2011	Cas-CT generation was not required for MG132-induced cell death, since expression of cleavage-resistant Cas mutants effectively increased sensitivity of Cas-/- MEFs to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	breast cancer anti-estrogen resistance 1	Mus musculus	104-107
22034875-6	2011	Cas-CT generation was not required for MG132-induced cell death, since expression of cleavage-resistant Cas mutants effectively increased sensitivity of Cas-/- MEFs to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	breast cancer anti-estrogen resistance 1	Mus musculus	104-107
22034875-8	2011	Interestingly, however, MG132 or Bortezomib treatment resulted in activation of autophagy in cells that lacked Cas, but not in cells that expressed Cas.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	breast cancer anti-estrogen resistance 1	Mus musculus	111-114
22034875-9	2011	Furthermore, autophagy was found to play a protective role in Cas-deficient cells, as inhibition of autophagy either by chemical or genetic means enhanced MG132-induced apoptosis in Cas-/- (EV) cells, but not in Cas-FL cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	breast cancer anti-estrogen resistance 1	Mus musculus	62-65
22034875-9	2011	Furthermore, autophagy was found to play a protective role in Cas-deficient cells, as inhibition of autophagy either by chemical or genetic means enhanced MG132-induced apoptosis in Cas-/- (EV) cells, but not in Cas-FL cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	breast cancer anti-estrogen resistance 1	Mus musculus	182-185
22034875-9	2011	Furthermore, autophagy was found to play a protective role in Cas-deficient cells, as inhibition of autophagy either by chemical or genetic means enhanced MG132-induced apoptosis in Cas-/- (EV) cells, but not in Cas-FL cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	breast cancer anti-estrogen resistance 1	Mus musculus	182-185
21924340-12	2011	The proteasome inhibitor, MG 132, blocked Gastrodia elata-mediated suppression of mutant Htt aggregations.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	huntingtin	Rattus norvegicus	89-92
22031102-4	2011	Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cyclin dependent kinase inhibitor 1A	Homo sapiens	85-88
22031102-4	2011	Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cyclin dependent kinase inhibitor 1A	Homo sapiens	89-93
22031102-4	2011	Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	97-100
21812426-4	2011	Meanwhile, proteasome inhibitor MG132 but not lysosome inhibitor chloroquine could restore Her2/neu and polyubiquitination of Her2/neu was augmented during emodin AMAD treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	91-99
21978374-9	2011	Co-treatment with protein synthesis inhibitor cycloheximide or proteasome inhibitor MG132 revealed that depletion of ERalpha by WA is post-translational, due to proteasome-dependent ERalpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	estrogen receptor 1	Homo sapiens	117-124
21812426-4	2011	Meanwhile, proteasome inhibitor MG132 but not lysosome inhibitor chloroquine could restore Her2/neu and polyubiquitination of Her2/neu was augmented during emodin AMAD treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	126-134
21706477-5	2011	By immunofluorescence staining, RPL41 induced ATF4 relocation from nuclei to cytoplasm, where ATF4 co-stained with a proteasome marker; the RPL41-induced ATF4 relocation and degradation were blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	ribosomal protein L41	Homo sapiens	32-37
21941087-8	2011	We found that FoxM1 knockdown sensitized the human cancer cells to apoptotic cell death induced by proteasome inhibitors, such as, MG132, bortezomib and thiostrepton, while it did not affect the levels of autophagy following treatment with these drugs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	forkhead box M1	Homo sapiens	14-19
21868755-11	2011	Proteasome inhibitor MG132 reversed the effects of GSK3 inhibition and increased c-FLIP ubiquitination, confirming that c-FLIP attenuation was mediated by proteasomal turnover as expected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	CASP8 and FADD like apoptosis regulator	Homo sapiens	81-87
21868755-11	2011	Proteasome inhibitor MG132 reversed the effects of GSK3 inhibition and increased c-FLIP ubiquitination, confirming that c-FLIP attenuation was mediated by proteasomal turnover as expected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	CASP8 and FADD like apoptosis regulator	Homo sapiens	120-126
21725586-6	2011	The proteasome inhibitor MG-132 increased the level of both A3G and Vif expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	60-63
21725586-6	2011	The proteasome inhibitor MG-132 increased the level of both A3G and Vif expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	Vif	Human immunodeficiency virus 1	68-71
21618595-10	2011	Consistent with these findings, hepaCAM decreased c-Myc stability by increasing the proportion of c-Myc phosphorylation on T58 which can be abrogated by a proteasomal inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-183	hepatic and glial cell adhesion molecule	Homo sapiens	32-39
21618595-10	2011	Consistent with these findings, hepaCAM decreased c-Myc stability by increasing the proportion of c-Myc phosphorylation on T58 which can be abrogated by a proteasomal inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-183	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	50-55
21618595-10	2011	Consistent with these findings, hepaCAM decreased c-Myc stability by increasing the proportion of c-Myc phosphorylation on T58 which can be abrogated by a proteasomal inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-183	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	98-103
21706477-5	2011	By immunofluorescence staining, RPL41 induced ATF4 relocation from nuclei to cytoplasm, where ATF4 co-stained with a proteasome marker; the RPL41-induced ATF4 relocation and degradation were blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	activating transcription factor 4	Homo sapiens	46-50
21706477-5	2011	By immunofluorescence staining, RPL41 induced ATF4 relocation from nuclei to cytoplasm, where ATF4 co-stained with a proteasome marker; the RPL41-induced ATF4 relocation and degradation were blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	activating transcription factor 4	Homo sapiens	94-98
21706477-5	2011	By immunofluorescence staining, RPL41 induced ATF4 relocation from nuclei to cytoplasm, where ATF4 co-stained with a proteasome marker; the RPL41-induced ATF4 relocation and degradation were blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	ribosomal protein L41	Homo sapiens	140-145
21706477-5	2011	By immunofluorescence staining, RPL41 induced ATF4 relocation from nuclei to cytoplasm, where ATF4 co-stained with a proteasome marker; the RPL41-induced ATF4 relocation and degradation were blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	activating transcription factor 4	Homo sapiens	94-98
21832068-6	2011	CRAG knockdown by siRNA or expression of a dominant negative mutant of CRAG significantly attenuated the c-Fos activation triggered by either polyQ or the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	ArfGAP with GTPase domain, ankyrin repeat and PH domain 3	Mus musculus	0-4
21832068-6	2011	CRAG knockdown by siRNA or expression of a dominant negative mutant of CRAG significantly attenuated the c-Fos activation triggered by either polyQ or the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	ArfGAP with GTPase domain, ankyrin repeat and PH domain 3	Mus musculus	71-75
21832068-6	2011	CRAG knockdown by siRNA or expression of a dominant negative mutant of CRAG significantly attenuated the c-Fos activation triggered by either polyQ or the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	FBJ osteosarcoma oncogene	Mus musculus	105-110
21832068-7	2011	Importantly, c-Fos expression partially rescued the enhanced cytotoxicity of CRAG knockdown in polyQ-expressing or MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	FBJ osteosarcoma oncogene	Mus musculus	13-18
21832068-7	2011	Importantly, c-Fos expression partially rescued the enhanced cytotoxicity of CRAG knockdown in polyQ-expressing or MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	ArfGAP with GTPase domain, ankyrin repeat and PH domain 3	Mus musculus	77-81
21712074-7	2011	In addition, inhibition of axonal transport by colchicine and inhibition of proteasomal activity by MG132 significantly prevented the decrease in orexin immunoreactivity by tunicamycin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	hypocretin neuropeptide precursor	Homo sapiens	146-152
21778238-4	2011	In normal human lung fibroblasts, cigarette smoke extract (CSE) caused cell death, accompanying degradation of total and phosphorylated Akt (p-Akt), which was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	AKT serine/threonine kinase 1	Homo sapiens	136-139
21778238-4	2011	In normal human lung fibroblasts, cigarette smoke extract (CSE) caused cell death, accompanying degradation of total and phosphorylated Akt (p-Akt), which was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	AKT serine/threonine kinase 1	Homo sapiens	143-146
22019639-3	2011	We used the proteasome inhibitor MG132 to show that proteolysis of Arabidopsis RETINOBLASTOMA-RELATED 1 (AtRBR1) and three E2Fs is mediated by the proteasome pathway during sucrose starvation in Arabidopsis suspension MM2d cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	retinoblastoma-related 1	Arabidopsis thaliana	105-111
21374733-8	2011	Interestingly, treatment of MG132 restored Mdm2 expression to the steady-state level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	MDM2 proto-oncogene	Homo sapiens	43-47
21929909-8	2011	RESULTS: Low levels of AR were demonstrable in alpha(2)beta(1)(hi) cells following inhibition of the proteasome using MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	androgen receptor	Homo sapiens	23-25
21723853-7	2011	In the presence of a proteasome inhibitor, MG132, the hyperoxia-mediated degradation of HIF-1alpha was deterred and hydroxylated HIF-1alpha was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	hypoxia inducible factor 1 subunit alpha	Homo sapiens	88-98
21723853-7	2011	In the presence of a proteasome inhibitor, MG132, the hyperoxia-mediated degradation of HIF-1alpha was deterred and hydroxylated HIF-1alpha was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	hypoxia inducible factor 1 subunit alpha	Homo sapiens	129-139
21620964-9	2011	Furthermore, other NF-kappaB inhibitors, such as pyrrolidine dithiocarbamate (PDTC) and MG132, also increased HO-1 mRNA and protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	heme oxygenase 1	Homo sapiens	110-114
21299413-5	2011	The inhibition of proteasome activity by proteasome inhibitor MG132 showed increase in protein levels of endogenous NANOG in a dose-dependent manner in human ESCs (hESCS).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	Nanog homeobox	Homo sapiens	116-121
21864408-9	2011	We treated the cells with proteasome inhibitor MG-132 and found that p21 may be degraded in the proteasome to regulate protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	H3 histone pseudogene 16	Homo sapiens	69-72
21700708-8	2011	Proteasome inhibitors, MG132 and lactacystin, blocked the NO donor-induced reduction in IRS-2 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	insulin receptor substrate 2	Homo sapiens	88-93
21299413-9	2011	Pretreatment of hESCs with proteasome inhibitor MG132 inhibits NANOG protein degradation and extends its half-life.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	Nanog homeobox	Homo sapiens	63-68
21843349-9	2011	RESULTS: In the present study, we showed that the proteasome inhibitor MG132 significantly inhibited IkappaBalpha degradation thus preventing NFkappaB activation in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	101-113
21843349-9	2011	RESULTS: In the present study, we showed that the proteasome inhibitor MG132 significantly inhibited IkappaBalpha degradation thus preventing NFkappaB activation in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	142-150
21843349-10	2011	MG132 preserved muscle and myofiber cross-sectional area by downregulating the muscle-specific ubiquitin ligases atrogin-1/MAFbx and MuRF-1 mRNA in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	F-box protein 32	Mus musculus	123-128
21843349-10	2011	MG132 preserved muscle and myofiber cross-sectional area by downregulating the muscle-specific ubiquitin ligases atrogin-1/MAFbx and MuRF-1 mRNA in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tripartite motif-containing 63	Mus musculus	133-139
21733854-6	2011	The decreased PGC-1alpha protein level was abolished by MG132, a potent proteasome inhibitor, suggesting that PGC-1alpha is degraded through the ubiquitin-proteasome pathway upon UV-irradiation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	PPARG coactivator 1 alpha	Homo sapiens	14-24
21646357-5	2011	Cell surface expression of G50C and G50A was rescued upon MG132 treatment as well as cyclosporine A, but not by FK506 or bile acids, suggesting that Gly(50) is involved in hASBT folding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	solute carrier family 10 member 2	Homo sapiens	172-177
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21737065-4	2011	Inhibition of endogenously expressed nNOS by 7-NI and ARR17477 enhanced the toxicity of MPP(+) and MG-132 in N1E-115 cells, whereas in transfected SH-SY5Y cells overexpressing nNOS, ARR17477 and 7-NI protected against MPP(+)- and MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	230-236	nitric oxide synthase 1, neuronal	Mus musculus	37-41
21733854-6	2011	The decreased PGC-1alpha protein level was abolished by MG132, a potent proteasome inhibitor, suggesting that PGC-1alpha is degraded through the ubiquitin-proteasome pathway upon UV-irradiation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	PPARG coactivator 1 alpha	Homo sapiens	110-120
21819345-8	2011	Goat testicular lysates spiked with recombinant human AIRE exhibited augmented cyclin B2 degradation in the presence of protease inhibitors, which was inhibited by MG-132, indicating the operation of proteasomal pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-170	autoimmune regulator	Homo sapiens	54-58
21819345-8	2011	Goat testicular lysates spiked with recombinant human AIRE exhibited augmented cyclin B2 degradation in the presence of protease inhibitors, which was inhibited by MG-132, indicating the operation of proteasomal pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-170	cyclin B2	Homo sapiens	79-88
21775096-10	2011	The MG-132-induced apoptosis may involve downregulation of E3 ubiquitin ligase, and upregulation of Grp78 and caspase-12.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-10	Cbl proto-oncogene like 2	Homo sapiens	59-78
21412219-9	2011	WT mice administered MG-132 (a proteasomal inhibitor of the N-end rule pathway) resulted in increased renal RGS4 protein and in an inhibition of renal dysfunction after IRI in WT but not in knockout mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	regulator of G-protein signaling 4	Mus musculus	108-112
21775096-10	2011	The MG-132-induced apoptosis may involve downregulation of E3 ubiquitin ligase, and upregulation of Grp78 and caspase-12.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-10	heat shock protein family A (Hsp70) member 5	Homo sapiens	100-105
21520056-9	2011	An increase in protein ubiquitination by Abeta(25-35), but not Abeta(35-25), treatment was examined, and Abeta-inhibited HSP90 and TERT protein expression and telomerase activity was reversed by adding proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	heat shock protein 90 alpha family class A member 1	Homo sapiens	121-126
21569124-4	2011	Our data show that cytochalasin B, LY294002, wortmannin, nocodazole, MG132 and XVA143 inhibitors reduced LVS uptake by &gt;50% in these assays without having significant cytotoxic effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	lacking vigorous sperm	Mus musculus	105-108
21525883-8	2011	The TRP-2 downregulation caused by A(3)B(5) may occur through proteasomal degradation because the A(3)B(5)-induced TRP-2 downregulation was inhibited by the ubiquitination inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	183-189	dopachrome tautomerase	Homo sapiens	4-9
21525883-8	2011	The TRP-2 downregulation caused by A(3)B(5) may occur through proteasomal degradation because the A(3)B(5)-induced TRP-2 downregulation was inhibited by the ubiquitination inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	183-189	dopachrome tautomerase	Homo sapiens	115-120
21477582-6	2011	The induction of UBE2M by Gem was accompanied by a reduction in p27(Kip1) protein levels, which could be restored by silencing UBE2M expression with siRNA or by treating cells with the proteasome inhibitor MG132, indicating that UBE2M mediates Gem-induced p27(Kip1) protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	ubiquitin conjugating enzyme E2 M	Homo sapiens	17-22
21576240-8	2011	Furthermore, inhibition of hypoxia-induced HIF-1alpha protein accumulation by AR inhibition was abolished in the presence of MG132, a potent inhibitor of the 26 S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	aldo-keto reductase family 1 member B	Homo sapiens	78-80
21627972-0	2011	Inhibition of NF-kappaB by MG132 through ER stress-mediated induction of LAP and LIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	LAP	Homo sapiens	73-76
21627972-0	2011	Inhibition of NF-kappaB by MG132 through ER stress-mediated induction of LAP and LIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	SMG1 nonsense mediated mRNA decay associated PI3K related kinase	Homo sapiens	81-84
21627972-4	2011	Through ER stress, MG132 up-regulated C/EBPbeta mRNA transiently and caused sustained accumulation of its translational products liver activating protein (LAP) and liver-enriched inhibitory protein (LIP), both of which were identified as suppressors of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	CCAAT enhancer binding protein beta	Homo sapiens	38-47
21627972-4	2011	Through ER stress, MG132 up-regulated C/EBPbeta mRNA transiently and caused sustained accumulation of its translational products liver activating protein (LAP) and liver-enriched inhibitory protein (LIP), both of which were identified as suppressors of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	LAP	Homo sapiens	155-158
21627972-4	2011	Through ER stress, MG132 up-regulated C/EBPbeta mRNA transiently and caused sustained accumulation of its translational products liver activating protein (LAP) and liver-enriched inhibitory protein (LIP), both of which were identified as suppressors of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	SMG1 nonsense mediated mRNA decay associated PI3K related kinase	Homo sapiens	164-197
21627972-4	2011	Through ER stress, MG132 up-regulated C/EBPbeta mRNA transiently and caused sustained accumulation of its translational products liver activating protein (LAP) and liver-enriched inhibitory protein (LIP), both of which were identified as suppressors of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	SMG1 nonsense mediated mRNA decay associated PI3K related kinase	Homo sapiens	199-202
21750559-9	2011	When cells were treated with MG-132, a proteasome inhibitor, Mcl-1 protein level increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	61-66
21477582-6	2011	The induction of UBE2M by Gem was accompanied by a reduction in p27(Kip1) protein levels, which could be restored by silencing UBE2M expression with siRNA or by treating cells with the proteasome inhibitor MG132, indicating that UBE2M mediates Gem-induced p27(Kip1) protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	cyclin dependent kinase inhibitor 1B	Homo sapiens	68-72
21477582-6	2011	The induction of UBE2M by Gem was accompanied by a reduction in p27(Kip1) protein levels, which could be restored by silencing UBE2M expression with siRNA or by treating cells with the proteasome inhibitor MG132, indicating that UBE2M mediates Gem-induced p27(Kip1) protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	interferon alpha inducible protein 27	Homo sapiens	256-259
21477582-6	2011	The induction of UBE2M by Gem was accompanied by a reduction in p27(Kip1) protein levels, which could be restored by silencing UBE2M expression with siRNA or by treating cells with the proteasome inhibitor MG132, indicating that UBE2M mediates Gem-induced p27(Kip1) protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	cyclin dependent kinase inhibitor 1B	Homo sapiens	260-264
21062782-10	2011	Only MG132 was able to rescue their steady-state levels, suggesting that B4GALT1- and ST6GAL1-induced degradation are likely the consequence of an accumulation in the endoplasmic reticulum (ER), followed by a retrotranslocation into the cytosol and proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	5-10	ST6 beta-galactoside alpha-2,6-sialyltransferase 1	Homo sapiens	86-93
21062782-10	2011	Only MG132 was able to rescue their steady-state levels, suggesting that B4GALT1- and ST6GAL1-induced degradation are likely the consequence of an accumulation in the endoplasmic reticulum (ER), followed by a retrotranslocation into the cytosol and proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	5-10	beta-1,4-galactosyltransferase 1	Homo sapiens	73-80
21623689-3	2011	The 9,10-PQ-mediated CHOP induction was strengthened by a proteasome inhibitor (MG132) and the MG132-induced cell sensitization to the 9,10-PQ toxicity was abolished by a ROS inhibitor, suggesting that ROS generation and consequent proteasomal dysfunction are responsible for the CHOP up-regulation caused by 9,10-PQ.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	DNA-damage inducible transcript 3	Rattus norvegicus	280-284
21554318-8	2011	Moreover, in muscle C2C12 cells mutant SOD1 remains soluble even when proteasome is inhibited with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	superoxide dismutase 1, soluble	Mus musculus	39-43
21561860-9	2011	Importantly, we show that inhibition of Bim degradation by the proteasome inhibitor MG132 sensitized resistant OV433 cells to cisplatin-induced death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	BCL2 like 11	Homo sapiens	40-43
21866623-4	2011	Constitutively-active RhoA nude mice models were established and treated with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	ras homolog family member A	Mus musculus	22-26
21866623-5	2011	The effect of RhoA and MG132 on expression of HIF-1alpha, VEGF and CD31 were detected by immunohistochemistry.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	hypoxia inducible factor 1, alpha subunit	Mus musculus	46-56
21866623-5	2011	The effect of RhoA and MG132 on expression of HIF-1alpha, VEGF and CD31 were detected by immunohistochemistry.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	vascular endothelial growth factor A	Mus musculus	58-62
21866623-5	2011	The effect of RhoA and MG132 on expression of HIF-1alpha, VEGF and CD31 were detected by immunohistochemistry.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	platelet/endothelial cell adhesion molecule 1	Mus musculus	67-71
21866623-6	2011	RESULTS: Cell line of stable-transfected constitutively-active RhoA was established and constitutively-active RhoA could stimulate secretion of VEGF but MG132 inhibited that.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	ras homolog family member A	Mus musculus	63-67
21866623-6	2011	RESULTS: Cell line of stable-transfected constitutively-active RhoA was established and constitutively-active RhoA could stimulate secretion of VEGF but MG132 inhibited that.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	ras homolog family member A	Mus musculus	110-114
21866623-8	2011	Constitutively-active RhoA could promote protein of HIF-1alpha, VEGF and CD31 but MG132 inhibited the function of RhoA (P &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	ras homolog family member A	Mus musculus	114-118
21866623-9	2011	CONCLUSION: Our studies indicates that MG132 could affect angiogenesis of tumors through inhibition the regulating function of RhoA on HIF-1alpha, VEGF and CD31.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	ras homolog family member A	Mus musculus	127-131
21866623-9	2011	CONCLUSION: Our studies indicates that MG132 could affect angiogenesis of tumors through inhibition the regulating function of RhoA on HIF-1alpha, VEGF and CD31.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	hypoxia inducible factor 1, alpha subunit	Mus musculus	135-145
21866623-9	2011	CONCLUSION: Our studies indicates that MG132 could affect angiogenesis of tumors through inhibition the regulating function of RhoA on HIF-1alpha, VEGF and CD31.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	vascular endothelial growth factor A	Mus musculus	147-151
21866623-9	2011	CONCLUSION: Our studies indicates that MG132 could affect angiogenesis of tumors through inhibition the regulating function of RhoA on HIF-1alpha, VEGF and CD31.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	platelet/endothelial cell adhesion molecule 1	Mus musculus	156-160
21620381-0	2011	MG132 enhances neurite outgrowth in neurons overexpressing mutant TAR DNA-binding protein-43 via increase of HO-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TAR DNA binding protein	Homo sapiens	66-92
21620381-0	2011	MG132 enhances neurite outgrowth in neurons overexpressing mutant TAR DNA-binding protein-43 via increase of HO-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heme oxygenase 1	Homo sapiens	109-113
21620381-3	2011	Subsequently, we tested the effect of MG132 on the mutant TDP-43 cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	TAR DNA binding protein	Homo sapiens	58-64
21620381-5	2011	Heme oxygenase-1 (HO-1) known as antioxidase was restored by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	heme oxygenase 1	Homo sapiens	0-16
21620381-5	2011	Heme oxygenase-1 (HO-1) known as antioxidase was restored by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	heme oxygenase 1	Homo sapiens	18-22
21620381-8	2011	However, MG132 increased the expression of HO-1 independent of the Nrf2 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	heme oxygenase 1	Homo sapiens	43-47
21463260-9	2011	Lastly, the proteasome inhibitor (MG132) rescues JDP2 degradation following cycloheximide treatment and increases the expression of the JDP2 phospho-mimetic T148E mutant.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	Jun dimerization protein 2	Homo sapiens	49-53
21540189-7	2011	GPER is ubiquitinated at the cell surface, exhibits a short half-life (t1/2;) &lt;1 h), and is protected from degradation by the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	G protein-coupled estrogen receptor 1	Homo sapiens	0-4
21693764-3	2011	To better understand the relationship between SUMO and protein degradation by the proteasome, we performed a quantitative proteomic analysis of SUMO-2 substrates after short- and long-term inhibition of the proteasome with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	223-228	small ubiquitin like modifier 2	Homo sapiens	144-150
21693764-4	2011	Comparisons with changes to the SUMO-2 conjugate subproteome in response to heat stress revealed qualitative and quantitative parallels between both conditions; however, in contrast to heat stress, the MG132-triggered increase in SUMO-2 conjugation depended strictly on protein synthesis, implying that the accumulation of newly synthesized, misfolded proteins destined for degradation by the proteasome triggered the SUMO conjugation response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	small ubiquitin like modifier 2	Homo sapiens	32-38
21693764-4	2011	Comparisons with changes to the SUMO-2 conjugate subproteome in response to heat stress revealed qualitative and quantitative parallels between both conditions; however, in contrast to heat stress, the MG132-triggered increase in SUMO-2 conjugation depended strictly on protein synthesis, implying that the accumulation of newly synthesized, misfolded proteins destined for degradation by the proteasome triggered the SUMO conjugation response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	small ubiquitin like modifier 2	Homo sapiens	230-236
21463260-9	2011	Lastly, the proteasome inhibitor (MG132) rescues JDP2 degradation following cycloheximide treatment and increases the expression of the JDP2 phospho-mimetic T148E mutant.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	Jun dimerization protein 2	Homo sapiens	136-140
21441465-8	2011	Lastly, down-regulation of ADAM10 using siRNA enhanced the growth-suppressing effects mediated by the proteasome inhibitors MG132 and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	ADAM metallopeptidase domain 10	Homo sapiens	27-33
21430051-6	2011	While loss of PML-NBs in response to Us3 expression was prevented by the proteasome inhibitor MG132, Us3-mediated degradation of PML was not observed in infected cells or in transfected cells expressing enhanced green fluorescent protein (EGFP)-tagged PML isoform IV.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	tegument protein	Human alphaherpesvirus 2	37-40
21619452-10	2011	Inhibition of proteosome function with MG-132 reversed the inhibitory effect of cAMP on p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	tumor protein p53	Homo sapiens	88-91
21411500-4	2011	DATS-mediated decline in XIAP protein level was partially reversible in the presence of proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	X-linked inhibitor of apoptosis	Homo sapiens	25-29
21811429-0	2011	Up-regulation of the DR5 expression by proteasome inhibitor MG132 augments TRAIL-induced apoptosis in soft tissue sarcoma cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	TNF receptor superfamily member 10b	Homo sapiens	21-24
21811429-0	2011	Up-regulation of the DR5 expression by proteasome inhibitor MG132 augments TRAIL-induced apoptosis in soft tissue sarcoma cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	TNF superfamily member 10	Homo sapiens	75-80
21811429-7	2011	Co-incubation of cells with TRAIL and a proteasome inhibitor, MG132, augmented the apoptotic effect of TRAIL in both TRAIL-sensitive and TRAIL-resistant cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	TNF superfamily member 10	Homo sapiens	28-33
21811429-7	2011	Co-incubation of cells with TRAIL and a proteasome inhibitor, MG132, augmented the apoptotic effect of TRAIL in both TRAIL-sensitive and TRAIL-resistant cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	TNF superfamily member 10	Homo sapiens	103-108
21811429-7	2011	Co-incubation of cells with TRAIL and a proteasome inhibitor, MG132, augmented the apoptotic effect of TRAIL in both TRAIL-sensitive and TRAIL-resistant cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	TNF superfamily member 10	Homo sapiens	103-108
21811429-7	2011	Co-incubation of cells with TRAIL and a proteasome inhibitor, MG132, augmented the apoptotic effect of TRAIL in both TRAIL-sensitive and TRAIL-resistant cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	TNF superfamily member 10	Homo sapiens	103-108
21811429-8	2011	This effect was due to up-regulation of TRAIL receptors and members of the pro-apoptotic BCL-2 family by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	TNF superfamily member 10	Homo sapiens	40-45
21811429-8	2011	This effect was due to up-regulation of TRAIL receptors and members of the pro-apoptotic BCL-2 family by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	BCL2 apoptosis regulator	Homo sapiens	89-94
21811429-9	2011	CONCLUSION: These data show that combining TRAIL with MG132 enhances apoptosis and overcomes TRAIL resistance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	TNF superfamily member 10	Homo sapiens	93-98
21310902-6	2011	On stress induction, HTRA1 and VEGFA were upregulated in human fetal RPE cells treated by tunicamycin and dithiothreitol, but reduced after treatment by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	HtrA serine peptidase 1	Homo sapiens	21-26
21310902-6	2011	On stress induction, HTRA1 and VEGFA were upregulated in human fetal RPE cells treated by tunicamycin and dithiothreitol, but reduced after treatment by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	vascular endothelial growth factor A	Homo sapiens	31-36
21430051-6	2011	While loss of PML-NBs in response to Us3 expression was prevented by the proteasome inhibitor MG132, Us3-mediated degradation of PML was not observed in infected cells or in transfected cells expressing enhanced green fluorescent protein (EGFP)-tagged PML isoform IV.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	PML nuclear body scaffold	Homo sapiens	14-17
21399877-0	2011	Proteasome inhibition by MG132 induces growth inhibition and death of human pulmonary fibroblast cells in a caspase-independent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	caspase 8	Homo sapiens	108-115
21399877-5	2011	However, all the tested caspase inhibitors intensified HPF growth inhibition by MG132 and caspase-9 inhibitor also enhanced cell death and MMP ( Psim) loss.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	caspase 8	Homo sapiens	24-31
21399877-6	2011	Moreover, the administration of Bcl-2 siRNA augmented HPF cell death by MG132 whereas p53, Bax, caspase-3 and -8 siRNAs did not strongly affect cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	BCL2 apoptosis regulator	Homo sapiens	32-37
21399877-8	2011	Caspase-8 and -9 inhibitors increased the number of GSH-depleted cells in MG132-treated HPF cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	caspase 8	Homo sapiens	0-16
21399877-9	2011	In conclusion, MG132 induced growth inhibition and death in HPF cells in a caspase-independent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	caspase 8	Homo sapiens	75-82
21318239-0	2011	Classical swine fever virus NS2 protein promotes interleukin-8 expression and inhibits MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	NS2	Homo sapiens	28-31
21444209-2	2011	We found that Arabidopsis retinoblastoma-related protein1 (AtRBR1) and three E2F proteins were degraded under limited sucrose conditions, while protein abundance increased in response to treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	retinoblastoma-related 1	Arabidopsis thaliana	26-57
21444209-2	2011	We found that Arabidopsis retinoblastoma-related protein1 (AtRBR1) and three E2F proteins were degraded under limited sucrose conditions, while protein abundance increased in response to treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	retinoblastoma-related 1	Arabidopsis thaliana	59-65
21270289-7	2011	Combination treatment of IFN-alpha and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	interferon alpha 1	Homo sapiens	25-34
21215737-0	2011	Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	aldo-keto reductase family 1 member C1	Homo sapiens	51-57
21215737-0	2011	Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	aldo-keto reductase family 1 member C3	Homo sapiens	59-65
21215737-0	2011	Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	aldo-keto reductase family 1 member B1	Ictalurus punctatus	67-73
21215737-0	2011	Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	aldo-keto reductase family 1 member B10	Homo sapiens	79-86
21215737-3	2011	Proteasome inhibitors bortezomib and MG-132 produce mild oxidative stress that activates Nrf2-mediated gene expression that in turn may have cytoprotective effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
21215737-5	2011	The present study investigated the effect of bortezomib and MG-132 on the expression of AKR1C1-1C4, AKR1B1, and AKR1B10 in colon cancer cell lines HT-29 and SW-480.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-66	aldo-keto reductase family 1 member C1	Homo sapiens	88-94
21215737-5	2011	The present study investigated the effect of bortezomib and MG-132 on the expression of AKR1C1-1C4, AKR1B1, and AKR1B10 in colon cancer cell lines HT-29 and SW-480.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-66	aldo-keto reductase family 1 member B1	Ictalurus punctatus	100-106
21215737-5	2011	The present study investigated the effect of bortezomib and MG-132 on the expression of AKR1C1-1C4, AKR1B1, and AKR1B10 in colon cancer cell lines HT-29 and SW-480.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-66	aldo-keto reductase family 1 member B10	Homo sapiens	112-119
21215737-12	2011	MG-132 increased mRNA amounts of AKR1C1, 1C3, 1B1, and 1B10 in a concentration-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	aldo-keto reductase family 1 member C1	Homo sapiens	33-39
21420391-0	2011	MG132 treatment attenuates cardiac remodeling and dysfunction following aortic banding in rats via the NF-kappaB/TGFbeta1 pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor, beta 1	Rattus norvegicus	113-121
21420391-11	2011	MG132 significantly inhibited NF-kappaB activity and down-regulate the levels of TGFbeta1 and Smad2 expression by 2 and still at 8 weeks (P&lt;0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor, beta 1	Rattus norvegicus	81-89
21420391-11	2011	MG132 significantly inhibited NF-kappaB activity and down-regulate the levels of TGFbeta1 and Smad2 expression by 2 and still at 8 weeks (P&lt;0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	SMAD family member 2	Rattus norvegicus	94-99
21420391-12	2011	Short- and long-term treatment with MG132 significantly attenuated hypertension-induced cardiac remodeling and dysfunction, which may be mediated by the NF-kappaB/TGFbeta1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	transforming growth factor, beta 1	Rattus norvegicus	163-171
21237244-7	2011	We also demonstrate that p27(Kip1) reduction is not due to transcriptional regulation and that the proteasome inhibitor MG132 affects p27(Kip1) degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	dynactin subunit 6	Homo sapiens	134-137
21237244-7	2011	We also demonstrate that p27(Kip1) reduction is not due to transcriptional regulation and that the proteasome inhibitor MG132 affects p27(Kip1) degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	cyclin dependent kinase inhibitor 1B	Homo sapiens	138-142
21262221-4	2011	Moreover, inducing p53 accumulation with MG132 reduced autophagic ratio, and repressed the expression and activation of NF-kappaB expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	tumor protein p53	Homo sapiens	19-22
21262221-4	2011	Moreover, inducing p53 accumulation with MG132 reduced autophagic ratio, and repressed the expression and activation of NF-kappaB expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	nuclear factor kappa B subunit 1	Homo sapiens	120-129
21320486-3	2011	MG132 treatment decreases APPL1 labeling of endosomes while the staining of the canonical early endosomes with EEA1 remains unaffected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1	Homo sapiens	26-31
21352276-6	2011	We also characterized their differential elimination from melanosomal compartments by Rab7 by utilizing a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	RAB7, member RAS oncogene family	Mus musculus	86-90
21270289-7	2011	Combination treatment of IFN-alpha and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	mitogen-activated protein kinase 3	Homo sapiens	110-114
21270289-7	2011	Combination treatment of IFN-alpha and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	mitogen-activated protein kinase 3	Homo sapiens	158-162
21270289-7	2011	Combination treatment of IFN-alpha and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	signal transducer and activator of transcription 1	Homo sapiens	164-169
21270289-7	2011	Combination treatment of IFN-alpha and the proteasome inhibitor MG-132 showed a time-dependent restoration of ERK1 protein levels and significant increase of ERK1, STAT1 and c-Jun phosphorylation in PLpro-expressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	174-179
21167122-6	2011	Treatment of 8B20 cells with the UPP inhibitors, MG132 and clasto-lactacystin-beta-lactone, led to an increase in levels of p53 while treatment with non-proteasomal inhibitors did not alter p53 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	tumor protein p53	Homo sapiens	124-127
21441410-5	2011	Mitotic slippage induced by SU6656 or geraldol was blocked by the proteasome inhibitor MG-132 and involved proteasome-dependent degradation of cyclin B1 and the mitotic checkpoint proteins budding uninhibited by benzimidazole related 1 (BubR1) and cell division cycle 20 (Cdc20) in T98G cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	BUB1 mitotic checkpoint serine/threonine kinase B	Homo sapiens	237-242
21441410-5	2011	Mitotic slippage induced by SU6656 or geraldol was blocked by the proteasome inhibitor MG-132 and involved proteasome-dependent degradation of cyclin B1 and the mitotic checkpoint proteins budding uninhibited by benzimidazole related 1 (BubR1) and cell division cycle 20 (Cdc20) in T98G cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	cell division cycle 20	Homo sapiens	272-277
21203833-0	2011	The proteasome inhibitor MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	mitogen-activated protein kinase 1	Homo sapiens	93-96
21203833-0	2011	The proteasome inhibitor MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	AKT serine/threonine kinase 1	Homo sapiens	101-104
21203833-0	2011	The proteasome inhibitor MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	mechanistic target of rapamycin kinase	Homo sapiens	105-109
21203833-5	2011	MG-132 induced reduction in ERK and Akt activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	mitogen-activated protein kinase 1	Homo sapiens	28-31
21203833-5	2011	MG-132 induced reduction in ERK and Akt activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	AKT serine/threonine kinase 1	Homo sapiens	36-39
21203833-6	2011	The transient transfection of constitutively active forms of MEK, an upstream of ERK, and Akt blocked the MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	mitogen-activated protein kinase kinase 7	Homo sapiens	61-64
21203833-6	2011	The transient transfection of constitutively active forms of MEK, an upstream of ERK, and Akt blocked the MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	mitogen-activated protein kinase 1	Homo sapiens	81-84
21203833-6	2011	The transient transfection of constitutively active forms of MEK, an upstream of ERK, and Akt blocked the MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	AKT serine/threonine kinase 1	Homo sapiens	90-93
21203833-7	2011	Similarly to down-regulation of Akt, expression levels of mTOR were inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	AKT serine/threonine kinase 1	Homo sapiens	32-35
21203833-7	2011	Similarly to down-regulation of Akt, expression levels of mTOR were inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	mechanistic target of rapamycin kinase	Homo sapiens	58-62
21203833-8	2011	Addition of rapamycin, an inhibitor of mTOR, caused stimulation of the MG-132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-77	mechanistic target of rapamycin kinase	Homo sapiens	39-43
21203833-10	2011	Overexpression of constitutively active forms of MEK and Akt blocked the MG-132-induced AIF nuclear translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-79	mitogen-activated protein kinase kinase 7	Homo sapiens	49-52
21203833-10	2011	Overexpression of constitutively active forms of MEK and Akt blocked the MG-132-induced AIF nuclear translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-79	AKT serine/threonine kinase 1	Homo sapiens	57-60
21203833-11	2011	These findings indicate that MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	mitogen-activated protein kinase 1	Homo sapiens	97-100
21203833-11	2011	These findings indicate that MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	AKT serine/threonine kinase 1	Homo sapiens	105-108
21203833-11	2011	These findings indicate that MG-132 induces AIF nuclear translocation through down-regulation of ERK and Akt/mTOR pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	mechanistic target of rapamycin kinase	Homo sapiens	109-113
21557901-9	2011	All the stimulating effects of anti-beta2GPI/beta2GPI complex (100 mg/L) on THP-1 cells were inhibited by MG-132 (5 mumol/L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	apolipoprotein H	Homo sapiens	36-44
21557901-9	2011	All the stimulating effects of anti-beta2GPI/beta2GPI complex (100 mg/L) on THP-1 cells were inhibited by MG-132 (5 mumol/L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	apolipoprotein H	Homo sapiens	45-53
21462205-5	2011	Increases in MuRF-1, MAFbx, and USP28 mRNA were largely repressed after MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	tripartite motif-containing 63	Mus musculus	13-19
21462205-5	2011	Increases in MuRF-1, MAFbx, and USP28 mRNA were largely repressed after MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	F-box protein 32	Mus musculus	21-26
21462205-5	2011	Increases in MuRF-1, MAFbx, and USP28 mRNA were largely repressed after MG132 administration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	ubiquitin specific peptidase 28	Mus musculus	32-37
21167122-9	2011	Treatment of 8B20 cells with MG132 led to an increase in the half-life of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	tumor protein p53	Homo sapiens	74-77
21167122-11	2011	In vivo studies showed that MG132 induced p53 overexpression and reduced tumor growth, suggesting an important role of p53 stabilization in controlling melanoma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	tumor protein p53	Homo sapiens	42-45
21167122-11	2011	In vivo studies showed that MG132 induced p53 overexpression and reduced tumor growth, suggesting an important role of p53 stabilization in controlling melanoma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	tumor protein p53	Homo sapiens	119-122
21067284-4	2011	Furthermore, proteasome inhibition with MG132 restored the expression of Rheb and increased mTOR activity, resulting in an increased viability of H2O2-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	Ras homolog enriched in brain	Mus musculus	73-77
21419099-7	2011	Predictably, a proteasome inhibitor, MG132, inhibited the Nutlin-induced decrease in the levels of Parp1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	poly (ADP-ribose) polymerase family, member 1	Mus musculus	99-104
21093098-5	2011	Moreover SAMe-induced reduction in Cx43 and beta-catenin was prevented by the proteasome inhibitor MG132, and was not mediated by GSK3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	gap junction protein, alpha 1	Mus musculus	35-39
21093098-5	2011	Moreover SAMe-induced reduction in Cx43 and beta-catenin was prevented by the proteasome inhibitor MG132, and was not mediated by GSK3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	catenin (cadherin associated protein), beta 1	Mus musculus	44-56
21067284-4	2011	Furthermore, proteasome inhibition with MG132 restored the expression of Rheb and increased mTOR activity, resulting in an increased viability of H2O2-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	mechanistic target of rapamycin kinase	Mus musculus	92-96
21199652-10	2011	In Caco-2/TC7 cells, the effect of hepcidin on the DMT1 protein level was completely abolished in the presence of a proteasome inhibitor (MG-132); DMT1 ubiquitination was induced by the addition of hepcidin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	hepcidin antimicrobial peptide	Homo sapiens	35-43
21242306-9	2011	MG132, a potent proteasome inhibitor and activator of ROS, markedly decreased degradation and increased nucleolar retention of NS mutants, whereas N-acetyl-L-cysteine largely prevented the effects of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	G protein nucleolar 3	Homo sapiens	127-129
21199652-10	2011	In Caco-2/TC7 cells, the effect of hepcidin on the DMT1 protein level was completely abolished in the presence of a proteasome inhibitor (MG-132); DMT1 ubiquitination was induced by the addition of hepcidin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	solute carrier family 11 member 2	Homo sapiens	51-55
21199652-10	2011	In Caco-2/TC7 cells, the effect of hepcidin on the DMT1 protein level was completely abolished in the presence of a proteasome inhibitor (MG-132); DMT1 ubiquitination was induced by the addition of hepcidin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	solute carrier family 11 member 2	Homo sapiens	147-151
21199652-10	2011	In Caco-2/TC7 cells, the effect of hepcidin on the DMT1 protein level was completely abolished in the presence of a proteasome inhibitor (MG-132); DMT1 ubiquitination was induced by the addition of hepcidin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	hepcidin antimicrobial peptide	Homo sapiens	198-206
21310827-7	2011	Addition of the proteasome inhibitor MG132 prevented the decrease of SKP2 in PKCiota silenced cells, and polyubiquitin-SKP2 was elevated after PKCiota depletion, showing that PKCiota might regulate the expression of SKP2 through the ubiquitin-proteasome pathway in suspended cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	S-phase kinase associated protein 2	Homo sapiens	69-73
21310827-7	2011	Addition of the proteasome inhibitor MG132 prevented the decrease of SKP2 in PKCiota silenced cells, and polyubiquitin-SKP2 was elevated after PKCiota depletion, showing that PKCiota might regulate the expression of SKP2 through the ubiquitin-proteasome pathway in suspended cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	protein kinase C iota	Homo sapiens	77-84
21256122-5	2011	In addition, hPc2 promotes the SUMOylation of alpha-synuclein in the presence of MG-132-induced proteasome inhibition, which consequently promotes alpha-synuclein aggregate formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	chromobox 4	Homo sapiens	13-17
21735595-11	2010	In contrast, the current state-of-the-art probe, MG132, inhibits degradation of both Wee1 and cyclin B in the same assays.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	WEE1 G2 checkpoint kinase	Homo sapiens	85-89
21256122-5	2011	In addition, hPc2 promotes the SUMOylation of alpha-synuclein in the presence of MG-132-induced proteasome inhibition, which consequently promotes alpha-synuclein aggregate formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	synuclein alpha	Homo sapiens	46-61
21252232-3	2011	Here we found that depletion of MYPT1 by siRNA led to precocious chromatid segregation when HeLa cells were arrested at metaphase by a proteasome inhibitor, MG132, or by Cdc20 depletion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	157-162	protein phosphatase 1 regulatory subunit 12A	Homo sapiens	32-37
21256122-5	2011	In addition, hPc2 promotes the SUMOylation of alpha-synuclein in the presence of MG-132-induced proteasome inhibition, which consequently promotes alpha-synuclein aggregate formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	synuclein alpha	Homo sapiens	147-162
21329675-4	2011	Co-treatment with the proteasome inhibitor MG132 or epoxomicin but not calpain inhibitor calpeptin inhibited etoposide-induced Ikaros downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	IKAROS family zinc finger 1	Homo sapiens	127-133
21418583-8	2011	MG132 in combination with resveratrol caused cell cycle blockade at G1/S transition via p27Kip1 accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1B	Homo sapiens	88-95
21233207-8	2011	Furthermore, the relative reduction of expression of Ca(V)2.2(W391A) compared with the WT channel was reversed by exposure to two proteasome inhibitors, MG132 and lactacystin, particularly in the somata.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	caveolin 2	Homo sapiens	53-59
21418583-10	2011	Resveratrol induced FOXO1 expression at the transcriptional level, while MG132 increased nuclear distribution of FOXO1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	forkhead box O1	Homo sapiens	113-118
21241714-7	2011	Increased p47phox and nitrotyrosine (NT) expressions in kidneys of DN rats were decreased after MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	NSFL1 cofactor	Rattus norvegicus	10-13
21418583-11	2011	MG132 in combination with resveratrol caused synergistic induction of p27Kip1 through increased recruitment of FOXO1 on the p27Kip1 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1B	Homo sapiens	70-77
21418583-11	2011	MG132 in combination with resveratrol caused synergistic induction of p27Kip1 through increased recruitment of FOXO1 on the p27Kip1 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	forkhead box O1	Homo sapiens	111-116
21418583-11	2011	MG132 in combination with resveratrol caused synergistic induction of p27Kip1 through increased recruitment of FOXO1 on the p27Kip1 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1B	Homo sapiens	124-131
21219885-5	2011	Consistent with this result, the application of proteasome inhibitor MG132 partly reversed HD-induced decrease of NF-M.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	neurofilament medium chain	Rattus norvegicus	114-118
21199866-6	2011	However, this substitution blocked ER exit and produced ABCB6 degradation, which was mostly reversed by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	56-61
21209077-6	2011	The agonist-induced down-regulation of RGS4 proteins was completely blocked by treatment with the proteasome inhibitors MG132 or lactacystin or high concentrations of leupeptin, indicating involvement of ubiquitin-proteasome and lysosomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	regulator of G protein signaling 4	Homo sapiens	39-43
21209077-7	2011	Polyubiquitinated RGS4 protein was observed in the presence of MG132 or the specific proteasome inhibitor lactacystin and promoted by opioid agonist.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	regulator of G protein signaling 4	Homo sapiens	18-22
21241714-8	2011	Renal mRNA and protein expressions of NF-E2 related factor 2 (Nrf2) were up-regulated by MG132 in comparison to DN alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	NFE2 like bZIP transcription factor 2	Rattus norvegicus	38-60
21241714-8	2011	Renal mRNA and protein expressions of NF-E2 related factor 2 (Nrf2) were up-regulated by MG132 in comparison to DN alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	NFE2 like bZIP transcription factor 2	Rattus norvegicus	62-66
21241714-9	2011	Decreased renal mRNA expression of superoxide dismutase 1 (SOD1), catalase (CAT) and glutathione peroxidase (GPx) in DN rats was heightened after MG132 intervention.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	superoxide dismutase 1	Rattus norvegicus	35-57
21241714-9	2011	Decreased renal mRNA expression of superoxide dismutase 1 (SOD1), catalase (CAT) and glutathione peroxidase (GPx) in DN rats was heightened after MG132 intervention.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	superoxide dismutase 1	Rattus norvegicus	59-63
21241714-9	2011	Decreased renal mRNA expression of superoxide dismutase 1 (SOD1), catalase (CAT) and glutathione peroxidase (GPx) in DN rats was heightened after MG132 intervention.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	catalase	Rattus norvegicus	66-74
21241714-9	2011	Decreased renal mRNA expression of superoxide dismutase 1 (SOD1), catalase (CAT) and glutathione peroxidase (GPx) in DN rats was heightened after MG132 intervention.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	catalase	Rattus norvegicus	76-79
21241714-10	2011	Depressed activities of renal SOD, CAT and GPx in DN rats were also improved by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	superoxide dismutase 1	Rattus norvegicus	30-33
21241714-10	2011	Depressed activities of renal SOD, CAT and GPx in DN rats were also improved by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	catalase	Rattus norvegicus	35-38
21148565-4	2011	Moreover, the ubiquitin-dependent degradation of Bcl-2 was found to be promoted after KA treatment, which could be suppressed by the proteasome inhibitor MG132 and the NO donors, sodium nitroprusside and S-nitrosoglutathione.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	BCL2 apoptosis regulator	Homo sapiens	49-54
21148565-8	2011	NS102, GSNO, sodium nitroprusside, and MG132 contribute to the survival of CA1 and CA3/DG pyramidal neurons by attenuating Bcl-2 denitrosylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	carbonic anhydrase 1	Homo sapiens	75-78
21148565-8	2011	NS102, GSNO, sodium nitroprusside, and MG132 contribute to the survival of CA1 and CA3/DG pyramidal neurons by attenuating Bcl-2 denitrosylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	carbonic anhydrase 3	Homo sapiens	83-86
21148565-8	2011	NS102, GSNO, sodium nitroprusside, and MG132 contribute to the survival of CA1 and CA3/DG pyramidal neurons by attenuating Bcl-2 denitrosylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	BCL2 apoptosis regulator	Homo sapiens	123-128
21191016-4	2011	Furthermore, depletion of a free-ubiquitin pool by the proteasome inhibitor MG132 abolished WNV endocytosis, suggesting that CBLL1 acts in concert with the ubiquitin proteasome system to mediate virus internalization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	Cbl proto-oncogene like 1	Homo sapiens	125-130
21429296-5	2011	We found that MG132 facilitated NGF-induced neurite outgrowth and potentiated the phosphorylation of the extracellular signal-regulated kinase/mitogen- activated protein kinase (ERK/MAPK) and phosphatidylinositol- 3-kinase (PI3K)/AKT pathways and TrkA receptors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	AKT serine/threonine kinase 1	Rattus norvegicus	230-233
21206980-7	2011	MG132 enhanced the expression of the TRAIL receptors DR4 and DR5, and neutralization of DR5 receptors showed a marked reduction of TRAIL-mediated apoptosis, whereas that of DR4 was a partial reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF superfamily member 10	Homo sapiens	37-42
21206980-7	2011	MG132 enhanced the expression of the TRAIL receptors DR4 and DR5, and neutralization of DR5 receptors showed a marked reduction of TRAIL-mediated apoptosis, whereas that of DR4 was a partial reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10a	Homo sapiens	53-56
21206980-7	2011	MG132 enhanced the expression of the TRAIL receptors DR4 and DR5, and neutralization of DR5 receptors showed a marked reduction of TRAIL-mediated apoptosis, whereas that of DR4 was a partial reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10b	Homo sapiens	61-64
21206980-5	2011	Furthermore, the inhibitors of caspase-3, caspase-8 and caspase-9 reduced the accelerative effect of MG132 on TRAIL-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	TNF superfamily member 10	Homo sapiens	110-115
21186403-6	2011	MG132 intensified apoptosis and PARP cleavage in PG-treated HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	collagen type XI alpha 2 chain	Homo sapiens	32-36
21206980-8	2011	MG132 also markedly reduced cellular FLICE-inhibitory protein (c-FLIP), cellular inhibitor of apoptosis protein-1 (cIAP-1), X-linked IAP (XIAP) and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	CASP8 and FADD like apoptosis regulator	Homo sapiens	63-69
21206980-3	2011	We found that the proteasome inhibitor MG132 markedly accelerated TRAIL-mediated apoptosis in OSCC cell lines HSC-2 and HSC-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	TNF superfamily member 10	Homo sapiens	66-71
21206980-8	2011	MG132 also markedly reduced cellular FLICE-inhibitory protein (c-FLIP), cellular inhibitor of apoptosis protein-1 (cIAP-1), X-linked IAP (XIAP) and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	baculoviral IAP repeat containing 2	Homo sapiens	72-113
21206980-3	2011	We found that the proteasome inhibitor MG132 markedly accelerated TRAIL-mediated apoptosis in OSCC cell lines HSC-2 and HSC-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	DnaJ heat shock protein family (Hsp40) member B7	Homo sapiens	120-125
21206980-8	2011	MG132 also markedly reduced cellular FLICE-inhibitory protein (c-FLIP), cellular inhibitor of apoptosis protein-1 (cIAP-1), X-linked IAP (XIAP) and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	baculoviral IAP repeat containing 2	Homo sapiens	115-121
21206980-4	2011	Addition of TRAIL to MG132-treated cells resulted in Bid cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF superfamily member 10	Homo sapiens	12-17
21206980-8	2011	MG132 also markedly reduced cellular FLICE-inhibitory protein (c-FLIP), cellular inhibitor of apoptosis protein-1 (cIAP-1), X-linked IAP (XIAP) and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	X-linked inhibitor of apoptosis	Homo sapiens	124-136
21206980-5	2011	Furthermore, the inhibitors of caspase-3, caspase-8 and caspase-9 reduced the accelerative effect of MG132 on TRAIL-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	caspase 3	Homo sapiens	31-40
21206980-8	2011	MG132 also markedly reduced cellular FLICE-inhibitory protein (c-FLIP), cellular inhibitor of apoptosis protein-1 (cIAP-1), X-linked IAP (XIAP) and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	X-linked inhibitor of apoptosis	Homo sapiens	138-142
21206980-5	2011	Furthermore, the inhibitors of caspase-3, caspase-8 and caspase-9 reduced the accelerative effect of MG132 on TRAIL-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	caspase 8	Homo sapiens	42-51
21206980-9	2011	Therefore, MG132 provides partial regulation of TRAIL-mediated apoptosis in OSCC cells via modulation of DR5, c-FLIP, cIAP-1, XIAP and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	TNF superfamily member 10	Homo sapiens	48-53
21206980-5	2011	Furthermore, the inhibitors of caspase-3, caspase-8 and caspase-9 reduced the accelerative effect of MG132 on TRAIL-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	caspase 9	Homo sapiens	56-65
21206980-9	2011	Therefore, MG132 provides partial regulation of TRAIL-mediated apoptosis in OSCC cells via modulation of DR5, c-FLIP, cIAP-1, XIAP and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	TNF receptor superfamily member 10b	Homo sapiens	105-108
21206980-9	2011	Therefore, MG132 provides partial regulation of TRAIL-mediated apoptosis in OSCC cells via modulation of DR5, c-FLIP, cIAP-1, XIAP and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	CASP8 and FADD like apoptosis regulator	Homo sapiens	110-116
21206980-9	2011	Therefore, MG132 provides partial regulation of TRAIL-mediated apoptosis in OSCC cells via modulation of DR5, c-FLIP, cIAP-1, XIAP and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	baculoviral IAP repeat containing 2	Homo sapiens	118-124
21206980-9	2011	Therefore, MG132 provides partial regulation of TRAIL-mediated apoptosis in OSCC cells via modulation of DR5, c-FLIP, cIAP-1, XIAP and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	X-linked inhibitor of apoptosis	Homo sapiens	126-130
21206980-10	2011	The proteasome inhibitor MG132 may therefore represent a novel strategy for overcoming resistance to TRAIL-mediated apoptosis in OSCC cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	TNF superfamily member 10	Homo sapiens	101-106
21293471-8	2011	In addition, the nuclear factor kappa B (NF-kappaB) inhibitors MG132 and PDTC completely blocked the high glucose-induced TNFalpha and MCP-1 secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	tumor necrosis factor	Rattus norvegicus	122-130
20717902-7	2011	The protease inhibitor MG132 inhibited the downregulation of AR protein which suggested that statins decreased AR protein levels by increasing AR proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	androgen receptor	Homo sapiens	61-63
20717902-7	2011	The protease inhibitor MG132 inhibited the downregulation of AR protein which suggested that statins decreased AR protein levels by increasing AR proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	androgen receptor	Homo sapiens	111-113
20717902-7	2011	The protease inhibitor MG132 inhibited the downregulation of AR protein which suggested that statins decreased AR protein levels by increasing AR proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	androgen receptor	Homo sapiens	111-113
21293471-8	2011	In addition, the nuclear factor kappa B (NF-kappaB) inhibitors MG132 and PDTC completely blocked the high glucose-induced TNFalpha and MCP-1 secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	C-C motif chemokine ligand 2	Rattus norvegicus	135-140
21094287-5	2011	Mechanically, such degradation of iNOS protein is due to ubiquitination and proteasome-dependency since it was almost completely blocked by N-benzoyloxycarbonyl-Leu-Leu-leucinal (MG132), a specific inhibitor of proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	179-184	nitric oxide synthase 2, inducible	Mus musculus	34-38
21360263-5	2011	The mechanism for PLC-gamma1-induced EpoR downregulation was analyzed by blockage of proteosomal degradation with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	phospholipase C, gamma 1	Rattus norvegicus	18-28
21360263-5	2011	The mechanism for PLC-gamma1-induced EpoR downregulation was analyzed by blockage of proteosomal degradation with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	erythropoietin receptor	Rattus norvegicus	37-41
21084425-8	2011	Specifically, treatment with MG-132 increases lifespan, enhances locomotive activity, enlarges muscle fiber diameter, reduces fibrosis, restores Akt phosphorylation and decreases apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	thymoma viral proto-oncogene 1	Mus musculus	145-148
21268072-7	2011	Furthermore, inhibition of proteasome activity by MG132 blocked GA-induced down-regulation of mutant p53, causing mutant p53 accumulation in detergent-insoluble cellular fractions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	tumor protein p53	Homo sapiens	101-104
21170508-4	2011	The BBR-induced downregulation of c-FLIP and Mcl-1 proteins were involved in proteasome dependent pathways, which was confirmed by the result that pre-treatment with the proteasome inhibitor MG132 inhibited berberine-induced downregulation of the c-FLIP and Mcl-1 proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	CASP8 and FADD like apoptosis regulator	Homo sapiens	34-40
21170508-4	2011	The BBR-induced downregulation of c-FLIP and Mcl-1 proteins were involved in proteasome dependent pathways, which was confirmed by the result that pre-treatment with the proteasome inhibitor MG132 inhibited berberine-induced downregulation of the c-FLIP and Mcl-1 proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	45-50
21170508-4	2011	The BBR-induced downregulation of c-FLIP and Mcl-1 proteins were involved in proteasome dependent pathways, which was confirmed by the result that pre-treatment with the proteasome inhibitor MG132 inhibited berberine-induced downregulation of the c-FLIP and Mcl-1 proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	CASP8 and FADD like apoptosis regulator	Homo sapiens	247-253
21170508-4	2011	The BBR-induced downregulation of c-FLIP and Mcl-1 proteins were involved in proteasome dependent pathways, which was confirmed by the result that pre-treatment with the proteasome inhibitor MG132 inhibited berberine-induced downregulation of the c-FLIP and Mcl-1 proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	191-196	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	258-263
21268072-7	2011	Furthermore, inhibition of proteasome activity by MG132 blocked GA-induced down-regulation of mutant p53, causing mutant p53 accumulation in detergent-insoluble cellular fractions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	tumor protein p53	Homo sapiens	121-124
21272366-12	2011	Caspase 8 protein expression was restored by MG-132 and IFN-gamma pretreatment, which also re-established sensitivity to rhTRAIL and agonistic DR4 antibody in SW948-TR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	caspase 8	Homo sapiens	0-9
21186355-4	2011	On treatment with the proteasomal inhibitor MG132, Cavbeta-free channels were rescued from degradation and trafficked to the plasma membrane.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	carbonic anhydrase 5B	Homo sapiens	51-58
21272366-12	2011	Caspase 8 protein expression was restored by MG-132 and IFN-gamma pretreatment, which also re-established sensitivity to rhTRAIL and agonistic DR4 antibody in SW948-TR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	major histocompatibility complex, class II, DR beta 4	Homo sapiens	143-146
21224428-4	2011	We demonstrate that bortezomib and MG132 suppress NF-kappaB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-kappaB p65 and p50 in the nucleus and inhibits NF-kappaB DNA binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	nuclear factor kappa B subunit 1	Homo sapiens	50-59
21224428-4	2011	We demonstrate that bortezomib and MG132 suppress NF-kappaB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-kappaB p65 and p50 in the nucleus and inhibits NF-kappaB DNA binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	NFKB inhibitor alpha	Homo sapiens	174-186
21224428-4	2011	We demonstrate that bortezomib and MG132 suppress NF-kappaB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-kappaB p65 and p50 in the nucleus and inhibits NF-kappaB DNA binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	NFKB inhibitor alpha	Homo sapiens	188-271
21224428-4	2011	We demonstrate that bortezomib and MG132 suppress NF-kappaB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-kappaB p65 and p50 in the nucleus and inhibits NF-kappaB DNA binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	nuclear factor kappa B subunit 1	Homo sapiens	301-310
21224428-4	2011	We demonstrate that bortezomib and MG132 suppress NF-kappaB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-kappaB p65 and p50 in the nucleus and inhibits NF-kappaB DNA binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	nuclear factor kappa B subunit 1	Homo sapiens	319-322
21224428-4	2011	We demonstrate that bortezomib and MG132 suppress NF-kappaB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IkappaBalpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-kappaB p65 and p50 in the nucleus and inhibits NF-kappaB DNA binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	nuclear factor kappa B subunit 1	Homo sapiens	301-310
21134392-7	2011	Molecular data showed that all these effects of Andro might be mediated via TGFbeta1/PHD2/HIF-1alpha pathway, as demonstrated by the transfection of TGFbeta1 overexpression vector and PHD2 siRNA, and the usage of a pharmacological MG132 inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	231-236	transforming growth factor beta 1	Homo sapiens	76-84
21134392-7	2011	Molecular data showed that all these effects of Andro might be mediated via TGFbeta1/PHD2/HIF-1alpha pathway, as demonstrated by the transfection of TGFbeta1 overexpression vector and PHD2 siRNA, and the usage of a pharmacological MG132 inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	231-236	egl-9 family hypoxia inducible factor 1	Homo sapiens	85-89
21134392-7	2011	Molecular data showed that all these effects of Andro might be mediated via TGFbeta1/PHD2/HIF-1alpha pathway, as demonstrated by the transfection of TGFbeta1 overexpression vector and PHD2 siRNA, and the usage of a pharmacological MG132 inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	231-236	hypoxia inducible factor 1 subunit alpha	Homo sapiens	90-100
21283566-9	2011	The proteasome inhibitor MG-132 augmented the decrease in c-FLIP levels and apoptosis induced by these derivatives.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	CASP8 and FADD like apoptosis regulator	Homo sapiens	58-64
21297867-4	2011	METHODOLOGY/PRINCIPAL FINDINGS: Here we show that proteasome inhibition with MG132, per se at non-lethal levels, sensitized vascular smooth muscle cells to caspase-3 activation and cell death during ER stress induced by tunicamycin (Tn).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	caspase 3	Homo sapiens	156-165
21062749-10	2011	Using the NF-kappaB inhibitors, MG-132 or Bay11-7082, we demonstrated that NF-kappaB activation mediated the up-regulation of miR-155 by alcohol in KCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-38	microRNA 155	Mus musculus	126-133
21418993-9	2011	After a pretreatment of PDTC (10 micromol/L), SB203580 (5 micromol/L) and MG132 (10 micromol/L), the levels of MCP-1 and IL-8 decreased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	C-C motif chemokine ligand 2	Rattus norvegicus	111-116
22087308-6	2011	The downregulation of Jak2 was inhibited by the proteasome inhibitor MG132 or by expression of both of loss-of-function mutants of c-Cbl and Cbl-b, E3 ubiquitin ligases which facilitated ubiquitination of Jak2-V617F when co-expressed in 293T cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	Janus kinase 2	Homo sapiens	22-26
20981255-3	2011	We demonstrate that Hsp90 inhibition by geldanamycin can effectively suppress proteasome inhibitor, MG-132-induced protein aggregation in a way that is independent of HDAC inhibition or the tubulin acetylation levels in ARPE-19 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-106	heat shock protein 90 alpha family class A member 1	Homo sapiens	20-25
21175982-7	2011	RESULTS: In cultured renal cells, both MG132 and lactacystin inhibited TGF-beta-induced alpha-smooth muscle actin (alpha-SMA) protein expression according to both western blotting and immunofluorescent study results.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	actin gamma 2, smooth muscle	Rattus norvegicus	88-113
21175982-7	2011	RESULTS: In cultured renal cells, both MG132 and lactacystin inhibited TGF-beta-induced alpha-smooth muscle actin (alpha-SMA) protein expression according to both western blotting and immunofluorescent study results.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	actin gamma 2, smooth muscle	Rattus norvegicus	115-124
21175982-8	2011	MG132 also suppressed TGF-beta-induced mRNA expression of alpha-SMA and upregulation of Smad-response element reporter activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	actin gamma 2, smooth muscle	Rattus norvegicus	58-67
22212933-5	2011	The processing of MAGE-A4 was inhibited by the proteasome inhibitors MG115, MG132, lactacystin and epoxamicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	MAGE family member A4	Homo sapiens	18-25
22216197-4	2011	PRINCIPAL FINDINGS: We found that proteasomal inhibitors MG-132 and clasto-lactacystin-beta-lactone stabilized the protein expression of full-length Nrf1 in both COS7 and WFF2002 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-63	nuclear respiratory factor 1	Homo sapiens	149-153
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	tumor protein p53	Homo sapiens	155-158
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	tumor protein p53	Homo sapiens	229-232
21200153-8	2011	We demonstrate that along with the epigenetic silencing of the p16INK4a gene, the complete inactivation of the locus is achieved by the improper turnover of INK4/ARF proteins by the ubiquitin-proteasome system (UPS), as the proteasome inhibitor MG-132 blocks p14(ARF) degradation and induces a dramatic stabilization of the p16(INK4a) protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-251	cyclin dependent kinase inhibitor 2A	Homo sapiens	63-71
21200153-8	2011	We demonstrate that along with the epigenetic silencing of the p16INK4a gene, the complete inactivation of the locus is achieved by the improper turnover of INK4/ARF proteins by the ubiquitin-proteasome system (UPS), as the proteasome inhibitor MG-132 blocks p14(ARF) degradation and induces a dramatic stabilization of the p16(INK4a) protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-251	cyclin dependent kinase inhibitor 2A	Homo sapiens	66-70
21200153-8	2011	We demonstrate that along with the epigenetic silencing of the p16INK4a gene, the complete inactivation of the locus is achieved by the improper turnover of INK4/ARF proteins by the ubiquitin-proteasome system (UPS), as the proteasome inhibitor MG-132 blocks p14(ARF) degradation and induces a dramatic stabilization of the p16(INK4a) protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-251	cyclin dependent kinase inhibitor 2A	Homo sapiens	63-66
21200153-8	2011	We demonstrate that along with the epigenetic silencing of the p16INK4a gene, the complete inactivation of the locus is achieved by the improper turnover of INK4/ARF proteins by the ubiquitin-proteasome system (UPS), as the proteasome inhibitor MG-132 blocks p14(ARF) degradation and induces a dramatic stabilization of the p16(INK4a) protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-251	cyclin dependent kinase inhibitor 2A	Homo sapiens	66-71
21912117-7	2011	Inhibition of proteasomes with MG-132 significantly elevated Rfc1 protein levels and induced colocalization of Rfc1 and ubiquitin particularly in submembranous cellular compartments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	replication factor C subunit 1	Homo sapiens	61-65
21912117-7	2011	Inhibition of proteasomes with MG-132 significantly elevated Rfc1 protein levels and induced colocalization of Rfc1 and ubiquitin particularly in submembranous cellular compartments.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	replication factor C subunit 1	Homo sapiens	111-115
20954830-5	2011	Treatment with MAPK (MEK, JNK, and p38) inhibitors showed a slight enhancement of cell-growth inhibition by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	mitogen-activated protein kinase 14	Bos taurus	35-38
21829535-2	2011	Here, we studied TDP-43 in primary neurons under different stress conditions and found that only proteasome inhibition by MG-132 or lactacystin could induce significant cytoplasmic accumulation of TDP-43, a histopathological hallmark in disease.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	TAR DNA binding protein	Homo sapiens	17-23
22132158-9	2011	Proteasome inhibition by MG-132 revealed that miR-135a regulated proteasomal degradation and potentially controlled the expression of chemokinesin DNA binding protein (Kid).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	heat shock transcription factor 4	Mus musculus	147-166
22132158-9	2011	Proteasome inhibition by MG-132 revealed that miR-135a regulated proteasomal degradation and potentially controlled the expression of chemokinesin DNA binding protein (Kid).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	kinesin family member 22	Mus musculus	168-171
21998680-9	2011	Data obtained from protein expression and ubiquitination analysis, in the presence of the proteasome inhibitor MG132, suggested that upon EGF stimuli EGR1 sumoylation enhanced its turnover, increasing ubiquitination and proteasome mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	epidermal growth factor	Homo sapiens	138-141
21998680-9	2011	Data obtained from protein expression and ubiquitination analysis, in the presence of the proteasome inhibitor MG132, suggested that upon EGF stimuli EGR1 sumoylation enhanced its turnover, increasing ubiquitination and proteasome mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	early growth response 1	Homo sapiens	150-154
21829535-2	2011	Here, we studied TDP-43 in primary neurons under different stress conditions and found that only proteasome inhibition by MG-132 or lactacystin could induce significant cytoplasmic accumulation of TDP-43, a histopathological hallmark in disease.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	TAR DNA binding protein	Homo sapiens	197-203
20837660-3	2010	The inefficacy of MG132 was due to its metabolism by CYP3A enzymes, as deduced from its rapid, ketoconazole-sensitive clearance by pooled human liver microsomes and cultured hepatocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	53-58
21738571-2	2011	In this, the first comprehensive analysis of gene expression changes in response to heat shock and MG132 (a proteasome inhibitor), both of which are known to induce heat shock proteins (Hsps), we compared the responses of normal mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant cell line, TR-RIF-1 (TR), to the two stresses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	replication timing regulatory factor 1	Mus musculus	259-264
21738571-2	2011	In this, the first comprehensive analysis of gene expression changes in response to heat shock and MG132 (a proteasome inhibitor), both of which are known to induce heat shock proteins (Hsps), we compared the responses of normal mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant cell line, TR-RIF-1 (TR), to the two stresses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	replication timing regulatory factor 1	Mus musculus	311-316
21041310-8	2010	The proteasome inhibitor MG132 abolished down-regulation of ERalpha by TPSF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	estrogen receptor 1	Homo sapiens	60-67
21093410-5	2010	MDM2-mediated degradation of p73 was inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	MDM2 proto-oncogene	Homo sapiens	0-4
21093410-5	2010	MDM2-mediated degradation of p73 was inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	tumor protein p73	Homo sapiens	29-32
20966391-8	2010	BK-beta(1) expression was suppressed by the FBXO activator doxorubicin but enhanced by FBXO-9 small interfering RNA or by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-153	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	0-10
20840860-7	2010	Treatment of the cells with the proteasome inhibitor MG-132 resulted in the accumulation of both p53 and PPP1R13L proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	tumor protein p53	Homo sapiens	97-100
20840860-7	2010	Treatment of the cells with the proteasome inhibitor MG-132 resulted in the accumulation of both p53 and PPP1R13L proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	protein phosphatase 1 regulatory subunit 13 like	Homo sapiens	105-113
20508647-5	2010	EVI1 protein was modulated by treatment with the proteasome inhibitors, MG132 and PS-341/Velcade, suggesting that degradation occurs through the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	MDS1 and EVI1 complex locus	Homo sapiens	0-4
21701587-6	2011	The protein levels of LMP1 could readily be detected after incubation with proteasome inhibitor, MG132 suggesting that LMP1 protein is rapidly degraded via proteasome-mediated proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	PDZ and LIM domain 7	Homo sapiens	22-26
21701587-6	2011	The protein levels of LMP1 could readily be detected after incubation with proteasome inhibitor, MG132 suggesting that LMP1 protein is rapidly degraded via proteasome-mediated proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	PDZ and LIM domain 7	Homo sapiens	119-123
20959456-9	2010	The short half-life of Ser-129-phosphorylated a-Syn was blocked by MG132 to a greater extent than okadaic acid.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	synemin	Homo sapiens	48-51
20940307-7	2010	Furthermore, the reduced level of PTEN in PLK3 null MEFs is stabilized by treatment with MG132, a proteosome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	phosphatase and tensin homolog	Mus musculus	34-38
20940307-7	2010	Furthermore, the reduced level of PTEN in PLK3 null MEFs is stabilized by treatment with MG132, a proteosome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	polo like kinase 3	Mus musculus	42-46
21108537-4	2010	Here we showed that exposure of the recipient oocyte to the proteasome inhibitor MG132 prior to fusion inhibited the degradation of cyclin B, which normally occurred immediately after activation by electro stimulation, and therefore sustained a high level of MPF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	mesothelin	Homo sapiens	259-262
21108537-8	2010	Investigation of the global nuclear organization by immunodetection of heterochromatin protein 1 (CBX1) showed that SCNT embryos derived from MG132-treated recipient oocytes displayed organization patterns similar to the ones observed in IVF embryos in contrast to the nontreated SCNT controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	chromobox 1	Homo sapiens	98-102
20869878-7	2010	Experiments with the NF-kappaB inhibitor, MG-132, demonstrated that NF-kappaB was involved in the induction of CCL2 but not CCL3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	21-30
20869878-7	2010	Experiments with the NF-kappaB inhibitor, MG-132, demonstrated that NF-kappaB was involved in the induction of CCL2 but not CCL3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-77
20869878-7	2010	Experiments with the NF-kappaB inhibitor, MG-132, demonstrated that NF-kappaB was involved in the induction of CCL2 but not CCL3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	chemokine (C-C motif) ligand 2	Mus musculus	111-115
20837660-4	2010	The efficacy of MG132 was increased by inclusion of ketoconazole in the hepatocyte incubations and decreased by prior treatment of the cultures with the CYP3A inducers phenobarbital or rifampicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	153-158
20830735-3	2010	Here we report unprecedented detection of endogenous p10, the smaller proteolytic fragment of the Cdk5 activator p35 in treated primary cortical neurons that underwent significant apoptosis, triggered by proteasome inhibitors MG132 and lactacystin, and protein kinase inhibitor staurosporine (STS).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-231	S100 calcium binding protein A10	Homo sapiens	53-56
20830735-3	2010	Here we report unprecedented detection of endogenous p10, the smaller proteolytic fragment of the Cdk5 activator p35 in treated primary cortical neurons that underwent significant apoptosis, triggered by proteasome inhibitors MG132 and lactacystin, and protein kinase inhibitor staurosporine (STS).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-231	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	113-116
20814167-6	2010	Under the selected optimal conditions, we subjected transient MG132-treated embryos to reverse transcription (RT)-PCR analysis of expression of four ZGA genes, i.e., the hsp70.1, MuERV-L, eif-1a and zscan4d genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	heat shock protein 1B	Mus musculus	170-177
20814167-6	2010	Under the selected optimal conditions, we subjected transient MG132-treated embryos to reverse transcription (RT)-PCR analysis of expression of four ZGA genes, i.e., the hsp70.1, MuERV-L, eif-1a and zscan4d genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	endogenous retroviral sequence 4 (with leucine tRNA primer)	Mus musculus	179-186
20814167-6	2010	Under the selected optimal conditions, we subjected transient MG132-treated embryos to reverse transcription (RT)-PCR analysis of expression of four ZGA genes, i.e., the hsp70.1, MuERV-L, eif-1a and zscan4d genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	eukaryotic translation initiation factor 1A	Mus musculus	188-194
20814167-6	2010	Under the selected optimal conditions, we subjected transient MG132-treated embryos to reverse transcription (RT)-PCR analysis of expression of four ZGA genes, i.e., the hsp70.1, MuERV-L, eif-1a and zscan4d genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	zinc finger and SCAN domain containing 4D	Mus musculus	199-206
20946870-4	2010	Regarding the proteasomal ubiquitination, a proteasome inhibitor MG-132 restored the reduced accumulation of HIF-1alpha in ECs from APA-KO mice similar to control mice under hypoxic conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	glutamyl aminopeptidase	Mus musculus	132-135
24198522-5	2010	Inhibition of Notch1 activation by the Notch inhibitor, MG132, led to enhanced expression of a serum-stimulated oligodendrocyte marker.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	notch receptor 1	Homo sapiens	14-20
24198522-5	2010	Inhibition of Notch1 activation by the Notch inhibitor, MG132, led to enhanced expression of a serum-stimulated oligodendrocyte marker.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	notch receptor 1	Homo sapiens	14-19
24198522-6	2010	This marker was undetectable in serum-deprived KP-hMSCs treated with MG132, suggesting that inhibition of Notch1 function is additive to serum-stimulated oligodendrocyte differentiation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	notch receptor 1	Homo sapiens	106-112
20946870-4	2010	Regarding the proteasomal ubiquitination, a proteasome inhibitor MG-132 restored the reduced accumulation of HIF-1alpha in ECs from APA-KO mice similar to control mice under hypoxic conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	hypoxia inducible factor 1, alpha subunit	Mus musculus	109-119
20843805-6	2010	The Nedd4-2 inhibitory effects on TRPV6 were partially blocked by proteasome inhibitor MG132 but not by the lysosome inhibitor chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	NEDD4 like E3 ubiquitin protein ligase S homeolog	Xenopus laevis	4-11
20665661-9	2010	Although EAG could activate NF-kappaB signaling, the proteasome inhibitor of MG-132 could effectively prevent NF-kappaB targeted gene expression induced by EAG and then sensitize LLC-1 cells to induce EAG-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-83	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	110-119
20665669-6	2010	After being treated with the proteasome inhibitor MG132, ubiquitinated DCN accumulated and displayed a prolonged half-life, accompanied by decreased TGF-beta1 expression and reduced collagen IV mRNA level in MC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	transforming growth factor, beta 1	Rattus norvegicus	149-158
20854249-7	2010	IL-1beta-induced brain endothelial expression of ICAM-1 and VCAM-1 was inhibited (80-88 %) by the proteasome inhibitor MG132 or the antioxidant caffeic acid phenethyl ester (CAPE), effects suggested to be NF-kB-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	interleukin 1 beta	Rattus norvegicus	0-8
20854249-7	2010	IL-1beta-induced brain endothelial expression of ICAM-1 and VCAM-1 was inhibited (80-88 %) by the proteasome inhibitor MG132 or the antioxidant caffeic acid phenethyl ester (CAPE), effects suggested to be NF-kB-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	intercellular adhesion molecule 1	Rattus norvegicus	49-55
20854249-7	2010	IL-1beta-induced brain endothelial expression of ICAM-1 and VCAM-1 was inhibited (80-88 %) by the proteasome inhibitor MG132 or the antioxidant caffeic acid phenethyl ester (CAPE), effects suggested to be NF-kB-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	vascular cell adhesion molecule 1	Rattus norvegicus	60-66
20854249-7	2010	IL-1beta-induced brain endothelial expression of ICAM-1 and VCAM-1 was inhibited (80-88 %) by the proteasome inhibitor MG132 or the antioxidant caffeic acid phenethyl ester (CAPE), effects suggested to be NF-kB-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	205-210
20854249-8	2010	IL-1beta-induced brain endothelial CXCL1 expression was partially inhibited by JNK MAP kinase or MG132 (62 or 56 %, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	interleukin 1 beta	Rattus norvegicus	0-8
20854249-8	2010	IL-1beta-induced brain endothelial CXCL1 expression was partially inhibited by JNK MAP kinase or MG132 (62 or 56 %, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	C-X-C motif chemokine ligand 1	Rattus norvegicus	35-40
20854249-9	2010	However, CXCL1 secretion from brain endothelium was reduced (65 %) only by MG132, and not MAP kinase inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	C-X-C motif chemokine ligand 1	Rattus norvegicus	9-14
20854249-10	2010	Similarly, IL-1beta-induced neutrophil transendothelial migration was reduced (77-89 %) by MG132, but not MAP kinase inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	interleukin 1 beta	Rattus norvegicus	11-19
20702393-6	2010	The results showed that Nucling is a short-lived protein, and its degradation was recovered by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	uveal autoantigen with coiled-coil domains and ankyrin repeats	Mus musculus	24-31
20810727-10	2010	CD1d protein levels were rescued by the proteasome inhibitor, MG132, indicating a role for proteasome-mediated degradation in HPV-associated CD1d downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	CD1d molecule	Homo sapiens	0-4
20719828-11	2010	CONCLUSIONS: These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-216	DNA damage inducible transcript 3	Homo sapiens	140-144
20719828-8	2010	siRNA for ORP150 stimulated MG132-mediated apoptosis and induction of CHOP, a transcription factor with apoptosis-inducing activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	hypoxia up-regulated 1	Homo sapiens	10-16
20719828-9	2010	In contrast, ORP150-overexpressing cells demonstrated less susceptibility to MG132-induced apoptosis and displayed less up-regulation of CHOP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	hypoxia up-regulated 1	Homo sapiens	13-19
20719828-11	2010	CONCLUSIONS: These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	hypoxia up-regulated 1	Homo sapiens	57-63
20719828-11	2010	CONCLUSIONS: These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	DNA damage inducible transcript 3	Homo sapiens	140-144
20719828-11	2010	CONCLUSIONS: These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-216	hypoxia up-regulated 1	Homo sapiens	57-63
20731760-5	2010	Furthermore, proteasomal inhibition with MG132 caused increased caspase-mediated TDP-43 fragmentation and accumulation of detergent-insoluble 35- and 25-kDa C-terminal fragments in Grn(-/-) neurons and mouse embryonic fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	TAR DNA binding protein	Mus musculus	81-87
20731760-5	2010	Furthermore, proteasomal inhibition with MG132 caused increased caspase-mediated TDP-43 fragmentation and accumulation of detergent-insoluble 35- and 25-kDa C-terminal fragments in Grn(-/-) neurons and mouse embryonic fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	granulin	Mus musculus	181-184
20731760-6	2010	Interestingly, full-length TDP-43 also accumulated in the detergent-insoluble fraction, and caspase-inhibition prevented MG132-induced generation of TDP-43 C-terminal fragments but did not block the pathological conversion of full-length TDP-43 from soluble to insoluble species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	TAR DNA binding protein	Mus musculus	27-33
20731760-6	2010	Interestingly, full-length TDP-43 also accumulated in the detergent-insoluble fraction, and caspase-inhibition prevented MG132-induced generation of TDP-43 C-terminal fragments but did not block the pathological conversion of full-length TDP-43 from soluble to insoluble species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	TAR DNA binding protein	Mus musculus	149-155
20731760-6	2010	Interestingly, full-length TDP-43 also accumulated in the detergent-insoluble fraction, and caspase-inhibition prevented MG132-induced generation of TDP-43 C-terminal fragments but did not block the pathological conversion of full-length TDP-43 from soluble to insoluble species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	TAR DNA binding protein	Mus musculus	149-155
20810727-10	2010	CD1d protein levels were rescued by the proteasome inhibitor, MG132, indicating a role for proteasome-mediated degradation in HPV-associated CD1d downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	CD1d molecule	Homo sapiens	141-145
20843941-9	2010	Higher nuclear localization was also observed when cells expressing IRS-1(WT) were incubated with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	insulin receptor substrate 1	Rattus norvegicus	68-73
20729194-5	2010	First, we showed that treatment of HEK 293T cells with the proteosome inhibitor MG132 resulted in an increase in both the polyubiquitination and the accumulation of Mps1 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	TTK protein kinase	Homo sapiens	165-169
20806931-9	2010	Proteasome inhibitors MG-132 (5 muM) and bortezomib (50 nM) dramatically increased the level of CBR3 mRNA, obviously because of the increase in the level of Nrf2 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	carbonyl reductase 3	Homo sapiens	96-100
20806931-9	2010	Proteasome inhibitors MG-132 (5 muM) and bortezomib (50 nM) dramatically increased the level of CBR3 mRNA, obviously because of the increase in the level of Nrf2 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	NFE2 like bZIP transcription factor 2	Homo sapiens	157-161
20570725-14	2010	Furthermore, replacing Thr-203 with alanine prevented the loss of MK3.2 following osmotic stress, as did pretreatment with the proteosome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	148-153	mitogen-activated protein kinase-activated protein kinase 3	Mus musculus	66-69
20599784-4	2010	MG132, a proteasome inhibitor, protected HIF-1alpha from LW6-induced proteasomal degradation, indicating that LW6 affects the stability of the HIF-1alpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	41-51
20599784-4	2010	MG132, a proteasome inhibitor, protected HIF-1alpha from LW6-induced proteasomal degradation, indicating that LW6 affects the stability of the HIF-1alpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	143-153
20860658-12	2010	Using a ubiquitin-proteasome inhibitor MG132, it was established that blocking PGC-1alpha degradation partially suppressed the reduction of mitochondrial mass.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	PPARG coactivator 1 alpha	Homo sapiens	79-89
20545600-0	2010	Treatment with p38 inhibitor intensifies the death of MG132-treated As4.1 juxtaglomerular cells via the enhancement of GSH depletion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	mitogen-activated protein kinase 14	Mus musculus	15-18
20545600-3	2010	MG132 inhibited the growth of As4.1 cells and induced cell death, accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)) and activation of caspase-3 and -8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Mus musculus	163-179
20545600-5	2010	The MEK inhibitor slightly reduced cell growth and caspase-3 activity in MG132-treated As4.1 cells and mildly increased MMP (DeltaPsi(m)) loss and O(2)(*-) level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	midkine	Mus musculus	4-7
20545600-5	2010	The MEK inhibitor slightly reduced cell growth and caspase-3 activity in MG132-treated As4.1 cells and mildly increased MMP (DeltaPsi(m)) loss and O(2)(*-) level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	caspase 3	Mus musculus	51-60
20545600-8	2010	Treatment with the p38 inhibitor magnified cell-growth inhibition and apoptosis by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	mitogen-activated protein kinase 14	Mus musculus	19-22
20545600-10	2010	Conclusively, the p38 inhibitor strongly intensified cell death in MG132-treated As4.1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	mitogen-activated protein kinase 14	Mus musculus	18-21
20957029-6	2010	Heat stress- and other HSP inducer (CdCl(2), celastrol, MG132)-induced HSP70 expression could be inhibited by AICAR, an AMPK specific activator.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	23-26
20849415-6	2010	Blocking the proteasomal degradation by MG132 stabilized the MBP-1 protein in cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	enolase 1	Homo sapiens	61-66
20406645-10	2010	The parasite proteasome seems to be involved in degradation of the enzyme, since Phytomonas ODC can be markedly stabilized by MG-132, a well known proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	ornithine decarboxylase 1	Homo sapiens	92-95
20957029-6	2010	Heat stress- and other HSP inducer (CdCl(2), celastrol, MG132)-induced HSP70 expression could be inhibited by AICAR, an AMPK specific activator.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	heat shock protein family A (Hsp70) member 4	Homo sapiens	71-76
20957029-6	2010	Heat stress- and other HSP inducer (CdCl(2), celastrol, MG132)-induced HSP70 expression could be inhibited by AICAR, an AMPK specific activator.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	110-115
20927194-10	2010	RESULTS: The two proinflammatory cytokines, TNF-alpha and IL-1beta, were able to activate the reporter system, translating the activation of the NF-kappaB signaling pathway and NF-kappaB inhibitors, BAY 11-7082, caffeic acid phenethyl ester and MG132 were efficient.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-250	tumor necrosis factor	Homo sapiens	44-53
20619429-7	2010	Moreover, MDM2 knockdown decreased the sensitivity of N-MLV infection to treatment with MG132 and As(2)O(3), two known TRIM5alpha pharmacological inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	MDM2 proto-oncogene	Homo sapiens	10-14
20619429-7	2010	Moreover, MDM2 knockdown decreased the sensitivity of N-MLV infection to treatment with MG132 and As(2)O(3), two known TRIM5alpha pharmacological inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	tripartite motif containing 5	Homo sapiens	119-129
20927194-10	2010	RESULTS: The two proinflammatory cytokines, TNF-alpha and IL-1beta, were able to activate the reporter system, translating the activation of the NF-kappaB signaling pathway and NF-kappaB inhibitors, BAY 11-7082, caffeic acid phenethyl ester and MG132 were efficient.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-250	interleukin 1 beta	Homo sapiens	58-66
20927194-10	2010	RESULTS: The two proinflammatory cytokines, TNF-alpha and IL-1beta, were able to activate the reporter system, translating the activation of the NF-kappaB signaling pathway and NF-kappaB inhibitors, BAY 11-7082, caffeic acid phenethyl ester and MG132 were efficient.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-250	nuclear factor kappa B subunit 1	Homo sapiens	145-154
20927194-10	2010	RESULTS: The two proinflammatory cytokines, TNF-alpha and IL-1beta, were able to activate the reporter system, translating the activation of the NF-kappaB signaling pathway and NF-kappaB inhibitors, BAY 11-7082, caffeic acid phenethyl ester and MG132 were efficient.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-250	nuclear factor kappa B subunit 1	Homo sapiens	177-186
21472326-10	2010	Treatment with the proteasome inhibitors lactacystine and MG-132 inhibited the statin-mediated down-regulation of SATB1, suggesting that regulation occurs at the post-translational level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-64	SATB homeobox 1	Homo sapiens	114-119
20595005-8	2010	Furthermore, the proteasome inhibitor MG132 was able to inhibit expression of FLIP mRNA and protein and upregulate the sensitivity of these cells to TRAIL treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	TNF superfamily member 10	Homo sapiens	149-154
20595005-10	2010	Therefore, the proteasome inhibitor MG132 should be further evaluated for combination therapy with TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	TNF superfamily member 10	Homo sapiens	99-104
20471435-11	2010	The down-regulation of PDCD4 by TPA was restored by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	programmed cell death 4	Homo sapiens	23-28
20681988-6	2010	We also found that hypoxia/SD induced the transcription and secretion of IL-10, which were significantly enhanced by lipopolysaccharide and the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	interleukin 10	Rattus norvegicus	73-78
20688878-7	2010	Site-directed mutagenesis of the NF-kappaB element in ADAM-12 promoter and inhibition of NF-kappaB activity by Bay-11-7085 and MG-132 significantly reduced TGF-beta1-mediated increase of ADAM-12 promoter-driven gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-133	nuclear factor kappa B subunit 1	Homo sapiens	33-42
20688878-7	2010	Site-directed mutagenesis of the NF-kappaB element in ADAM-12 promoter and inhibition of NF-kappaB activity by Bay-11-7085 and MG-132 significantly reduced TGF-beta1-mediated increase of ADAM-12 promoter-driven gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-133	nuclear factor kappa B subunit 1	Homo sapiens	89-98
20688878-7	2010	Site-directed mutagenesis of the NF-kappaB element in ADAM-12 promoter and inhibition of NF-kappaB activity by Bay-11-7085 and MG-132 significantly reduced TGF-beta1-mediated increase of ADAM-12 promoter-driven gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-133	transforming growth factor beta 1	Homo sapiens	156-165
20688878-7	2010	Site-directed mutagenesis of the NF-kappaB element in ADAM-12 promoter and inhibition of NF-kappaB activity by Bay-11-7085 and MG-132 significantly reduced TGF-beta1-mediated increase of ADAM-12 promoter-driven gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-133	ADAM metallopeptidase domain 12	Homo sapiens	187-194
20696002-6	2010	As an effective suppressor, the amount of AGO1 accumulated in the presence of P25 was dramatically lower than that infiltrated with HcPro, but was restored when treated with a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	197-202	argonaute RISC component 1	Homo sapiens	42-46
20449726-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4 microM at 48 h and induced cell death, accompanied by the loss of mitochondrial membrane potential (MMP; Psi(m)), Bcl-2 decrease, activations of caspase-3 and caspase-8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	B cell leukemia/lymphoma 2	Mus musculus	196-201
20449726-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4 microM at 48 h and induced cell death, accompanied by the loss of mitochondrial membrane potential (MMP; Psi(m)), Bcl-2 decrease, activations of caspase-3 and caspase-8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Mus musculus	227-236
20449726-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4 microM at 48 h and induced cell death, accompanied by the loss of mitochondrial membrane potential (MMP; Psi(m)), Bcl-2 decrease, activations of caspase-3 and caspase-8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 8	Mus musculus	241-250
20449726-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4 microM at 48 h and induced cell death, accompanied by the loss of mitochondrial membrane potential (MMP; Psi(m)), Bcl-2 decrease, activations of caspase-3 and caspase-8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	poly (ADP-ribose) polymerase family, member 1	Mus musculus	256-260
20449726-5	2010	However, caspase inhibitors, especially Z-VAD (pan-caspase inhibitor) intensified cell growth inhibition, cell death, MMP (Psi(m)) loss, and Bcl-2 decrease in MG132-treated As4.1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	B cell leukemia/lymphoma 2	Mus musculus	141-146
20182834-8	2010	The proteasome inhibitor, MG132, partially restored HSP70 protein levels in ESP-challenged haemocytes, demonstrating that the decrease in HSP70 was in part due to intracellular degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	heat shock protein 70 B2-like	Biomphalaria glabrata	52-57
20182834-8	2010	The proteasome inhibitor, MG132, partially restored HSP70 protein levels in ESP-challenged haemocytes, demonstrating that the decrease in HSP70 was in part due to intracellular degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	heat shock protein 70 B2-like	Biomphalaria glabrata	138-143
20473778-10	2010	Addition of the proteasome inhibitor, MG132, reverses the loss of telomerase activity; therefore, reductions in telomerase activity are dynamic, ongoing, and correlated with robust up-regulation of MKRN1 as the cells terminally differentiate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	makorin ring finger protein 1	Homo sapiens	198-203
20696002-6	2010	As an effective suppressor, the amount of AGO1 accumulated in the presence of P25 was dramatically lower than that infiltrated with HcPro, but was restored when treated with a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	197-202	transmembrane p24 trafficking protein 9	Homo sapiens	78-81
20530983-9	2010	Inhibition of beta-catenin degradation by inhibition of glycogen synthase kinase 3-beta with lithium chloride (LiCl) or inhibition of proteasome with z-Leu-Leu-Leu-CHO (MG132) accelerated the decrease of type II collagen expression in the chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-167	LOC100125986	Oryctolagus cuniculus	14-26
20865169-8	2010	Pharmacological treatment of Rh1(P37H) flies with the VCP/ERAD inhibitor Eeyarestatin I or with the proteasome inhibitor MG132 also led to a strong suppression of retinal degeneration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	neither inactivation nor afterpotential E	Drosophila melanogaster	29-33
20385228-6	2010	This repressive effect is at least partially mediated via stimulating proteasome-dependent TxNIP degradation, since the proteasomal inhibitor MG132, but not the lysosomal inhibitor chloroquine, significantly blocked the repressive effect of forskolin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	thioredoxin interacting protein	Rattus norvegicus	91-96
20522648-3	2010	In a tissue culture system, the LPS-induced decrease in the AQP5 mRNA level was blocked completely by pyrrolidine dithiocarbamate, MG132, tyrphostin AG126, SP600125, and partially by SB203580, which are inhibitors for IkappaB kinase, 26S proteasome, ERK1/2, JNK, and p38 MAPK, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	aquaporin 5	Mus musculus	60-64
20089131-6	2010	Our data show that the proteasomal inhibitor MG-132 promotes Hsp27 phosphorylation by activation of p38 mitogen activated protein kinase and leads to the formation of small oligomers.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	heat shock protein family B (small) member 1	Rattus norvegicus	61-66
20089131-6	2010	Our data show that the proteasomal inhibitor MG-132 promotes Hsp27 phosphorylation by activation of p38 mitogen activated protein kinase and leads to the formation of small oligomers.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	mitogen activated protein kinase 14	Rattus norvegicus	100-103
20530983-9	2010	Inhibition of beta-catenin degradation by inhibition of glycogen synthase kinase 3-beta with lithium chloride (LiCl) or inhibition of proteasome with z-Leu-Leu-Leu-CHO (MG132) accelerated the decrease of type II collagen expression in the chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	LOC100125986	Oryctolagus cuniculus	14-26
20506183-9	2010	The elevated DNA-binding activity of the NF-kappaB/p50 homodimer and p50, as well as the neuronal expression of SP and CGRP, observed in the ankle joints of arthritic rats were normalized after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	209-214	calcitonin-related polypeptide alpha	Rattus norvegicus	119-123
20621833-2	2010	6-Aminonicotinamide (6-AN), an inhibitor of the pentose phosphate pathway (PPP), also inhibited the increase of HIF-1alpha protein under hypoxic conditions, while the reduced protein levels of HIF-1alpha by low glucose were apparently recovered by the addition of MG-132 or NADPH.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	264-270	hypoxia inducible factor 1 subunit alpha	Homo sapiens	112-122
20621833-2	2010	6-Aminonicotinamide (6-AN), an inhibitor of the pentose phosphate pathway (PPP), also inhibited the increase of HIF-1alpha protein under hypoxic conditions, while the reduced protein levels of HIF-1alpha by low glucose were apparently recovered by the addition of MG-132 or NADPH.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	264-270	hypoxia inducible factor 1 subunit alpha	Homo sapiens	193-203
20452984-6	2010	Expression of the Fad3 proteins in tobacco cells incubated with the proteasomal inhibitor MG132 further confirmed that they were degraded via the proteasomal pathway in plants.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	omega-3 fatty acid desaturase, endoplasmic reticulum	Nicotiana tabacum	18-22
20418385-6	2010	The decrease in MYPT1 protein caused by 48-h DETA NO incubation was prevented by ODQ, an inhibitor of guanylyl cyclase, and by inhibitors of proteasomes (MG-132 and lactacystin) but was not affected by the inhibitor of protein synthesis, cycloheximide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-160	protein phosphatase 1 regulatory subunit 12A	Homo sapiens	16-21
20682972-4	2010	At least one mechanism to stabilize and destabilize XPC involves ubiquitin-mediated degradation of XPC, as the ubiquitin ligase inhibitor MG-132 blocked XPC degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	52-55
20682972-4	2010	At least one mechanism to stabilize and destabilize XPC involves ubiquitin-mediated degradation of XPC, as the ubiquitin ligase inhibitor MG-132 blocked XPC degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	99-102
20682972-4	2010	At least one mechanism to stabilize and destabilize XPC involves ubiquitin-mediated degradation of XPC, as the ubiquitin ligase inhibitor MG-132 blocked XPC degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-144	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	99-102
20373002-9	2010	Pretreatment of these cells with MG132, an inhibitor of nuclear factor kappa B (NF-kappaB) pathway, abolished TNF-alpha-induced reduction in mRNA levels of dystrophin and titin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	titin	Homo sapiens	171-176
20373002-9	2010	Pretreatment of these cells with MG132, an inhibitor of nuclear factor kappa B (NF-kappaB) pathway, abolished TNF-alpha-induced reduction in mRNA levels of dystrophin and titin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	nuclear factor kappa B subunit 1	Homo sapiens	56-78
20206143-9	2010	Further studies demonstrated that DHA accelerated the degradation of c-MYC protein and this process was blocked by pretreatment with the proteasome inhibitor MG-132 or GSK 3beta inhibitor LiCl in HCT116 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-164	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	69-74
20410141-7	2010	Inhibition of proteasome activity by MG132 abolished DPC repair in both XPA-null and XPA-complemented cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	XPA, DNA damage recognition and repair factor	Homo sapiens	72-75
20374429-7	2010	Decreased levels of Tra2beta, an RNA splicing factor responsible for tau exon 10 inclusion, were detected both in cortical cell cultures exposed to MG132 and in cerebral cortex after ischemic injury.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	148-153	transformer 2 beta homolog	Homo sapiens	20-28
20373002-9	2010	Pretreatment of these cells with MG132, an inhibitor of nuclear factor kappa B (NF-kappaB) pathway, abolished TNF-alpha-induced reduction in mRNA levels of dystrophin and titin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	nuclear factor kappa B subunit 1	Homo sapiens	80-89
20373002-9	2010	Pretreatment of these cells with MG132, an inhibitor of nuclear factor kappa B (NF-kappaB) pathway, abolished TNF-alpha-induced reduction in mRNA levels of dystrophin and titin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	tumor necrosis factor	Homo sapiens	110-119
20373002-9	2010	Pretreatment of these cells with MG132, an inhibitor of nuclear factor kappa B (NF-kappaB) pathway, abolished TNF-alpha-induced reduction in mRNA levels of dystrophin and titin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	dystrophin	Homo sapiens	156-166
20155807-4	2010	MG-132, a proteasome inhibitor, increased the amount of HO-1 protein mainly in astrocytes of primary mesencephalic cultures.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	heme oxygenase 1	Homo sapiens	56-60
20155807-6	2010	Proteasome inhibition with MG132 also increased the cytomegalovirus promoter-driven expression of Flag-HO-1 protein and resulted in an accumulation of ubiquitinated Flag-HO-1 in Flag-HO-1-overexpressing PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	heme oxygenase 1	Homo sapiens	103-107
20155807-6	2010	Proteasome inhibition with MG132 also increased the cytomegalovirus promoter-driven expression of Flag-HO-1 protein and resulted in an accumulation of ubiquitinated Flag-HO-1 in Flag-HO-1-overexpressing PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	heme oxygenase 1	Homo sapiens	170-174
20155807-6	2010	Proteasome inhibition with MG132 also increased the cytomegalovirus promoter-driven expression of Flag-HO-1 protein and resulted in an accumulation of ubiquitinated Flag-HO-1 in Flag-HO-1-overexpressing PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	heme oxygenase 1	Homo sapiens	170-174
20421417-7	2010	BubR1 and Mad2 can bind to Cdc20 independently, and the interactions are enhanced after cells are arrested at mitosis by the depletion of Cdc27 using RNA interference (RNAi) in S2 cells or by MG132 treatment in syncytial embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	Bub1-related kinase	Drosophila melanogaster	0-5
20421417-7	2010	BubR1 and Mad2 can bind to Cdc20 independently, and the interactions are enhanced after cells are arrested at mitosis by the depletion of Cdc27 using RNA interference (RNAi) in S2 cells or by MG132 treatment in syncytial embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	mad2	Drosophila melanogaster	10-14
20421417-7	2010	BubR1 and Mad2 can bind to Cdc20 independently, and the interactions are enhanced after cells are arrested at mitosis by the depletion of Cdc27 using RNA interference (RNAi) in S2 cells or by MG132 treatment in syncytial embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	fizzy	Drosophila melanogaster	27-32
20410141-7	2010	Inhibition of proteasome activity by MG132 abolished DPC repair in both XPA-null and XPA-complemented cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	XPA, DNA damage recognition and repair factor	Homo sapiens	85-88
20348135-5	2010	The proteasome inhibitor MG132 prevents DNMT1 degradation and reduces hypomethylation induced by 5-aza-dC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	DNA methyltransferase (cytosine-5) 1	Mus musculus	40-45
20651358-3	2010	MG132 induced cell growth inhibition and apoptosis in HeLa cells, which was accompanied by the loss of mitochondrial membrane potential (MMP; Delta Psi(m)), activation of caspase-3 and poly (ADP-ribose) polymerase (PARP) cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	171-213
20514451-12	2010	Chemotherapeutics induced apoptosis of SGC-7901 and activated Akt and NF-kappaB, combined use of wortmannin or MG-132 induced apoptosis further and attenuated the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-117	AKT serine/threonine kinase 1	Homo sapiens	62-65
20514451-12	2010	Chemotherapeutics induced apoptosis of SGC-7901 and activated Akt and NF-kappaB, combined use of wortmannin or MG-132 induced apoptosis further and attenuated the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-117	nuclear factor kappa B subunit 1	Homo sapiens	70-79
20514451-12	2010	Chemotherapeutics induced apoptosis of SGC-7901 and activated Akt and NF-kappaB, combined use of wortmannin or MG-132 induced apoptosis further and attenuated the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-117	nuclear factor kappa B subunit 1	Homo sapiens	177-186
20394812-7	2010	Pre-treatment of cells with a proteasome inhibitor (MG132) suppressed PCB-153 induced decrease in cyclin D1 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	pyruvate carboxylase	Homo sapiens	70-73
20394812-7	2010	Pre-treatment of cells with a proteasome inhibitor (MG132) suppressed PCB-153 induced decrease in cyclin D1 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	cyclin D1	Homo sapiens	98-107
20410161-0	2010	Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	peroxiredoxin 1	Homo sapiens	44-59
20410161-0	2010	Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	81-85
20651355-7	2010	MG132, an established NF-kappaB inhibitor, suppressed NF-kappaB activity without causing alterations of lysosome permeability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	22-31
20651355-7	2010	MG132, an established NF-kappaB inhibitor, suppressed NF-kappaB activity without causing alterations of lysosome permeability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	54-63
19597128-7	2010	One hundred micromoles of H(2)O(2) enhanced the translocation of nuclear factor (NF)-kappaB p65, but not that of interferon regulatory factor-3 (IRF-3), into the nucleus and the NF-kappaB DNA binding activity after poly(I:C) stimulation, which effect was inhibited not by the silencing of IRF-3 but by MG132, a proteasome inhibitor, or dexamethasone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	302-307	nuclear factor kappa B subunit 1	Homo sapiens	65-91
20651358-3	2010	MG132 induced cell growth inhibition and apoptosis in HeLa cells, which was accompanied by the loss of mitochondrial membrane potential (MMP; Delta Psi(m)), activation of caspase-3 and poly (ADP-ribose) polymerase (PARP) cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	poly(ADP-ribose) polymerase 1	Homo sapiens	215-219
20188206-7	2010	Simultaneous exposure of cells with celastrol plus either mild heat shock or the proteasome inhibitor, MG132, produced an enhanced accumulation of HSP30 that was greater than the sum of the individual stressors alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	heat shock protein 30E L homeolog	Xenopus laevis	147-152
20138027-7	2010	This study identified five lead compounds such as thapsigargin, tunicamycine, MG132, kaempferol and camptothecin that could induce cytochrome C release in both wild type and Bax deficient cells with equal potency.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	cytochrome c, somatic	Homo sapiens	131-143
20138027-7	2010	This study identified five lead compounds such as thapsigargin, tunicamycine, MG132, kaempferol and camptothecin that could induce cytochrome C release in both wild type and Bax deficient cells with equal potency.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	BCL2 associated X, apoptosis regulator	Homo sapiens	174-177
20471510-0	2010	Treatment with p38 inhibitor partially prevents Calu-6 lung cancer cell death by a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	mitogen-activated protein kinase 14	Homo sapiens	15-18
20471510-8	2010	Furthermore, MG132 increased the phosphorylation of p38 in Calu-6 cells at 1 and 24 hours.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 14	Homo sapiens	52-55
20471510-9	2010	Treatment with p38 inhibitor significantly prevented cell growth inhibition, MMP (DeltaPsi(m)) loss and apoptosis in MG132-treated Calu-6 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	mitogen-activated protein kinase 14	Homo sapiens	15-18
20471510-11	2010	In conclusion, p38 inhibitor partially prevented Calu-6 cell death by MG132, which might be affected by GSH level changes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	mitogen-activated protein kinase 14	Homo sapiens	15-18
20392068-7	2010	Finally, MITF down-regulation by 1 was clearly restored by both chloroquine, a lysosomal proteolysis inhibitor, and MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	melanogenesis associated transcription factor	Mus musculus	9-13
20862209-7	2010	In contrast, proteasomal inhibitors bortezomib and MG-132 completely suppressed ricin-induced IL-1beta release from macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-57	interleukin 1 beta	Mus musculus	94-102
19838833-2	2010	In this study, we report that proteasome inhibitors, lactacystin and carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132), induced the accumulation of ubiquitinated proteins as well as a dose- and time-dependent increase in the relative levels of heat shock protein (HSP)30 and HSP70 and their respective mRNAs in Xenopus laevis A6 kidney epithelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	heat shock protein 30E L homeolog	Xenopus laevis	244-270
20075985-7	2010	However, treatment with the inhibitor MG132 restored HIF-1alpha levels, suggesting that reovirus-induced HIF-1alpha decrease needs proteosomal activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	hypoxia inducible factor 1 subunit alpha	Homo sapiens	53-63
20075985-7	2010	However, treatment with the inhibitor MG132 restored HIF-1alpha levels, suggesting that reovirus-induced HIF-1alpha decrease needs proteosomal activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	hypoxia inducible factor 1 subunit alpha	Homo sapiens	105-115
19997094-11	2010	Protein extracts from IBS patients but not from controls degraded recombinant occludin (20% over 160 min), which was blocked by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	occludin	Homo sapiens	78-86
19838833-2	2010	In this study, we report that proteasome inhibitors, lactacystin and carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132), induced the accumulation of ubiquitinated proteins as well as a dose- and time-dependent increase in the relative levels of heat shock protein (HSP)30 and HSP70 and their respective mRNAs in Xenopus laevis A6 kidney epithelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	heat shock 70kDa protein L homeolog	Xenopus laevis	275-280
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	heat shock protein 30E L homeolog	Xenopus laevis	44-49
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	heat shock 70kDa protein L homeolog	Xenopus laevis	54-59
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	heat shock factor protein	Xenopus laevis	156-175
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	heat shock factor protein	Xenopus laevis	177-181
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock protein 30E L homeolog	Xenopus laevis	44-49
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock 70kDa protein L homeolog	Xenopus laevis	54-59
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock factor protein	Xenopus laevis	156-175
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock factor protein	Xenopus laevis	177-181
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock factor protein	Xenopus laevis	264-268
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock protein 30E L homeolog	Xenopus laevis	310-315
19838833-3	2010	In A6 cells recovering from MG132 exposure, HSP30 and HSP70 levels were still elevated after 24 h but decreased substantially after 48 h. The activation of heat shock factor 1 (HSF1) may be involved in MG132-induced hsp gene expression in A6 cells since KNK437, a HSF1 inhibitor, repressed the accumulation of HSP30 and HSP70.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	heat shock 70kDa protein L homeolog	Xenopus laevis	320-325
19838833-4	2010	Exposing A6 cells to simultaneous MG132 and mild heat shock enhanced the accumulation of HSP30 and HSP70 to a much greater extent than with each stressor alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	heat shock protein 30E L homeolog	Xenopus laevis	89-94
19838833-4	2010	Exposing A6 cells to simultaneous MG132 and mild heat shock enhanced the accumulation of HSP30 and HSP70 to a much greater extent than with each stressor alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	heat shock 70kDa protein L homeolog	Xenopus laevis	99-104
19838833-5	2010	Immunocytochemical studies determined that HSP30 was localized primarily in the cytoplasm of lactacystin- or MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	heat shock protein 30E L homeolog	Xenopus laevis	43-48
19838833-6	2010	In some cells treated with higher concentrations of MG132 or lactacystin, we observed in the cortical cytoplasm (1) relatively large HSP30 staining structures, (2) colocalization of actin and HSP30, and (3) cytoplasmic areas that were devoid of HSP30.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	heat shock protein 30E L homeolog	Xenopus laevis	133-138
19838833-6	2010	In some cells treated with higher concentrations of MG132 or lactacystin, we observed in the cortical cytoplasm (1) relatively large HSP30 staining structures, (2) colocalization of actin and HSP30, and (3) cytoplasmic areas that were devoid of HSP30.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	actin like 6A S homeolog	Xenopus laevis	182-187
19838833-6	2010	In some cells treated with higher concentrations of MG132 or lactacystin, we observed in the cortical cytoplasm (1) relatively large HSP30 staining structures, (2) colocalization of actin and HSP30, and (3) cytoplasmic areas that were devoid of HSP30.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	heat shock protein 30E L homeolog	Xenopus laevis	192-197
19838833-6	2010	In some cells treated with higher concentrations of MG132 or lactacystin, we observed in the cortical cytoplasm (1) relatively large HSP30 staining structures, (2) colocalization of actin and HSP30, and (3) cytoplasmic areas that were devoid of HSP30.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	heat shock protein 30E L homeolog	Xenopus laevis	192-197
20332106-5	2010	When cells were treated with the proteasome inhibitor MG132, the size and frequency of p53-containing nucleolar cavities increased, and the protein partially colocalized with inactivated proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	tumor protein p53	Homo sapiens	87-90
20409024-7	2010	A pharmacological inhibitor of nuclear factor (NF)-kappaB, MG132, inhibited LPS-induced CTGF mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	nuclear factor kappa B subunit 1	Homo sapiens	31-57
20409024-7	2010	A pharmacological inhibitor of nuclear factor (NF)-kappaB, MG132, inhibited LPS-induced CTGF mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cellular communication network factor 2	Homo sapiens	88-92
20331971-3	2010	Proteasome inhibitor MG132 treatment induced an accumulation of ubiquitinated K-cyclin in these cells, and co-expression of CDK6 prevented K-cyclin ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	cyclin dependent kinase 6	Homo sapiens	124-128
20233849-8	2010	In cells deficient for SENP1 or in wild-type cells treated with the proteasome inhibitor MG132, there is considerable accumulation of N4BP1 at PML NBs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	SUMO specific peptidase 1	Homo sapiens	23-28
20233849-8	2010	In cells deficient for SENP1 or in wild-type cells treated with the proteasome inhibitor MG132, there is considerable accumulation of N4BP1 at PML NBs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	NEDD4 binding protein 1	Homo sapiens	134-139
20304029-4	2010	RESULTS: We show herein that BCR-ABL downregulates SHIP, but not SHIP2 or PTEN, and this can be blocked with the Src kinase inhibitor PP2, which inhibits the tyrosine phosphorylation of SHIP, or with the proteasomal inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-232	inositol polyphosphate-5-phosphatase D	Mus musculus	51-55
20304029-4	2010	RESULTS: We show herein that BCR-ABL downregulates SHIP, but not SHIP2 or PTEN, and this can be blocked with the Src kinase inhibitor PP2, which inhibits the tyrosine phosphorylation of SHIP, or with the proteasomal inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-232	Rous sarcoma oncogene	Mus musculus	113-116
20304029-4	2010	RESULTS: We show herein that BCR-ABL downregulates SHIP, but not SHIP2 or PTEN, and this can be blocked with the Src kinase inhibitor PP2, which inhibits the tyrosine phosphorylation of SHIP, or with the proteasomal inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	226-232	neuropeptide Y receptor Y6	Mus musculus	134-137
20304029-7	2010	In bone marrow-derived macrophages, IL-4 also leads to the proteasomal degradation of SHIP but, unlike in Ba/F3(p210-tetOFF) cells, SHIP2 is also proteasomally degraded and the degradation of both inositol phosphatases can be prevented with PP2 or MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	248-254	interleukin 4	Mus musculus	36-40
20112289-6	2010	Most of these effects were partially prevented by the NADPH oxidase inhibitor apocynin or the NFkappaB inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	nuclear factor kappa B subunit 1	Homo sapiens	94-102
20158498-7	2010	Whereas numerous mammalian protease inhibitors have no effect on MLK3 proteolysis, blockade of the proteasome through epoxomicin or MG132 abolishes PMA-induced production of the CTF of MLK3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	nuclear factor I C	Homo sapiens	178-181
20158498-7	2010	Whereas numerous mammalian protease inhibitors have no effect on MLK3 proteolysis, blockade of the proteasome through epoxomicin or MG132 abolishes PMA-induced production of the CTF of MLK3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	185-189
20043954-3	2010	Because some cytokines are involved in the regulation of sleep, this study was designed to determine if tumor necrosis factor (TNF) and interleukin-1beta (IL-1beta), mediate daytime somnolence in the proteasome inhibitor (MG-132)-induced hemiparkinsonian rat model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-228	interleukin 1 beta	Rattus norvegicus	155-163
20442774-7	2010	Moreover, LBH589 decreased c-FLIP stability and the presence of the proteasome inhibitor MG132 prevented c-FLIP from reduction by LBH589.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	CASP8 and FADD like apoptosis regulator	Homo sapiens	105-111
20405034-4	2010	The cleavage of GAD67 was sensitive to the proteasome inhibitors MG132, YU102 and lactacystin, and was also abrogated by the E1 ubiquitin ligase inhibitor UBEI-41.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	glutamate decarboxylase 1	Homo sapiens	16-21
20405034-5	2010	In contrast, MG132 and UBEI-41 were the only inhibitors tested that showed an effect on GAD65 cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	glutamate decarboxylase 2	Homo sapiens	88-93
20043954-3	2010	Because some cytokines are involved in the regulation of sleep, this study was designed to determine if tumor necrosis factor (TNF) and interleukin-1beta (IL-1beta), mediate daytime somnolence in the proteasome inhibitor (MG-132)-induced hemiparkinsonian rat model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-228	tumor necrosis factor-like	Rattus norvegicus	104-125
20043954-3	2010	Because some cytokines are involved in the regulation of sleep, this study was designed to determine if tumor necrosis factor (TNF) and interleukin-1beta (IL-1beta), mediate daytime somnolence in the proteasome inhibitor (MG-132)-induced hemiparkinsonian rat model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-228	interleukin 1 beta	Rattus norvegicus	136-153
20167927-9	2010	Consistently, we found that genetic deletion of AMPKalpha2 in low-density lipoprotein receptor knockout (LDLr(-/-)) strain markedly increased 26S proteasome activity, IkappaB degradation, NF-kappaB transactivation, NAD(P)H oxidase subunit overexpression, oxidative stress, and endothelial dysfunction, all of which were largely suppressed by chronic administration of MG132, a potent cell permeable proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	368-373	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	48-58
20043954-4	2010	Our results indicated that microglial activation caused the loss of dopaminergic neurons in the substantia nigra, and the expression of TNF-alpha, but not IL-1beta, increased in the midbrain and hypothalamus in MG-132-induced hemiparkinsonian rats.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-217	tumor necrosis factor	Rattus norvegicus	136-145
20043954-7	2010	Increased nuclear translocation of NF-kappaB in the midbrain, and the blockade of SWS enhancement in MG-132-induced hemiparkinsonian rats by an inhibitor of NF-kappaB activation indicate that the TNF-NF-kappaB cascade is a critical mediator of MG-132 hemiparkinsonian-induced sleep alteration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-107	tumor necrosis factor-like	Rattus norvegicus	196-199
20043954-7	2010	Increased nuclear translocation of NF-kappaB in the midbrain, and the blockade of SWS enhancement in MG-132-induced hemiparkinsonian rats by an inhibitor of NF-kappaB activation indicate that the TNF-NF-kappaB cascade is a critical mediator of MG-132 hemiparkinsonian-induced sleep alteration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-250	tumor necrosis factor-like	Rattus norvegicus	196-199
20139075-9	2010	Finally, CUL7-induced loss of E-cadherin expression was partially reversed by treatment of CUL7-expressing cells with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	cullin 7	Homo sapiens	9-13
20139075-9	2010	Finally, CUL7-induced loss of E-cadherin expression was partially reversed by treatment of CUL7-expressing cells with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	cadherin 1	Homo sapiens	30-40
20139075-9	2010	Finally, CUL7-induced loss of E-cadherin expression was partially reversed by treatment of CUL7-expressing cells with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	cullin 7	Homo sapiens	91-95
20332299-7	2010	Pretreatment with either the lysosomal inhibitor chloroquine or the proteosomal inhibitor MG132 blocked sulindac metabolite-induced downregulation of EGFR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	epidermal growth factor receptor	Homo sapiens	150-154
20383463-8	2010	The elevated phosphorylation levels of ERK1/2 and JNK1 in AAB rats were significantly reversed by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	mitogen activated protein kinase 3	Rattus norvegicus	39-45
20383463-9	2010	In conclusion, our results suggested that long-term treatment with MG132 attenuates pressureoverload-induced cardiac hypertrophy and improves cardiac function in AAB rats through regulation of ERK1/2 and JNK1 signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	mitogen activated protein kinase 3	Rattus norvegicus	193-199
20304949-3	2010	Previously, we demonstrated that treatment with the proteasome inhibitor MG-132 rescues the cell membrane localization of dystrophin and the dystrophin glycoprotein complex in mdx mice, a natural genetic mouse model of DMD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-79	dystrophin, muscular dystrophy	Mus musculus	122-132
20304949-3	2010	Previously, we demonstrated that treatment with the proteasome inhibitor MG-132 rescues the cell membrane localization of dystrophin and the dystrophin glycoprotein complex in mdx mice, a natural genetic mouse model of DMD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-79	dystrophin	Homo sapiens	141-151
20305374-6	2010	Moreover, the combination of celecoxib with MG132 synergistically inhibited cell viability and increased apoptosis, as documented by caspase 3 and 7 activation, PARP cleavage, and down-regulation of Bcl-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	caspase 3	Homo sapiens	133-142
20305374-6	2010	Moreover, the combination of celecoxib with MG132 synergistically inhibited cell viability and increased apoptosis, as documented by caspase 3 and 7 activation, PARP cleavage, and down-regulation of Bcl-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	collagen type XI alpha 2 chain	Homo sapiens	161-165
19399612-0	2010	Proteasome inhibitor MG132 inhibits angiogenesis in pancreatic cancer by blocking NF-kappaB activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	nuclear factor kappa B subunit 1	Homo sapiens	82-91
20305374-6	2010	Moreover, the combination of celecoxib with MG132 synergistically inhibited cell viability and increased apoptosis, as documented by caspase 3 and 7 activation, PARP cleavage, and down-regulation of Bcl-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	BCL2 apoptosis regulator	Homo sapiens	199-204
20305374-7	2010	Celecoxib and MG132, both alone and synergistically in combination, induced expression of the endoplasmic reticulum (ER) stress genes ATF4, CHOP, TRB3 and promoted the splicing of XBP1 mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	activating transcription factor 4	Homo sapiens	134-138
20305374-7	2010	Celecoxib and MG132, both alone and synergistically in combination, induced expression of the endoplasmic reticulum (ER) stress genes ATF4, CHOP, TRB3 and promoted the splicing of XBP1 mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	DNA damage inducible transcript 3	Homo sapiens	140-144
20305374-7	2010	Celecoxib and MG132, both alone and synergistically in combination, induced expression of the endoplasmic reticulum (ER) stress genes ATF4, CHOP, TRB3 and promoted the splicing of XBP1 mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	tribbles pseudokinase 3	Homo sapiens	146-150
20305374-7	2010	Celecoxib and MG132, both alone and synergistically in combination, induced expression of the endoplasmic reticulum (ER) stress genes ATF4, CHOP, TRB3 and promoted the splicing of XBP1 mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	X-box binding protein 1	Homo sapiens	180-184
19399612-6	2010	Collectively, MG132 blocked PaCa-derived VEGF and IL-8 production through inhibition of NF-kappaB activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	vascular endothelial growth factor A	Homo sapiens	41-45
19399612-6	2010	Collectively, MG132 blocked PaCa-derived VEGF and IL-8 production through inhibition of NF-kappaB activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	C-X-C motif chemokine ligand 8	Homo sapiens	50-54
19399612-6	2010	Collectively, MG132 blocked PaCa-derived VEGF and IL-8 production through inhibition of NF-kappaB activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	nuclear factor kappa B subunit 1	Homo sapiens	88-97
19399612-8	2010	Our studies show that MG132, a proteasome inhibitor, significantly blocked pancreatic-cancer-associated angiogenesis through inhibition of NF-kappaB and NF-kappaB-dependent proangiogenic gene products VEGF and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	nuclear factor kappa B subunit 1	Homo sapiens	139-148
19399612-8	2010	Our studies show that MG132, a proteasome inhibitor, significantly blocked pancreatic-cancer-associated angiogenesis through inhibition of NF-kappaB and NF-kappaB-dependent proangiogenic gene products VEGF and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	nuclear factor kappa B subunit 1	Homo sapiens	153-162
19399612-8	2010	Our studies show that MG132, a proteasome inhibitor, significantly blocked pancreatic-cancer-associated angiogenesis through inhibition of NF-kappaB and NF-kappaB-dependent proangiogenic gene products VEGF and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	vascular endothelial growth factor A	Homo sapiens	201-205
19399612-8	2010	Our studies show that MG132, a proteasome inhibitor, significantly blocked pancreatic-cancer-associated angiogenesis through inhibition of NF-kappaB and NF-kappaB-dependent proangiogenic gene products VEGF and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	C-X-C motif chemokine ligand 8	Homo sapiens	210-214
20419542-8	2010	Our data also showed that MG132 (inhibitor of NF-kappaB) and NG-nitro-l-arginine methyl ester (inhibitor of iNOS) inhibited hepatocyte apoptosis induced by d-GaIN.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	nuclear factor kappa B subunit 1	Homo sapiens	46-55
19907029-12	2010	These effects of TNF-alpha were inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	tumor necrosis factor	Homo sapiens	17-26
19907029-13	2010	MG132 also attenuated the TNF-alpha-induced inhibition of GJIC in these cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Homo sapiens	26-35
20436219-10	2010	DCA caused stronger than UDCA stimulation of the COX-2 mRNA expression in these cells and this effect was significantly attenuated by the addition of inhibitor of NF kappaB activity (proteosome inhibitor MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	204-210	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	49-54
20054823-7	2010	In this regard, proteasome inhibitor MG-132 mimicked the effect of LL-37 by up-regulating BMP4 expression and Smad1/5 phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	cathelicidin antimicrobial peptide	Homo sapiens	67-72
20054823-7	2010	In this regard, proteasome inhibitor MG-132 mimicked the effect of LL-37 by up-regulating BMP4 expression and Smad1/5 phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	bone morphogenetic protein 4	Homo sapiens	90-94
20054823-7	2010	In this regard, proteasome inhibitor MG-132 mimicked the effect of LL-37 by up-regulating BMP4 expression and Smad1/5 phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	SMAD family member 1	Homo sapiens	110-117
20089134-5	2010	Incubating cells over-expressing parkin with the proteasomal inhibitor, MG-132, restores 1B-DMT1 levels emphasizing that the observed changes are caused by degradation via the proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	solute carrier family 11 member 2	Homo sapiens	92-96
20604839-8	2010	Moreover, inhibition of melanoma cell migration by imidazole was restored by MG132, a proteasome inhibitor, via inhibition of beta-catenin degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	catenin (cadherin associated protein), beta 1	Mus musculus	126-138
20436219-10	2010	DCA caused stronger than UDCA stimulation of the COX-2 mRNA expression in these cells and this effect was significantly attenuated by the addition of inhibitor of NF kappaB activity (proteosome inhibitor MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	204-210	nuclear factor kappa B subunit 1	Homo sapiens	163-172
20646542-12	2010	(2) MG132 could induce the inhibition and apoptosis of HCE1/MCS cells and partially reverse the natural resistance of HCE1/MCS to cisplatin, of which partially reverse the natural resistance may be in relation to the down-regulation of NF-kappaB and bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	55-59
20026589-9	2010	The proteasome inhibitor MG132 strongly stabilized SUMO-2-conjugated HIF-2alpha during hypoxia but did not affect the total level of HIF-2alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	small ubiquitin like modifier 2	Homo sapiens	51-57
20026589-9	2010	The proteasome inhibitor MG132 strongly stabilized SUMO-2-conjugated HIF-2alpha during hypoxia but did not affect the total level of HIF-2alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	endothelial PAS domain protein 1	Homo sapiens	69-79
20005289-7	2010	In addition, MG132 reduced ERK phosphorylation, increased caspase-3 activation, Fas-L expression and Bcl-2 cleavage in evodiamine-treated A375-S2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	caspase 3	Homo sapiens	58-67
20005289-7	2010	In addition, MG132 reduced ERK phosphorylation, increased caspase-3 activation, Fas-L expression and Bcl-2 cleavage in evodiamine-treated A375-S2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	Fas ligand	Homo sapiens	80-85
20005289-7	2010	In addition, MG132 reduced ERK phosphorylation, increased caspase-3 activation, Fas-L expression and Bcl-2 cleavage in evodiamine-treated A375-S2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	BCL2 apoptosis regulator	Homo sapiens	101-106
20646542-0	2010	[Reversion of resistance to cisplatin induced by MG132 in cervical cancer line HCE1 multicellular spheroid].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	79-83
20646542-1	2010	OBJECTIVE: To investigate the effect of the ubiquitin-proteasome pathway inhibitor MG132 on the natural resistance to cisplatin in the human cervical cancer line (HCE1) multicellular spheroid (HCE1/MCS) model and to probe it if MG132 could reverse the HCE1/MCS resistance to cisplatin, as well as the possible mechanism of drug resistance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	163-167
20646542-9	2010	(3) The rate of apoptosis of HCE1/MC and HCE1/MCS were: in MG132 group, 8.14% and 5.97%; in MG132+cisplatin group, 99.01% and 95.22%; in cisplatin group, 33.61% and 0.88%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	29-33
20646542-9	2010	(3) The rate of apoptosis of HCE1/MC and HCE1/MCS were: in MG132 group, 8.14% and 5.97%; in MG132+cisplatin group, 99.01% and 95.22%; in cisplatin group, 33.61% and 0.88%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	41-45
20080137-6	2010	Further, we demonstrate that inhibition of HRSV in Vero cells by MG-132 corresponds with an increase in eIF2alpha phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	eukaryotic translation initiation factor 2A	Chlorocebus sabaeus	104-113
20080137-7	2010	Phosphorylation of eIF2alpha during MG-132 treatment only occurred in HRSV infected Vero cells, and not in GFP transfected controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	eukaryotic translation initiation factor 2A	Chlorocebus sabaeus	19-28
20646542-12	2010	(2) MG132 could induce the inhibition and apoptosis of HCE1/MCS cells and partially reverse the natural resistance of HCE1/MCS to cisplatin, of which partially reverse the natural resistance may be in relation to the down-regulation of NF-kappaB and bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	Miles-Carpenter X-linked mental retardation syndrome	Homo sapiens	60-63
20100472-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4microM at 48h and induced cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)), Bcl-2 decrease, activation of caspase-3 and -8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	B cell leukemia/lymphoma 2	Mus musculus	209-214
20100472-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4microM at 48h and induced cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)), Bcl-2 decrease, activation of caspase-3 and -8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Mus musculus	239-255
20100472-3	2010	MG132 inhibited the growth of As4.1 cells with an IC(50) of approximately 0.3-0.4microM at 48h and induced cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)), Bcl-2 decrease, activation of caspase-3 and -8, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	poly (ADP-ribose) polymerase family, member 1	Mus musculus	261-265
20100472-6	2010	NAC also decreased the caspase-3 activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	caspase 3	Mus musculus	23-32
20646542-9	2010	(3) The rate of apoptosis of HCE1/MC and HCE1/MCS were: in MG132 group, 8.14% and 5.97%; in MG132+cisplatin group, 99.01% and 95.22%; in cisplatin group, 33.61% and 0.88%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	Miles-Carpenter X-linked mental retardation syndrome	Homo sapiens	46-49
20646542-9	2010	(3) The rate of apoptosis of HCE1/MC and HCE1/MCS were: in MG132 group, 8.14% and 5.97%; in MG132+cisplatin group, 99.01% and 95.22%; in cisplatin group, 33.61% and 0.88%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	29-33
20646542-12	2010	(2) MG132 could induce the inhibition and apoptosis of HCE1/MCS cells and partially reverse the natural resistance of HCE1/MCS to cisplatin, of which partially reverse the natural resistance may be in relation to the down-regulation of NF-kappaB and bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	RNA guanylyltransferase and 5'-phosphatase	Homo sapiens	118-122
20646542-10	2010	(4) The expression level of NF-kappaB and the high expression rate of bcl-2 were: in HCE1/MCS of control group, 0.67 and 60%; in HCE1/MCS of cisplatin group, 0.85 and 83%; in HCE1/MCS of MG132 group, 0.39 and 20%; in HCE1/MCS of MG132+cisplatin group, 0.47 and 33%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	187-192	BCL2 apoptosis regulator	Homo sapiens	70-75
20646542-10	2010	(4) The expression level of NF-kappaB and the high expression rate of bcl-2 were: in HCE1/MCS of control group, 0.67 and 60%; in HCE1/MCS of cisplatin group, 0.85 and 83%; in HCE1/MCS of MG132 group, 0.39 and 20%; in HCE1/MCS of MG132+cisplatin group, 0.47 and 33%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	229-234	BCL2 apoptosis regulator	Homo sapiens	70-75
20646542-12	2010	(2) MG132 could induce the inhibition and apoptosis of HCE1/MCS cells and partially reverse the natural resistance of HCE1/MCS to cisplatin, of which partially reverse the natural resistance may be in relation to the down-regulation of NF-kappaB and bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	Miles-Carpenter X-linked mental retardation syndrome	Homo sapiens	123-126
20646542-12	2010	(2) MG132 could induce the inhibition and apoptosis of HCE1/MCS cells and partially reverse the natural resistance of HCE1/MCS to cisplatin, of which partially reverse the natural resistance may be in relation to the down-regulation of NF-kappaB and bcl-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-9	BCL2 apoptosis regulator	Homo sapiens	250-255
20171192-6	2010	Consistent with our previous findings from parkin knockout mice, rat models of PD (6-hydroxydopamine-, rotenone-, or MG132-induced PD) were also associated with an increase in soluble and insoluble PINK1 levels as well as enhanced formation of parkin aggregates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	PTEN induced kinase 1	Rattus norvegicus	198-203
20450628-0	2010	[Effect of MG-132 upon the expression of intercellular adhesion molecule-1 in cerulein-induced acute pancreatitis in mice].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	intercellular adhesion molecule 1	Mus musculus	41-74
20148946-6	2010	Ubiquitinated forms of BAF60b were found to accumulate upon treatment with the proteasome inhibitor MG132, indicating that BAF60b ubiquitination is of the degradative type and could regulate the level of BAF60b in SWI/SNF complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily d, member 2	Homo sapiens	23-29
20152813-7	2010	ABP1 was poly-ubiquitinated in tobacco cells and its stability was significantly increased in the presence of MG132, a 26S proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	endoplasmic reticulum auxin binding protein 1	Arabidopsis thaliana	0-4
20093492-9	2010	Furthermore, BMP-7 had no effect on Smad3 signaling after siRNA-mediated SnoN knockdown, whereas prevention of SnoN degradation with the proteasome inhibitor MG132 reproduced the inhibitory action of BMP-7 on Smad3 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	SKI like proto-oncogene	Homo sapiens	111-115
20093492-9	2010	Furthermore, BMP-7 had no effect on Smad3 signaling after siRNA-mediated SnoN knockdown, whereas prevention of SnoN degradation with the proteasome inhibitor MG132 reproduced the inhibitory action of BMP-7 on Smad3 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	bone morphogenetic protein 7	Homo sapiens	200-205
20093492-9	2010	Furthermore, BMP-7 had no effect on Smad3 signaling after siRNA-mediated SnoN knockdown, whereas prevention of SnoN degradation with the proteasome inhibitor MG132 reproduced the inhibitory action of BMP-7 on Smad3 signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	SMAD family member 3	Homo sapiens	209-214
20393010-0	2010	MG132, a proteasome inhibitor, induced death of calf pulmonary artery endothelial cells via caspase-dependent apoptosis and GSH depletion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 8	Bos taurus	92-99
20393010-5	2010	All the tested caspase inhibitors (pan-caspase, caspase-3, -8 and -9 inhibitor) significantly rescued CPAECs from MG132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	caspase 8	Bos taurus	15-22
20393010-5	2010	All the tested caspase inhibitors (pan-caspase, caspase-3, -8 and -9 inhibitor) significantly rescued CPAECs from MG132-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	caspase 3	Bos taurus	48-68
20045449-4	2010	Here we demonstrate that overexpression of wt PINK1 inhibits activation of Bax and release of cytochrome c, thereby diminishing caspase 9 processing and effector caspase activity after induction of proteasomal stress with the proteasome inhibitor (PI) MG132 in SHEP cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	252-257	PTEN induced kinase 1	Homo sapiens	46-51
20045449-4	2010	Here we demonstrate that overexpression of wt PINK1 inhibits activation of Bax and release of cytochrome c, thereby diminishing caspase 9 processing and effector caspase activity after induction of proteasomal stress with the proteasome inhibitor (PI) MG132 in SHEP cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	252-257	BCL2 associated X, apoptosis regulator	Homo sapiens	75-78
20053998-8	2010	Although the molecular mechanism(s) by which p38 promotes the degradation of melanogenic enzymes remain to be determined, the involvement of the ubiquitin-proteasome pathway was demonstrated by co-treatment with the proteasome-specific inhibitor MG132 and the relative decrease in the ubiquitination of tyrosinase in cells transfected with p38-specific small interfering RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	246-251	mitogen-activated protein kinase 14	Mus musculus	45-48
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	interleukin 6	Homo sapiens	64-68
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	interleukin 6	Homo sapiens	64-68
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	tumor necrosis factor	Homo sapiens	150-158
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	interleukin 6	Homo sapiens	167-171
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	NFKB inhibitor alpha	Homo sapiens	190-203
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	dual specificity phosphatase 1	Homo sapiens	310-315
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	mitogen-activated protein kinase 14	Homo sapiens	365-368
20043958-6	2010	Investigating the effect of MG-132 on secretion of the cytokine IL-6 we show that while short-term pretreatment with MG-132 (30min) partially reduced TNFalpha-induced IL-6 via inhibition of IkappaB-alpha degradation and the NF-kappaB pathway, longer-term proteasome inhibition (up to 24h) robustly upregulated MKP-1 and was temporally correlated with repression of p38-mediated IL-6 secretion from ASM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	interleukin 6	Homo sapiens	167-171
20043958-8	2010	Taken together, our results demonstrate that MG-132 upregulates MKP-1 and represses cytokine secretion from ASM and highlight the potential of the proteasome as a therapeutic target in asthma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	dual specificity phosphatase 1	Homo sapiens	64-69
19961488-5	2010	Incubation of Hepa-1c1c7 cells with the proteasome inhibitor MG132 elevated the levels of gap junction protein connexin 43 (Cx43) and promoted gap junctional intercellular communication.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	gap junction protein, alpha 1	Mus musculus	111-122
19961488-5	2010	Incubation of Hepa-1c1c7 cells with the proteasome inhibitor MG132 elevated the levels of gap junction protein connexin 43 (Cx43) and promoted gap junctional intercellular communication.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	gap junction protein, alpha 1	Mus musculus	124-128
19961488-7	2010	The elevated Cx43 contributed to MG132-induced cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	gap junction protein, alpha 1	Mus musculus	13-17
19961488-8	2010	This is shown by the observations that: (i) overexpression of Cx43 in the gap junction-deficient LLC-PK1 cells rendered them vulnerable to MG132-elicited cell injury; (ii) fibroblasts derived from Cx43-null mice were more resistant to MG-132 compared with Cx43 wild-type control; and (iii) the gap junction inhibitor flufenamic acid significantly attenuated cell damage caused by MG132 in Hepa-1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	gap junction protein alpha 1	Sus scrofa	62-66
19961488-8	2010	This is shown by the observations that: (i) overexpression of Cx43 in the gap junction-deficient LLC-PK1 cells rendered them vulnerable to MG132-elicited cell injury; (ii) fibroblasts derived from Cx43-null mice were more resistant to MG-132 compared with Cx43 wild-type control; and (iii) the gap junction inhibitor flufenamic acid significantly attenuated cell damage caused by MG132 in Hepa-1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	235-241	gap junction protein alpha 1	Sus scrofa	62-66
19961488-8	2010	This is shown by the observations that: (i) overexpression of Cx43 in the gap junction-deficient LLC-PK1 cells rendered them vulnerable to MG132-elicited cell injury; (ii) fibroblasts derived from Cx43-null mice were more resistant to MG-132 compared with Cx43 wild-type control; and (iii) the gap junction inhibitor flufenamic acid significantly attenuated cell damage caused by MG132 in Hepa-1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	380-385	gap junction protein alpha 1	Sus scrofa	62-66
19961488-11	2010	These results suggested that elevated Cx43 sensitizes cells to MG132-induced cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	gap junction protein, alpha 1	Mus musculus	38-42
19969553-6	2010	Studies using proteosome inhibitor MG132 suggested that omega-3 PUFAs induce degradation of the PcG protein EZH2 through posttranslational mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	108-112
20148946-6	2010	Ubiquitinated forms of BAF60b were found to accumulate upon treatment with the proteasome inhibitor MG132, indicating that BAF60b ubiquitination is of the degradative type and could regulate the level of BAF60b in SWI/SNF complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily d, member 2	Homo sapiens	123-129
20148946-6	2010	Ubiquitinated forms of BAF60b were found to accumulate upon treatment with the proteasome inhibitor MG132, indicating that BAF60b ubiquitination is of the degradative type and could regulate the level of BAF60b in SWI/SNF complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily d, member 2	Homo sapiens	123-129
20091742-10	2010	In addition, through the use of cycloheximide and the proteasome inhibitor MG132, we showed that hyperosmolarity significantly increased the half-life and inhibited the protein level of TGF-beta RI by polyubiquitination and proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	transforming growth factor beta 1	Homo sapiens	186-194
19996297-11	2010	AD-induced increases in beta-arrestin2 ubiquitinylation led to its degradation by the proteasomal pathway, as the proteasome inhibitor N-[(phenylmethoxy)carbonyl]-l-leucyl-N-[(1S)-1-formyl-3-methylbutyl]-l-leucinamide (MG-132) prevented antidepressant-induced decreases in beta-arrestin2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	219-225	arrestin, beta 2, pseudogene	Rattus norvegicus	24-38
20122816-8	2010	In contrast, treatment with PMA and IFNgamma reduced the RARgamma and RXRalpha protein expression (preventable by the proteasome inhibitor MG132), increased the accumulation of [(3)H]RA and/or [(3)H]ddRA in the cells, and changed the CRABPII transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	interferon gamma	Homo sapiens	36-44
20122816-8	2010	In contrast, treatment with PMA and IFNgamma reduced the RARgamma and RXRalpha protein expression (preventable by the proteasome inhibitor MG132), increased the accumulation of [(3)H]RA and/or [(3)H]ddRA in the cells, and changed the CRABPII transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	retinoic acid receptor gamma	Homo sapiens	57-65
20122816-8	2010	In contrast, treatment with PMA and IFNgamma reduced the RARgamma and RXRalpha protein expression (preventable by the proteasome inhibitor MG132), increased the accumulation of [(3)H]RA and/or [(3)H]ddRA in the cells, and changed the CRABPII transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	retinoid X receptor alpha	Homo sapiens	70-78
19781773-7	2010	Furthermore, proteasome inhibitor MG132 prevented the down-regulation of survivin expression and STAT3 dephosphorylation by deguelin, suggesting that the action mechanism of deguelin involves the degradation of survivin and phosphorylated STAT3 through the ubiquitin/proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	signal transducer and activator of transcription 3	Homo sapiens	97-102
19781773-7	2010	Furthermore, proteasome inhibitor MG132 prevented the down-regulation of survivin expression and STAT3 dephosphorylation by deguelin, suggesting that the action mechanism of deguelin involves the degradation of survivin and phosphorylated STAT3 through the ubiquitin/proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	signal transducer and activator of transcription 3	Homo sapiens	239-244
19769945-4	2010	Western blotting demonstrated that WA inhibited Hsp90 chaperone activity to induce degradation of Hsp90 client proteins (Akt, Cdk4 and glucocorticoid receptor), which was reversed by the proteasomal inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	210-215	heat shock protein 90 alpha family class A member 1	Homo sapiens	48-53
20064569-6	2010	Upon treatment with a proteasome inhibitor, MG132, the ubiquitinylated species of NR1 subunit were detected, suggesting that NR1 is being targeted for endoplasmic reticulum-associated proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	82-85
20064569-6	2010	Upon treatment with a proteasome inhibitor, MG132, the ubiquitinylated species of NR1 subunit were detected, suggesting that NR1 is being targeted for endoplasmic reticulum-associated proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	125-128
19646807-0	2010	The pharmacological NFkappaB inhibitors BAY117082 and MG132 induce cell arrest and apoptosis in leukemia cells through ROS-mitochondria pathway activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	nuclear factor kappa B subunit 1	Homo sapiens	20-28
19646807-2	2010	In this work, we evaluated the effects of the pharmacological NFkappaB inhibitors BAY117082 and MG132 on leukemia cells apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	nuclear factor kappa B subunit 1	Homo sapiens	62-70
19646807-3	2010	BAY117082 and MG132 presented potent apoptotic effects compared to inhibitors of MAPKs, EGFR, PI3K/Akt, PKC and PKA signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	AKT serine/threonine kinase 1	Homo sapiens	99-102
19646807-5	2010	BAY117082 and MG132-induced apoptosis was dependent on their ability to increase ROS as a prelude to mitochondria membrane potential (MMP) depolarization, permeability transition pore opening and cytochrome c release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	cytochrome c, somatic	Homo sapiens	196-208
19646807-8	2010	In contrast, MG132 induced classical apoptosis through ROS-mitochondria and subsequent caspase-9/caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	caspase 9	Homo sapiens	87-96
19646807-8	2010	In contrast, MG132 induced classical apoptosis through ROS-mitochondria and subsequent caspase-9/caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	caspase 3	Homo sapiens	97-106
19646807-9	2010	At sub-apoptotic concentrations, BAY117082 and MG132 arrested cells in G2/M phase of the cell cycle and blocked doxorubicin-induced NFkappaB, which sensitized doxorubicin-resistant cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	nuclear factor kappa B subunit 1	Homo sapiens	132-140
19646807-10	2010	Data suggest that the NFkappaB inhibitors MG132 and BAY117082 are potential anti-leukemia agents.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	nuclear factor kappa B subunit 1	Homo sapiens	22-30
19769945-4	2010	Western blotting demonstrated that WA inhibited Hsp90 chaperone activity to induce degradation of Hsp90 client proteins (Akt, Cdk4 and glucocorticoid receptor), which was reversed by the proteasomal inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	210-215	heat shock protein 90 alpha family class A member 1	Homo sapiens	98-103
19769945-4	2010	Western blotting demonstrated that WA inhibited Hsp90 chaperone activity to induce degradation of Hsp90 client proteins (Akt, Cdk4 and glucocorticoid receptor), which was reversed by the proteasomal inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	210-215	AKT serine/threonine kinase 1	Homo sapiens	121-124
19769945-4	2010	Western blotting demonstrated that WA inhibited Hsp90 chaperone activity to induce degradation of Hsp90 client proteins (Akt, Cdk4 and glucocorticoid receptor), which was reversed by the proteasomal inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	210-215	cyclin dependent kinase 4	Homo sapiens	126-130
19769945-4	2010	Western blotting demonstrated that WA inhibited Hsp90 chaperone activity to induce degradation of Hsp90 client proteins (Akt, Cdk4 and glucocorticoid receptor), which was reversed by the proteasomal inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	210-215	nuclear receptor subfamily 3 group C member 1	Homo sapiens	135-158
19796682-7	2010	The UV-dependent loss of nuclear BARD1 was blocked by the proteasome inhibitor MG132, but not by leptomycin B, indicating a change in BARD1 nuclear degradation rather than nuclear export.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	BRCA1 associated RING domain 1	Homo sapiens	33-38
20104019-3	2010	Three widely used ER stress inducers including tunicamycin, DTT and MG132 led to the conversion of LC3-I to LC3-II , a commonly used marker of autophagy, as well as the downregulation of mTOR concurrently.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	mechanistic target of rapamycin kinase	Homo sapiens	187-191
20087064-5	2010	Abolition of macroautophagy by knockdown of Class III phosphatidylinositol-3 kinase Vps34 or ATG5/7 sensitized gastric cancer cells to the antiproliferative effect of MG-132 by promoting G(2)/M cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	167-173	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	84-89
20087064-5	2010	Abolition of macroautophagy by knockdown of Class III phosphatidylinositol-3 kinase Vps34 or ATG5/7 sensitized gastric cancer cells to the antiproliferative effect of MG-132 by promoting G(2)/M cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	167-173	autophagy related 5	Homo sapiens	93-97
20087064-6	2010	In addition, MG-132 increased ERK phosphorylation whose inhibition by MEK inhibitor significantly enhanced the antiproliferative effect of proteasome inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	EPH receptor B2	Homo sapiens	30-33
20087064-6	2010	In addition, MG-132 increased ERK phosphorylation whose inhibition by MEK inhibitor significantly enhanced the antiproliferative effect of proteasome inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	mitogen-activated protein kinase kinase 7	Homo sapiens	70-73
19796682-7	2010	The UV-dependent loss of nuclear BARD1 was blocked by the proteasome inhibitor MG132, but not by leptomycin B, indicating a change in BARD1 nuclear degradation rather than nuclear export.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	BRCA1 associated RING domain 1	Homo sapiens	134-139
19796682-8	2010	MG132 also blocked the dispersal of BARD1/BRCA1 nuclear foci at 6h after UV, implicating the proteasome in repair foci disassembly.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BRCA1 associated RING domain 1	Homo sapiens	36-41
19796682-8	2010	MG132 also blocked the dispersal of BARD1/BRCA1 nuclear foci at 6h after UV, implicating the proteasome in repair foci disassembly.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BRCA1 DNA repair associated	Homo sapiens	42-47
19859909-7	2010	While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	growth factor, augmenter of liver regeneration	Rattus norvegicus	46-49
20074015-12	2010	Moreover, it was found that well-known proteasome inhibitors, such as MG115, MG132 and bortezomib, inhibit FoxM1 transcriptional activity and FoxM1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	forkhead box M1	Homo sapiens	107-112
20074015-12	2010	Moreover, it was found that well-known proteasome inhibitors, such as MG115, MG132 and bortezomib, inhibit FoxM1 transcriptional activity and FoxM1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	forkhead box M1	Homo sapiens	142-147
20043067-9	2010	Proteasome inhibitor MG132 disturbed the reduction of RRM1 expression in tranilast treated KP4 cells, indicating protein degradation by the activated proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	ribonucleotide reductase catalytic subunit M1	Homo sapiens	54-58
19859909-7	2010	While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	mitogen activated protein kinase 14	Rattus norvegicus	82-85
19859909-7	2010	While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	growth factor, augmenter of liver regeneration	Rattus norvegicus	46-49
19859909-7	2010	While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	growth factor, augmenter of liver regeneration	Rattus norvegicus	122-125
19859909-7	2010	While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	tumor necrosis factor	Rattus norvegicus	134-143
19859909-7	2010	While inhibitor of NFkappaB (MG132) inhibited ALR-induced NO synthesis, MG132 and p38-MAPK inhibitor (SB203580) abrogated ALR-induced TNF-alpha and IL-6 synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	interleukin 6	Rattus norvegicus	148-152
20487197-8	2010	Treatment with the proteasome inhibitor MG132 blocked the decrease in MITF by sphingosylphosphorylcholine, but sphingosylphosphorylcholine did not decrease the level of MITF mRNA, indicating that the reduction in the level of MITF results from MITF degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	melanogenesis associated transcription factor	Mus musculus	70-74
20181055-5	2010	Blocking NFkappaB with MG-132 also inhibited pro-coagulant activation of monocytes by fibrinogen.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-29	fibrinogen beta chain	Homo sapiens	86-96
20006625-8	2010	KEY FINDINGS: Both bortezomib and another proteasome inhibitor, MG-132, significantly reduced FAK expression, suppressed cancer cell migration and increased cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	protein tyrosine kinase 2	Homo sapiens	94-97
19813265-8	2010	MG132-treated embryos showed increased expression of POU5F1, DPPA2, DPPA3, DPPA5, and NDP52l1 genes compared to control embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	POU domain, class 5, transcription factor 1	Sus scrofa	53-59
19813265-8	2010	MG132-treated embryos showed increased expression of POU5F1, DPPA2, DPPA3, DPPA5, and NDP52l1 genes compared to control embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	developmental pluripotency associated 2	Sus scrofa	61-66
19813265-8	2010	MG132-treated embryos showed increased expression of POU5F1, DPPA2, DPPA3, DPPA5, and NDP52l1 genes compared to control embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	developmental pluripotency-associated protein 3	Sus scrofa	68-73
19813265-8	2010	MG132-treated embryos showed increased expression of POU5F1, DPPA2, DPPA3, DPPA5, and NDP52l1 genes compared to control embryos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	developmental pluripotency associated 5	Sus scrofa	75-80
19699182-4	2010	Proteasome inhibitors PS-341 and MG-132 blocked cisplatin-induced Mcl-1 depletion and markedly prevented mitochondrial release of AIF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	myeloid cell leukemia sequence 1	Mus musculus	66-71
19944744-4	2010	In this study, we demonstrated that the protein levels of TDP-43 and TDP-25 were increased in cells treated with a proteasome inhibitor, MG132, or an autophagy inhibitor, 3-MA, whereas, they were decreased in cells treated with an enhancer of autophagy, trehalose.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	TAR DNA binding protein	Homo sapiens	58-64
19699182-4	2010	Proteasome inhibitors PS-341 and MG-132 blocked cisplatin-induced Mcl-1 depletion and markedly prevented mitochondrial release of AIF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	130-133
19887452-9	2010	SIRT1 degradation is markedly blocked by SB203589 or MG132 after IR treatment, suggesting that cleavage occurs as a result of binding with p38 kinase, followed by processing via the 26 S proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	sirtuin 1	Homo sapiens	0-5
19699182-10	2010	In an in vivo model of cisplatin nephrotoxicity, proteasome inhibitor MG-132 prevented mitochondrial release of AIF and markedly attenuated acute kidney injury as assessed by renal function and histology.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	112-115
19769966-5	2010	We determined that MORF4 protein was unstable and that addition of the proteasome inhibitor MG132 resulted in the accumulation of the protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	mortality factor 4 (pseudogene)	Homo sapiens	19-24
20016288-9	2010	Pretreatment of the cells with MG132, a proteasome inhibitor, abolished the IFN-alpha2b-mediated p21 degradation, suggesting that IFN-alpha2b accelerated the ubiquitin-proteasome dependent degradation of p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	cyclin dependent kinase inhibitor 1A	Homo sapiens	97-100
20016288-9	2010	Pretreatment of the cells with MG132, a proteasome inhibitor, abolished the IFN-alpha2b-mediated p21 degradation, suggesting that IFN-alpha2b accelerated the ubiquitin-proteasome dependent degradation of p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	cyclin dependent kinase inhibitor 1A	Homo sapiens	204-207
20798512-5	2010	Reversion studies and activation of GCN2 by tRNA and the proteasome inhibitor MG-132 showed a correlation between GCN2 phosphorylation and diminished ROS levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	36-40
20798512-5	2010	Reversion studies and activation of GCN2 by tRNA and the proteasome inhibitor MG-132 showed a correlation between GCN2 phosphorylation and diminished ROS levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	114-118
21220940-12	2010	The addition of MG132 further enhanced the mechanical strain induced activation of Smad proteins and the increased expression of ALP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	SMAD family member 1	Mus musculus	83-87
21127388-11	2010	The ET-induced expression of MMP9, but not MMP2, was inhibited by pyrrolidine dithiocarbamate, proteasome inhibitor I, and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	matrix metallopeptidase 9	Rattus norvegicus	29-33
20061635-8	2010	Moreover, specific proteasome inhibitors, MG132 and lactacystin, blocked the turnover of NEP, whereas inhibitors of lysosome had no significant effect, suggesting that Cu2+-induced degradation of NEP is via a proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	membrane metallo endopeptidase	Mus musculus	89-92
20061635-8	2010	Moreover, specific proteasome inhibitors, MG132 and lactacystin, blocked the turnover of NEP, whereas inhibitors of lysosome had no significant effect, suggesting that Cu2+-induced degradation of NEP is via a proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	immunoglobulin kappa variable 1-35	Mus musculus	168-171
20061635-8	2010	Moreover, specific proteasome inhibitors, MG132 and lactacystin, blocked the turnover of NEP, whereas inhibitors of lysosome had no significant effect, suggesting that Cu2+-induced degradation of NEP is via a proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	membrane metallo endopeptidase	Mus musculus	196-199
19737590-7	2010	Geldanamycin-induced decrease of insulin receptor substrate-1 was attenuated by lactacystin, beta-lactone or MG132 (proteasome inhibitor), but not by calpastatin (calpain inhibitor) or leupeptin (lysosome inhibitor); geldanamycin did not affect heteroprotein complex formation between insulin receptor substrate-1 or -2 and Hsp90.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	insulin receptor substrate 1	Bos taurus	33-61
19765735-3	2010	In this study, we investigate the ability of MG-132, a proteasome inhibitor, to inhibit carcinoid growth, the neuroendocrine phenotype, and its association with GSK-3beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	glycogen synthase kinase 3 beta	Homo sapiens	161-170
19765735-7	2010	RESULTS: Treating carcinoid cells with MG-132 resulted in growth inhibition, a dose-dependent inhibition of CgA and ASCL1, as well as an increase in the levels of cleaved PARP and cleaved caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	chromogranin A	Homo sapiens	108-111
19765735-7	2010	RESULTS: Treating carcinoid cells with MG-132 resulted in growth inhibition, a dose-dependent inhibition of CgA and ASCL1, as well as an increase in the levels of cleaved PARP and cleaved caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	achaete-scute family bHLH transcription factor 1	Homo sapiens	116-121
19765735-7	2010	RESULTS: Treating carcinoid cells with MG-132 resulted in growth inhibition, a dose-dependent inhibition of CgA and ASCL1, as well as an increase in the levels of cleaved PARP and cleaved caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	poly(ADP-ribose) polymerase 1	Homo sapiens	171-175
20377132-0	2010	The attenuation of MG132, a proteasome inhibitor, induced A549 lung cancer cell death by p38 inhibitor in ROS-independent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	mitogen-activated protein kinase 14	Homo sapiens	89-92
20377132-2	2010	In this study, we investigated the effects of MAPK (MEK, JNK, and p38) inhibitors on MG132-treated A549 lung cancer cells in relation to cell growth, cell death, ROS, and glutathione (GSH) levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	mitogen-activated protein kinase kinase 7	Homo sapiens	52-55
20377132-2	2010	In this study, we investigated the effects of MAPK (MEK, JNK, and p38) inhibitors on MG132-treated A549 lung cancer cells in relation to cell growth, cell death, ROS, and glutathione (GSH) levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	mitogen-activated protein kinase 8	Homo sapiens	57-60
20377132-2	2010	In this study, we investigated the effects of MAPK (MEK, JNK, and p38) inhibitors on MG132-treated A549 lung cancer cells in relation to cell growth, cell death, ROS, and glutathione (GSH) levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	mitogen-activated protein kinase 14	Homo sapiens	66-69
20377132-7	2010	In contrast, p38 inhibitor reduced cell growth inhibition, apoptosis, and MMP (deltapsi(m)) loss by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	mitogen-activated protein kinase 14	Homo sapiens	13-16
20377132-10	2010	Treatment with p38 inhibitor rescued some cells from MG132-induced apotposis, which was not affected by ROS and GSH level changes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	mitogen-activated protein kinase 14	Homo sapiens	15-18
19824885-6	2009	The proteasome inhibitor MG132 partially restored Fas expression and resensitized the cells to FasL, but not to ALP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	Fas ligand (TNF superfamily, member 6)	Mus musculus	95-99
20007772-8	2009	RAB3B overexpression in BE (2)-M17 cells was protective against toxins that simulate aspects of PD in vitro, including an oxidative stressor 6-hydroxydopamine (6-OHDA) and a proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	195-201	RAB3B, member RAS oncogene family	Rattus norvegicus	0-5
19909340-8	2009	Immunoblotting with anti-ubiquitin IgG1k after immunoprecipitation of ABCG2 revealed that the N596Q protein was ubiquitinated at levels that were significantly enhanced by treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	187-192	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	70-75
19952428-3	2009	Pretreatment with MG132 blocked hypoxia-induced degradation of ERalpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	estrogen receptor 1	Homo sapiens	63-70
19909340-9	2009	Immunofluorescence microscopy demonstrated that treatment with MG132 increased the level of ABCG2 N596Q protein both in intracellular compartments and in the plasma membrane.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	92-97
19681889-8	2009	KEY RESULTS: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 1	Homo sapiens	81-118
19739101-10	2009	Proteasome inhibition by MG132 stabilizes Runx2 protein levels in late G(1) and S in MC3T3-E1 cells, but not in ROS17/2.8 and SaOS-2 osteosarcoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	runt related transcription factor 2	Mus musculus	42-47
20078948-2	2009	METHOD: The degradation pathway of SNF5 was identified with protein synthesis inhibitor cycloheximide (CHX) and a potent proteasome inhibitor MG132, and then the PIH1D1 eukaryotic expression plasmid was transfected to explore its effect on the stability of SNF5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	35-39
19681889-9	2009	Induction of BAG3 by MG132 was inhibited by blocking JNK, but not ERK1/2 and p38 MAPK signalling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	mitogen-activated protein kinase 8	Homo sapiens	53-56
19681889-11	2009	Furthermore, activation of the JNK pathway induced BAG in kidney cancer cells after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	mitogen-activated protein kinase 8	Homo sapiens	31-34
19681889-8	2009	KEY RESULTS: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 1	Homo sapiens	120-123
19681889-8	2009	KEY RESULTS: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 8	Homo sapiens	126-149
19681889-8	2009	KEY RESULTS: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 8	Homo sapiens	151-154
19681889-8	2009	KEY RESULTS: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 14	Homo sapiens	160-196
19681889-8	2009	KEY RESULTS: MG132 activated several key mitogenic signalling pathways including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 3	Homo sapiens	198-202
19681889-9	2009	Induction of BAG3 by MG132 was inhibited by blocking JNK, but not ERK1/2 and p38 MAPK signalling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	BAG cochaperone 3	Homo sapiens	13-17
19711372-8	2009	Furthermore, pH 6.6-induced detachment of E-cadherin from AJs was blocked by pretreatment with MG132 or NH(4)Cl, indicating the involvement of ubiquitin-proteasomal/lysosomal degradation of E-cadherin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	cadherin 1	Homo sapiens	42-52
19330846-10	2009	MG-132 promotes the formation of small oligomers of HSP25, which have been connected to the protection of the microfilament system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	heat shock protein family B (small) member 1	Homo sapiens	52-57
19330846-12	2009	Hence, HSP25 enables astrocytes to prevent irreversible damage and to recover after removal of the proteasomal inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	heat shock protein family B (small) member 1	Homo sapiens	7-12
19446037-6	2009	Using proteosome inhibitor MG132 and I kappaB overexpression we demonstrated that an NF-kappaB-dependent mechanism was involved in both the activation of IL-8 and the repression of MCP-1 mRNA expression in response to hypoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	nuclear factor kappa B subunit 1	Homo sapiens	85-94
19446037-6	2009	Using proteosome inhibitor MG132 and I kappaB overexpression we demonstrated that an NF-kappaB-dependent mechanism was involved in both the activation of IL-8 and the repression of MCP-1 mRNA expression in response to hypoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	C-X-C motif chemokine ligand 8	Homo sapiens	154-158
19446037-6	2009	Using proteosome inhibitor MG132 and I kappaB overexpression we demonstrated that an NF-kappaB-dependent mechanism was involved in both the activation of IL-8 and the repression of MCP-1 mRNA expression in response to hypoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	C-C motif chemokine ligand 2	Homo sapiens	181-186
19787264-9	2009	Supporting the notion, siRNA-mediated knockdown of BRD8 induced cell death or growth delay in colorectal cancer cell lines, and surviving BRD8-knockdown cells were particularly sensitive to spindle poisons and a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	233-238	bromodomain containing 8	Homo sapiens	51-55
19787264-9	2009	Supporting the notion, siRNA-mediated knockdown of BRD8 induced cell death or growth delay in colorectal cancer cell lines, and surviving BRD8-knockdown cells were particularly sensitive to spindle poisons and a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	233-238	bromodomain containing 8	Homo sapiens	138-142
19711372-8	2009	Furthermore, pH 6.6-induced detachment of E-cadherin from AJs was blocked by pretreatment with MG132 or NH(4)Cl, indicating the involvement of ubiquitin-proteasomal/lysosomal degradation of E-cadherin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	cadherin 1	Homo sapiens	190-200
19699254-5	2009	The proteasome inhibitor MG132 completely blocked capsaicin-induced p53 degradation and enhanced apoptotic cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	68-71
19565657-4	2009	Washout of proteasome inhibitor (MG132) results in an enhancement of ERK1/2 activation and amelioration of JNK activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	mitogen-activated protein kinase 3	Mus musculus	69-75
19565657-4	2009	Washout of proteasome inhibitor (MG132) results in an enhancement of ERK1/2 activation and amelioration of JNK activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	mitogen-activated protein kinase 8	Mus musculus	107-110
19724054-6	2009	A proteasome inhibitor, MG132, suppresses secretion of AQP-1, implying that ubiquitination is a sorting signal for its release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	aquaporin 1	Mus musculus	55-60
19934380-7	2009	Protein gel blot analysis showed that the decrease in WRKY6 protein induced by low Pi treatment was inhibited by a 26S proteosome inhibitor, MG132, suggesting that low Pi-induced release of PHO1 repression may result from 26S proteosome-mediated proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	WRKY family transcription factor	Arabidopsis thaliana	54-59
19934380-7	2009	Protein gel blot analysis showed that the decrease in WRKY6 protein induced by low Pi treatment was inhibited by a 26S proteosome inhibitor, MG132, suggesting that low Pi-induced release of PHO1 repression may result from 26S proteosome-mediated proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	phosphate 1	Arabidopsis thaliana	190-194
19631348-5	2009	Proteasomal inhibition using MG-132 increased the proportion of phosphorylated IkappaB-alpha in nondystrophic diaphragm, but did not significantly increase this proportion in the mdx diaphragm.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	NFKB inhibitor alpha	Homo sapiens	79-92
19665001-6	2009	The proteasomal inhibitors MG132, epoxomicin, lactacystin, and ALLN suppressed T0070907-mediated tubulin loss, although epoxomicin and lactacystin were less effective than MG132, even at concentrations that completely inhibited TNFalpha-induced IkappaBalpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	tumor necrosis factor	Homo sapiens	228-236
19665001-6	2009	The proteasomal inhibitors MG132, epoxomicin, lactacystin, and ALLN suppressed T0070907-mediated tubulin loss, although epoxomicin and lactacystin were less effective than MG132, even at concentrations that completely inhibited TNFalpha-induced IkappaBalpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	NFKB inhibitor alpha	Homo sapiens	245-257
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 3	Arabidopsis thaliana	60-64
19729027-9	2009	In NCI-H292 cells, the LPS-enhanced downregulation of GR expression was recovered by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-116	nuclear receptor subfamily 3 group C member 1	Homo sapiens	54-56
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 5	Arabidopsis thaliana	66-70
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 7	Arabidopsis thaliana	72-76
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 16	Arabidopsis thaliana	78-83
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 17	Arabidopsis thaliana	88-93
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 3	Arabidopsis thaliana	104-108
19621034-8	2009	We found that the accumulation of a subset of ARR proteins (ARR3, ARR5, ARR7, ARR16 and ARR17; possibly ARR8 and ARR15) is increased by MG132, a specific proteasomal inhibitor, indicating that stability of these proteins is regulated by proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	response regulator 15	Arabidopsis thaliana	113-118
19295495-6	2009	NOS2 protein expression and the LPS/IFN-gamma-induced fall in phosphorylated S6 were prevented by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	nitric oxide synthase 2	Homo sapiens	0-4
19295495-6	2009	NOS2 protein expression and the LPS/IFN-gamma-induced fall in phosphorylated S6 were prevented by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	interferon regulatory factor 6	Homo sapiens	32-45
19631210-4	2009	MAFbx overexpression resulted in MG132-sensitive reduction of myogenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	F-box protein 32	Homo sapiens	0-5
19540199-8	2009	Knockdown of raptor, a structural component of mTOR complex 1, mimicked the anti-proliferative effect of MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	mechanistic target of rapamycin kinase	Homo sapiens	47-51
19631210-4	2009	MAFbx overexpression resulted in MG132-sensitive reduction of myogenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	myogenin	Homo sapiens	62-70
19597039-7	2009	Finally, Ang II infusion in mice decreased the levels of both BH4 and GTP cyclohydrolase I and impaired endothelial-dependent relaxation in isolated aortas, and all of these effects were prevented by the administration of MG132, a potent inhibitor for 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-227	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	9-15
19597039-7	2009	Finally, Ang II infusion in mice decreased the levels of both BH4 and GTP cyclohydrolase I and impaired endothelial-dependent relaxation in isolated aortas, and all of these effects were prevented by the administration of MG132, a potent inhibitor for 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-227	GTP cyclohydrolase 1	Mus musculus	70-90
19552924-8	2009	MG132 treatment also caused increased p21(Waf1/Cip1) and decreased cyclin D1 expression, suggesting that growth suppression may occur through cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1A	Homo sapiens	38-41
19298529-8	2009	Activation of PI3K-Akt signalling resulted in a decrease in the protein level of the transcription factor p53 via mouse double minute 2 (MDM2), an effect that was prevented by MG-132, an inhibitor of the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	thymoma viral proto-oncogene 1	Mus musculus	19-22
19298529-8	2009	Activation of PI3K-Akt signalling resulted in a decrease in the protein level of the transcription factor p53 via mouse double minute 2 (MDM2), an effect that was prevented by MG-132, an inhibitor of the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	transformation related protein 53, pseudogene	Mus musculus	106-109
19298529-8	2009	Activation of PI3K-Akt signalling resulted in a decrease in the protein level of the transcription factor p53 via mouse double minute 2 (MDM2), an effect that was prevented by MG-132, an inhibitor of the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	transformed mouse 3T3 cell double minute 2	Mus musculus	137-141
19017362-9	2009	The proteasome inhibitor MG-132 evoked the accumulation of perinuclear aggregates positive for Hsp70, ubiquitin-protein conjugates and the lysosomal membrane protein LAMP-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	heat shock protein family A (Hsp70) member 4	Homo sapiens	95-100
19017362-9	2009	The proteasome inhibitor MG-132 evoked the accumulation of perinuclear aggregates positive for Hsp70, ubiquitin-protein conjugates and the lysosomal membrane protein LAMP-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	lysosomal associated membrane protein 2	Homo sapiens	166-172
19552924-8	2009	MG132 treatment also caused increased p21(Waf1/Cip1) and decreased cyclin D1 expression, suggesting that growth suppression may occur through cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1A	Homo sapiens	42-46
19552924-8	2009	MG132 treatment also caused increased p21(Waf1/Cip1) and decreased cyclin D1 expression, suggesting that growth suppression may occur through cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1A	Homo sapiens	47-51
19552924-8	2009	MG132 treatment also caused increased p21(Waf1/Cip1) and decreased cyclin D1 expression, suggesting that growth suppression may occur through cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin D1	Homo sapiens	67-76
19541767-6	2009	The ER stress-induced reduction in IR cellular levels was greatly alleviated by the autophagy inhibitor 3-methyladenine but not by the proteasome inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	199-204	insulin receptor	Mus musculus	35-37
19520899-4	2009	However, MG132 has been reported to suppress P450s 3A as a result of impaired nuclear factor-kappaB activation and consequently reduced CYP3A protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	136-141
19520899-6	2009	We found a biphasic MG132 concentration effect on CYP3A turnover: Stabilization at 5 to 10 muM with marked suppression at &gt;100 microM.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	50-55
19520899-8	2009	At these high MG132 concentrations, such CYP3A suppression could be due to ER stress induction, so we monitored the activity of PERK [PKR (RNA-dependent protein kinase)-like ER kinase (EIF2AK3)], the ER stress-activated eukaryotic initiation factor 2alpha (eIF2alpha) kinase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	41-46
19263435-8	2009	Finally, studies with the proteasome inhibitor MG132 revealed that overexpression of PPP1R13L causes faster p53 degradation, a likely explanation for the depletion of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	protein phosphatase 1, regulatory subunit 13 like	Mus musculus	85-93
19675674-4	2009	However, JNK2-mediated downregulation of beta-catenin was blocked by the proteasome inhibitor MG132 and GSK3beta inhibitor lithium chloride.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	mitogen-activated protein kinase 9	Homo sapiens	9-13
19549782-6	2009	Inhibition of the proteasome with MG132 reveals that both mutant neuroserpin and alpha(1)-antitrypsin are degraded predominantly by endoplasmic reticulum-associated degradation (ERAD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	serpin family I member 1	Rattus norvegicus	65-76
19520899-10	2009	In parallel, MG132 also activated GCN2 [general control nonderepressible-2 (EIF2AK4)] eIF2alpha kinase in a concentration-dependent manner, but not the heme-regulated inhibitor eIF2alpha kinase [(EIF2AK1)].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	eukaryotic translation initiation factor 2 alpha kinase 4	Rattus norvegicus	76-83
19520899-10	2009	In parallel, MG132 also activated GCN2 [general control nonderepressible-2 (EIF2AK4)] eIF2alpha kinase in a concentration-dependent manner, but not the heme-regulated inhibitor eIF2alpha kinase [(EIF2AK1)].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	eukaryotic translation initiation factor 2A	Rattus norvegicus	86-95
19520899-10	2009	In parallel, MG132 also activated GCN2 [general control nonderepressible-2 (EIF2AK4)] eIF2alpha kinase in a concentration-dependent manner, but not the heme-regulated inhibitor eIF2alpha kinase [(EIF2AK1)].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	eukaryotic translation initiation factor 2 alpha kinase 1	Rattus norvegicus	196-203
19520899-12	2009	These findings reveal that at high concentrations, MG132 is indeed cytotoxic and can suppress CYP3A synthesis, a result confirmed by confocal immunofluorescence analyses of MG132-treated hepatocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	94-99
19675674-4	2009	However, JNK2-mediated downregulation of beta-catenin was blocked by the proteasome inhibitor MG132 and GSK3beta inhibitor lithium chloride.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	catenin beta 1	Homo sapiens	41-53
19481953-2	2009	The results indicated that PCF, ROS scavenger NAC and NF-kappaB inhibitor MG132 effectively inhibited UVB-induced HaCaT cells apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	nuclear factor kappa B subunit 1	Homo sapiens	54-63
19672316-5	2009	More importantly, we also found that well-known proteasome inhibitors such as MG115, MG132 and bortezomib inhibit FoxM1 transcriptional activity and FoxM1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	forkhead box M1	Homo sapiens	114-119
19672316-5	2009	More importantly, we also found that well-known proteasome inhibitors such as MG115, MG132 and bortezomib inhibit FoxM1 transcriptional activity and FoxM1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	forkhead box M1	Homo sapiens	149-154
19379726-6	2009	In contrast, other NF-kappaB inhibitors, such as fenofibrate, N-acetylcysteine and MG132, decreased MMP expression in IL-1beta-stimulated FLSs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	nuclear factor kappa B subunit 1	Homo sapiens	19-28
19365810-4	2009	Disruption of the proteosome pathway using selective inhibitors (MG-132, MG-115, and epoxomicin) resulted in the accumulation of p62 and CYLD, and altered the subcellular targeting and distribution of p62 and TRAF6 in osteoclast-like cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	nucleoporin 62	Homo sapiens	129-132
19365810-4	2009	Disruption of the proteosome pathway using selective inhibitors (MG-132, MG-115, and epoxomicin) resulted in the accumulation of p62 and CYLD, and altered the subcellular targeting and distribution of p62 and TRAF6 in osteoclast-like cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	CYLD lysine 63 deubiquitinase	Homo sapiens	137-141
19365810-4	2009	Disruption of the proteosome pathway using selective inhibitors (MG-132, MG-115, and epoxomicin) resulted in the accumulation of p62 and CYLD, and altered the subcellular targeting and distribution of p62 and TRAF6 in osteoclast-like cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	nucleoporin 62	Homo sapiens	201-204
19365810-4	2009	Disruption of the proteosome pathway using selective inhibitors (MG-132, MG-115, and epoxomicin) resulted in the accumulation of p62 and CYLD, and altered the subcellular targeting and distribution of p62 and TRAF6 in osteoclast-like cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	TNF receptor associated factor 6	Homo sapiens	209-214
19433583-8	2009	S6K1 reduction was blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	0-4
19464253-4	2009	We show that treatment with 25-OH or 7-KC results in the accumulation of poly-ubiquitinated Akt, an effect that is enhanced by co-treatment with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-176	thymoma viral proto-oncogene 1	Mus musculus	92-95
19508391-6	2009	Further, LPS + IFNgamma-induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFkappaB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	234-239	interferon gamma	Mus musculus	15-23
19508391-6	2009	Further, LPS + IFNgamma-induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFkappaB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	234-239	nitric oxide synthase 2, inducible	Mus musculus	46-50
19508391-6	2009	Further, LPS + IFNgamma-induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFkappaB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	234-239	NADPH oxidase 1	Mus musculus	55-59
19508391-6	2009	Further, LPS + IFNgamma-induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFkappaB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	234-239	mitogen-activated protein kinase kinase 1	Mus musculus	82-125
19508391-6	2009	Further, LPS + IFNgamma-induced expression of iNOS and Nox1 was attenuated by the mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor PD98059, the JNK inhibitor SP600125, the Jak2 inhibitor AG490 and the NFkappaB inhibitor MG132, but not by the p38 mitogen-activated protein kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	234-239	mitogen-activated protein kinase kinase 1	Mus musculus	127-133
19457084-8	2009	Furthermore, when HO-1 over-expressing cells were treated with the proteosome inhibitors, lactacystin and MG132, level of alpha-synuclein was almost completely restored.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	heme oxygenase 1	Homo sapiens	18-22
19457084-8	2009	Furthermore, when HO-1 over-expressing cells were treated with the proteosome inhibitors, lactacystin and MG132, level of alpha-synuclein was almost completely restored.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	synuclein alpha	Homo sapiens	122-137
19557642-0	2009	Proteasome inhibitor MG-132 mediated expression of p27Kip1 via S-phase kinase protein 2 degradation induces cell cycle coupled apoptosis in primary effusion lymphoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	cyclin dependent kinase inhibitor 1B	Homo sapiens	51-58
19557642-0	2009	Proteasome inhibitor MG-132 mediated expression of p27Kip1 via S-phase kinase protein 2 degradation induces cell cycle coupled apoptosis in primary effusion lymphoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	S-phase kinase associated protein 2	Homo sapiens	63-87
19557642-3	2009	Treatment of PEL cells with MG-132 results in downregulation of S-phase kinase protein 2 (SKP2) and accumulation of p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	S-phase kinase associated protein 2	Homo sapiens	64-88
19557642-3	2009	Treatment of PEL cells with MG-132 results in downregulation of S-phase kinase protein 2 (SKP2) and accumulation of p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	S-phase kinase associated protein 2	Homo sapiens	90-94
19557642-3	2009	Treatment of PEL cells with MG-132 results in downregulation of S-phase kinase protein 2 (SKP2) and accumulation of p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	cyclin dependent kinase inhibitor 1B	Homo sapiens	116-123
19557642-4	2009	Furthermore, MG-132 treatment of PEL cells causes Bax conformational changes, leading to loss of mitochondrial membrane potential and release of cytochrome c to the cytosole.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
19557642-4	2009	Furthermore, MG-132 treatment of PEL cells causes Bax conformational changes, leading to loss of mitochondrial membrane potential and release of cytochrome c to the cytosole.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	cytochrome c, somatic	Homo sapiens	145-157
19557642-5	2009	Such cytochrome c release results in sequential activation of caspases and apoptosis, while pretreatment of PEL cells with universal inhibitor of caspases, z-VAD-fmk prevents cell death induced by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	197-203	cytochrome c, somatic	Homo sapiens	5-17
19557642-6	2009	Finally, our data demonstrated in PEL cells that MG-132 downregulates the expression of inhibitor of apoptosis proteins XIAP, cIAP1 and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	X-linked inhibitor of apoptosis	Homo sapiens	120-124
19557642-6	2009	Finally, our data demonstrated in PEL cells that MG-132 downregulates the expression of inhibitor of apoptosis proteins XIAP, cIAP1 and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	baculoviral IAP repeat containing 2	Homo sapiens	126-131
19557642-7	2009	Altogether, these findings suggest that MG-132 is a potent inducer of apoptosis of PEL cells via downregulation of SKP2 leading to accumulation of p27Kip1, resulting in cell cycle arrest and apoptosis and strongly suggest that targeting the proteasomal pathway may provide a novel therapeutic approach for the treatment of PEL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	S-phase kinase associated protein 2	Homo sapiens	115-119
19557642-7	2009	Altogether, these findings suggest that MG-132 is a potent inducer of apoptosis of PEL cells via downregulation of SKP2 leading to accumulation of p27Kip1, resulting in cell cycle arrest and apoptosis and strongly suggest that targeting the proteasomal pathway may provide a novel therapeutic approach for the treatment of PEL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	cyclin dependent kinase inhibitor 1B	Homo sapiens	147-154
19373773-9	2009	Defects in oscillations are not due simply to multipolarity or loss of centrosome focus in the TOGp-depleted cells, since kinetochore oscillations appear normal in cells treated with the proteosome inhibitor MG132, which also results in multipolar spindles and centrosome fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	208-213	cytoskeleton associated protein 5	Homo sapiens	95-99
19528375-10	2009	Consistently, inhibition of the proteasome by MG132 abolished high-glucose-induced reduction of GTPCH I in human umbilical vein endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	GTP cyclohydrolase 1	Homo sapiens	96-103
19528375-12	2009	Finally, either administration of MG132 or supplementation of l-sepiapterin normalized the impaired endothelium-dependent relaxation in aortas isolated from AMPKalpha2(-/-) mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	157-167
19358268-8	2009	Treatment of Nmi expressors with the proteosome inhibitor MG132, resulted in elevated beta-catenin levels with concomitant elevation of c-Myc levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	N-myc and STAT interactor	Homo sapiens	13-16
19358268-8	2009	Treatment of Nmi expressors with the proteosome inhibitor MG132, resulted in elevated beta-catenin levels with concomitant elevation of c-Myc levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	catenin beta 1	Homo sapiens	86-98
19358268-8	2009	Treatment of Nmi expressors with the proteosome inhibitor MG132, resulted in elevated beta-catenin levels with concomitant elevation of c-Myc levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	136-141
19389809-9	2009	Class II CaSR mutants show increased expression and/or enhanced plasma membrane localization upon treatment with MG132 or the pharmacochaperone NPS R-568, permitting assay of functional activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	calcium sensing receptor	Homo sapiens	9-13
19379726-6	2009	In contrast, other NF-kappaB inhibitors, such as fenofibrate, N-acetylcysteine and MG132, decreased MMP expression in IL-1beta-stimulated FLSs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	interleukin 1 beta	Homo sapiens	118-126
19376148-7	2009	The decrease in LPS-induced iNOS protein by ZnPP was reversed by adding the proteasome inhibitors MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	nitric oxide synthase 2, inducible	Mus musculus	28-32
19409913-7	2009	Co-incubation with TNFalpha and the proteasome inhibitor MG132 resulted in dose-dependent improvement of endothelium-dependent vasorelaxation in comparison to rings treated with TNFalpha alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor necrosis factor	Rattus norvegicus	19-27
19409913-7	2009	Co-incubation with TNFalpha and the proteasome inhibitor MG132 resulted in dose-dependent improvement of endothelium-dependent vasorelaxation in comparison to rings treated with TNFalpha alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor necrosis factor	Rattus norvegicus	178-186
19409913-8	2009	Levels of eNOS mRNA and protein were reduced despite improved vascular function after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	nitric oxide synthase 3	Rattus norvegicus	10-14
19409913-9	2009	MG132 markedly suppressed mRNA levels of NADPH oxidase subunits and increased SOD1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	superoxide dismutase 1	Rattus norvegicus	78-82
19409913-11	2009	TNFalpha-induced upregulation of the potent vasoconstrictor endothelin was abolished by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	tumor necrosis factor	Rattus norvegicus	0-8
19527497-10	2009	The H2O2-potentiated IL-8 release was suppressed by MG-132, a proteosome inhibitor, and by dexamethasone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-58	C-X-C motif chemokine ligand 8	Homo sapiens	21-25
19636403-5	2009	In contrast, cells treated with 10, 50 nM Epx or MG132 displayed changes in ubiquitin or beta-catenin immunoblotting profiles and extensive tau degradation/truncation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	catenin beta 1	Homo sapiens	89-101
19363130-4	2009	The NF-kappaB antagonist MG-132 or the IKK-beta inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Lepr(db) mice, but the responses in mLepr(db) mice were unaffected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	leptin receptor	Mus musculus	179-183
19363130-5	2009	The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	180-186	conserved helix-loop-helix ubiquitous kinase	Mus musculus	26-35
19363130-5	2009	The protein expression of IKK-alpha and IKK-beta were higher in Lepr(db) than in mLepr(db) mice; the expression of IKK-beta, but not the expression of IKK-alpha, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF-alpha in diabetic mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	180-186	inhibitor of kappaB kinase beta	Mus musculus	115-123
19376888-10	2009	Endotoxin increased diaphragm caspase-3 activity (P &lt;0.01); caspase-3 activity remained high when either MG132, epoxomicin, or bortezomib were given.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	caspase 3	Rattus norvegicus	63-72
19363130-9	2009	MG-132 or the neutralization of TNF-alpha reduced superoxide production in Lepr(db) mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	leptin receptor	Mus musculus	75-79
19725468-11	2009	Degradation of PARP and p53 by lidamycin as a substitute for SIRT1 and Akt was confirmed with caspase inhibitor Q-VD-OPh and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	collagen type XI alpha 2 chain	Homo sapiens	15-19
19201384-7	2009	Moreover, Western blotting analysis revealed that MG132 induced c-Jun phosphorylation in all three CNS-derived cell lines, whereas a high level of activating transcription factor-2 (ATF-2) phosphorylation was observed only in IMR-32 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-69
19493001-7	2009	We found that the reduction in tyrosinase levels that was induced by terrein was clearly recovered by MG-132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	tyrosinase	Mus musculus	31-41
19493001-8	2009	Moreover, ubiquitination of tyrosinase increased following treatment with terrein in the presence of MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-107	tyrosinase	Mus musculus	28-38
19154794-4	2009	Downregulation of Cdc6 was completely restored by pretreatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	cell division cycle 6	Homo sapiens	18-22
19201384-8	2009	Finally, MG132-induced MIE protein expression was suppressed by JNK inhibitor that reduced the phosphorylation levels of both c-Jun and ATF-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	mitogen-activated protein kinase 8	Homo sapiens	64-67
19549366-10	2009	It is concluded that the MG-132 may induce K562 cell apoptosis and proliferation inhibition through up-regulation of NF-kappaB activity and down-regulation of GR expression both in dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	nuclear receptor subfamily 3 group C member 1	Homo sapiens	159-161
19201384-8	2009	Finally, MG132-induced MIE protein expression was suppressed by JNK inhibitor that reduced the phosphorylation levels of both c-Jun and ATF-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	126-131
19201384-8	2009	Finally, MG132-induced MIE protein expression was suppressed by JNK inhibitor that reduced the phosphorylation levels of both c-Jun and ATF-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	activating transcription factor 2	Homo sapiens	136-141
19287004-6	2009	IFN-gamma enhanced the association between JAK2 and ASK1, and the ASK1-JAK2 complex was labile and was stabilized by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	interferon gamma	Mus musculus	0-9
19417133-7	2009	MG132 blocked SGI-1027-induced depletion of DNMT1, indicating the involvement of proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	chromogranin B	Rattus norvegicus	14-17
19417133-7	2009	MG132 blocked SGI-1027-induced depletion of DNMT1, indicating the involvement of proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA methyltransferase 1	Rattus norvegicus	44-49
19287004-6	2009	IFN-gamma enhanced the association between JAK2 and ASK1, and the ASK1-JAK2 complex was labile and was stabilized by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	Janus kinase 2	Mus musculus	43-47
19372735-7	2009	We found that proteasome inhibitors epoxomicin and MG132 attenuated NFkappaB induction much more effectively than the IKK inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	nuclear factor kappa B subunit 1	Homo sapiens	68-76
19287004-6	2009	IFN-gamma enhanced the association between JAK2 and ASK1, and the ASK1-JAK2 complex was labile and was stabilized by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	mitogen-activated protein kinase kinase kinase 5	Mus musculus	66-70
19287004-6	2009	IFN-gamma enhanced the association between JAK2 and ASK1, and the ASK1-JAK2 complex was labile and was stabilized by the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	Janus kinase 2	Mus musculus	71-75
19223597-8	2009	High-glucose treatment increased CREB polyubiquitination, while treatment of INS-1E cells with the proteasome inhibitor MG-132 prevented the decrease in CREB content.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-126	cAMP responsive element binding protein 1	Rattus norvegicus	153-157
19393171-2	2009	Different from other GTFs, decrease of TFIIB during the differentiation was suppressed by addition of a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	general transcription factor IIB	Homo sapiens	39-44
19095738-9	2009	Both these cytokines activated GPB5 transcription by 2- to 3-fold, and their effects were abolished by the addition of MG132, a NF-kappaB inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	glycoprotein hormone subunit beta 5	Homo sapiens	31-35
19415549-8	2009	In addition, the tyrosine kinase inhibitor AG 17 and the proteasome inhibitor MG132 significantly reduced IL-8 and CINC-1 expression induced by GPCR ligands.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	C-X-C motif chemokine ligand 1	Rattus norvegicus	115-121
19460723-9	2009	Hyperoxic exposure also caused obviously enhanced MPO activity and expressions of NF-kappaB, TNF-alpha, and IL-6 (P&lt;0.01), which were all reduced by MG-132 treatment (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	myeloperoxidase	Rattus norvegicus	50-53
19229559-6	2009	In lymphoblastoid cells carrying SCA8 large alleles, treatment of MG-132 or staurosporine significantly increases the cell death or caspase 3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	ataxin 8	Homo sapiens	33-37
19229559-6	2009	In lymphoblastoid cells carrying SCA8 large alleles, treatment of MG-132 or staurosporine significantly increases the cell death or caspase 3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	caspase 3	Homo sapiens	132-141
19137541-10	2009	Proteasome inhibition by MG132 caused stabilization and accumulation of all CLU protein products, including the nuclear form of CLU (nCLU), and committing cells to caspase-dependent death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	clusterin	Homo sapiens	76-79
19137541-10	2009	Proteasome inhibition by MG132 caused stabilization and accumulation of all CLU protein products, including the nuclear form of CLU (nCLU), and committing cells to caspase-dependent death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	clusterin	Homo sapiens	128-131
19460723-9	2009	Hyperoxic exposure also caused obviously enhanced MPO activity and expressions of NF-kappaB, TNF-alpha, and IL-6 (P&lt;0.01), which were all reduced by MG-132 treatment (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	tumor necrosis factor	Rattus norvegicus	93-102
19460723-9	2009	Hyperoxic exposure also caused obviously enhanced MPO activity and expressions of NF-kappaB, TNF-alpha, and IL-6 (P&lt;0.01), which were all reduced by MG-132 treatment (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	interleukin 6	Rattus norvegicus	108-112
19400951-7	2009	These proteins were rescued by the proteasome inhibitor MG132, indicating the autocatalytic degradation of F-box proteins upon loss of CSN2 or CSN5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	casein beta	Homo sapiens	135-139
19435936-5	2009	Treatment with the proteasome inhibitor MG132 led to accumulation of GFP-eIF4A-III mainly in the nucleolus, suggesting that transition of eIF4A-III between subnuclear domains and/or accumulation in nuclear speckles is controlled by proteolysis-labile factors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	eukaryotic initiation factor 4A-III	Arabidopsis thaliana	73-82
19435936-5	2009	Treatment with the proteasome inhibitor MG132 led to accumulation of GFP-eIF4A-III mainly in the nucleolus, suggesting that transition of eIF4A-III between subnuclear domains and/or accumulation in nuclear speckles is controlled by proteolysis-labile factors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	eukaryotic initiation factor 4A-III	Arabidopsis thaliana	138-147
19400951-7	2009	These proteins were rescued by the proteasome inhibitor MG132, indicating the autocatalytic degradation of F-box proteins upon loss of CSN2 or CSN5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	COP9 signalosome subunit 5	Homo sapiens	143-147
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	mitogen-activated protein kinase 8	Homo sapiens	4-7
19268428-4	2009	CSN2 and CSN5, subunits of COP9 CSN complex, were coprecipitated with ABCA1 when coexpressed in HEK293 cells and proteasomal degradation was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	casein beta	Homo sapiens	0-4
19268428-4	2009	CSN2 and CSN5, subunits of COP9 CSN complex, were coprecipitated with ABCA1 when coexpressed in HEK293 cells and proteasomal degradation was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	COP9 signalosome subunit 5	Homo sapiens	9-13
19268428-4	2009	CSN2 and CSN5, subunits of COP9 CSN complex, were coprecipitated with ABCA1 when coexpressed in HEK293 cells and proteasomal degradation was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	COP9 signalosome subunit 8	Homo sapiens	27-31
19268428-4	2009	CSN2 and CSN5, subunits of COP9 CSN complex, were coprecipitated with ABCA1 when coexpressed in HEK293 cells and proteasomal degradation was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	ATP binding cassette subfamily A member 1	Homo sapiens	70-75
19245796-3	2009	Here, we show that endocytosis of cell surface E-cadherin during EMT induced by TGF-beta and during scattering induced by hepatocyte growth factor (HGF) can be blocked by inhibiting proteasome with lactacystin and MG132 in normal epithelial cells and in cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	cadherin 1	Homo sapiens	47-57
19245796-3	2009	Here, we show that endocytosis of cell surface E-cadherin during EMT induced by TGF-beta and during scattering induced by hepatocyte growth factor (HGF) can be blocked by inhibiting proteasome with lactacystin and MG132 in normal epithelial cells and in cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	hepatocyte growth factor	Homo sapiens	122-146
19245796-3	2009	Here, we show that endocytosis of cell surface E-cadherin during EMT induced by TGF-beta and during scattering induced by hepatocyte growth factor (HGF) can be blocked by inhibiting proteasome with lactacystin and MG132 in normal epithelial cells and in cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	hepatocyte growth factor	Homo sapiens	148-151
19318567-4	2009	Endogenous nucleostemin protein is completely stabilized by MG132, an inhibitor of the 26S proteasome, as are the levels of expressed enhanced green fluorescent protein-tagged nucleostemin, both wild-type protein and protein containing mutations at the G(1) GTP binding site.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	G protein nucleolar 3	Homo sapiens	11-23
19220323-7	2009	MG132 ameliorated intestinal inflammation of IL-10(-/-) mice by decreasing TNF-alpha mRNA expression in the colonic tissues, which was associated with suppression of NF-kappaB activation, and reduced significantly the number of Ki-67-positive intestinal epithelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Mus musculus	75-84
19220323-9	2009	MG132 also suppressed significantly epithelial cell proliferation, cell migration and MDR1 gene expression in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	86-90
19254699-4	2009	D-glucosamine inhibited HIF-1alpha accumulation induced by proteasome inhibitor MG132 and prolyl hydroxylase inhibitor DMOG suggesting D-glucosamine reduces HIF-1alpha protein expression through proteasome-independent pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	hypoxia inducible factor 1 subunit alpha	Homo sapiens	24-34
19218244-10	2009	The proteasome inhibitor MG132 reduced CPT-induced Tra2 degradation and TAF1 alternative splicing, and mutation of evolutionarily conserved Tra2 lysine 81, a potential ubiquitin conjugation site, to arginine inhibited CPT-induced Tra2 degradation, supporting a proteasome-dependent alternative splicing mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	transformer 2	Drosophila melanogaster	51-55
19218244-10	2009	The proteasome inhibitor MG132 reduced CPT-induced Tra2 degradation and TAF1 alternative splicing, and mutation of evolutionarily conserved Tra2 lysine 81, a potential ubiquitin conjugation site, to arginine inhibited CPT-induced Tra2 degradation, supporting a proteasome-dependent alternative splicing mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	TBP-associated factor 1	Drosophila melanogaster	72-76
19220323-7	2009	MG132 ameliorated intestinal inflammation of IL-10(-/-) mice by decreasing TNF-alpha mRNA expression in the colonic tissues, which was associated with suppression of NF-kappaB activation, and reduced significantly the number of Ki-67-positive intestinal epithelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interleukin 10	Mus musculus	45-50
18987671-8	2009	These findings demonstrate that ABT-737 combined with MG-132 synergistically induced Noxa-dependent mitochondrial-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-60	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	85-89
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	60-64
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	DNA damage inducible transcript 3	Homo sapiens	66-70
19374806-9	2009	MG-132 treatment decreased the mRNA and protein expression of NF-kappaB, and increased the protein expression of caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor kappa B subunit 1	Homo sapiens	62-71
19287990-3	2009	Nevertheless, the reduction of the c-Myc gene expression was not accompanied by corresponding reduction of mRNAs but protein, which can be abrogated by a proteosome inhibitor (MG132), suggesting that the reduction was associated with their increased degradation rather than transcriptional controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	35-40
19374806-9	2009	MG-132 treatment decreased the mRNA and protein expression of NF-kappaB, and increased the protein expression of caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 3	Homo sapiens	113-122
19374806-10	2009	CONCLUSIONS: MG-132 can induce apoptosis of human erythroleukemia cell line K562 through the down-regulation of NF-kappaB expression and up-regulation of caspase-3 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	nuclear factor kappa B subunit 1	Homo sapiens	112-121
19374806-10	2009	CONCLUSIONS: MG-132 can induce apoptosis of human erythroleukemia cell line K562 through the down-regulation of NF-kappaB expression and up-regulation of caspase-3 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	caspase 3	Homo sapiens	154-163
19059469-6	2009	The addition of the proteasomal inhibitor MG132 increased the apoptotic activity of both the disulfide conjugate and free Cyt c, but not the thioether conjugate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	cytochrome c, somatic	Homo sapiens	122-127
19144635-5	2009	Nedd4-2 strongly down-regulates ACK1 levels when coexpressed, and this process can be blocked by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	0-7
19144635-5	2009	Nedd4-2 strongly down-regulates ACK1 levels when coexpressed, and this process can be blocked by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	tyrosine kinase non receptor 2	Homo sapiens	32-36
19147500-9	2009	We further observed in vivo a post-translational modification of TIR1 dependent on the proteasome inhibitor MG-132 and provide evidence for proteasome-mediated degradation of TIR1, CUL1, and ASK1 (Arabidopsis SKP1 homolog).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	F-box/RNI-like superfamily protein	Arabidopsis thaliana	65-69
19006120-0	2009	Proteasome inhibitor MG132 induces BAG3 expression through activation of heat shock factor 1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	BAG cochaperone 3	Homo sapiens	35-39
18930432-4	2009	We found that the proteasome inhibitors, MG132 and lactacystin, induced neurite outgrowth and also activated extracellular signal-regulated kinase/mitogen activated protein kinase and phosphatidylinositol-3-kinase/AKT pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	AKT serine/threonine kinase 1	Homo sapiens	214-217
19233177-4	2009	Consistent with this, treating cells with the proteasome inhibitor MG-132 significantly increases C18Y Bmi-1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-73	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	103-108
19006120-5	2009	In the current study, we provide evidence that heat shock transcription factor 1 (HSF1) is involved in BAG3 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	heat shock transcription factor 1	Homo sapiens	47-80
19006120-5	2009	In the current study, we provide evidence that heat shock transcription factor 1 (HSF1) is involved in BAG3 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	heat shock transcription factor 1	Homo sapiens	82-86
19006120-5	2009	In the current study, we provide evidence that heat shock transcription factor 1 (HSF1) is involved in BAG3 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	BAG cochaperone 3	Homo sapiens	103-107
19006120-8	2009	Chromatin immunoprecipitation assay demonstrated that HSF1 directly bound to the MG132-responsive site on the BAG3 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	heat shock transcription factor 1	Homo sapiens	54-58
19006120-8	2009	Chromatin immunoprecipitation assay demonstrated that HSF1 directly bound to the MG132-responsive site on the BAG3 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	BAG cochaperone 3	Homo sapiens	110-114
19006120-9	2009	Activation of HSF1 occurred with MG132 along with BAG3 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	heat shock transcription factor 1	Homo sapiens	14-18
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	heat shock transcription factor 1	Homo sapiens	23-27
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	BAG cochaperone 3	Homo sapiens	68-72
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	BAG cochaperone 3	Homo sapiens	166-170
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	heat shock transcription factor 1	Homo sapiens	23-27
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	BAG cochaperone 3	Homo sapiens	68-72
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	BAG cochaperone 3	Homo sapiens	166-170
19006120-10	2009	Furthermore, knockdown HSF1 by small interfering RNA attenuated the BAG3 upregulation due to MG132.These results indicate that the proteasome inhibitor MG132 induces BAG3 expression through HSF1 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	heat shock transcription factor 1	Homo sapiens	190-194
19212627-9	2009	The decreased expression of Bcl-XL protein after UVB treatment was partially restored in the presence of MG132, which is an inhibitor of proteasome, implying that the down-regulation of Bcl-XL may be regulated by the proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	BCL2 like 1	Homo sapiens	28-34
19041327-8	2009	Wild type but not enzyme-deficient HDAC2 promotes the degradation of CIITA protein, whereas TSA and the proteasome inhibitor MG132 restore CIITA activity by stabilizing CIITA protein and increasing its association with target promoters.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	class II major histocompatibility complex transactivator	Homo sapiens	139-144
19041327-8	2009	Wild type but not enzyme-deficient HDAC2 promotes the degradation of CIITA protein, whereas TSA and the proteasome inhibitor MG132 restore CIITA activity by stabilizing CIITA protein and increasing its association with target promoters.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-130	class II major histocompatibility complex transactivator	Homo sapiens	139-144
18602823-6	2009	At SUL doses &lt;30 muM, the SUL-induced suppression of ERalpha protein was reversed by preincubation with the proteasome inhibitor MG132 and was accompanied by an increase in protein levels of the 20S catalytic core subunit PSMB5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	estrogen receptor 1	Homo sapiens	56-63
19212627-9	2009	The decreased expression of Bcl-XL protein after UVB treatment was partially restored in the presence of MG132, which is an inhibitor of proteasome, implying that the down-regulation of Bcl-XL may be regulated by the proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	BCL2 like 1	Homo sapiens	186-192
19201892-6	2009	MG132 and clasto-lactacystin beta-lactone inhibited the loss of immunoreactivity of FcgammaRIIa, suggesting that this receptor was down-regulated via the proteasomal pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	Fc gamma receptor IIa	Homo sapiens	84-95
19164785-9	2009	This change, unlike NCX1, was exerted at the posttranscriptional level because it was prevented by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	solute carrier family 8 member A1	Homo sapiens	20-24
18951928-5	2009	We show that Zn/PDTC induces p53 proteasomal degradation and that the proteasome inhibitor MG132 further increases fibroblast growth inhibition by Zn/PDTC, suggesting that p53 degradation plays an important role in fibroblast resistance to Zn/PDTC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	tumor protein p53	Homo sapiens	172-175
18987329-9	2009	MG-132, not CI, suppressed cellular MMP13 fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	matrix metallopeptidase 13	Homo sapiens	36-41
18832097-10	2009	In STS-treated LNCaP cells and human skin fibroblasts, the proteasome inhibitor MG-132 protected the VDR caspase cleavage fragment from further degradation by the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-86	vitamin D receptor	Homo sapiens	101-104
19176375-5	2009	Bioluminescence analysis further showed that proteasome inhibition with bortezomib or MG132 attenuated overall ligand-induced degradation of EGFR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	epidermal growth factor receptor	Homo sapiens	141-145
19141650-6	2009	Treatment of Panc-1 cells with a proteasome inhibitor, MG132, increased the HPK1 protein levels in a dose-dependent manner, suggesting that alteration in proteasome activity contributes to the loss of HPK1 protein expression in pancreatic cancer.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens	76-80
19141650-6	2009	Treatment of Panc-1 cells with a proteasome inhibitor, MG132, increased the HPK1 protein levels in a dose-dependent manner, suggesting that alteration in proteasome activity contributes to the loss of HPK1 protein expression in pancreatic cancer.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens	201-205
19141650-8	2009	After MG132 withdrawal, wild-type HPK1 protein expression was markedly decreased within 24 hours, but kinase-dead HPK1 mutant protein expression was sustained for up to 96 hours.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	mitogen-activated protein kinase kinase kinase kinase 1	Homo sapiens	34-38
18832104-8	2009	These results are related to proteosomal activation because MG132, a proteasome inhibitor, abolished BMP-2-mediated degradation of TGF-beta RI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	bone morphogenetic protein 2	Rattus norvegicus	101-106
18832104-8	2009	These results are related to proteosomal activation because MG132, a proteasome inhibitor, abolished BMP-2-mediated degradation of TGF-beta RI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	transforming growth factor, beta 1	Rattus norvegicus	131-139
19100675-9	2009	Treatment with a proteasome inhibitor, MG-132, also blocked degradation of phosphorylated BIM.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	BCL2-like 11 (apoptosis facilitator)	Mus musculus	90-93
19147768-8	2009	MG132, an inhibitor of 26S proteosome, blocked the Poly E-induced down-regulation of cyclin D1, and Poly E promoted cyclin D1 polyubiquitination, suggesting that Poly E also inhibits cyclin D1 expression by promoting its degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin D1	Homo sapiens	85-94
19148524-8	2009	In addition, the decrease in the levels of Cyclin D1/Cdk4 and Cyclin B1, but not of Cdc2, is similarly prevented by co-treatment of cells with MG-132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	cyclin D1	Homo sapiens	43-52
19148524-8	2009	In addition, the decrease in the levels of Cyclin D1/Cdk4 and Cyclin B1, but not of Cdc2, is similarly prevented by co-treatment of cells with MG-132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	cyclin dependent kinase 4	Homo sapiens	53-57
19148524-8	2009	In addition, the decrease in the levels of Cyclin D1/Cdk4 and Cyclin B1, but not of Cdc2, is similarly prevented by co-treatment of cells with MG-132, a potent proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	cyclin B1	Homo sapiens	62-71
18830882-4	2009	The concentration required for 50% inhibition (IC(50)) by ZLLLal was 88 nM for cathepsin B and 163 nM for cathepsin L.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-64	cathepsin B	Rattus norvegicus	79-90
18830882-4	2009	The concentration required for 50% inhibition (IC(50)) by ZLLLal was 88 nM for cathepsin B and 163 nM for cathepsin L.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-64	cathepsin L	Rattus norvegicus	106-117
18710428-6	2009	Inhibition studies using SB203580 (inhibitor of p38MAPK), U0126 (inhibitor of mitogen-activated or extracellular signal-regulated protein kinase 1/2) and MG132 (inhibitor of NF-kappaB) showed that the phosphorylation of Erk1/2 and p38MAPK with activation of NF-kappaB was closely related to MMP-9 upregulation in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	nuclear factor kappa B subunit 1	Homo sapiens	174-183
18710428-6	2009	Inhibition studies using SB203580 (inhibitor of p38MAPK), U0126 (inhibitor of mitogen-activated or extracellular signal-regulated protein kinase 1/2) and MG132 (inhibitor of NF-kappaB) showed that the phosphorylation of Erk1/2 and p38MAPK with activation of NF-kappaB was closely related to MMP-9 upregulation in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	mitogen-activated protein kinase 3	Homo sapiens	220-226
18710428-6	2009	Inhibition studies using SB203580 (inhibitor of p38MAPK), U0126 (inhibitor of mitogen-activated or extracellular signal-regulated protein kinase 1/2) and MG132 (inhibitor of NF-kappaB) showed that the phosphorylation of Erk1/2 and p38MAPK with activation of NF-kappaB was closely related to MMP-9 upregulation in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	mitogen-activated protein kinase 14	Homo sapiens	231-238
18710428-6	2009	Inhibition studies using SB203580 (inhibitor of p38MAPK), U0126 (inhibitor of mitogen-activated or extracellular signal-regulated protein kinase 1/2) and MG132 (inhibitor of NF-kappaB) showed that the phosphorylation of Erk1/2 and p38MAPK with activation of NF-kappaB was closely related to MMP-9 upregulation in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	nuclear factor kappa B subunit 1	Homo sapiens	258-267
18710428-6	2009	Inhibition studies using SB203580 (inhibitor of p38MAPK), U0126 (inhibitor of mitogen-activated or extracellular signal-regulated protein kinase 1/2) and MG132 (inhibitor of NF-kappaB) showed that the phosphorylation of Erk1/2 and p38MAPK with activation of NF-kappaB was closely related to MMP-9 upregulation in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	matrix metallopeptidase 9	Homo sapiens	291-296
19095772-4	2009	GnRH-stimulated activity of an LHbeta reporter gene was prevented by proteasome inhibitors MG-132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-97	gonadotropin releasing hormone 1	Homo sapiens	0-4
19095772-4	2009	GnRH-stimulated activity of an LHbeta reporter gene was prevented by proteasome inhibitors MG-132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-97	luteinizing hormone subunit beta	Homo sapiens	31-37
19095772-6	2009	Increased endogenous LHbeta transcription after GnRH treatment was also prevented by MG-132, as measured by primary transcript assays.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-91	luteinizing hormone subunit beta	Homo sapiens	21-27
19095772-6	2009	Increased endogenous LHbeta transcription after GnRH treatment was also prevented by MG-132, as measured by primary transcript assays.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-91	gonadotropin releasing hormone 1	Homo sapiens	48-52
19095772-10	2009	MG-132 disrupted GnRH-induced Egr-1 and SF-1 binding and prevented phosphorylated RNA polymerase II association with the LHbeta promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	gonadotropin releasing hormone 1	Homo sapiens	17-21
19095772-10	2009	MG-132 disrupted GnRH-induced Egr-1 and SF-1 binding and prevented phosphorylated RNA polymerase II association with the LHbeta promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	early growth response 1	Homo sapiens	30-35
19095772-10	2009	MG-132 disrupted GnRH-induced Egr-1 and SF-1 binding and prevented phosphorylated RNA polymerase II association with the LHbeta promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	splicing factor 1	Homo sapiens	40-44
19095772-10	2009	MG-132 disrupted GnRH-induced Egr-1 and SF-1 binding and prevented phosphorylated RNA polymerase II association with the LHbeta promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	luteinizing hormone subunit beta	Homo sapiens	121-127
19095772-11	2009	Egr-1, but not SF-1, protein was induced by GnRH and accumulated with MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	early growth response 1	Homo sapiens	0-5
19234086-7	2009	This Rma1H1-induced reduction of PIP2;1 was inhibited by MG132, an inhibitor of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	plasma membrane intrinsic protein 2A	Arabidopsis thaliana	33-39
19094209-11	2008	Pre-treatment with the proteasome inhibitor MG132 prevented EVOO polyphenols-induced HER2 depletion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	erb-b2 receptor tyrosine kinase 2	Homo sapiens	85-89
18787018-6	2009	Furthermore, a proteosome inhibitor, MG132, blocked Ago2 protein turnover.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	argonaute RISC catalytic component 2	Homo sapiens	52-56
18983819-3	2008	Pretreatment of cells with the proteasome inhibitor MG132 inhibited the loss of TCF-1 and TCF-4 induced by celecoxib, suggesting that celecoxib induced the proteasome-dependent degradation of TCF-1 and TCF-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	transcription factor 7	Homo sapiens	80-85
18983819-3	2008	Pretreatment of cells with the proteasome inhibitor MG132 inhibited the loss of TCF-1 and TCF-4 induced by celecoxib, suggesting that celecoxib induced the proteasome-dependent degradation of TCF-1 and TCF-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	transcription factor 4	Homo sapiens	90-95
18983819-3	2008	Pretreatment of cells with the proteasome inhibitor MG132 inhibited the loss of TCF-1 and TCF-4 induced by celecoxib, suggesting that celecoxib induced the proteasome-dependent degradation of TCF-1 and TCF-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	transcription factor 7	Homo sapiens	192-197
18983819-3	2008	Pretreatment of cells with the proteasome inhibitor MG132 inhibited the loss of TCF-1 and TCF-4 induced by celecoxib, suggesting that celecoxib induced the proteasome-dependent degradation of TCF-1 and TCF-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	transcription factor 4	Homo sapiens	202-207
18983819-4	2008	Beta-catenin/TCF-dependent transcriptional activity was significantly decreased after the treatment with celecoxib for 6 h and the pretreatment of the cells with MG132 attenuated the effect of celecoxib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	162-167	catenin beta 1	Homo sapiens	0-12
18983819-4	2008	Beta-catenin/TCF-dependent transcriptional activity was significantly decreased after the treatment with celecoxib for 6 h and the pretreatment of the cells with MG132 attenuated the effect of celecoxib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	162-167	hepatocyte nuclear factor 4 alpha	Homo sapiens	13-16
19218821-8	2009	Pretreatment with the NF-kappaB inhibitors caffeic acid phenylethyl ester and MG-132 inhibited MCP-1 production by CysLTs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	nuclear factor kappa B subunit 1	Homo sapiens	22-31
19218821-8	2009	Pretreatment with the NF-kappaB inhibitors caffeic acid phenylethyl ester and MG-132 inhibited MCP-1 production by CysLTs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	C-C motif chemokine ligand 2	Homo sapiens	95-100
19764654-11	2009	Treatment of cells with proteasomal inhibition MG132 blocked the loss of Cbl only partially.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	Cbl proto-oncogene	Homo sapiens	73-76
18952597-5	2008	But beta-catenin inhibition was significantly reduced by GSK3beta RNA interference or GSK3beta inhibitor lithium chloride and proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	catenin (cadherin associated protein), beta 1	Mus musculus	4-16
18794801-4	2008	We found that hNAT5/hNAT3 silencing in HeLa cells results in inhibition of cell proliferation and increased sensitivity to the pro-apoptotic agent MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	N-alpha-acetyltransferase 20, NatB catalytic subunit	Homo sapiens	14-19
18794801-4	2008	We found that hNAT5/hNAT3 silencing in HeLa cells results in inhibition of cell proliferation and increased sensitivity to the pro-apoptotic agent MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	N-alpha-acetyltransferase 20, NatB catalytic subunit	Homo sapiens	20-25
18492488-4	2008	MG132 and ALLN inhibited the release of cytochrome c from mitochondria into the cytosol in the absence of survival factors and suppressed the cleavage of pro-caspase-9 and -3 to its active forms induced by etoposide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cytochrome c, somatic	Homo sapiens	40-52
18492488-4	2008	MG132 and ALLN inhibited the release of cytochrome c from mitochondria into the cytosol in the absence of survival factors and suppressed the cleavage of pro-caspase-9 and -3 to its active forms induced by etoposide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	154-174
18492488-5	2008	In addition, MG132 and ALLN enhanced the phosphorylation of Akt and ERK in osteoclasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	AKT serine/threonine kinase 1	Homo sapiens	60-63
18492488-5	2008	In addition, MG132 and ALLN enhanced the phosphorylation of Akt and ERK in osteoclasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 1	Homo sapiens	68-71
19033390-3	2008	We recently showed that p53 localizes to the nucleolus after proteasome inhibition with MG132 and this localization requires sequences within its carboxyl terminus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	tumor protein p53	Homo sapiens	24-27
19033390-4	2008	In the present study, we found that after treatment with MG132, p53 associates with a discrete sub-nucleolar component, the fibrillar center (FC), a region mainly enriched with RNA polymerase I.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	64-67
18660828-8	2008	KEY RESULTS: The proteasome inhibitors, MG132, PSI, lactacystin and epoxomicin, induced BAG2 at the transcriptional level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	BAG cochaperone 2	Homo sapiens	88-92
18563798-6	2008	Treatment of oligodendrocytes with the proteasomal inhibitor MG-132 (1 micaroM; 18 h) caused an increase in the amount of TPPP/p25alpha by about 40%, a decrease in its solubility, and led to the appearance of TPPP/p25alpha-positive cytoplasmic inclusions, which stained with thioflavin S and resembled inclusion bodies.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	tubulin polymerization promoting protein	Rattus norvegicus	122-135
18563798-6	2008	Treatment of oligodendrocytes with the proteasomal inhibitor MG-132 (1 micaroM; 18 h) caused an increase in the amount of TPPP/p25alpha by about 40%, a decrease in its solubility, and led to the appearance of TPPP/p25alpha-positive cytoplasmic inclusions, which stained with thioflavin S and resembled inclusion bodies.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	tubulin polymerization promoting protein	Rattus norvegicus	209-222
18298651-3	2008	Inhibition of proteasome function by MG-132 in dopaminergic neuronal cell model (N27 cells) rapidly depolarized mitochondria independent of ROS generation to activate the apoptotic cascade involving cytochrome c release, and caspase-9 and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	cytochrome c, somatic	Homo sapiens	199-211
18298651-3	2008	Inhibition of proteasome function by MG-132 in dopaminergic neuronal cell model (N27 cells) rapidly depolarized mitochondria independent of ROS generation to activate the apoptotic cascade involving cytochrome c release, and caspase-9 and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	caspase 9	Homo sapiens	225-234
18298651-3	2008	Inhibition of proteasome function by MG-132 in dopaminergic neuronal cell model (N27 cells) rapidly depolarized mitochondria independent of ROS generation to activate the apoptotic cascade involving cytochrome c release, and caspase-9 and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	caspase 3	Homo sapiens	239-248
18298651-4	2008	PKCdelta was a key downstream effector of caspase-3 because the kinase was proteolytically cleaved by caspase-3 following exposure to proteasome inhibitors MG-132 or lactacystin, resulting in a persistent increase in the kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-162	protein kinase C delta	Homo sapiens	0-8
18298651-4	2008	PKCdelta was a key downstream effector of caspase-3 because the kinase was proteolytically cleaved by caspase-3 following exposure to proteasome inhibitors MG-132 or lactacystin, resulting in a persistent increase in the kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-162	caspase 3	Homo sapiens	42-51
18298651-4	2008	PKCdelta was a key downstream effector of caspase-3 because the kinase was proteolytically cleaved by caspase-3 following exposure to proteasome inhibitors MG-132 or lactacystin, resulting in a persistent increase in the kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-162	caspase 3	Homo sapiens	102-111
18298651-5	2008	Notably MG-132 treatment resulted in translocation of proteolytically cleaved PKCdelta fragments to mitochondria in a time-dependent fashion, and the PKCdelta inhibition effectively blocked the activation of caspase-9 and caspase-3, indicating that the accumulation of the PKCdelta catalytic fragment in the mitochondrial fraction possibly amplifies mitochondria-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-14	protein kinase C delta	Homo sapiens	78-86
18298651-5	2008	Notably MG-132 treatment resulted in translocation of proteolytically cleaved PKCdelta fragments to mitochondria in a time-dependent fashion, and the PKCdelta inhibition effectively blocked the activation of caspase-9 and caspase-3, indicating that the accumulation of the PKCdelta catalytic fragment in the mitochondrial fraction possibly amplifies mitochondria-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-14	caspase 9	Homo sapiens	208-217
18298651-5	2008	Notably MG-132 treatment resulted in translocation of proteolytically cleaved PKCdelta fragments to mitochondria in a time-dependent fashion, and the PKCdelta inhibition effectively blocked the activation of caspase-9 and caspase-3, indicating that the accumulation of the PKCdelta catalytic fragment in the mitochondrial fraction possibly amplifies mitochondria-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-14	caspase 3	Homo sapiens	222-231
18298651-7	2008	Furthermore, inhibition of PKCdelta proteolytic cleavage by a caspase-3 cleavage-resistant mutant (PKCdelta-CRM) or suppression of PKCdelta expression by siRNA significantly attenuated MG-132-induced caspase-9 and -3 activation and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	protein kinase C delta	Homo sapiens	27-35
18298651-7	2008	Furthermore, inhibition of PKCdelta proteolytic cleavage by a caspase-3 cleavage-resistant mutant (PKCdelta-CRM) or suppression of PKCdelta expression by siRNA significantly attenuated MG-132-induced caspase-9 and -3 activation and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	protein kinase C delta	Homo sapiens	99-107
18298651-7	2008	Furthermore, inhibition of PKCdelta proteolytic cleavage by a caspase-3 cleavage-resistant mutant (PKCdelta-CRM) or suppression of PKCdelta expression by siRNA significantly attenuated MG-132-induced caspase-9 and -3 activation and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	protein kinase C delta	Homo sapiens	99-107
18298651-7	2008	Furthermore, inhibition of PKCdelta proteolytic cleavage by a caspase-3 cleavage-resistant mutant (PKCdelta-CRM) or suppression of PKCdelta expression by siRNA significantly attenuated MG-132-induced caspase-9 and -3 activation and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	caspase 9	Homo sapiens	200-216
18941459-7	2008	In contrast, blocking proteasome-mediated protein degradation using MG-132 significantly enhances the ability of IP6 to reduce cellular metabolic activity in both PC3 and DU145 AIPCa cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-74	keratin 6A	Homo sapiens	163-166
18941459-9	2008	The enhanced effect of combined MG132/IP6 treatment is almost completely inhibited by cycloheximide and correlates with changes in BCL-2 family protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	BCL2 apoptosis regulator	Homo sapiens	131-136
18835339-0	2008	MG-132 inhibits the TCDD-mediated induction of Cyp1a1 at the catalytic activity but not the mRNA or protein levels in Hepa 1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	47-53
18835339-1	2008	Previous studies have shown that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced degradation of aryl hydrocarbon receptor (AhR) is inhibited by MG-132, a potent inhibitor of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-153	aryl-hydrocarbon receptor	Mus musculus	99-124
18835339-1	2008	Previous studies have shown that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced degradation of aryl hydrocarbon receptor (AhR) is inhibited by MG-132, a potent inhibitor of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-153	aryl-hydrocarbon receptor	Mus musculus	126-129
18835339-2	2008	Therefore, the current study aims to address the effect of MG-132 on the AhR-regulated gene, cytochrome P450 1a1 (Cyp1a1), using murine hepatoma Hepa 1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	aryl-hydrocarbon receptor	Mus musculus	73-76
18835339-2	2008	Therefore, the current study aims to address the effect of MG-132 on the AhR-regulated gene, cytochrome P450 1a1 (Cyp1a1), using murine hepatoma Hepa 1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	93-112
18835339-2	2008	Therefore, the current study aims to address the effect of MG-132 on the AhR-regulated gene, cytochrome P450 1a1 (Cyp1a1), using murine hepatoma Hepa 1c1c7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-65	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	114-120
18835339-3	2008	Our results showed that MG-132 at the highest concentration tested, 10 microM significantly increased the Cyp1a1 at mRNA, protein and catalytic activity levels through a transcriptional mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	106-112
18835339-4	2008	On the other hand, MG-132 further potentiated the TCDD-mediated induction of Cyp1a1 at mRNA but not at protein level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	77-83
18835339-5	2008	In contrast, MG-132 significantly inhibited the TCDD-mediated induction of Cyp1a1 catalytic activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	75-81
18835339-6	2008	In addition, we showed that the decrease in Cyp1a1 catalytic activity is not Cyp specific, as MG-132 significantly inhibited Cyp2b1 and total cytochrome P450 catalytic activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-100	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	44-50
18835339-6	2008	In addition, we showed that the decrease in Cyp1a1 catalytic activity is not Cyp specific, as MG-132 significantly inhibited Cyp2b1 and total cytochrome P450 catalytic activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-100	peptidyl-prolyl isomerase G (cyclophilin G)	Mus musculus	44-47
18835339-9	2008	Furthermore, MG-132 potentiated the induction of HO-1 mRNA by TCDD in a concentration-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	heme oxygenase 1	Mus musculus	49-53
18835339-11	2008	In conclusion, the present study demonstrates for the first time that MG-132, despite of increasing Cyp1a1 mRNA expression, it decreases its activity probably through decreasing its heme content.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	100-106
19093261-0	2008	MG-132 inhibits telomerase activity, induces apoptosis and G(1) arrest associated with upregulated p27kip1 expression and downregulated survivin expression in gastric carcinoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	cyclin dependent kinase inhibitor 1B	Homo sapiens	99-106
19093261-18	2008	Our results suggest that MG-132 inhibits telomerase activity, induces apoptosis and G(1) arrest which is associated with upregulated p27kip1 expression and downregulated survivin expression in gastric carcinoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	cyclin dependent kinase inhibitor 1B	Homo sapiens	133-140
18956947-11	2008	Taken together, MG132 treatment during SCNT increases survival and pronuclear numbers in reconstructed rat embryos via maintenance of high CSF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	colony stimulating factor 2	Rattus norvegicus	139-142
18064564-2	2008	As acetylation regulates the activity of the anti-apoptotic transcription factor NF-kappaB, we investigated whether the proteasome inhibitor MG-132 would inhibit NF-kappaB activation and as a consequence potentiate HDACi-dependent apoptosis in breast cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-147	nuclear factor kappa B subunit 1	Homo sapiens	162-171
18064564-4	2008	This increase of NF-kappaB activity was strongly reduced by the addition of MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-82	nuclear factor kappa B subunit 1	Homo sapiens	17-26
18064564-5	2008	Moreover, MG-132 potentiates the HDACi-induced cell death that was associated with caspase-3 activation, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-16	caspase 3	Homo sapiens	83-92
18064564-5	2008	Moreover, MG-132 potentiates the HDACi-induced cell death that was associated with caspase-3 activation, and PARP cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-16	poly(ADP-ribose) polymerase 1	Homo sapiens	109-113
18064564-6	2008	Induction of the stress related kinases JNK and p38 and the up-regulation of p21 and p27 were also observed after co-treatment of cells with HDACi and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-157	mitogen-activated protein kinase 14	Homo sapiens	48-51
18064564-6	2008	Induction of the stress related kinases JNK and p38 and the up-regulation of p21 and p27 were also observed after co-treatment of cells with HDACi and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-157	H3 histone pseudogene 16	Homo sapiens	77-80
18064564-6	2008	Induction of the stress related kinases JNK and p38 and the up-regulation of p21 and p27 were also observed after co-treatment of cells with HDACi and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-157	dynactin subunit 6	Homo sapiens	85-88
18064564-7	2008	Disruption of the NF-kappaB pathway by BAY 11-7085 or IkappaB-SR mimicked the action of MG-132 in promoting HDACi-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	nuclear factor kappa B subunit 1	Homo sapiens	18-27
18660828-9	2008	MG132-induced apoptosis was significantly suppressed by BAG2 knockdown using RNA interference.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BAG cochaperone 2	Homo sapiens	56-60
18491227-5	2008	Either MG132 or DMM could efficiently block degradation of M4 E-cadherin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	7-12	cadherin 1	Homo sapiens	62-72
18787399-4	2008	Pretreatment of HCT116 cells with the proteasome inhibitors MG132 or lactacystin prevented Chk1 decline induced by R16, accompanied by significant accumulation of ubiquitinated Chk1 protein, indicating the involvement of ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	checkpoint kinase 1	Homo sapiens	91-95
18787399-4	2008	Pretreatment of HCT116 cells with the proteasome inhibitors MG132 or lactacystin prevented Chk1 decline induced by R16, accompanied by significant accumulation of ubiquitinated Chk1 protein, indicating the involvement of ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	checkpoint kinase 1	Homo sapiens	177-181
18768981-4	2008	The overexpression of viperin significantly decreased the production of SIN, but not of JEV, whereas the proteasome inhibitor MG132 sustained the protein level and antiviral effect of viperin in JEV-infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	radical S-adenosyl methionine domain containing 2	Homo sapiens	184-191
18697743-8	2008	Additionally, UV treatment potently increased c-Myc degradation, which was reduced by co-treatment with the proteasomal inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-137	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	46-51
18404646-7	2008	Furthermore, treatment of cells with proteosome inhibitor MG132 reversed the downregulation of geminin by apigenin, supporting our hypothesis that the degradation pathway is another mechanism by which apigenin affects geminin expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	geminin DNA replication inhibitor	Homo sapiens	95-102
18404646-7	2008	Furthermore, treatment of cells with proteosome inhibitor MG132 reversed the downregulation of geminin by apigenin, supporting our hypothesis that the degradation pathway is another mechanism by which apigenin affects geminin expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	geminin DNA replication inhibitor	Homo sapiens	218-225
19001438-7	2008	SHetA2 increased ubiquitination of c-FLIP and the consequent degradation was abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	115-120	CASP8 and FADD like apoptosis regulator	Homo sapiens	35-41
18706882-2	2008	Treatment of differentiated PC12 cells with MG132, a proteasome inhibitor, elicited a dose- and time-dependent increase in neuronal nitric oxide synthase (nNOS) protein levels, decreased cell viability, and increased cytotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	nitric oxide synthase 1	Rattus norvegicus	123-153
18706882-4	2008	Nitric oxide/peroxynitrite formation was increased upon treatment of PC12 cells with MG132 and decreased upon treatment with the combination of MG132 and 7-NI (a specific inhibitor of nNOS).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	nitric oxide synthase 1	Rattus norvegicus	184-188
18706882-2	2008	Treatment of differentiated PC12 cells with MG132, a proteasome inhibitor, elicited a dose- and time-dependent increase in neuronal nitric oxide synthase (nNOS) protein levels, decreased cell viability, and increased cytotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	nitric oxide synthase 1	Rattus norvegicus	155-159
18706882-6	2008	These effects are strengthened by the activation of caspase-9 along with increased caspase-3 activity upon treatment of PC12 cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	caspase 9	Rattus norvegicus	52-61
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	tyrosine hydroxylase	Rattus norvegicus	136-156
18706882-6	2008	These effects are strengthened by the activation of caspase-9 along with increased caspase-3 activity upon treatment of PC12 cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	caspase 3	Rattus norvegicus	83-92
18550891-4	2008	Degradation was abolished when HepG2 cytosol was removed by digitonin permeabilization, and treatment of intact cells with the proteasome inhibitor MG132 caused accumulation of ubiquitinated apoB protein in the cytosol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	148-153	apolipoprotein B	Homo sapiens	191-195
18922894-5	2008	However, the proteasome inhibitor MG132 potentiated, while DCC counteracted, netrin-1-induced TAp73alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	netrin 1	Homo sapiens	77-85
18827362-4	2008	Potentiated expression of COX-2 and iNOS by troglitazone was inhibited by MG-132, a specific inhibitor of inhibitory factor kappaB (IkappaB) activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-80	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	26-31
18827362-4	2008	Potentiated expression of COX-2 and iNOS by troglitazone was inhibited by MG-132, a specific inhibitor of inhibitory factor kappaB (IkappaB) activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-80	nitric oxide synthase 2	Rattus norvegicus	36-40
18700866-6	2008	By contrast, proteasome inhibitor-1 (Pro1) and MG132 enhanced the HBx-induced ER-stress response and the subsequent activation of caspase-12, -9 and -3 and reduced cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	X protein	Hepatitis B virus	66-69
18700866-6	2008	By contrast, proteasome inhibitor-1 (Pro1) and MG132 enhanced the HBx-induced ER-stress response and the subsequent activation of caspase-12, -9 and -3 and reduced cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	caspase 9	Homo sapiens	130-151
18599551-6	2008	Proteasome inhibitors, N-acetyl-L-leucyl-L-leucyl-L-norleucinal and MG132 prevented the 5alpha-DHT- dependent enhancement of HERG, as did the lysosome inhibitor, bafilomycin A1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	potassium voltage-gated channel subfamily H member 2	Homo sapiens	125-129
18655187-6	2008	When the proteasome pathway was blocked by MG-132 during quercetin treatment, accumulation of the NP-40 insoluble form of Her-2/neu occurred.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	erb-b2 receptor tyrosine kinase 2	Homo sapiens	122-131
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	tyrosine hydroxylase	Rattus norvegicus	158-160
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	tyrosine hydroxylase	Rattus norvegicus	136-156
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	tyrosine hydroxylase	Rattus norvegicus	158-160
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	tyrosine hydroxylase	Rattus norvegicus	241-243
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	tyrosine hydroxylase	Rattus norvegicus	136-156
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	tyrosine hydroxylase	Rattus norvegicus	158-160
18665911-4	2008	In rats received systemic injection of MG-132, hMSCs treatment in MG-132-treated rats dramatically reduced the decline in the number of tyrosine hydroxylase (TH)-immunoreactive cells, showing an approximately 50% increase in the survival of TH-immunoreactive cells in the substantia nigra compared with the MG-132-treated group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	tyrosine hydroxylase	Rattus norvegicus	241-243
18567003-3	2008	Proteasome inhibition by MG132 sensitized cervical cancer cell lines to recombinant human (rh)TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	TNF superfamily member 10	Homo sapiens	94-99
18644859-8	2008	Furthermore, inhibition of proteasome with MG132 elicited robust nuclear accumulation of SUMO2/3- and ubiquitin-modified BMAL1 that was restricted to the transcriptionally active stage of the circadian cycle.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	small ubiquitin like modifier 2	Homo sapiens	89-96
18644859-8	2008	Furthermore, inhibition of proteasome with MG132 elicited robust nuclear accumulation of SUMO2/3- and ubiquitin-modified BMAL1 that was restricted to the transcriptionally active stage of the circadian cycle.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	121-126
18483465-7	2008	Moreover, down-regulation of ER alpha by TNF alpha was not inhibited in cells that were pretreated with the proteasome inhibitors, MG132 and MG152, which suggests that proteasome-dependent proteolysis does not significantly influence TNF alpha-induced down-regulation of ER alpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	estrogen receptor 1	Homo sapiens	29-37
18617527-6	2008	Inhibition of Cdk2 (roscovitine) or proteasome (MG132) was associated with an enhanced nuclear punctuate distribution of SHP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	121-126
18586292-6	2008	Polyubiquitination of Bcl-xL was detected after incubation with 100 microM clivorine for 40 h in the presence of proteasome specific inhibitor MG132, indicating possible degradation of Bcl-xL protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	BCL2-like 1	Mus musculus	22-28
18586292-6	2008	Polyubiquitination of Bcl-xL was detected after incubation with 100 microM clivorine for 40 h in the presence of proteasome specific inhibitor MG132, indicating possible degradation of Bcl-xL protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	BCL2-like 1	Mus musculus	185-191
18586292-7	2008	Furthermore, pretreatment with MG132 or calpain inhibitor I for 2 h significantly enhanced clivorine-decreased Bcl-xL level and cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	BCL2-like 1	Mus musculus	111-117
18617527-9	2008	Treatment with MG132 led to an increase in expression of the full-length SHP-1 protein while concomitantly leading to a decrease in the levels of the lower mass 45-kDa molecular species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	73-78
18586895-5	2008	Treatment of cells with proteasome inhibitors MG-132 and lactacystin strongly upregulated endogenous MRTF-A protein levels and resulted in a substantial increase in ubiquitin immunoreactivity in MRTF-A immunoprecipitants.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-52	myocardin related transcription factor A	Mus musculus	101-107
18421014-6	2008	The proteasomal inhibitor, MG132, also blocked CSE-induced HDAC2 degradation, increasing the levels of ubiquitinated HDAC2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	histone deacetylase 2	Homo sapiens	59-64
18421014-6	2008	The proteasomal inhibitor, MG132, also blocked CSE-induced HDAC2 degradation, increasing the levels of ubiquitinated HDAC2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	histone deacetylase 2	Homo sapiens	117-122
18586895-5	2008	Treatment of cells with proteasome inhibitors MG-132 and lactacystin strongly upregulated endogenous MRTF-A protein levels and resulted in a substantial increase in ubiquitin immunoreactivity in MRTF-A immunoprecipitants.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-52	myocardin related transcription factor A	Mus musculus	195-201
18457675-8	2008	Overexpression of p38, treatment with Chrysin, MG132, or dimethylformamide shows dependence of TC on p38 as partner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	mitogen-activated protein kinase 14	Homo sapiens	101-104
18567580-6	2008	In the presence of the proteasome inhibitor MG132, TNF increased accumulation of ubiquitinated Smad1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	tumor necrosis factor	Mus musculus	51-54
18615632-8	2008	Inhibition of proteasome function using MG132 led to accumulation of excess N-RAP, and the secondary decrease in N-RAP that otherwise accompanied NMHC IIB knockdown was abolished.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	nebulin-related anchoring protein	Mus musculus	76-81
18697835-3	2008	Full-length ADPH was unstable and could not be detected on CLDs unless cultures were incubated with oleic acid (OA) to stimulate triglyceride synthesis, or were treated with MG132 to block proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	perilipin 2	Homo sapiens	12-16
18724031-5	2008	MG132 increased both p300 and p53 protein levels in these cells, suggesting that ubiquitin-dependent degradation is involved in the homeostasis of these proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	30-33
18795123-5	2008	We found that as low as 0.5 microM MG132 caused a significant apoptosis in both cell lines as evidenced by DNA damage, cleavage of poly ADP-ribose polymerase and caspases 3, 7, and 9, and mitochondrial release of Smac/DIABLO and Cytochrome c.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	diablo IAP-binding mitochondrial protein	Homo sapiens	213-217
18795123-5	2008	We found that as low as 0.5 microM MG132 caused a significant apoptosis in both cell lines as evidenced by DNA damage, cleavage of poly ADP-ribose polymerase and caspases 3, 7, and 9, and mitochondrial release of Smac/DIABLO and Cytochrome c.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	diablo IAP-binding mitochondrial protein	Homo sapiens	218-224
18795123-5	2008	We found that as low as 0.5 microM MG132 caused a significant apoptosis in both cell lines as evidenced by DNA damage, cleavage of poly ADP-ribose polymerase and caspases 3, 7, and 9, and mitochondrial release of Smac/DIABLO and Cytochrome c.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	cytochrome c, somatic	Homo sapiens	229-241
18795123-7	2008	Mcl-1, among the Bcl-2 and IAP (inhibitor of apoptosis protein) antiapoptotic family proteins tested, was proved to be a major inhibitor of the MG132-induced apoptosis in MPM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5
18795123-7	2008	Mcl-1, among the Bcl-2 and IAP (inhibitor of apoptosis protein) antiapoptotic family proteins tested, was proved to be a major inhibitor of the MG132-induced apoptosis in MPM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	BCL2 apoptosis regulator	Homo sapiens	17-22
18795123-7	2008	Mcl-1, among the Bcl-2 and IAP (inhibitor of apoptosis protein) antiapoptotic family proteins tested, was proved to be a major inhibitor of the MG132-induced apoptosis in MPM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	magnesium transporter 1	Homo sapiens	27-30
18795123-7	2008	Mcl-1, among the Bcl-2 and IAP (inhibitor of apoptosis protein) antiapoptotic family proteins tested, was proved to be a major inhibitor of the MG132-induced apoptosis in MPM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	magnesium transporter 1	Homo sapiens	32-62
18795123-8	2008	Meanwhile, subapoptotic doses of MG132 inhibited the invasion of both MPM cell lines through reducing Rac1 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	Rac family small GTPase 1	Homo sapiens	102-106
18567580-6	2008	In the presence of the proteasome inhibitor MG132, TNF increased accumulation of ubiquitinated Smad1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	SMAD family member 1	Mus musculus	95-100
18680593-7	2008	Consistently, treatment of cells with a proteasome inhibitor MG132 alleviated protein degradation of APOBEC3G and APOBEC3G-UBA2 fusion proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	101-109
18680593-7	2008	Consistently, treatment of cells with a proteasome inhibitor MG132 alleviated protein degradation of APOBEC3G and APOBEC3G-UBA2 fusion proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	114-122
18680593-7	2008	Consistently, treatment of cells with a proteasome inhibitor MG132 alleviated protein degradation of APOBEC3G and APOBEC3G-UBA2 fusion proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	ubiquitin like modifier activating enzyme 2	Homo sapiens	123-127
18539754-7	2008	We also observed in diabetic mice that augmented RAGE signaling augmented expression of TNF-alpha, because this increase was attenuated by sRAGE or NF-kappaB inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	advanced glycosylation end product-specific receptor	Mus musculus	49-53
18539754-7	2008	We also observed in diabetic mice that augmented RAGE signaling augmented expression of TNF-alpha, because this increase was attenuated by sRAGE or NF-kappaB inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	tumor necrosis factor	Mus musculus	88-97
18554923-6	2008	Pre-treatment of ts20 transfectants with either chloroquine or MG132 inhibited ligand-induced G-CSFR degradation, suggesting a role for both lysosomes and proteasomes in regulating G-CSFR surface expression in this cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	colony stimulating factor 3 receptor	Homo sapiens	94-100
18554923-6	2008	Pre-treatment of ts20 transfectants with either chloroquine or MG132 inhibited ligand-induced G-CSFR degradation, suggesting a role for both lysosomes and proteasomes in regulating G-CSFR surface expression in this cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	colony stimulating factor 3 receptor	Homo sapiens	181-187
18539596-7	2008	Under an in vivo condition, chronic morphine exposure also induced posttranscriptional down-regulation of the glutamate transporter EAAC1, which was prevented by MG-132, and transcriptional up-regulation of PTEN and Nedd4 within the spinal cord dorsal horn.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	162-168	solute carrier family 1 member 1	Homo sapiens	132-137
18298552-5	2008	We also analysed the effects of MG132 on the activation of NF-kappaB and AP-1 and on the IkappaB molecule.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	nuclear factor kappa B subunit 1	Homo sapiens	59-68
18298552-5	2008	We also analysed the effects of MG132 on the activation of NF-kappaB and AP-1 and on the IkappaB molecule.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-77
18298552-7	2008	MG132 increased the release of the soluble receptors TNF-R1 and IL-1R1 from U937 cells and decreased their cell-surface expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 1A	Homo sapiens	53-59
18298552-7	2008	MG132 increased the release of the soluble receptors TNF-R1 and IL-1R1 from U937 cells and decreased their cell-surface expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interleukin 1 receptor type 1	Homo sapiens	64-70
18298552-8	2008	MG132 also increased IL-6R cell-surface expression and decreased its release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interleukin 6 receptor	Homo sapiens	21-26
18539596-3	2008	Here we show that chronic morphine exposure induced posttranscriptional down-regulation of the glutamate transporter EAAC1 in C6 glioma cells with a concurrent decrease in glutamate uptake and increase in proteasome activity, which were blocked by the selective proteasome inhibitor MG-132 or lactacystin but not the lysosomal inhibitor chloroquin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	283-289	solute carrier family 1 member 1	Homo sapiens	117-122
18346979-6	2008	Adenoviral transfer of atrogin-1 induced a reduction in cell size that was ameliorated by the ubiquitin proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	F-box protein 32	Rattus norvegicus	23-32
18469159-7	2008	Proteasome inhibitors MG132 (N-[(phenylmethoxy)-carbonyl]-L-leucyl-N-[(1S)-1-formyl-3-methylbutyl]-L-leucinamide) and lactacystin increased TTP protein levels and abolished the effects of cAMP-enhancing compounds on TTP protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	zinc finger protein 36	Mus musculus	140-143
18469159-7	2008	Proteasome inhibitors MG132 (N-[(phenylmethoxy)-carbonyl]-L-leucyl-N-[(1S)-1-formyl-3-methylbutyl]-L-leucinamide) and lactacystin increased TTP protein levels and abolished the effects of cAMP-enhancing compounds on TTP protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	zinc finger protein 36	Mus musculus	216-219
18656624-10	2008	Exogenous OPN or MG132 restored Ub-P-Stat1 and iNOS to levels seen in WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	signal transducer and activator of transcription 1	Mus musculus	37-42
18656624-10	2008	Exogenous OPN or MG132 restored Ub-P-Stat1 and iNOS to levels seen in WT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	nitric oxide synthase 2, inducible	Mus musculus	47-51
18641315-7	2008	Ro52-mediated IRF3 degradation significantly inhibits IFN-beta promoter activity, an effect that is reversed in the presence of the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	tripartite motif-containing 21	Mus musculus	0-4
18641315-7	2008	Ro52-mediated IRF3 degradation significantly inhibits IFN-beta promoter activity, an effect that is reversed in the presence of the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	interferon regulatory factor 3	Homo sapiens	14-18
18641315-7	2008	Ro52-mediated IRF3 degradation significantly inhibits IFN-beta promoter activity, an effect that is reversed in the presence of the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	interferon beta 1	Homo sapiens	54-62
18515798-5	2008	Interestingly, Top1 down-regulation, induction of DNA SSBs and ATM autophosphorylation were all abolished by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	134-139	ATM serine/threonine kinase	Homo sapiens	63-66
18644116-8	2008	Thus, HIPK2 could induce beta-catenin protein degradation that was prevented by cell treatment with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	homeodomain interacting protein kinase 2	Homo sapiens	6-11
18644116-8	2008	Thus, HIPK2 could induce beta-catenin protein degradation that was prevented by cell treatment with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	catenin beta 1	Homo sapiens	25-37
18538797-7	2008	TRPC4 downregulation was also achieved by increasing extracellular calcium and was attenuated by gadolinium and MG132, suggesting that TRPC4 protein is regulated by intracellular calcium concentration and/or the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	transient receptor potential cation channel, subfamily C, member 4	Rattus norvegicus	0-5
18538797-7	2008	TRPC4 downregulation was also achieved by increasing extracellular calcium and was attenuated by gadolinium and MG132, suggesting that TRPC4 protein is regulated by intracellular calcium concentration and/or the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	transient receptor potential cation channel, subfamily C, member 4	Rattus norvegicus	135-140
18566389-8	2008	Use of proteasome inhibitor, MG-132 or a PPARgamma agonist, pioglitazone, prevented LPS-mediated M-CSF induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	colony stimulating factor 1 (macrophage)	Mus musculus	97-102
18645030-7	2008	The down-regulation of c-FLIP by honokiol could be prevented by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	CASP8 and FADD like apoptosis regulator	Homo sapiens	23-29
18466318-0	2008	Adaptation to chronic MG132 reduces oxidative toxicity by a CuZnSOD-dependent mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	superoxide dismutase 1	Rattus norvegicus	60-67
18466318-6	2008	Chronic MG132 resulted in elevated antioxidant proteins CuZn superoxide dismutase (SOD; +55%), MnSOD (+21%), and catalase (+15%), as well as chaperone heat-shock protein 70 (+42%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-13	superoxide dismutase 2	Rattus norvegicus	95-100
18466318-6	2008	Chronic MG132 resulted in elevated antioxidant proteins CuZn superoxide dismutase (SOD; +55%), MnSOD (+21%), and catalase (+15%), as well as chaperone heat-shock protein 70 (+42%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-13	catalase	Rattus norvegicus	113-121
18466318-6	2008	Chronic MG132 resulted in elevated antioxidant proteins CuZn superoxide dismutase (SOD; +55%), MnSOD (+21%), and catalase (+15%), as well as chaperone heat-shock protein 70 (+42%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-13	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	151-172
18410509-8	2008	The late decline in Ha-Ras levels observed after 60 min was prevented by the proteasome inhibitor, MG132, as well as by the selective mitogen-activated protein kinase (MAPK) inhibitor, PD98059.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	Harvey rat sarcoma virus oncogene	Mus musculus	20-26
18466927-6	2008	As previously reported, yeast cells overexpressing Cdc34 were resistant to cadmium even in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	SCF E2 ubiquitin-protein ligase catalytic subunit CDC34	Saccharomyces cerevisiae S288C	51-56
21479433-4	2008	Treatment of the cells with the proteasome inhibitor MG132 protected the HIF-1alpha protein from Zeb-mediated epigenetic regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	hypoxia inducible factor 1 subunit alpha	Homo sapiens	73-83
18435911-0	2008	Proteasome inhibitor MG-132 lowers gastric adenocarcinoma TMK1 cell proliferation via bone morphogenetic protein signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	bone morphogenetic protein 1	Homo sapiens	86-112
18435911-7	2008	Knockdown of BMP receptor II by RNA interference abolished Smad1/5/8 phosphorylation, p21(Waf1/Cip1) induction, and the inhibition of cell proliferation induced by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-170	bone morphogenetic protein 1	Homo sapiens	13-16
18435911-8	2008	Further analysis revealed that MG-132 up-regulated the expression of BMP1 and BMP4 and suppressed the expression of Smad6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	bone morphogenetic protein 1	Homo sapiens	69-73
18435911-8	2008	Further analysis revealed that MG-132 up-regulated the expression of BMP1 and BMP4 and suppressed the expression of Smad6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	bone morphogenetic protein 4	Homo sapiens	78-82
18435911-8	2008	Further analysis revealed that MG-132 up-regulated the expression of BMP1 and BMP4 and suppressed the expression of Smad6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	SMAD family member 6	Homo sapiens	116-121
18435911-9	2008	Knockdown of Smad6 also mimicked the effect of MG-132 on BMP signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	SMAD family member 6	Homo sapiens	13-18
18435911-9	2008	Knockdown of Smad6 also mimicked the effect of MG-132 on BMP signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	bone morphogenetic protein 1	Homo sapiens	57-60
18523266-7	2008	The protein stability, Ser(392) phosphorylation and Lys(373)/Lys(382) acetylation of p53 were enhanced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	tumor protein p53	Homo sapiens	85-88
18523266-10	2008	Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	tumor protein p53	Homo sapiens	92-95
18381294-6	2008	Using cycloheximide and MG132, we demonstrated that the Cyr61-mediated HIF-1alpha up-regulation was through de novo protein synthesis, rather than increased protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	cellular communication network factor 1	Homo sapiens	56-61
18381294-6	2008	Using cycloheximide and MG132, we demonstrated that the Cyr61-mediated HIF-1alpha up-regulation was through de novo protein synthesis, rather than increased protein stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	hypoxia inducible factor 1 subunit alpha	Homo sapiens	71-81
18466927-7	2008	However, the acquired resistance to cadmium by overexpression of Ubc4 was not observed in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	E2 ubiquitin-conjugating protein UBC4	Saccharomyces cerevisiae S288C	65-69
18407463-6	2008	The Galpha(o/i)-induced decrease in RGS20 can be blocked by proteasomal inhibitors lactacystin or MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	G protein subunit alpha o1	Homo sapiens	4-14
18414391-0	2008	Bone morphogenetic protein signalling is required for the anti-mitogenic effect of the proteasome inhibitor MG-132 on colon cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	bone morphogenetic protein 1	Homo sapiens	0-26
18414391-5	2008	The involvement of BMP signalling in the action of MG-132 was elucidated by western blot, real-time PCR, immunofluorescence and RNA interference.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-57	bone morphogenetic protein 1	Homo sapiens	19-22
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	bone morphogenetic protein 1	Homo sapiens	33-36
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	SMAD family member 1	Homo sapiens	90-97
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	136-139
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	140-144
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	145-149
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	dynactin subunit 6	Homo sapiens	155-158
18414391-7	2008	In this regard, MG-132 activated BMP signalling and this was manifested as an increase in Smad1/5/8 phosphorylation and upregulation of p21(Waf1/Cip1) and p27(Kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	cyclin dependent kinase inhibitor 1B	Homo sapiens	159-163
18414391-8	2008	Knockdown of BMP receptor II abolished Smad1/5/8 phosphorylation, the induction of p21(Waf1/Cip1) and p27(Kip1) and inhibition of cell proliferation induced by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	160-166	bone morphogenetic protein 1	Homo sapiens	13-16
18414391-10	2008	Moreover, the expression of Smad6, an intracellular inhibitor of BMP signalling, was suppressed by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	SMAD family member 6	Homo sapiens	28-33
18414391-10	2008	Moreover, the expression of Smad6, an intracellular inhibitor of BMP signalling, was suppressed by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	bone morphogenetic protein 1	Homo sapiens	65-68
18407463-6	2008	The Galpha(o/i)-induced decrease in RGS20 can be blocked by proteasomal inhibitors lactacystin or MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	regulator of G protein signaling 20	Homo sapiens	36-41
18334598-5	2008	Similar to results in primary hepatocytes, the inhibition of the proteasome with N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132) suppresses CYP3A4 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-129	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	142-148
18334598-6	2008	We also found that MG132 treatment had a broad affect on the NF-kappaB pathway, including down-regulation of NF-kappaB DNA binding activity and IkappaB kinase (IKK)alpha levels and up-regulation of IKKbeta and inhibitory kappaB levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	144-169
18334598-6	2008	We also found that MG132 treatment had a broad affect on the NF-kappaB pathway, including down-regulation of NF-kappaB DNA binding activity and IkappaB kinase (IKK)alpha levels and up-regulation of IKKbeta and inhibitory kappaB levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	198-205
18506934-8	2008	RESULTS: MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-alpha level, pancreatic and pulmonary MPO activity (P &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	tumor necrosis factor	Rattus norvegicus	96-105
18313411-9	2008	Interestingly, proteasome inhibitors (MG132 and Lactacystin) and an autophagy inhibitor (3-methyladenine) reversed CO influence iNOS levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	inositol-3-phosphate synthase 1	Homo sapiens	128-132
18359185-3	2008	To examine the effect of DEPs on eosinophils, we measured the cytokine products and activity of nuclear factor-kappa B (NF-kappa B) after addition of the proteasomal inhibitor MG132 in HL-60 clone 15 cells differentiated into eosinophils.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	nuclear factor kappa B subunit 1	Homo sapiens	96-118
18359185-3	2008	To examine the effect of DEPs on eosinophils, we measured the cytokine products and activity of nuclear factor-kappa B (NF-kappa B) after addition of the proteasomal inhibitor MG132 in HL-60 clone 15 cells differentiated into eosinophils.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	nuclear factor kappa B subunit 1	Homo sapiens	120-130
18506934-8	2008	RESULTS: MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-alpha level, pancreatic and pulmonary MPO activity (P &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	myeloperoxidase	Rattus norvegicus	138-141
18337245-5	2008	HeLa cells treated with the proteasome inhibitor MG-132 showed delayed phosphorylation of ATM substrates in response to UV light.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	ATM serine/threonine kinase	Homo sapiens	90-93
18178165-4	2008	The expression and ubiquitination of CAD was remarkably increased by MG132 treatment in the absence of ICAD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	DNA fragmentation factor subunit beta	Homo sapiens	37-40
17638069-6	2008	The proteasome inhibitor MG132 blocks OPDA-mediated decrease in cyclin D1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cyclin D1	Homo sapiens	64-73
18237272-5	2008	Immunoprecipitation followed by immunoblot analysis showed that the ABCG2 F208S and S441N variant proteins were endogenously ubiquitinated in Flp-In-293 cells, and treatment with MG132 significantly enhanced the level of these ubiquitinated variants.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	179-184	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	68-73
18237272-6	2008	Immunofluorescence microscopy demonstrated that MG132 greatly affected the ABCG2 F208S and S441N variants in terms of both protein levels and intracellular distribution.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	75-80
18237272-4	2008	Interestingly, protein expression levels of the ABCG2 F208S and S441N variants increased 6- to 12-fold when Flp-In-293 cells were treated with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-53
18436832-12	2008	In HLE B-3 cells, TGF-beta(2) increased MMP-2 mRNA and protein levels; these increases were inhibited by MG132 cotreatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	transforming growth factor beta 2	Homo sapiens	18-29
18436832-12	2008	In HLE B-3 cells, TGF-beta(2) increased MMP-2 mRNA and protein levels; these increases were inhibited by MG132 cotreatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	matrix metallopeptidase 2	Homo sapiens	40-45
18436832-13	2008	Medium from HLE B-3 cultures showed MMP-2 and -9 activities, which were induced by TGF-beta(2) treatment and inhibited by MG132 co-treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	matrix metallopeptidase 2	Homo sapiens	36-48
18064628-8	2008	The proteasome inhibitor, MG132, potently increased Bim protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	BCL2 like 11	Homo sapiens	52-55
18505931-4	2008	Cotreatment with the proteasomal inhibitor MG-132 abolishes the ability of LBH589 to reduce DNMT1, suggesting that the proteasomal pathway mediates DNMT1 degradation on HDAC inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	LBH regulator of WNT signaling pathway	Homo sapiens	75-78
18313049-8	2008	HAP95 is ubiquitylated and subjected to a proteasome-dependent degradation pathway, however, the experiments in which 293 cells expressing both RNF43 and HAP95 were treated with a proteasome inhibitor, MG132, show that HAP95 is unlikely to serve as a substrate of RNF43 ubiquitin ligase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	A-kinase anchoring protein 8 like	Homo sapiens	0-5
18505931-4	2008	Cotreatment with the proteasomal inhibitor MG-132 abolishes the ability of LBH589 to reduce DNMT1, suggesting that the proteasomal pathway mediates DNMT1 degradation on HDAC inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	DNA methyltransferase 1	Homo sapiens	92-97
18505931-4	2008	Cotreatment with the proteasomal inhibitor MG-132 abolishes the ability of LBH589 to reduce DNMT1, suggesting that the proteasomal pathway mediates DNMT1 degradation on HDAC inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	DNA methyltransferase 1	Homo sapiens	148-153
18505931-4	2008	Cotreatment with the proteasomal inhibitor MG-132 abolishes the ability of LBH589 to reduce DNMT1, suggesting that the proteasomal pathway mediates DNMT1 degradation on HDAC inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	histone deacetylase 9	Homo sapiens	169-173
18313049-8	2008	HAP95 is ubiquitylated and subjected to a proteasome-dependent degradation pathway, however, the experiments in which 293 cells expressing both RNF43 and HAP95 were treated with a proteasome inhibitor, MG132, show that HAP95 is unlikely to serve as a substrate of RNF43 ubiquitin ligase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	ring finger protein 43	Homo sapiens	144-149
18313049-8	2008	HAP95 is ubiquitylated and subjected to a proteasome-dependent degradation pathway, however, the experiments in which 293 cells expressing both RNF43 and HAP95 were treated with a proteasome inhibitor, MG132, show that HAP95 is unlikely to serve as a substrate of RNF43 ubiquitin ligase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	ring finger protein 43	Homo sapiens	264-269
18208356-3	2008	Pulse-chase labeling and a ubiquitination experiment using MG132, a proteasomal inhibitor, indicate that Smurf1 induces proteasomal degradation of hPEM-2 in cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	SMAD specific E3 ubiquitin protein ligase 1	Homo sapiens	105-111
18208356-3	2008	Pulse-chase labeling and a ubiquitination experiment using MG132, a proteasomal inhibitor, indicate that Smurf1 induces proteasomal degradation of hPEM-2 in cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	Cdc42 guanine nucleotide exchange factor 9	Homo sapiens	147-153
18236383-5	2008	Furthermore, MG132 increased antioxidant enzyme activities of SOD, CAT, and GSH-Px.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	catalase	Rattus norvegicus	67-70
18236383-6	2008	(2) In vitro, MG132 increased free radical oxygen species in hepatocytes; this effect disappeared in the presence of CAT or mannitol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	catalase	Rattus norvegicus	117-120
17927769-8	2008	Plasma LDH and AST levels were decreased by MG132 during both ischemia and reperfusion, while ALT values were decreased only after 30 min of reperfusion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	15-18
18341587-4	2008	Interestingly, the proteasome inhibitors MG132 and epoxomicin were capable of potentiating TRAIL-induced apoptosis in TRAIL-sensitive U87 and U251 cells and of reactivating apoptosis in TRAIL-resistant U343 and U373 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	TNF superfamily member 10	Homo sapiens	91-96
18341587-4	2008	Interestingly, the proteasome inhibitors MG132 and epoxomicin were capable of potentiating TRAIL-induced apoptosis in TRAIL-sensitive U87 and U251 cells and of reactivating apoptosis in TRAIL-resistant U343 and U373 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	TNF superfamily member 10	Homo sapiens	118-123
18341587-4	2008	Interestingly, the proteasome inhibitors MG132 and epoxomicin were capable of potentiating TRAIL-induced apoptosis in TRAIL-sensitive U87 and U251 cells and of reactivating apoptosis in TRAIL-resistant U343 and U373 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	TNF superfamily member 10	Homo sapiens	118-123
18296917-0	2008	Proteasome inhibitor MG132 reverses multidrug resistance of gastric cancer through enhancing apoptosis and inhibiting P-gp.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	phosphoglycolate phosphatase	Homo sapiens	118-122
18296917-4	2008	In the present study, we found that, in vincristine-resistant human gastric cancer cell line SGC7901/VCR, proteasome inhibitor MG132 was an effective inducer of apoptosis, and also had the capacity of downregulating the expression of anti-apoptotic Bcl-2 and MDR1 (P-gp), by which MG132 resensitized tumor cells to the apoptosis induced by anticancer drugs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	BCL2 apoptosis regulator	Homo sapiens	249-254
18296917-4	2008	In the present study, we found that, in vincristine-resistant human gastric cancer cell line SGC7901/VCR, proteasome inhibitor MG132 was an effective inducer of apoptosis, and also had the capacity of downregulating the expression of anti-apoptotic Bcl-2 and MDR1 (P-gp), by which MG132 resensitized tumor cells to the apoptosis induced by anticancer drugs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	ATP binding cassette subfamily B member 1	Homo sapiens	259-263
18296917-4	2008	In the present study, we found that, in vincristine-resistant human gastric cancer cell line SGC7901/VCR, proteasome inhibitor MG132 was an effective inducer of apoptosis, and also had the capacity of downregulating the expression of anti-apoptotic Bcl-2 and MDR1 (P-gp), by which MG132 resensitized tumor cells to the apoptosis induced by anticancer drugs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	phosphoglycolate phosphatase	Homo sapiens	265-269
18296917-5	2008	Data presented by drug sensitivity assay further demonstrated that MG132 could reverse the resistant phenotype of gastric cancer cells effectively through both enhancing drug-induced apoptosis and inhibiting P-gp.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	phosphoglycolate phosphatase	Homo sapiens	208-212
18395088-12	2008	In the presence of an NF-kappaB inhibitor MG132, IL-8 transcription was inhibited, but not that of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	nuclear factor kappa B subunit 1	Homo sapiens	22-31
18395088-12	2008	In the presence of an NF-kappaB inhibitor MG132, IL-8 transcription was inhibited, but not that of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	C-X-C motif chemokine ligand 8	Homo sapiens	49-53
18227168-11	2008	The decreased alpha(v)beta(3) level was restored by treatment with the proteasome inhibitor MG132, suggesting a SPE B-mediated endocytosis of integrin alpha(v)beta(3) via the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	integrin subunit alpha V	Homo sapiens	142-166
17906695-4	2008	In both Hep3B and HEK293 cells, a proteasome inhibitor MG132 noticeably attenuated hypoxic induction of erythropoietin and VEGF mRNAs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	erythropoietin	Homo sapiens	104-118
17906695-4	2008	In both Hep3B and HEK293 cells, a proteasome inhibitor MG132 noticeably attenuated hypoxic induction of erythropoietin and VEGF mRNAs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	vascular endothelial growth factor A	Homo sapiens	123-127
17906695-5	2008	MG132 inactivated HIF-1alpha C-terminal transactivation domain (CAD), independently of factor inhibiting HIF-1 (FIH) and inhibited p300 recruitment by HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	18-28
17906695-5	2008	MG132 inactivated HIF-1alpha C-terminal transactivation domain (CAD), independently of factor inhibiting HIF-1 (FIH) and inhibited p300 recruitment by HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	E1A binding protein p300	Homo sapiens	131-135
17906695-5	2008	MG132 inactivated HIF-1alpha C-terminal transactivation domain (CAD), independently of factor inhibiting HIF-1 (FIH) and inhibited p300 recruitment by HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	151-161
17906695-8	2008	Both the activity and the p300 binding of HIF-1alpha were inhibited by CITED2 expression and recovered by CITED2 siRNA in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	E1A binding protein p300	Homo sapiens	26-30
17906695-8	2008	Both the activity and the p300 binding of HIF-1alpha were inhibited by CITED2 expression and recovered by CITED2 siRNA in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	hypoxia inducible factor 1 subunit alpha	Homo sapiens	42-52
17906695-8	2008	Both the activity and the p300 binding of HIF-1alpha were inhibited by CITED2 expression and recovered by CITED2 siRNA in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2	Homo sapiens	106-112
18199655-6	2008	Treatment with the proteasome inhibitor MG132 partially relieved TRIM5alpha-mediated restriction of RMT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	tripartite motif containing 5	Homo sapiens	65-75
18325350-5	2008	The proteasome inhibitors, epoxomicin and MG132, significantly inhibited degradation of Bach1 by ZnMP in a dose-dependent fashion, indicating that the degradation of Bach1 by ZnMP is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	BTB domain and CNC homolog 1	Homo sapiens	88-93
18325350-5	2008	The proteasome inhibitors, epoxomicin and MG132, significantly inhibited degradation of Bach1 by ZnMP in a dose-dependent fashion, indicating that the degradation of Bach1 by ZnMP is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	BTB domain and CNC homolog 1	Homo sapiens	166-171
18077709-4	2008	This indicates that viral RT products rescued from restriction by either heat shock treatment or the presence of MG132 are on a productive pathway, supporting a model in which TRIM5alpha proteins restrict retroviruses in multiple phases that are differentially sensitive to heat shock and proteasome inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	tripartite motif containing 5	Homo sapiens	176-186
18094054-8	2008	We also found that treatment with the proteasome inhibitor MG132 partially rescued the severe mitotic phenotype observed in response to release from nocodazole block in CENP-50-deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	centromere protein U	Gallus gallus	169-176
18078967-7	2008	SPI-serum-stimulated AhR degradation was inhibited by treating the cells with the proteasome inhibitor, MG132, and was observed to be preceded by ubiquitination of the receptor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	aryl hydrocarbon receptor	Rattus norvegicus	21-24
18339263-3	2008	However, inhibition of proteasomal proteolytic activity by clasto-lactacystin beta-lactone (CLBL) and Z-Leu-Leu-Leu-CHO (MG132), which are specific inhibitors of the 20S proteasomal core proteases, led to a significant (P &lt; 0.05) inhibition of induction of acrosome reaction mediated by both recombinant human ZP3 and ZP4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	zona pellucida glycoprotein 3	Homo sapiens	313-316
18339263-3	2008	However, inhibition of proteasomal proteolytic activity by clasto-lactacystin beta-lactone (CLBL) and Z-Leu-Leu-Leu-CHO (MG132), which are specific inhibitors of the 20S proteasomal core proteases, led to a significant (P &lt; 0.05) inhibition of induction of acrosome reaction mediated by both recombinant human ZP3 and ZP4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	zona pellucida glycoprotein 4	Homo sapiens	321-324
17603062-7	2008	The NFkappaB inhibitor MG-132 and heat inactivation significantly reversed Adipo-stimulated monocyte adhesion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-29	nuclear factor kappa B subunit 1	Homo sapiens	4-12
18164817-4	2008	MG132, a blocker of nuclear factor kappaB (NF-kappaB) activation, did not apparently affect LPS-induced GDNF gene expression, whereas it attenuated the up-regulation of iNOS genes via Toll-like receptor (TLR) 4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	toll-like receptor 4	Rattus norvegicus	204-210
18283158-4	2008	RESULTS: In cells that express E6, proteasome inhibition with MG132 restored p53 protein levels and decreased proliferation in a dose-dependent fashion that was significantly more pronounced compared with controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	tumor protein p53	Homo sapiens	77-80
18726001-7	2008	Exogenous application of different plant growth hormones revealed that BIN2 depletion is specifically induced by BR through a functional BR receptor, while treatment of a proteasome inhibitor, MG132, not only prevented the BR-induced BIN2 depletion but also nullified the inhibitory effect of BR on the BIN2 kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-198	Protein kinase superfamily protein	Arabidopsis thaliana	234-238
18726001-7	2008	Exogenous application of different plant growth hormones revealed that BIN2 depletion is specifically induced by BR through a functional BR receptor, while treatment of a proteasome inhibitor, MG132, not only prevented the BR-induced BIN2 depletion but also nullified the inhibitory effect of BR on the BIN2 kinase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-198	Protein kinase superfamily protein	Arabidopsis thaliana	234-238
18063576-4	2008	Inhibition of the 26 S proteasome with MG132 rescued cyclin D1 protein levels, indicating that rather than inhibiting translation, PKR and PERK act to increase cyclin D1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	cyclin D1	Homo sapiens	53-62
18174273-10	2008	The effect of TNF-alpha was prevented by the lysosomal protease inhibitors leupeptin or chloroquine or by the proteasome inhibitors MG132 or lactacystin, suggesting a cytokine-induced AQP8 proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	tumor necrosis factor	Rattus norvegicus	14-23
18083835-5	2008	We show that eRF3a forms altered in their eRF1-binding site have a decreased stability, which increases upon cell treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	G1 to S phase transition 1	Homo sapiens	13-18
18235224-5	2008	Inhibition of the 26S proteasome by MG132 leads to the rapid inhibition of phosphorylation of the mTORC1 substrates S6 kinase and 4E-BP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	CREB regulated transcription coactivator 1	Mus musculus	98-104
18235224-5	2008	Inhibition of the 26S proteasome by MG132 leads to the rapid inhibition of phosphorylation of the mTORC1 substrates S6 kinase and 4E-BP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	BP1	Homo sapiens	133-136
18057259-5	2008	Levels of unconjugated RIG-I also decreased when 26S proteasome activity was blocked by treatment with MG132, ALLN, or Lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	DExD/H-box helicase 58	Homo sapiens	23-28
18057259-6	2008	In the presence of MG132, ISG15 conjugation to RIG-I increased, and hence, the unconjugated form of RIG-I was reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	ISG15 ubiquitin like modifier	Homo sapiens	26-31
18057259-6	2008	In the presence of MG132, ISG15 conjugation to RIG-I increased, and hence, the unconjugated form of RIG-I was reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	DExD/H-box helicase 58	Homo sapiens	47-52
18057259-6	2008	In the presence of MG132, ISG15 conjugation to RIG-I increased, and hence, the unconjugated form of RIG-I was reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	DExD/H-box helicase 58	Homo sapiens	100-105
18069942-3	2008	Changes observed for XND1 knockout plants compared with wild-type Arabidopsis thaliana included a reduction in both plant height and tracheary element length and an increase in metaxylem relative to protoxylem in roots of plants treated with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	267-272	xylem NAC domain 1	Arabidopsis thaliana	21-25
18083835-5	2008	We show that eRF3a forms altered in their eRF1-binding site have a decreased stability, which increases upon cell treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	eukaryotic translation termination factor 1	Homo sapiens	42-46
17653084-4	2008	In Jurkat cells inhibition of proteasomal activity by MG132 enhances the level of hypophosphorylated, unmodified 4E-BP1 but only modestly increases the accumulation of high-molecular-weight, phosphorylated forms of 4E-BP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	113-119
17653084-4	2008	In Jurkat cells inhibition of proteasomal activity by MG132 enhances the level of hypophosphorylated, unmodified 4E-BP1 but only modestly increases the accumulation of high-molecular-weight, phosphorylated forms of 4E-BP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	215-221
18039666-6	2008	We also show that production of the short Tgs1 isoform is inhibited by MG132, suggesting that it results from proteasomal limited processing of the full-length Tgs1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	trimethylguanosine synthase 1	Homo sapiens	42-46
18039666-6	2008	We also show that production of the short Tgs1 isoform is inhibited by MG132, suggesting that it results from proteasomal limited processing of the full-length Tgs1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	trimethylguanosine synthase 1	Homo sapiens	160-164
18155168-3	2008	Here we show that prolonged hsp90 inhibition in different cell types reduces protein levels of both sGC subunits by about half, an effect that was prevented by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	heat shock protein 90 alpha family class A member 1	Homo sapiens	28-33
17928529-3	2008	RANKL induced Jak1 ubiquitination, and a proteasome inhibitor MG132 efficiently blocked the RANKL-induced degradation of Jak1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	Janus kinase 1	Mus musculus	14-18
17928529-3	2008	RANKL induced Jak1 ubiquitination, and a proteasome inhibitor MG132 efficiently blocked the RANKL-induced degradation of Jak1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	92-97
17928529-3	2008	RANKL induced Jak1 ubiquitination, and a proteasome inhibitor MG132 efficiently blocked the RANKL-induced degradation of Jak1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	Janus kinase 1	Mus musculus	121-125
17996194-5	2008	Moreover, we demonstrated that BAG3 knockdown by siRNA sensitized cancer cells to MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	BAG cochaperone 3	Homo sapiens	31-35
17923481-7	2008	However, PDC activity could be restored in cells from this patient following treatment with MG132, a specific proteasome inhibitor, and normal levels of E1beta could be detected in MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	181-186	branched chain keto acid dehydrogenase E1 subunit beta	Homo sapiens	153-159
17928629-10	2008	In cells transiently transfected with a luciferase reporter bearing a portion (-597/+33) of the human PTGES gene promoter, interleukin-1beta (IL1B) produced a moderate increase in luciferase activity; this effect was abrogated in the presence of an indirect NFkappaB inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	278-284	prostaglandin E synthase	Homo sapiens	102-107
17928629-10	2008	In cells transiently transfected with a luciferase reporter bearing a portion (-597/+33) of the human PTGES gene promoter, interleukin-1beta (IL1B) produced a moderate increase in luciferase activity; this effect was abrogated in the presence of an indirect NFkappaB inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	278-284	interleukin 1 beta	Homo sapiens	123-140
17928629-10	2008	In cells transiently transfected with a luciferase reporter bearing a portion (-597/+33) of the human PTGES gene promoter, interleukin-1beta (IL1B) produced a moderate increase in luciferase activity; this effect was abrogated in the presence of an indirect NFkappaB inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	278-284	interleukin 1 beta	Homo sapiens	142-146
18175929-3	2008	TNFalpha treatment of HC11 cells also induced expression of SAA genes, and the effect on SAA1 and SAA2 expression was suppressed by treatment with MG132, and in cells transfected with a dominant negative mutant form of IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	tumor necrosis factor	Homo sapiens	0-8
19065031-1	2008	AIM: to determine if chondrocytic Hsp70 induction, via intra-articular injections of a reversible proteasome inhibitor (MG132), can protect articular chondrocytes from cellular death in experimental rat OA knee induced surgically by anterior cruciate ligament transection (ACLT).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-125	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	34-39
19065031-8	2008	The expression of Hsp70 increased 11-fold in the MG132-treated group versus 2-3-fold in ACLT-control rats on D28.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	18-23
19065031-9	2008	Concomitantly, cells expressing caspase-3 increased 4-fold in ACLT model and decreased 2-fold with MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	caspase 3	Rattus norvegicus	32-41
19065031-10	2008	CONCLUSIONS: Intra-articular induction of Hsp70 by MG132 could be a safe and interesting tool in chondrocytes protection from cellular injuries and thus might be a novel chondroprotective modality in rat OA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	42-47
18175929-3	2008	TNFalpha treatment of HC11 cells also induced expression of SAA genes, and the effect on SAA1 and SAA2 expression was suppressed by treatment with MG132, and in cells transfected with a dominant negative mutant form of IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	C-C motif chemokine ligand 2	Homo sapiens	22-26
18175929-3	2008	TNFalpha treatment of HC11 cells also induced expression of SAA genes, and the effect on SAA1 and SAA2 expression was suppressed by treatment with MG132, and in cells transfected with a dominant negative mutant form of IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	serum amyloid A1	Homo sapiens	89-93
18175929-3	2008	TNFalpha treatment of HC11 cells also induced expression of SAA genes, and the effect on SAA1 and SAA2 expression was suppressed by treatment with MG132, and in cells transfected with a dominant negative mutant form of IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	serum amyloid A2	Homo sapiens	98-102
17764071-7	2008	MG132, a proteasome inhibitor, protected the hypoxia- or IGF-induced HIF-1alpha protein from deguelin-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	hypoxia inducible factor 1 subunit alpha	Homo sapiens	69-79
17828282-5	2008	Treatment of ovarian (2008) and lung (H1299) tumor cells with adenoviral delivery of mda-7 (Ad-mda7) or Ad-mda7 plus the proteosome inhibitor MG132 showed that MDA-7 protein expression was dependent upon proteosome activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	interleukin 24	Homo sapiens	160-165
17828282-6	2008	Western blot and immunoprecipitation analyses verified that the MDA-7 protein was ubiquitinated and that ubiquitinated-MDA-7 levels were increased in MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	interleukin 24	Homo sapiens	64-69
17828282-6	2008	Western blot and immunoprecipitation analyses verified that the MDA-7 protein was ubiquitinated and that ubiquitinated-MDA-7 levels were increased in MG132-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	interleukin 24	Homo sapiens	119-124
17828282-8	2008	Furthermore, ubiquitinated MDA-7 protein was degraded by the 26S proteasome, as MDA-7 accumulation was observed only when cells were treated with MG132 but not with lysosome or protease inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	interleukin 24	Homo sapiens	27-32
17828282-8	2008	Furthermore, ubiquitinated MDA-7 protein was degraded by the 26S proteasome, as MDA-7 accumulation was observed only when cells were treated with MG132 but not with lysosome or protease inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	interleukin 24	Homo sapiens	80-85
18005266-5	2008	IL-4 also increased suppressor of cytokine signalling 3 (SOCS3) protein level in the presence of the proteasome inhibitor MG132 exclusively in PLB-985D cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	interleukin 4	Homo sapiens	0-4
18005266-5	2008	IL-4 also increased suppressor of cytokine signalling 3 (SOCS3) protein level in the presence of the proteasome inhibitor MG132 exclusively in PLB-985D cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	suppressor of cytokine signaling 3	Homo sapiens	20-55
18005266-5	2008	IL-4 also increased suppressor of cytokine signalling 3 (SOCS3) protein level in the presence of the proteasome inhibitor MG132 exclusively in PLB-985D cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	suppressor of cytokine signaling 3	Homo sapiens	57-62
17912641-0	2007	Absence of Bax switched MG132-induced apoptosis to non-apoptotic cell death that could be suppressed by transcriptional or translational inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	BCL2 associated X, apoptosis regulator	Homo sapiens	11-14
17959680-11	2008	Ubiquitination of UL84 occurred in the presence and absence of the proteasome activity inhibitor MG132 in infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	protein UL84	Human betaherpesvirus 5	18-22
18377959-0	2008	The proteasome inhibitor MG132 induces nuclear translocation of erythroid transcription factor Nrf2 and cyclooxygenase-2 expression in human vascular endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	NFE2 like bZIP transcription factor 2	Homo sapiens	95-99
18377959-0	2008	The proteasome inhibitor MG132 induces nuclear translocation of erythroid transcription factor Nrf2 and cyclooxygenase-2 expression in human vascular endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	104-120
18037126-4	2007	However, our previous studies using U937 cells showed that HNE-modified glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is degraded by an enzyme that is sensitive to a serine protease inhibitor, diisopropyl fluorophosphate (DFP), but not a proteasome inhibitor, MG-132, and that its degradation is not catalyzed in the acidic pH range where lysosomal enzymes are active.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	263-269	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	72-112
18037126-4	2007	However, our previous studies using U937 cells showed that HNE-modified glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is degraded by an enzyme that is sensitive to a serine protease inhibitor, diisopropyl fluorophosphate (DFP), but not a proteasome inhibitor, MG-132, and that its degradation is not catalyzed in the acidic pH range where lysosomal enzymes are active.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	263-269	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	114-119
17912641-4	2007	We previously showed that proteasome inhibitors including MG132 and Bortezomib could induce apoptosis in a Bax- and caspase-dependent way.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	BCL2 associated X, apoptosis regulator	Homo sapiens	107-110
17891158-10	2007	Treatment with the proteasome inhibitors, lactacystin or MG132, reversed the decrease in iNOS protein levels caused by PPARalpha agonists.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	nitric oxide synthase 2, inducible	Mus musculus	89-93
17927689-7	2007	The protection degradation of HDAC1 and p300 by MG-132 could be partially reversed by curcumin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	histone deacetylase 1	Homo sapiens	30-35
17927689-7	2007	The protection degradation of HDAC1 and p300 by MG-132 could be partially reversed by curcumin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	E1A binding protein p300	Homo sapiens	40-44
17891158-10	2007	Treatment with the proteasome inhibitors, lactacystin or MG132, reversed the decrease in iNOS protein levels caused by PPARalpha agonists.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	peroxisome proliferator activated receptor alpha	Mus musculus	119-128
17597106-10	2007	Tamoxifen-induced MGMT degradation could be blocked by MG-132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	O-6-methylguanine-DNA methyltransferase	Homo sapiens	18-22
18025182-4	2007	Ligation of several NK cell activation receptors including NKp30 induced a similar response and was blocked by pretreatment with the proteosome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	natural cytotoxicity triggering receptor 3	Homo sapiens	59-64
18158999-4	2007	RESULTS: MG-132 significantly decreased serum amylase, pancreatic weight/body weight ratio, and pancreatic and pulmonary myeloperoxidase activity (P&lt;0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	myeloperoxidase	Rattus norvegicus	121-136
17976382-3	2007	We showed that the proteasome inhibitor MG-132 increases Nrf3 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	NFE2 like bZIP transcription factor 3	Homo sapiens	57-61
18025303-2	2007	Cdk1 inhibition by roscovitine is known to induce premature mitotic exit, whereas inhibition of the APC/C-dependent degradation of cyclin B1 by MG132 induces mitotic arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	cyclin B1	Homo sapiens	131-140
17716627-6	2007	Furthermore, MG-132--a specific inhibitor of the proteasome--blocked the degradation of repp86 in Siah2 overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	TPX2 microtubule nucleation factor	Homo sapiens	88-94
17855340-10	2007	Further, FN potentiated Caco2-BBE cell attachment and wound healing, which was inhibited by RGD peptide as well as NF-kappaB inhibitors MG-132 and 1-pyrrolidinecarbodithioic acid, ammonium salt.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-142	fibronectin 1	Homo sapiens	9-11
17855769-7	2007	All Bsep mutants accumulate in perinuclear aggresome-like structures in the presence of the proteasome inhibitor MG-132, suggesting that mutations are associated with protein instability and ubiquitin-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	ATP binding cassette subfamily B member 11	Homo sapiens	4-8
17639599-11	2007	Furthermore, the NF-kappaB inhibitors MG132 (10 microM) or PDTC (5 microM) completely blocked the high glucose-induced GRO secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	C-X-C motif chemokine ligand 1	Rattus norvegicus	119-122
17707122-3	2007	Overexpression of wild-type PINK1 blocked mitochondrial release of apoptogenic cytochrome c, caspase-3 activation and apoptotic cell death induced by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	171-176	PTEN induced kinase 1	Homo sapiens	28-33
17720143-9	2007	Using MG132, a proteasome inhibitor, reFIP-gts also prevents hTERT translocation from proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-11	telomerase reverse transcriptase	Homo sapiens	61-66
17873020-4	2007	Transient overexpression of CHIP in COS-7 cells degraded heterologous sGC in a concentration-related manner; this downregulation of sGC was abrogated by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-184	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	70-73
17873020-4	2007	Transient overexpression of CHIP in COS-7 cells degraded heterologous sGC in a concentration-related manner; this downregulation of sGC was abrogated by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-184	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	132-135
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	heat shock protein 90 alpha family class A member 1	Homo sapiens	20-25
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	52-57
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	188-193
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	heat shock protein 90 alpha family class A member 1	Homo sapiens	226-231
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	188-193
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	heat shock protein 90 alpha family class A member 1	Homo sapiens	226-231
17978573-5	2007	We also showed that HSP90 prolongs the half-life of c-Jun by stabilizing the protein; the proteasome inhibitor N-benzoyloxy-carbonyl (Z)-Leu-Leu-leucinal (MG132) blocks the degradation of c-Jun promoted by GA. Transfection of HSP90 plasmids did not obviously alter phosphorylation of c-Jun, and a Jun-2 luciferase activity assay indicated that over-expression of HSP90 elevated the total protein activity of c-Jun in HEK293 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	188-193
17716627-6	2007	Furthermore, MG-132--a specific inhibitor of the proteasome--blocked the degradation of repp86 in Siah2 overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	siah E3 ubiquitin protein ligase 2	Homo sapiens	98-103
17698841-8	2007	HDM2 was stabilized in the HCMV-infected cells by MG132, indicating a shift from p53 to HDM2 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	MDM2 proto-oncogene	Homo sapiens	0-4
17407140-7	2007	Proteasome inhibitor (MG132) treatment of the cells indicated that proteasome mediated degradation of p27, and Skp2-dependent degradation might be prevented.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	dynactin subunit 6	Homo sapiens	102-105
17407140-7	2007	Proteasome inhibitor (MG132) treatment of the cells indicated that proteasome mediated degradation of p27, and Skp2-dependent degradation might be prevented.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	S-phase kinase associated protein 2	Homo sapiens	111-115
17698841-8	2007	HDM2 was stabilized in the HCMV-infected cells by MG132, indicating a shift from p53 to HDM2 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	tumor protein p53	Homo sapiens	81-84
17493842-0	2007	Caspase-8 dependent osteosarcoma cell apoptosis induced by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	caspase 8	Homo sapiens	0-9
17493842-8	2007	This suggests that the apoptosis induced by MG132 in MG63 cells is caspase-8 dependent, p27 and bcl-2 family related.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	caspase 8	Homo sapiens	67-76
17493842-8	2007	This suggests that the apoptosis induced by MG132 in MG63 cells is caspase-8 dependent, p27 and bcl-2 family related.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	dynactin subunit 6	Homo sapiens	88-91
17493842-8	2007	This suggests that the apoptosis induced by MG132 in MG63 cells is caspase-8 dependent, p27 and bcl-2 family related.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	BCL2 apoptosis regulator	Homo sapiens	96-101
17609434-5	2007	Indeed, under this condition, ERalpha protein was rescued using the proteasome inhibitor MG132 in presence of the protein synthesis inhibitor cycloheximide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	estrogen receptor 1	Homo sapiens	30-37
17646573-9	2007	In addition, proteasome inhibitor MG132 (1 micromol/L) prevented insulin receptor substrate-1 degradation (n=4).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	insulin receptor substrate 1	Homo sapiens	65-93
17982228-5	2007	In addition, pretreatment of cells with NF-kappaB inhibitor (MG-132) or JNK inhibitor (SP600125) significantly inhibited ICAM-1 expression promoted by HDM extract.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	intercellular adhesion molecule 1	Homo sapiens	121-127
17443676-4	2007	The stability of gp130 protein was mediated by NFkappaB activity, as the inhibitors quinazoline and MG132 not only blocked the increase induced by 6 h of TNF treatment, but also reduced its basal level of expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	interleukin 6 cytokine family signal transducer	Rattus norvegicus	17-22
17443676-4	2007	The stability of gp130 protein was mediated by NFkappaB activity, as the inhibitors quinazoline and MG132 not only blocked the increase induced by 6 h of TNF treatment, but also reduced its basal level of expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	tumor necrosis factor	Rattus norvegicus	154-157
17609434-6	2007	In addition, strong accumulation of ubiquitinated ERalpha was obtained after GSK-3 silencing in the presence of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	estrogen receptor 1	Homo sapiens	50-57
17686774-5	2007	Interestingly, the protein levels of those ABCG2 variants were remarkably enhanced by treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
17786340-6	2007	Moreover, MG132, an inhibitor of AIF release from mitochondria, blocked the induction of cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	apoptosis inducing factor mitochondria associated 1	Homo sapiens	33-36
17635918-7	2007	Specifically, the effect of low concentration of GS-HCl (1 mM) or of tunicamycin (0.1 microg/ml) to produce the aglycosylated COX-2 was rescued by the proteasomal inhibitor MG132 but not by the lysosomal or caspase inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-178	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	126-131
17635918-9	2007	Notably, GS-HCl (5 mM) also facilitated degradation of the higher molecular species of COX-2 in IL-1beta-treated A549 cells that was retarded by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92
17635918-9	2007	Notably, GS-HCl (5 mM) also facilitated degradation of the higher molecular species of COX-2 in IL-1beta-treated A549 cells that was retarded by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	interleukin 1 beta	Homo sapiens	96-104
17869053-8	2007	Inhibitors of NF-kappaB and stabilizers of I-kappaBalpha (e.g., MG-132, lactacystin, etc) prevented NF-kappaB activation while protecting against EtOH-induced injury.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	NFKB inhibitor alpha	Homo sapiens	43-56
17631504-5	2007	Degradation of T-Cad was blocked upon treatment of PC12 cells with the proteasomal inhibitor ZLLL or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-97	cadherin 13	Rattus norvegicus	15-20
17724800-4	2007	RESULTS: Administering the proteasome inhibitor MG132 (at a dose of 10 mg/kg, ip) 90 min after the onset of pancreatic inflammation induced the expression of cell-protective 72 kDa heat shock protein (HSP72) and decreased DNA-binding of nuclear factor-kappaB (NF-kappaB).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	selenoprotein K	Rattus norvegicus	181-199
17724800-4	2007	RESULTS: Administering the proteasome inhibitor MG132 (at a dose of 10 mg/kg, ip) 90 min after the onset of pancreatic inflammation induced the expression of cell-protective 72 kDa heat shock protein (HSP72) and decreased DNA-binding of nuclear factor-kappaB (NF-kappaB).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	201-206
17869053-8	2007	Inhibitors of NF-kappaB and stabilizers of I-kappaBalpha (e.g., MG-132, lactacystin, etc) prevented NF-kappaB activation while protecting against EtOH-induced injury.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	nuclear factor kappa B subunit 1	Homo sapiens	100-109
17617377-15	2007	Additionally, inhibition of 26S proteasome by MG132 revealed production of DBC2 protein in the resistant cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	Rho related BTB domain containing 2	Homo sapiens	75-79
17579211-6	2007	In vitro assays using purified proteins showed that Lon-mediated degradation of StAR was ATP-dependent and blocked by the proteasome inhibitors MG132 (IC(50) = 20 microm) and clasto-lactacystin beta-lactone (cLbetaL, IC(50) = 3 microm); by contrast, epoxomicin, representing a different class of proteasome inhibitors, had no effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	lon peptidase 1, mitochondrial	Homo sapiens	52-55
17579211-6	2007	In vitro assays using purified proteins showed that Lon-mediated degradation of StAR was ATP-dependent and blocked by the proteasome inhibitors MG132 (IC(50) = 20 microm) and clasto-lactacystin beta-lactone (cLbetaL, IC(50) = 3 microm); by contrast, epoxomicin, representing a different class of proteasome inhibitors, had no effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	steroidogenic acute regulatory protein	Homo sapiens	80-84
17541959-8	2007	AR protein expression in alpha2beta1hi cells became detectable when its degradation was repressed by the proteosomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	androgen receptor	Homo sapiens	0-2
17579211-7	2007	Such inhibition is consistent with results in cultured rat ovarian granulosa cells demonstrating that degradation of StAR in the mitochondrial matrix is blocked by MG132 and cLbetaL but not by epoxomicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	steroidogenic acute regulatory protein	Rattus norvegicus	117-121
17705854-8	2007	Experiments using cycloheximde and MG132 further confirmed its indispensable role for the protein stability of T beta RI.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	transforming growth factor beta receptor 1	Homo sapiens	111-120
17679617-6	2007	Inhibition of the 26S proteasome with either MG132 or PR-11 prevented the high glucose-triggered reduction of GTPCH and BH4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	GTP cyclohydrolase 1	Homo sapiens	110-115
17679617-9	2007	Finally, administration of MG132 or a superoxide dismutase mimetic, tempol, reversed the diabetes mellitus-induced reduction of GTPCH and BH4 and endothelial dysfunction in streptozotocin-induced diabetes mellitus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	GTP cyclohydrolase 1	Homo sapiens	128-133
17641041-6	2007	A high rate of NF-kappaB/p65 degradation in LNK cells correlates with Pro1 activity, since treatment with the proteasome inhibitor MG132 increased levels of NF-kappaB/p65 protein and decreased Pro1 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	25-28
17516915-9	2007	Induction of PTGS2 protein by 4beta-PMA in the absence of a PPAR ligand was decreased by the NF-kappaB (nuclear factor kappaB) inhibitors MG132 and parthenolide, suggesting that PKC acted through NF-kappaB in addition to PPAR phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	prostaglandin-endoperoxide synthase 2	Bos taurus	13-18
17505054-7	2007	Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	gastric inhibitory polypeptide receptor	Homo sapiens	18-23
17505054-7	2007	Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-114	gastric inhibitory polypeptide	Homo sapiens	18-21
17458898-6	2007	MG-132, a proteasome inhibitor, induced endogenous and ectopic [cytomegalovirus promoter (CMV)-driven] maspin expression, and maspin siRNA attenuated MG-132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	serpin family B member 5	Homo sapiens	103-109
17458898-6	2007	MG-132, a proteasome inhibitor, induced endogenous and ectopic [cytomegalovirus promoter (CMV)-driven] maspin expression, and maspin siRNA attenuated MG-132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-156	serpin family B member 5	Homo sapiens	126-132
17641041-6	2007	A high rate of NF-kappaB/p65 degradation in LNK cells correlates with Pro1 activity, since treatment with the proteasome inhibitor MG132 increased levels of NF-kappaB/p65 protein and decreased Pro1 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	proline dehydrogenase	Mus musculus	70-74
17437535-7	2007	Blockade of the proteasome pathway by MG132 prevented OGD-induced decrease of GRK2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	G protein-coupled receptor kinase 2	Rattus norvegicus	78-82
17641041-6	2007	A high rate of NF-kappaB/p65 degradation in LNK cells correlates with Pro1 activity, since treatment with the proteasome inhibitor MG132 increased levels of NF-kappaB/p65 protein and decreased Pro1 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	167-170
17641041-6	2007	A high rate of NF-kappaB/p65 degradation in LNK cells correlates with Pro1 activity, since treatment with the proteasome inhibitor MG132 increased levels of NF-kappaB/p65 protein and decreased Pro1 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	proline dehydrogenase	Mus musculus	193-197
17297446-7	2007	Proteasomal degradation appears responsible for the decrease of both Mdm2 and p21(CIP1/WAF1), as MG-132 prevented their degradation and revealed AF-induced Mdm2 polyubiquitylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-103	MDM2 proto-oncogene	Homo sapiens	69-73
17606337-7	2007	The metal-mediated induction of Cyp1a1 mRNA was further potentiated by the protein synthesis inhibitor, cycloheximide and the 26S proteasome inhibitor, MG-132, but completely inhibited by the RNA transcription inhibitor, actinomycin-D, implying a transcriptional regulation of the Cyp1a1 gene by the heavy metals.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-158	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	32-38
17670978-5	2007	Overexpression of G-substrate protected dopaminergic BE(2)-M17 cells against toxins, including 6-OHDA and MG-132 (carbobenzoxy-L-leucyl- L-leucyl-L-leucinal), whereas RNA interference (RNAi)-mediated knockdown of endogenous G-substrate increased their vulnerability to these toxins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	protein phosphatase 1 regulatory subunit 17	Homo sapiens	18-29
17473057-8	2007	The effects of 5-AED on survival and G-CSF secretion were blocked by the NFkappaB inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	135-140	colony stimulating factor 3	Homo sapiens	37-42
17473057-8	2007	The effects of 5-AED on survival and G-CSF secretion were blocked by the NFkappaB inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	135-140	nuclear factor kappa B subunit 1	Homo sapiens	73-81
17602818-9	2007	The treatment of the proteasome inhibitor MG132 greatly increased Cdc25A protein in abundance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	cell division cycle 25A	Homo sapiens	66-72
17297446-7	2007	Proteasomal degradation appears responsible for the decrease of both Mdm2 and p21(CIP1/WAF1), as MG-132 prevented their degradation and revealed AF-induced Mdm2 polyubiquitylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-103	cyclin dependent kinase inhibitor 1A	Homo sapiens	78-81
17297446-7	2007	Proteasomal degradation appears responsible for the decrease of both Mdm2 and p21(CIP1/WAF1), as MG-132 prevented their degradation and revealed AF-induced Mdm2 polyubiquitylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-103	cyclin dependent kinase inhibitor 1A	Homo sapiens	82-86
17297446-7	2007	Proteasomal degradation appears responsible for the decrease of both Mdm2 and p21(CIP1/WAF1), as MG-132 prevented their degradation and revealed AF-induced Mdm2 polyubiquitylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-103	cyclin dependent kinase inhibitor 1A	Homo sapiens	87-91
17615180-9	2007	Proteasome inhibition by lactacystin or MG-132 partially blocked the decrease in p63, suggesting a posttranslational degradation mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	tumor protein p63	Homo sapiens	81-84
17442736-7	2007	A role for hypoxia-inducible factor (HIF)-1 was suggested by the increase in HIF-1alpha as a result of hypoxia and by the increase in GLUT1 expression following treatment of BeWo with MG-132, a proteasomal inhibitor that increases HIF-1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	hypoxia inducible factor 1 subunit alpha	Homo sapiens	11-43
17442736-7	2007	A role for hypoxia-inducible factor (HIF)-1 was suggested by the increase in HIF-1alpha as a result of hypoxia and by the increase in GLUT1 expression following treatment of BeWo with MG-132, a proteasomal inhibitor that increases HIF-1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	hypoxia inducible factor 1 subunit alpha	Homo sapiens	77-87
17442736-7	2007	A role for hypoxia-inducible factor (HIF)-1 was suggested by the increase in HIF-1alpha as a result of hypoxia and by the increase in GLUT1 expression following treatment of BeWo with MG-132, a proteasomal inhibitor that increases HIF-1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	solute carrier family 2 member 1	Homo sapiens	134-139
17442736-7	2007	A role for hypoxia-inducible factor (HIF)-1 was suggested by the increase in HIF-1alpha as a result of hypoxia and by the increase in GLUT1 expression following treatment of BeWo with MG-132, a proteasomal inhibitor that increases HIF-1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-190	hypoxia inducible factor 1 subunit alpha	Homo sapiens	77-82
17442736-9	2007	In contrast to BeWo cells, hypoxia produced minimal increases in GLUT1 expression in explants; however, treatment with MG-132 did upregulate syncytial basal membrane GLUT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-125	solute carrier family 2 member 1	Homo sapiens	166-171
17224908-6	2007	Proteasome inhibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	58-61
17224908-6	2007	Proteasome inhibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor protein p53	Homo sapiens	73-76
17224908-6	2007	Proteasome inhibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	H3 histone pseudogene 16	Homo sapiens	88-91
17565155-9	2007	The proteasome inhibitor MG132 was used to investigate deguelin"s effect on the induction of ubiquitin-mediated proteasomal degradation of HIF-1alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	hypoxia inducible factor 1, alpha subunit	Mus musculus	139-149
17445767-6	2007	The inhibitor of NF-kappaB (MG132) also significantly reduced Hcy-induced IgG secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	17-26
17521826-4	2007	Here we study the effect of a UPS inhibitor, MG132, on long-term memory consolidation and NF-kappaB activation in the learning paradigm of the crab Chasmagnathus, a model in which this transcription factor plays a key role.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	nuclear factor kappa B subunit 1	Homo sapiens	90-99
17521826-6	2007	Then we studied the effect of the UPS inhibitor on NF-kappaB pathway, finding that MG132 blocks the activation of NF-kappaB induced by training.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	nuclear factor kappa B subunit 1	Homo sapiens	51-60
17521826-6	2007	Then we studied the effect of the UPS inhibitor on NF-kappaB pathway, finding that MG132 blocks the activation of NF-kappaB induced by training.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	nuclear factor kappa B subunit 1	Homo sapiens	114-123
17475277-7	2007	Moreover, the proteasome inhibitor, MG132, inhibited NF-kappaB activation and strongly inhibited iNOS/NO induction, ROS production, and loss of DeltaPsim induced by TNF-alpha/IFN-gamma, thereby inhibiting apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	53-62
17475277-7	2007	Moreover, the proteasome inhibitor, MG132, inhibited NF-kappaB activation and strongly inhibited iNOS/NO induction, ROS production, and loss of DeltaPsim induced by TNF-alpha/IFN-gamma, thereby inhibiting apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	nitric oxide synthase 2, inducible	Mus musculus	97-101
17475277-7	2007	Moreover, the proteasome inhibitor, MG132, inhibited NF-kappaB activation and strongly inhibited iNOS/NO induction, ROS production, and loss of DeltaPsim induced by TNF-alpha/IFN-gamma, thereby inhibiting apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	tumor necrosis factor	Mus musculus	165-174
17475277-7	2007	Moreover, the proteasome inhibitor, MG132, inhibited NF-kappaB activation and strongly inhibited iNOS/NO induction, ROS production, and loss of DeltaPsim induced by TNF-alpha/IFN-gamma, thereby inhibiting apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	interferon gamma	Mus musculus	175-184
17894019-5	2007	Some mice in each group were infused with 10 microM MG132 (an inhibitor of NF-kappaB).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
17311906-10	2007	Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	116-121
17311906-10	2007	Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	162-167
17311906-10	2007	Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	BCL2 apoptosis regulator	Homo sapiens	205-210
17311906-10	2007	Preincubating cells with the proteasome inhibitor MG-132 or lactacystin not only restored cisplatin-induced loss of Mcl-1 but also resulted in an accumulation of Mcl-1 that exceeded basal levels; however, Bcl-2 and BclxL levels did not change in response to MG-132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	BCL2 like 1	Homo sapiens	215-220
17183061-5	2007	Conversely, the proteasomal inhibitors MG132 and lactacystin prevented DHA-induced beta-catenin decrease, suggesting that DHA may regulate the proteasomal degradation of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	catenin beta 1	Homo sapiens	83-95
17183061-5	2007	Conversely, the proteasomal inhibitors MG132 and lactacystin prevented DHA-induced beta-catenin decrease, suggesting that DHA may regulate the proteasomal degradation of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	catenin beta 1	Homo sapiens	170-182
17275031-10	2007	The IL-1beta-induced ICAM-1 was also inhibited by a potent inhibitor of NF-kappaB, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	interleukin 1 beta	Homo sapiens	4-12
17314023-7	2007	Inhibition of PARP and the proteasome by 3-aminobenzamide and MG-132, respectively, revealed about 90% of apoptotic cells by cell cycle analysis at the time of retrodifferentiation whereas control cells doubled.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	poly(ADP-ribose) polymerase 1	Homo sapiens	14-18
17513391-3	2007	Glutamine appears to act by changing the stability of the glutamine synthetase protein, and the effect was partially blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	glutamate-ammonia ligase (glutamine synthetase)	Mus musculus	58-78
17275031-10	2007	The IL-1beta-induced ICAM-1 was also inhibited by a potent inhibitor of NF-kappaB, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	intercellular adhesion molecule 1	Homo sapiens	21-27
17275031-10	2007	The IL-1beta-induced ICAM-1 was also inhibited by a potent inhibitor of NF-kappaB, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	nuclear factor kappa B subunit 1	Homo sapiens	72-81
17317665-4	2007	The degradation of p12 is due to an accelerated rate of proteolysis that is inhibited by the proteasome inhibitors, MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	DNA polymerase delta 4, accessory subunit	Homo sapiens	19-22
17417665-5	2007	In cultured BECs, CDX2 and MUC2 were expressed following treatment with PAMPs and inhibitors (anti-Toll-like receptor (TLR)2/TLR4 antibody, nuclear factor-kappaB (NF-kappaB) inhibitor MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-189	caudal type homeo box 2	Rattus norvegicus	18-22
17417665-5	2007	In cultured BECs, CDX2 and MUC2 were expressed following treatment with PAMPs and inhibitors (anti-Toll-like receptor (TLR)2/TLR4 antibody, nuclear factor-kappaB (NF-kappaB) inhibitor MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	184-189	mucin 2, oligomeric mucus/gel-forming	Rattus norvegicus	27-31
17417665-8	2007	In cultured BECs, treatment with PAMPs induced upregulation of CDX2 and MUC2 expression, and this effect was abolished by pretreatment with anti-TLR2 and anti-TLR4 antibody and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	caudal type homeo box 2	Rattus norvegicus	63-67
17417665-8	2007	In cultured BECs, treatment with PAMPs induced upregulation of CDX2 and MUC2 expression, and this effect was abolished by pretreatment with anti-TLR2 and anti-TLR4 antibody and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	mucin 2, oligomeric mucus/gel-forming	Rattus norvegicus	72-76
17499743-4	2007	MG-132 and lactacystin, proteasome inhibitors, increased cell-surface expression of TP beta, but not TP alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta	Homo sapiens	84-91
17302910-6	2007	The effect of p45 on ataxin-3 degradation is blocked by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	nuclear factor, erythroid 2	Homo sapiens	14-17
17302910-6	2007	The effect of p45 on ataxin-3 degradation is blocked by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	ataxin 3	Homo sapiens	21-29
17264307-9	2007	The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo-synthesized in response to IL-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	interleukin 4	Homo sapiens	14-18
17146438-6	2007	Inhibition of EGFR degradation, by either pretreatment with the EGFR tyrosine kinase inhibitor gefitinib or by exposure to the proteosome/lysosome inhibitor MG132, significantly reduced gemcitabine-induced cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	157-162	epidermal growth factor receptor	Homo sapiens	14-18
17324379-10	2007	Cdc2 and cyclin B1 were ubiquitinated by GA. MG132 abrogated the GA-induced decrease of Cdc2 and cyclin B1 indicating that these proteins were degraded by proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	cyclin dependent kinase 1	Homo sapiens	0-4
17324379-10	2007	Cdc2 and cyclin B1 were ubiquitinated by GA. MG132 abrogated the GA-induced decrease of Cdc2 and cyclin B1 indicating that these proteins were degraded by proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	cyclin B1	Homo sapiens	9-18
17324379-10	2007	Cdc2 and cyclin B1 were ubiquitinated by GA. MG132 abrogated the GA-induced decrease of Cdc2 and cyclin B1 indicating that these proteins were degraded by proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	cyclin dependent kinase 1	Homo sapiens	88-92
17324379-10	2007	Cdc2 and cyclin B1 were ubiquitinated by GA. MG132 abrogated the GA-induced decrease of Cdc2 and cyclin B1 indicating that these proteins were degraded by proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	cyclin B1	Homo sapiens	97-106
17495527-3	2007	Indeed, treatment with the proteasome inhibitor MG-132 of skeletal muscles from mdx mice--a spontaneous mouse model of DMD--as well as from DMD patients, effectively rescued the expression and correct cellular localization of dystrophin and associated proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	dystrophin	Homo sapiens	226-236
17264307-9	2007	The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo-synthesized in response to IL-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	suppressor of cytokine signaling 3	Homo sapiens	22-27
17264307-9	2007	The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo-synthesized in response to IL-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	suppressor of cytokine signaling 3	Homo sapiens	190-195
17264307-9	2007	The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo-synthesized in response to IL-4.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	interleukin 4	Homo sapiens	234-238
17475341-6	2007	Using MG-132, helenalin and SN50 [inhibitors of the transcription factor, nuclear factor (NF)-kappaB], we determined that NF-kappaB activation is instrumental in TNFalpha-induced CXCL10 expression in A172 astroglia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-12	nuclear factor kappa B subunit 1	Homo sapiens	122-131
17475341-6	2007	Using MG-132, helenalin and SN50 [inhibitors of the transcription factor, nuclear factor (NF)-kappaB], we determined that NF-kappaB activation is instrumental in TNFalpha-induced CXCL10 expression in A172 astroglia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-12	tumor necrosis factor	Homo sapiens	162-170
17475341-6	2007	Using MG-132, helenalin and SN50 [inhibitors of the transcription factor, nuclear factor (NF)-kappaB], we determined that NF-kappaB activation is instrumental in TNFalpha-induced CXCL10 expression in A172 astroglia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	6-12	C-X-C motif chemokine ligand 10	Homo sapiens	179-185
17349974-7	2007	Interestingly, GFP-mPrp19 fusion protein was co-localized with mSUG1 protein in cytoplasm as the formation of the speckle-like structures in the presence of a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	180-185	pre-mRNA processing factor 19	Mus musculus	19-25
17349974-7	2007	Interestingly, GFP-mPrp19 fusion protein was co-localized with mSUG1 protein in cytoplasm as the formation of the speckle-like structures in the presence of a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	180-185	protease (prosome, macropain) 26S subunit, ATPase 5	Mus musculus	63-68
17374988-4	2007	Isobologram analysis showed that both MG132 and bortezomib interacted synergistically with IDA to induce apoptosis of THP1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	GLI family zinc finger 2	Homo sapiens	118-122
17350042-9	2007	EB1 is ubiquitinated and its proteolysis can be inhibited by MG132, demonstrating that it is a substrate of the UPS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	microtubule associated protein RP/EB family member 1	Homo sapiens	0-3
17135302-6	2007	In contrast, NF-kappaB inhibition by pyrrolidine dithiocarbamate and MG132 prevented the suppression of ABCA1 by IL-1beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	nuclear factor kappa B subunit 1	Homo sapiens	13-22
17135302-6	2007	In contrast, NF-kappaB inhibition by pyrrolidine dithiocarbamate and MG132 prevented the suppression of ABCA1 by IL-1beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	ATP binding cassette subfamily A member 1	Homo sapiens	104-109
17135302-6	2007	In contrast, NF-kappaB inhibition by pyrrolidine dithiocarbamate and MG132 prevented the suppression of ABCA1 by IL-1beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	interleukin 1 beta	Homo sapiens	113-121
17374988-8	2007	These data show that MG132 and bortezomib specifically sensitize leukemic cells to IDA through an increase in BIM and Bax pro-apoptotic Bcl-2 family proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	BCL2 associated X, apoptosis regulator	Homo sapiens	118-121
17219422-4	2007	Treatment with the proteasomal inhibitor MG132 blocked the retinol-induced decrease in beta-catenin indicating retinol decreases beta-catenin by increasing proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	catenin beta 1	Homo sapiens	87-99
17219422-4	2007	Treatment with the proteasomal inhibitor MG132 blocked the retinol-induced decrease in beta-catenin indicating retinol decreases beta-catenin by increasing proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	catenin beta 1	Homo sapiens	129-141
17303129-3	2007	We show that proteasome activation occurs in early phase of HS-PCD upstream of the caspase-like proteases activation; moreover inhibition of proteasome function by MG132 results in prevention of PCD perhaps due to the prevention of ROS production, cytochrome c release and caspase-3-like protease activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	164-169	cytochrome c	Nicotiana tabacum	248-260
17242182-4	2007	Thus, exposure of H1299 cells to ferric ammonium citrate reduced the half-life of transfected IRP1(C437S) from approximately 24 h to approximately 10 h. The iron-dependent degradation of IRP1(C437S) involved ubiquitination, required ongoing transcription and translation, and could be efficiently blocked by the proteasomal inhibitors MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	335-340	aconitase 1	Homo sapiens	94-98
17242182-4	2007	Thus, exposure of H1299 cells to ferric ammonium citrate reduced the half-life of transfected IRP1(C437S) from approximately 24 h to approximately 10 h. The iron-dependent degradation of IRP1(C437S) involved ubiquitination, required ongoing transcription and translation, and could be efficiently blocked by the proteasomal inhibitors MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	335-340	aconitase 1	Homo sapiens	187-191
17237497-10	2007	S1P1 degradation is blocked by MG132, a proteasomal inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	sphingosine-1-phosphate receptor 1	Homo sapiens	0-4
17291686-7	2007	The effects of ATRA were reversed by proteasome inhibitor MG-132, implying ligand-dependent RARalpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-64	retinoic acid receptor, alpha	Rattus norvegicus	92-100
17284438-6	2007	First we characterized the sensitivity of loss- or gain-of-function CaR mutants to proteasome inhibition by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	calcium sensing receptor	Homo sapiens	68-71
17553313-0	2007	[Role of MG132, a proteasome inhibitor, in inducing expression of costimulatory molecules CD86 in leukemic cells and its effect on allogeneic mixed lymphocyte reaction].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	CD86 molecule	Homo sapiens	90-94
17553313-1	2007	OBJECTIVE: To investigate the role of proteasome inhibitors MG132 in the inducing the expression of the costimulatory molecules CD80 and CD86 in leukemia cells and its effect on allogeneic mixed lymphocyte reaction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	CD80 molecule	Homo sapiens	128-132
17553313-1	2007	OBJECTIVE: To investigate the role of proteasome inhibitors MG132 in the inducing the expression of the costimulatory molecules CD80 and CD86 in leukemia cells and its effect on allogeneic mixed lymphocyte reaction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	CD86 molecule	Homo sapiens	137-141
17553313-6	2007	The mRNA expression of CD86 in the HL-60 cells treated with 1 micromol/L MG132 was examined by RT-PCR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	CD86 molecule	Homo sapiens	23-27
17553313-12	2007	Before MG132 treatment K562 cells did not express CD86, and the CD86 expression of the HL-60 cells was up-regulated time-dependently (all P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	7-12	CD86 molecule	Homo sapiens	64-68
17553313-13	2007	The mRNA expression of CD86 in the HL-60 treated with MG132 was up-regulated time-dependently (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	CD86 molecule	Homo sapiens	23-27
17553313-16	2007	CONCLUSION: MG132 induces the expression of costimulatory molecule CD86 in the HL-60 cells, thus improving the proliferation of PBMNC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	CD86 molecule	Homo sapiens	67-71
17553314-1	2007	OBJECTIVE: To investigate the highly specific proteasomal inhibitor MG132-induced apoptosis and its effect on nuclear factor (NF)-kappaB activation and survivin expression in leukemic K562 cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	nuclear factor kappa B subunit 1	Homo sapiens	110-136
17553314-7	2007	Compared with the control group, K562 cell treated with MG132 at the concentrations of 2, 4, 6, and 8 micromol/L for 24 hours showed the decrease of NF-kappaB activation to 75.0% +/- 3.7%, 59.9% +/- 5.3%, 45.4% +/- 5.7%, and 25.0% +/- 4.2% respectively, and decrease of survivin expression to 90.9% +/- 10.1%, 66.7% +/- 5.2%, 45.4% +/- 5.7%, and 30.3% +/- 6.6% respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	nuclear factor kappa B subunit 1	Homo sapiens	149-158
17553314-9	2007	CONCLUSION: MG132 induces apoptosis of leukemic cells, and effectively inhibits the NF-kappaB activation accompanied by the downregulation of survivin expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	nuclear factor kappa B subunit 1	Homo sapiens	84-93
17082223-7	2007	MG-132 but not bafilomycin A(1) extended the half-life, suggesting a role for the proteasome in Bsep degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	ATP binding cassette subfamily B member 11	Rattus norvegicus	96-100
17207582-3	2007	Down-regulation of GRIP1 by glutamate was blocked by carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132), a proteasome inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	glutamate receptor interacting protein 1	Rattus norvegicus	19-24
17207582-6	2007	Furthermore, MG132 prevented glutamate-stimulated reduction in surface amount of GluR2, and knockdown of GRIP1 by RNAi against GRIP1 reduced surface GluR2 in neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	81-86
17229476-0	2007	Expression of a mutant p193/CUL7 molecule confers resistance to MG132- and etoposide-induced apoptosis independent of p53 or Parc binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	poly(ADP-ribose) polymerase family member 4	Homo sapiens	23-27
17229476-0	2007	Expression of a mutant p193/CUL7 molecule confers resistance to MG132- and etoposide-induced apoptosis independent of p53 or Parc binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	cullin 7	Homo sapiens	28-32
17229476-2	2007	Expression of a dominant interfering variant of mouse p193/CUL7 (designated 1152stop) conferred resistance to MG132- and etoposide-induced apoptosis in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	cullin 7	Mus musculus	54-58
17229476-2	2007	Expression of a dominant interfering variant of mouse p193/CUL7 (designated 1152stop) conferred resistance to MG132- and etoposide-induced apoptosis in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	cullin 7	Mus musculus	59-63
17312389-6	2007	Indeed, API59-Cl induced p27 degradation was dependent on ubiquitin-proteasome pathway, particularly E3 ubiquitin ligase component, Skp2, but not Cullin-4A/4B, and can be largely blocked by proteasome inhibitors MG132 or PS341.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	cyclin-dependent kinase inhibitor 1B	Mus musculus	25-28
17287633-4	2007	Blocking nuclear factor-kappaB by MG132 or aurine tricarboxylic acid effectively inhibited the lipopolysaccharide-induced surface thrombomodulin down-regulation of monocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	thrombomodulin	Homo sapiens	130-144
17005371-8	2007	Proteasome inhibitor MG132 also caused cerebellar neuronal death by decreasing Bcl-x(L) expression and activating caspase-9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	BCL2 like 1	Homo sapiens	79-87
17332355-0	2007	MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating c-Fos/c-Jun heterodimers and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	TNF superfamily member 10	Homo sapiens	18-23
17332355-0	2007	MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating c-Fos/c-Jun heterodimers and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75
17332355-0	2007	MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating c-Fos/c-Jun heterodimers and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-81
17332355-0	2007	MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating c-Fos/c-Jun heterodimers and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	CASP8 and FADD like apoptosis regulator	Homo sapiens	110-116
17332355-6	2007	Here, we report that MG-132, a small-molecule inhibitor of the proteasome, sensitizes TRAIL-resistant prostate cancer cells by inducing c-Fos and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	TNF superfamily member 10	Homo sapiens	86-91
17332355-6	2007	Here, we report that MG-132, a small-molecule inhibitor of the proteasome, sensitizes TRAIL-resistant prostate cancer cells by inducing c-Fos and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	136-141
17332355-6	2007	Here, we report that MG-132, a small-molecule inhibitor of the proteasome, sensitizes TRAIL-resistant prostate cancer cells by inducing c-Fos and repressing c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	CASP8 and FADD like apoptosis regulator	Homo sapiens	157-166
17332355-7	2007	c-Fos, which is activated by MG-132, negatively regulates c-FLIP(L) by direct binding to the putative promoter region of the c-FLIP(L) gene.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
17332355-7	2007	c-Fos, which is activated by MG-132, negatively regulates c-FLIP(L) by direct binding to the putative promoter region of the c-FLIP(L) gene.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	CASP8 and FADD like apoptosis regulator	Homo sapiens	58-67
17332355-7	2007	c-Fos, which is activated by MG-132, negatively regulates c-FLIP(L) by direct binding to the putative promoter region of the c-FLIP(L) gene.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	CASP8 and FADD like apoptosis regulator	Homo sapiens	125-134
17332355-8	2007	In addition to activating c-Fos, MG-132 activates another AP-1 family member, c-Jun.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	26-31
17332355-8	2007	In addition to activating c-Fos, MG-132 activates another AP-1 family member, c-Jun.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-62
17332355-8	2007	In addition to activating c-Fos, MG-132 activates another AP-1 family member, c-Jun.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-83
17332355-10	2007	Therefore, MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating the AP-1 family members c-Fos and c-Jun, which, in turn, repress the antiapoptotic molecule c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	TNF superfamily member 10	Homo sapiens	29-34
17332355-10	2007	Therefore, MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating the AP-1 family members c-Fos and c-Jun, which, in turn, repress the antiapoptotic molecule c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-89
17332355-10	2007	Therefore, MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating the AP-1 family members c-Fos and c-Jun, which, in turn, repress the antiapoptotic molecule c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-110
17332355-10	2007	Therefore, MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating the AP-1 family members c-Fos and c-Jun, which, in turn, repress the antiapoptotic molecule c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	115-120
17332355-10	2007	Therefore, MG-132 sensitizes TRAIL-resistant prostate cancer cells by activating the AP-1 family members c-Fos and c-Jun, which, in turn, repress the antiapoptotic molecule c-FLIP(L).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	CASP8 and FADD like apoptosis regulator	Homo sapiens	173-179
17005371-8	2007	Proteasome inhibitor MG132 also caused cerebellar neuronal death by decreasing Bcl-x(L) expression and activating caspase-9.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	caspase 9	Homo sapiens	114-123
17005371-9	2007	Both ataxin-7-Q75 and MG132 caused the cytosolic accumulation of IkappaBalpha in cerebellar neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	NFKB inhibitor alpha	Homo sapiens	65-77
17005371-10	2007	Mutant ataxin-7-Q75 or MG132 increased the cytosolic level of NF-kappaB p65 and decreased the nuclear NF-kappaB p65 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	nuclear factor kappa B subunit 1	Homo sapiens	62-71
17005371-10	2007	Mutant ataxin-7-Q75 or MG132 increased the cytosolic level of NF-kappaB p65 and decreased the nuclear NF-kappaB p65 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	RELA proto-oncogene, NF-kB subunit	Homo sapiens	72-75
17005371-10	2007	Mutant ataxin-7-Q75 or MG132 increased the cytosolic level of NF-kappaB p65 and decreased the nuclear NF-kappaB p65 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	nuclear factor kappa B subunit 1	Homo sapiens	102-111
17005371-10	2007	Mutant ataxin-7-Q75 or MG132 increased the cytosolic level of NF-kappaB p65 and decreased the nuclear NF-kappaB p65 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-28	RELA proto-oncogene, NF-kB subunit	Homo sapiens	112-115
17028057-4	2007	STP-A11-mediated processing of p100 to p52 protein requires proteosome-mediated proteolysis because MG132 treatment clearly blocked p52 production in spite of the expression of STP-A11.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	thyroid hormone receptor interactor 10	Homo sapiens	0-3
17166173-3	2007	Inactivation of DJ-1 in zebrafish, Danio rerio, resulted in loss of dopaminergic neurons after exposure to hydrogen peroxide and the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	154-159	parkinson protein 7	Danio rerio	16-20
17166173-6	2007	Pharmacological p53 inhibition either before or during MG132 exposure in vivo prevented dopaminergic neuronal cell death in both cases.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	tumor protein p53	Danio rerio	16-19
17028057-4	2007	STP-A11-mediated processing of p100 to p52 protein requires proteosome-mediated proteolysis because MG132 treatment clearly blocked p52 production in spite of the expression of STP-A11.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	DXS435E	Homo sapiens	4-7
17028057-4	2007	STP-A11-mediated processing of p100 to p52 protein requires proteosome-mediated proteolysis because MG132 treatment clearly blocked p52 production in spite of the expression of STP-A11.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	nuclear factor kappa B subunit 2	Homo sapiens	39-42
17028057-4	2007	STP-A11-mediated processing of p100 to p52 protein requires proteosome-mediated proteolysis because MG132 treatment clearly blocked p52 production in spite of the expression of STP-A11.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	nuclear factor kappa B subunit 2	Homo sapiens	132-135
17142836-6	2007	5-HT promotes the association of RhoA with the E3 ubiquitin ligase Smurf1, and 5-HT-induced RhoA depletion was inhibited by the proteasome inhibitor MG132 and the RhoA inhibitor Tat-C3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-154	ras homolog family member A	Rattus norvegicus	33-37
17327906-6	2007	PA28gamma also improved cell viability in mutant huntingtin-expressing striatal neurons exposed to pathological stressors, such as the excitotoxin quinolinic acid and the reversible proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	203-208	proteasome activator subunit 3	Homo sapiens	0-9
17327906-6	2007	PA28gamma also improved cell viability in mutant huntingtin-expressing striatal neurons exposed to pathological stressors, such as the excitotoxin quinolinic acid and the reversible proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	203-208	huntingtin	Homo sapiens	49-59
17142836-6	2007	5-HT promotes the association of RhoA with the E3 ubiquitin ligase Smurf1, and 5-HT-induced RhoA depletion was inhibited by the proteasome inhibitor MG132 and the RhoA inhibitor Tat-C3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-154	SMAD specific E3 ubiquitin protein ligase 1	Rattus norvegicus	67-73
17142836-6	2007	5-HT promotes the association of RhoA with the E3 ubiquitin ligase Smurf1, and 5-HT-induced RhoA depletion was inhibited by the proteasome inhibitor MG132 and the RhoA inhibitor Tat-C3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-154	ras homolog family member A	Rattus norvegicus	92-96
17142836-6	2007	5-HT promotes the association of RhoA with the E3 ubiquitin ligase Smurf1, and 5-HT-induced RhoA depletion was inhibited by the proteasome inhibitor MG132 and the RhoA inhibitor Tat-C3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	149-154	ras homolog family member A	Rattus norvegicus	92-96
17142836-8	2007	In contrast, inhibition of 5-HT-mediated RhoA degradation by MG132 prevented 5-HT-induced Akt activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	ras homolog family member A	Rattus norvegicus	41-45
17212817-8	2007	Lastly, the effect of Vpx overlaps with that of the proteasome inhibitor MG132 in DCs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	vpx protein	Simian immunodeficiency virus	22-25
17027076-6	2007	The treatment with proteasome inhibitor, MG132 or Ca2+-chelator, BAPTA-AM, overcame the spontaneous degradation of both Mos and cyclin B1 in a dose-dependent manner in Wistar oocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	MOS proto-oncogene, serine/threonine kinase	Rattus norvegicus	120-123
17027076-6	2007	The treatment with proteasome inhibitor, MG132 or Ca2+-chelator, BAPTA-AM, overcame the spontaneous degradation of both Mos and cyclin B1 in a dose-dependent manner in Wistar oocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cyclin B1	Rattus norvegicus	128-137
16909127-3	2007	We now demonstrate that E2A proteins are primarily localized in the nucleus in both C2C12 myoblasts and myotubes, and are degraded by the ubiquitin proteasome system evidenced by stabilization following treatment with the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	transcription factor 3	Homo sapiens	24-27
17107743-7	2007	MG132, a specific inhibitor of NF-kappaB, eliminated the NO synthesis in IFN-gamma plus hydrolysate/oligomixture-induced RAW264.7 macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	31-40
17107743-7	2007	MG132, a specific inhibitor of NF-kappaB, eliminated the NO synthesis in IFN-gamma plus hydrolysate/oligomixture-induced RAW264.7 macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interferon gamma	Mus musculus	73-82
17108041-2	2007	We report here that the addition of MG132 or lactacystin, each a specific inhibitor of cellular proteasome activity, preferentially enhances cellular permissiveness to infection by Nef-defective versus wild-type HIV-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	Nef	Human immunodeficiency virus 1	181-184
17218054-5	2007	Unexpectedly, mitochondrial StAR turnover can be inhibited by two proteasome inhibitors, i.e., MG132 and clasto-lactacystin beta-lactone, but not epoxomicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	steroidogenic acute regulatory protein	Homo sapiens	28-32
16909119-6	2007	Similarly, inhibition of NF-kappaB by the proteasome inhibitor MG132 did not increase doxorubicin (Doxo)-induced apoptosis of glioblastoma cells, although it prevented DNA binding of NF-kappaB complexes in response to Doxo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	nuclear factor kappa B subunit 1	Homo sapiens	25-34
16909119-6	2007	Similarly, inhibition of NF-kappaB by the proteasome inhibitor MG132 did not increase doxorubicin (Doxo)-induced apoptosis of glioblastoma cells, although it prevented DNA binding of NF-kappaB complexes in response to Doxo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	nuclear factor kappa B subunit 1	Homo sapiens	183-192
17213309-4	2007	Treatment with the proteasome inhibitors MG132 and bortezomib increased WASP levels in T cells from WIP(-/-) mice and in T and B lymphocytes from two WAS patients with missense mutations (R86H and T45M) that disrupt WIP binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	Wiskott-Aldrich syndrome	Mus musculus	72-76
17213309-4	2007	Treatment with the proteasome inhibitors MG132 and bortezomib increased WASP levels in T cells from WIP(-/-) mice and in T and B lymphocytes from two WAS patients with missense mutations (R86H and T45M) that disrupt WIP binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	WAS/WASL interacting protein family, member 1	Mus musculus	100-103
17213309-4	2007	Treatment with the proteasome inhibitors MG132 and bortezomib increased WASP levels in T cells from WIP(-/-) mice and in T and B lymphocytes from two WAS patients with missense mutations (R86H and T45M) that disrupt WIP binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	WAS/WASL interacting protein family member 1	Homo sapiens	216-219
17105721-6	2007	Treatment of proteasome inhibitors, MG-132 or proteasome-specific inhibitor 1, prevented the Dox-mediated decrease of NFAT5 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	nuclear factor of activated T cells 5	Homo sapiens	118-123
17079230-8	2007	PDGFRalpha degradation by 17-AAG is inhibited by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	platelet derived growth factor receptor alpha	Homo sapiens	0-10
17079230-8	2007	PDGFRalpha degradation by 17-AAG is inhibited by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	N-methylpurine DNA glycosylase	Homo sapiens	29-32
17386086-11	2007	Similarly, inhibitors of NF-kappaB signaling (pyrrolidine dithiocarbamate, MG-132, and SN-50) abolished the suppressive effect of IL-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	interleukin 1 beta	Homo sapiens	130-134
16905641-5	2007	Proteasome inhibitors lactacystin and MG132 reduced the levels of SP-A, SP-B, and SP-C mRNAs in a concentration-dependent manner in H441 and MLE-12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	surfactant protein A1	Homo sapiens	66-70
16905641-5	2007	Proteasome inhibitors lactacystin and MG132 reduced the levels of SP-A, SP-B, and SP-C mRNAs in a concentration-dependent manner in H441 and MLE-12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	surfactant protein B	Homo sapiens	72-76
16905641-5	2007	Proteasome inhibitors lactacystin and MG132 reduced the levels of SP-A, SP-B, and SP-C mRNAs in a concentration-dependent manner in H441 and MLE-12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	surfactant protein C	Homo sapiens	82-86
16905641-6	2007	In H441 cells, lactacystin and MG132 inhibition of SP-B mRNA was associated with similar decreases in SP-B protein, and the inhibition was due to inhibition of gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	surfactant protein B	Homo sapiens	51-55
16905641-6	2007	In H441 cells, lactacystin and MG132 inhibition of SP-B mRNA was associated with similar decreases in SP-B protein, and the inhibition was due to inhibition of gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	surfactant protein B	Homo sapiens	102-106
16774932-4	2007	The use of Ro-318220 and GO-6983, general PKC inhibitors as well as MG-132, a proteasome-specific inhibitor, abrogated PMA-induced degradation of IKK-gamma and recovered the activation of IKK by TNF, suggesting that IKK complex is predominantly degraded by the proteasome pathway in a PKC-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-74	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	146-155
16774932-4	2007	The use of Ro-318220 and GO-6983, general PKC inhibitors as well as MG-132, a proteasome-specific inhibitor, abrogated PMA-induced degradation of IKK-gamma and recovered the activation of IKK by TNF, suggesting that IKK complex is predominantly degraded by the proteasome pathway in a PKC-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-74	tumor necrosis factor	Homo sapiens	195-198
17108132-6	2006	DDP-induced loss of hCTR1 was blocked by the proteasome inhibitors lactacystin, proteasome inhibitor 1, and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	solute carrier family 31 member 1	Homo sapiens	20-25
17200344-5	2007	Moreover, we assessed whether MG132, a proteasome inhibitor, affected the SMAD4 protein level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	SMAD family member 4	Homo sapiens	74-79
17200344-10	2007	SMAD4 protein levels were also affected in certain gastric carcinoma cell lines following incubation with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	SMAD family member 4	Homo sapiens	0-5
17083955-3	2006	The proteasome inhibitor, MG132, inhibited proteasome activity, but also decreased CYP3A23 mRNA and protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	83-90
17008592-4	2006	TNF-alpha-mediated induction of vascular cell adhesion molecule-1 (VCAM-1) was attenuated by all of these inhibitors, whereas in contrast, stimulation of intercellular adhesion molecule-1 (ICAM-1) was blocked by MG-132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-218	tumor necrosis factor	Homo sapiens	0-9
17008592-4	2006	TNF-alpha-mediated induction of vascular cell adhesion molecule-1 (VCAM-1) was attenuated by all of these inhibitors, whereas in contrast, stimulation of intercellular adhesion molecule-1 (ICAM-1) was blocked by MG-132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-218	intercellular adhesion molecule 1	Homo sapiens	154-187
17008592-4	2006	TNF-alpha-mediated induction of vascular cell adhesion molecule-1 (VCAM-1) was attenuated by all of these inhibitors, whereas in contrast, stimulation of intercellular adhesion molecule-1 (ICAM-1) was blocked by MG-132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-218	intercellular adhesion molecule 1	Homo sapiens	189-195
16413676-3	2006	Our study demonstrated that proteasome inhibitor MG132 (carbobenzoxy-L-leucyle-L-leucyl-L-leucinal) was a potent death-inducing agent for PC3 prostate cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	chromobox 8	Homo sapiens	138-141
16413676-5	2006	To understand the signaling pathways of proteasome inhibitor-induced cell death, we performed gene profiling study using Affymetrix human DNA microarrays to identify the genes whose expression was affected by proteasome inhibitor MG132 in PC3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	230-235	chromobox 8	Homo sapiens	239-242
17052676-4	2006	Both proteasome inhibitor MG-132 and selective p38 MAPK inhibitor SB 203580 could significantly decrease the expression of ICAM-1 on BEAS-2B cells and CD18 on eosinophils upon co-culture with or without TNF-alpha treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	intercellular adhesion molecule 1	Homo sapiens	123-129
17052676-4	2006	Both proteasome inhibitor MG-132 and selective p38 MAPK inhibitor SB 203580 could significantly decrease the expression of ICAM-1 on BEAS-2B cells and CD18 on eosinophils upon co-culture with or without TNF-alpha treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	integrin subunit beta 2	Homo sapiens	151-155
17052676-4	2006	Both proteasome inhibitor MG-132 and selective p38 MAPK inhibitor SB 203580 could significantly decrease the expression of ICAM-1 on BEAS-2B cells and CD18 on eosinophils upon co-culture with or without TNF-alpha treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	tumor necrosis factor	Homo sapiens	203-212
17041027-8	2006	Treating healthy seedlings and infected leaves with the proteasome inhibitor MG132 resulted in higher GRIK1 and GRIK2 protein levels, whereas treatment with the translation inhibitor cycloheximide reduced both kinases, demonstrating that their accumulation is modulated by posttranscriptional processes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	geminivirus rep interacting kinase 1	Arabidopsis thaliana	102-107
17041027-8	2006	Treating healthy seedlings and infected leaves with the proteasome inhibitor MG132 resulted in higher GRIK1 and GRIK2 protein levels, whereas treatment with the translation inhibitor cycloheximide reduced both kinases, demonstrating that their accumulation is modulated by posttranscriptional processes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	geminivirus rep interacting kinase 2	Arabidopsis thaliana	112-117
17079446-6	2006	Furthermore, exemestane-induced aromatase degradation can be completely blocked by 10 micromol/L MG132, indicating that the degradation is mediated by proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	32-41
16855208-7	2006	Inhibition of NFkappaB activation with either the proteasome inhibitor MG132 or phenethyl caffeiate reduced PTGFR mRNA levels, which indicates that this transcription factor is important for basal transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	nuclear factor kappa B subunit 1	Homo sapiens	14-22
16855208-7	2006	Inhibition of NFkappaB activation with either the proteasome inhibitor MG132 or phenethyl caffeiate reduced PTGFR mRNA levels, which indicates that this transcription factor is important for basal transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	prostaglandin F receptor	Homo sapiens	108-113
16825495-4	2006	Expression of SHP1 in these 2 cell lines also resulted in marked decreases in the protein levels of JAK3 and NPM-ALK, and these effects were reversible by proteosome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	14-18
16954375-9	2006	Similarly, the proteasome inhibitor MG132 stabilized interleukin-6 mRNA probably through an increase of AUF1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	interleukin 6	Homo sapiens	53-66
16954375-9	2006	Similarly, the proteasome inhibitor MG132 stabilized interleukin-6 mRNA probably through an increase of AUF1 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	heterogeneous nuclear ribonucleoprotein D	Homo sapiens	104-108
16883594-7	2006	However, MG132 (the proteasome inhibitor) rescued the inhibition of HIF-1alpha protein expression by 2-oxoglutarate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	hypoxia inducible factor 1 subunit alpha	Homo sapiens	68-78
16825495-4	2006	Expression of SHP1 in these 2 cell lines also resulted in marked decreases in the protein levels of JAK3 and NPM-ALK, and these effects were reversible by proteosome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	Janus kinase 3	Homo sapiens	100-104
16825495-4	2006	Expression of SHP1 in these 2 cell lines also resulted in marked decreases in the protein levels of JAK3 and NPM-ALK, and these effects were reversible by proteosome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	nucleophosmin 1	Homo sapiens	109-112
16825495-4	2006	Expression of SHP1 in these 2 cell lines also resulted in marked decreases in the protein levels of JAK3 and NPM-ALK, and these effects were reversible by proteosome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	ALK receptor tyrosine kinase	Homo sapiens	113-116
16965564-8	2006	MG-132 treatment resulted in lower increase in IL-1, TNF-alpha and IL-10 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 1 complex	Mus musculus	47-51
17167531-7	2006	Moreover, we found that PIMT expression returned to the basal level when cells were replated on a substratum after detachment, though downregulation of PIMT expression could be partly prevented by the PI3K inhibitors LY294002 and wortmannin, as well as by the proteasome inhibitors MG-132, lactacystin, and beta-lactone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-288	protein-L-isoaspartate (D-aspartate) O-methyltransferase	Bos taurus	24-28
17167531-7	2006	Moreover, we found that PIMT expression returned to the basal level when cells were replated on a substratum after detachment, though downregulation of PIMT expression could be partly prevented by the PI3K inhibitors LY294002 and wortmannin, as well as by the proteasome inhibitors MG-132, lactacystin, and beta-lactone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-288	protein-L-isoaspartate (D-aspartate) O-methyltransferase	Bos taurus	152-156
16939498-5	2006	Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	Janus kinase 3	Homo sapiens	73-77
16939498-5	2006	Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	nucleophosmin 1	Homo sapiens	82-95
16939498-5	2006	Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	nucleophosmin 1	Homo sapiens	97-100
16939498-5	2006	Interestingly, JSI-124 also dramatically decreased the protein levels of JAK3 and nucleophosmin (NPM)-ALK, and these effects were reversible by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	ALK receptor tyrosine kinase	Homo sapiens	102-105
16965564-8	2006	MG-132 treatment resulted in lower increase in IL-1, TNF-alpha and IL-10 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	tumor necrosis factor	Mus musculus	53-62
16965564-8	2006	MG-132 treatment resulted in lower increase in IL-1, TNF-alpha and IL-10 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 10	Mus musculus	67-72
16965564-11	2006	We conclude that MG-132 treatment decreases inflammatory response and prolongs survival in the CLP model of sepsis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-23	hyaluronan and proteoglycan link protein 1	Mus musculus	95-98
16870259-6	2006	MG-132 treatment also induced increases in caspase-3 activity in a time-dependent manner, with significant activation occurring between 90 and 150 min.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 3	Mus musculus	43-52
17003443-10	2006	Proteasome inhibitor (MG132) treatment strongly inhibited the proliferation of LECs, either alone or in the presence of TGF-beta2, FGF-2, or HGF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	transforming growth factor beta 2	Homo sapiens	120-129
17003443-10	2006	Proteasome inhibitor (MG132) treatment strongly inhibited the proliferation of LECs, either alone or in the presence of TGF-beta2, FGF-2, or HGF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	fibroblast growth factor 2	Homo sapiens	131-136
17003443-10	2006	Proteasome inhibitor (MG132) treatment strongly inhibited the proliferation of LECs, either alone or in the presence of TGF-beta2, FGF-2, or HGF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	hepatocyte growth factor	Homo sapiens	141-144
17003443-14	2006	MG132 caused a significant increase in p21 and p27 protein and decrease in CDK2, but no change in p53, p57, CDK4, or CDK6 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	H3 histone pseudogene 16	Homo sapiens	39-42
17003443-14	2006	MG132 caused a significant increase in p21 and p27 protein and decrease in CDK2, but no change in p53, p57, CDK4, or CDK6 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	dynactin subunit 6	Homo sapiens	47-50
17003443-14	2006	MG132 caused a significant increase in p21 and p27 protein and decrease in CDK2, but no change in p53, p57, CDK4, or CDK6 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase 2	Homo sapiens	75-79
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	H3 histone pseudogene 16	Homo sapiens	93-96
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	dynactin subunit 6	Homo sapiens	101-104
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	H3 histone pseudogene 16	Homo sapiens	126-129
16936098-5	2006	These pressure-induced changes in IL-6 were largely insensitive to MG132 in astrocytes, but were largely MG132-sensitive in microglia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	interleukin 6	Rattus norvegicus	34-38
16936098-7	2006	Elevated pressure also increased MG132-sensitive expression of IL-6 mRNA by microglia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	interleukin 6	Rattus norvegicus	63-67
16936098-9	2006	In contrast, pressure-induced regulation of IL-6 protein and mRNA by microglia is preceded by NFkappaB translocation and is sensitive to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	interleukin 6	Rattus norvegicus	44-48
17003263-5	2006	Indeed, overexpression of the mutant UbcH7 was sufficient to augment GR transactivation to levels achieved using the proteasome inhibitor MG132, but there was no further induction when MG132 and the UbcH7 mutant were used together.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	ubiquitin conjugating enzyme E2 L3	Homo sapiens	37-42
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	dynactin subunit 6	Homo sapiens	134-137
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	H3 histone pseudogene 16	Homo sapiens	93-96
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	dynactin subunit 6	Homo sapiens	101-104
17003443-15	2006	The antiproliferative effect of MG132 was significantly reversed in samples transfected with p21 and p27 siRNA, which reduced p21 and p27 protein expression to very low levels that remained below basal control levels, even after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	dynactin subunit 6	Homo sapiens	134-137
16897471-10	2006	Furthermore, MG132 treatment significantly enhanced the fluorescence of GFP-TOE(LE-ACS3) in the roots of wild-type Arabidopsis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	ACS3	Arabidopsis thaliana	83-87
17003263-5	2006	Indeed, overexpression of the mutant UbcH7 was sufficient to augment GR transactivation to levels achieved using the proteasome inhibitor MG132, but there was no further induction when MG132 and the UbcH7 mutant were used together.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	ubiquitin conjugating enzyme E2 L3	Homo sapiens	37-42
17003263-5	2006	Indeed, overexpression of the mutant UbcH7 was sufficient to augment GR transactivation to levels achieved using the proteasome inhibitor MG132, but there was no further induction when MG132 and the UbcH7 mutant were used together.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	nuclear receptor subfamily 3 group C member 1	Homo sapiens	69-71
16871283-7	2006	Importantly, the decrease in JAK3 was abrogated by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	Janus kinase 3	Homo sapiens	29-33
16822479-1	2006	Treatment of cells with estrogens and several pure ERalpha antagonists rapidly induces down-regulation of the alpha-type estrogen receptor (ERalpha) in the nucleus by mechanisms that are sensitive to the proteasome inhibitors, MG132 and clasto-lactacystin-beta-lactone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	estrogen receptor 1	Homo sapiens	51-58
16822479-1	2006	Treatment of cells with estrogens and several pure ERalpha antagonists rapidly induces down-regulation of the alpha-type estrogen receptor (ERalpha) in the nucleus by mechanisms that are sensitive to the proteasome inhibitors, MG132 and clasto-lactacystin-beta-lactone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	227-232	estrogen receptor 1	Homo sapiens	140-147
16822479-4	2006	The 4,4"-DHS-induced down-regulation of ERalpha in MCF-7 cells involved a mechanism that was insensitive to the two most specific proteasome inhibitors, clasto-lactacystin-beta-lactone and epoxomycin, but sensitive to MG132 at concentrations exceeding that required for maximal inhibition of the proteasome in MCF-7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	218-223	estrogen receptor 1	Homo sapiens	40-47
16965676-11	2006	The decrease of ERalpha and Cyclin D1 expression was inhibited by MG132, an inhibitor of 26S proteosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	estrogen receptor 1	Homo sapiens	16-23
16873546-7	2006	In vitro degradation of reduced GhCesA1 ZnBD is inhibited by proteosome inhibitor MG132 and also by E64 and EGTA, suggesting that proteolysis is initiated by cysteine protease activity rather than the proteosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	cellulose synthase A catalytic subunit 8 [UDP-forming]-like	Gossypium hirsutum	32-39
16965676-11	2006	The decrease of ERalpha and Cyclin D1 expression was inhibited by MG132, an inhibitor of 26S proteosome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	cyclin D1	Homo sapiens	28-37
16849502-5	2006	When overexpressed in EC, HO-1 targeted specifically the p38alpha but not the p38beta MAPK isoform for degradation by the 26S proteasome, an effect reversed by the 26S proteasome inhibitors MG-132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	heme oxygenase 1	Homo sapiens	26-30
16921258-7	2006	The pool of cyclins B remaining after CDK1 inactivation in the presence of MG132 is mitotically inert, while exogenous or newly synthesized cyclin B activates CDK1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	cyclin-dependent kinase 1 L homeolog	Xenopus laevis	38-42
16849502-5	2006	When overexpressed in EC, HO-1 targeted specifically the p38alpha but not the p38beta MAPK isoform for degradation by the 26S proteasome, an effect reversed by the 26S proteasome inhibitors MG-132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	mitogen-activated protein kinase 14	Homo sapiens	57-65
16849502-9	2006	The antiapoptotic effect of HO-1 was impaired when p38alpha expression was restored ectopically or when its degradation by the 26S proteasome was inhibited by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-165	heme oxygenase 1	Homo sapiens	28-32
16569768-3	2006	We demonstrate that the proteasome inhibitor MG132, but not the nuclear export inhibitor leptomycin B (LMB), stabilizes active nuclear Stat5A, whereas MG132 only partially stabilizes active cytoplasmic Stat5A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	signal transducer and activator of transcription 5A	Homo sapiens	135-141
16583136-6	2006	Using a reporter system, we found that MINT-mediated transcription suppression was sensitive to MG132, an inhibitor of the proteosome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	spen family transcriptional repressor	Homo sapiens	39-43
16672643-6	2006	Furthermore, cotreatment with the proteasome inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132) blocked SU9516-mediated Mcl-1 down-regulation, implicating proteasomal degradation in diminished expression of this protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	129-134
16910871-8	2006	We also observed that human DEHAL1B and DEHAL1C proteins are rapidly degraded in stably transfected HEK293 cells, unlike the DEHAL1 protein, and that exposure to the proteasome inhibitor MG132 resulted in accumulation of these proteins that was markedly time- and concentration-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	187-192	iodotyrosine deiodinase	Homo sapiens	28-34
16569768-3	2006	We demonstrate that the proteasome inhibitor MG132, but not the nuclear export inhibitor leptomycin B (LMB), stabilizes active nuclear Stat5A, whereas MG132 only partially stabilizes active cytoplasmic Stat5A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	signal transducer and activator of transcription 5A	Homo sapiens	202-208
16569768-3	2006	We demonstrate that the proteasome inhibitor MG132, but not the nuclear export inhibitor leptomycin B (LMB), stabilizes active nuclear Stat5A, whereas MG132 only partially stabilizes active cytoplasmic Stat5A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	signal transducer and activator of transcription 5A	Homo sapiens	202-208
16849522-3	2006	Introduction of wild-type PTEN into these cells also blunted HIF-1alpha induction in response to hypoxia and decreased HIF-1alpha accumulation in the presence of the proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	188-193	phosphatase and tensin homolog	Homo sapiens	26-30
16699949-5	2006	MG-132 treatment increases binding of DR5 to the adaptor protein FADD, and causes caspase-8 activation and cleavage of pro-apoptotic BID.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	TNF receptor superfamily member 10b	Homo sapiens	38-41
16699949-5	2006	MG-132 treatment increases binding of DR5 to the adaptor protein FADD, and causes caspase-8 activation and cleavage of pro-apoptotic BID.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	Fas associated via death domain	Homo sapiens	65-69
16699949-5	2006	MG-132 treatment increases binding of DR5 to the adaptor protein FADD, and causes caspase-8 activation and cleavage of pro-apoptotic BID.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	caspase 8	Homo sapiens	82-91
16699949-5	2006	MG-132 treatment increases binding of DR5 to the adaptor protein FADD, and causes caspase-8 activation and cleavage of pro-apoptotic BID.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	BH3 interacting domain death agonist	Homo sapiens	133-136
16699949-7	2006	MG-132 also increases apoptosis and DR5 expression in normal B-cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	TNF receptor superfamily member 10b	Homo sapiens	36-39
16537561-2	2006	A proteaosome inhibitor, MG132, mediated cell cycle arrest at G2/M and apoptosis through p38 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	mitogen-activated protein kinase 14	Homo sapiens	89-92
16537561-3	2006	Interestingly, FLIP was stabilized by MG132 and interacted with Raf-1, resulting in enhancement of p38 signals and cytotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	64-69
16537561-3	2006	Interestingly, FLIP was stabilized by MG132 and interacted with Raf-1, resulting in enhancement of p38 signals and cytotoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	mitogen-activated protein kinase 14	Homo sapiens	99-102
16761312-8	2006	GIA promoted phosphorylation and degradation of IkappaB and inhibition of NF-kappaB by MG-132 and 6-amino-4-phenoxyphenylethylamino-quinazoline suppressed the production of TNF-alpha and CXCL8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	tumor necrosis factor	Homo sapiens	173-182
16761312-8	2006	GIA promoted phosphorylation and degradation of IkappaB and inhibition of NF-kappaB by MG-132 and 6-amino-4-phenoxyphenylethylamino-quinazoline suppressed the production of TNF-alpha and CXCL8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	C-X-C motif chemokine ligand 8	Homo sapiens	187-192
16699949-3	2006	Herein, we have demonstrated that the induction of apoptosis by the proteasome inhibitors, MG-132 and PS-341 (bortezomib, Velcade), in primary CLL cells and the Burkitt lymphoma cell line, BJAB, is associated with up-regulation of TRAIL and its death receptors, DR4 and DR5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-97	TNF superfamily member 10	Homo sapiens	231-236
16699949-3	2006	Herein, we have demonstrated that the induction of apoptosis by the proteasome inhibitors, MG-132 and PS-341 (bortezomib, Velcade), in primary CLL cells and the Burkitt lymphoma cell line, BJAB, is associated with up-regulation of TRAIL and its death receptors, DR4 and DR5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-97	major histocompatibility complex, class II, DR beta 4	Homo sapiens	262-265
16699949-3	2006	Herein, we have demonstrated that the induction of apoptosis by the proteasome inhibitors, MG-132 and PS-341 (bortezomib, Velcade), in primary CLL cells and the Burkitt lymphoma cell line, BJAB, is associated with up-regulation of TRAIL and its death receptors, DR4 and DR5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-97	TNF receptor superfamily member 10b	Homo sapiens	270-273
16829709-9	2006	To delineate the mechanisms of the decrease in Cx43 under hypoxia, cells were pretreated with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	gap junction protein, alpha 1	Rattus norvegicus	47-51
16754861-8	2006	NudCL was shown to bind to the dynein complex, and its depletion induces degradation of dynein intermediate chain, a process suppressed by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	NudC domain containing 3	Homo sapiens	0-5
16784539-5	2006	Treatments with the histone deacetylase inhibitor TSA, the demethylating agent 5-aza-2"-deoxycytodine or the proteasome inhibitor MG132 significantly induced expression of hCdc14A in cell lines expressing low or undetectable levels of hCdc14A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	cell division cycle 14A	Homo sapiens	172-178
16784539-5	2006	Treatments with the histone deacetylase inhibitor TSA, the demethylating agent 5-aza-2"-deoxycytodine or the proteasome inhibitor MG132 significantly induced expression of hCdc14A in cell lines expressing low or undetectable levels of hCdc14A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	130-135	cell division cycle 14A	Homo sapiens	172-179
16778187-5	2006	We have found that PTEN protein is down-regulated under proteasome dysfunction induced by proteasome inhibitor MG132 in both human lymphoblast cells and MCF7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	phosphatase and tensin homolog	Homo sapiens	19-23
16434550-6	2006	The insulin-induced IR reduction was greatly reversed by MG-132, a proteasomal inhibitor, but not by chloroquine, a lysosomal inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-63	insulin	Homo sapiens	4-11
16551633-6	2006	Pretreatment with the proteasome inhibitor MG132 blocks IL-1beta-mediated reductions in nuclear RXRalpha levels while increasing accumulation in the cytoplasm.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	interleukin 1 beta	Homo sapiens	56-64
16551633-6	2006	Pretreatment with the proteasome inhibitor MG132 blocks IL-1beta-mediated reductions in nuclear RXRalpha levels while increasing accumulation in the cytoplasm.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	retinoid X receptor alpha	Homo sapiens	96-104
16738331-11	2006	Finally, treating cells with MG132 leads to accumulation of polyubiquitinated SENP2, indicating that SENP2 is degraded through the 26S proteolysis pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	SUMO specific peptidase 2	Homo sapiens	78-83
16734619-9	2006	Both ICAM-1 and VCAM-1 expression by HGF was inhibited by nuclear factor-kappaB (NF-kappaB) activation inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	intercellular adhesion molecule 1	Homo sapiens	5-11
16734619-9	2006	Both ICAM-1 and VCAM-1 expression by HGF was inhibited by nuclear factor-kappaB (NF-kappaB) activation inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	vascular cell adhesion molecule 1	Homo sapiens	16-22
16734619-9	2006	Both ICAM-1 and VCAM-1 expression by HGF was inhibited by nuclear factor-kappaB (NF-kappaB) activation inhibitor (MG-132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	hepatocyte growth factor	Homo sapiens	37-40
16609961-5	2006	Our data show that the proteasomal inhibitor MG-132 causes oxidative stress, as indicated by the upregulation of the small heat shock protein heme oxygenase-1 (HO-1) and the appearance of oxidized proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	heme oxygenase 1	Rattus norvegicus	142-158
16609961-5	2006	Our data show that the proteasomal inhibitor MG-132 causes oxidative stress, as indicated by the upregulation of the small heat shock protein heme oxygenase-1 (HO-1) and the appearance of oxidized proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	heme oxygenase 1	Rattus norvegicus	160-164
16702304-7	2006	In the presence of a proteasome inhibitor (MG132), the ubiquitin-IkappaBalpha complex expression was not significantly modified by glutamine under basal conditions but decreased significantly under proinflammatory conditions (P &lt; 0.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	NFKB inhibitor alpha	Homo sapiens	65-77
16617327-3	2006	We show that a selective inhibitor of p38alpha, SCIO-469, enhances the ability of MG132 and bortezomib to induce the apoptosis of MM cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	mitogen-activated protein kinase 14	Mus musculus	38-46
16738331-11	2006	Finally, treating cells with MG132 leads to accumulation of polyubiquitinated SENP2, indicating that SENP2 is degraded through the 26S proteolysis pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	SUMO specific peptidase 2	Homo sapiens	101-106
16051428-4	2006	DIM (20 microM) also decreased cyclin D1 in MCF-7 (24 h) and MDA-MB-231 (12 h), and the DIM/5,5"-diBrDIM-induced degradation of cyclin D1 was blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	178-183	cyclin D1	Homo sapiens	128-137
16181708-11	2006	MG132 treatment increased the intracellular RT-ODC content 20-fold (up the level of the MG132-treated wtRT; 60-80 fg/cell), and epoxomicin treatment, 10-fold as compared to non-treated samples.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	ornithine decarboxylase 1	Homo sapiens	47-50
16181708-11	2006	MG132 treatment increased the intracellular RT-ODC content 20-fold (up the level of the MG132-treated wtRT; 60-80 fg/cell), and epoxomicin treatment, 10-fold as compared to non-treated samples.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	ornithine decarboxylase 1	Homo sapiens	47-50
16723032-7	2006	The experiment using two NF-kappaB inhibitors, PDTC and MG132, confirmed that this increase of hBD-2 expression following DEP exposure was regulated through NF-kappaB-mediated pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	defensin beta 4A	Homo sapiens	95-100
16723032-7	2006	The experiment using two NF-kappaB inhibitors, PDTC and MG132, confirmed that this increase of hBD-2 expression following DEP exposure was regulated through NF-kappaB-mediated pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	nuclear factor kappa B subunit 1	Homo sapiens	157-166
16524876-5	2006	Inhibition of the proteasome by MG132 caused the prevention of Daxx degradation in parallel with the accumulation of ubiquitinated Daxx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	death domain associated protein	Homo sapiens	63-67
16707792-7	2006	The hormone-induced decline was inhibited by MG132 (benzyloxycarbonyl-leucyl-leucyl-leucinal), showing an involvement of the ubiquitin proteasome system, In keeping with this, dexamethasone increased the ubiquitination of cyclin D1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	cyclin D1	Rattus norvegicus	222-231
16527807-8	2006	Degradation of DDB2 could be blocked by silencing CUL-4A using small interference RNA or by treating cells with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	damage specific DNA binding protein 2	Homo sapiens	15-19
16524876-5	2006	Inhibition of the proteasome by MG132 caused the prevention of Daxx degradation in parallel with the accumulation of ubiquitinated Daxx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	death domain associated protein	Homo sapiens	131-135
16731754-10	2006	The proteasome inhibitor MG-132 blocked FD-mediated reduction of XIAP and AKT and antagonized apoptosis, suggesting that the activation of the proteasome pathway is one of the mechanisms involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	X-linked inhibitor of apoptosis	Homo sapiens	65-69
16804021-0	2006	Preincubation with the proteasome inhibitor MG-132 enhances proteasome activity via the Nrf2 transcription factor in aging human skin fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
16804021-4	2006	We examined the role of the nuclear factor-E2-related factor 2 (Nrf2) in fibroblasts, a key transactivator of the antioxidant response pathway, in the regulation of the proteasome by its inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	197-203	NFE2 like bZIP transcription factor 2	Homo sapiens	64-68
16804021-5	2006	Here, we demonstrate that the stimulation of the proteasome by low levels of MG-132 can be abrogated by small interfering RNAs (siRNAs) targeted against Nrf2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-83	NFE2 like bZIP transcription factor 2	Homo sapiens	153-157
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	NFKB inhibitor alpha	Homo sapiens	60-72
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	nuclear factor kappa B subunit 1	Homo sapiens	176-185
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	tumor necrosis factor	Homo sapiens	189-197
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	nuclear factor kappa B subunit 1	Homo sapiens	176-185
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	nuclear factor kappa B subunit 1	Homo sapiens	176-185
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	tumor necrosis factor	Homo sapiens	189-197
16408291-10	2006	Furthermore, the proteasome inhibitor MG-132 caused loss of IkappaBalpha, and an increase of it is phosphorylated form, but basal NF-kappaB was unchanged, whilst activation of NF-kappaB by TNFalpha was completely inhibited, suggesting that MG-132 activity is independent of constitutive NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	nuclear factor kappa B subunit 1	Homo sapiens	176-185
16504308-4	2006	Inhibition of HIF-1alpha degradation by proteasome inhibitor, MG-132, potentiated hypoxia-induced IL-1beta release from human astrocytes, and this response was blocked in the presence of CdCl2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	hypoxia inducible factor 1 subunit alpha	Homo sapiens	14-24
16504308-4	2006	Inhibition of HIF-1alpha degradation by proteasome inhibitor, MG-132, potentiated hypoxia-induced IL-1beta release from human astrocytes, and this response was blocked in the presence of CdCl2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	interleukin 1 beta	Homo sapiens	98-106
16464966-6	2006	The cytosolic phospholipase A(2) (cPLA(2)) inhibitor 1,1,1-trifluoro-6Z,9Z, 12Z,15Z-heneicosateraen-2-one significantly (p &lt; 0.05) inhibited the relaxation to LPS, whereas the NF-kappaB proteasomal inhibitor Z-Leu-Leu-Leu-aldehyde (MG-132) had no affect on the relaxation in the first 20 min, after which it reversed the response to a contraction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-233	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	34-41
16464966-6	2006	The cytosolic phospholipase A(2) (cPLA(2)) inhibitor 1,1,1-trifluoro-6Z,9Z, 12Z,15Z-heneicosateraen-2-one significantly (p &lt; 0.05) inhibited the relaxation to LPS, whereas the NF-kappaB proteasomal inhibitor Z-Leu-Leu-Leu-aldehyde (MG-132) had no affect on the relaxation in the first 20 min, after which it reversed the response to a contraction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	235-241	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	34-41
16731754-10	2006	The proteasome inhibitor MG-132 blocked FD-mediated reduction of XIAP and AKT and antagonized apoptosis, suggesting that the activation of the proteasome pathway is one of the mechanisms involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	AKT serine/threonine kinase 1	Homo sapiens	74-77
16596199-4	2006	MG-132 was associated with decreased cell viability (between 24% and 33%) and clonogenic survival (between 71% and 88%) alone and in combination with radiation in PC3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	chromobox 8	Homo sapiens	163-166
16596199-7	2006	Furthermore, MG-132 at concentrations associated with reductions in cell viability and clongenic survival inhibited NF-kappaB binding activity in PC3 cells with no effect in URO-tsa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	nuclear factor kappa B subunit 1	Homo sapiens	116-125
16513638-5	2006	Ubiquitination of CaR was observed in the presence of the proteasomal inhibitor MG132; mutation of all putative intracellular loop and carboxyl-terminal lysine residues abolished ubiquitination of CaR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	calcium sensing receptor	Homo sapiens	18-21
16596199-7	2006	Furthermore, MG-132 at concentrations associated with reductions in cell viability and clongenic survival inhibited NF-kappaB binding activity in PC3 cells with no effect in URO-tsa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	chromobox 8	Homo sapiens	146-149
16467309-6	2006	Thrombin- and SLIGKV-induced COX-2 expression and 6-keto-PGF1alpha generation were markedly attenuated by the NF-kappaB inhibitor PG490 and partially inhibited by the proteasome pathway inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-202	coagulation factor II, thrombin	Homo sapiens	0-8
16467309-6	2006	Thrombin- and SLIGKV-induced COX-2 expression and 6-keto-PGF1alpha generation were markedly attenuated by the NF-kappaB inhibitor PG490 and partially inhibited by the proteasome pathway inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-202	prostaglandin-endoperoxide synthase 2	Homo sapiens	29-34
16513638-8	2006	Treatment with tunicamycin, an inhibitor of N-linked glycosylation, induced the appearance of the unglycosylated 115-kDa CaR form, which was further increased by exposure to MG132, or upon transfection with a dorfin dominant negative construct, suggesting that dorfin-mediated proteasomal degradation of immature CaR occurs from the endoplasmic reticulum.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	calcium sensing receptor	Homo sapiens	121-124
16516846-3	2006	We investigated the effect of MG132 on the expression of cyclooxygenase-2 (COX-2), the rate-limiting enzyme in the synthesis of PGE(2), using macrophage cell line, Raw264.7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	prostaglandin-endoperoxide synthase 2	Mus musculus	57-73
16516846-3	2006	We investigated the effect of MG132 on the expression of cyclooxygenase-2 (COX-2), the rate-limiting enzyme in the synthesis of PGE(2), using macrophage cell line, Raw264.7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	prostaglandin-endoperoxide synthase 2	Mus musculus	75-80
16516846-4	2006	Our results showed that COX-2 expression is up-regulated by MG132 treatment and that this induction of COX-2 is regulated in part at the transcriptional level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	prostaglandin-endoperoxide synthase 2	Mus musculus	24-29
16516846-5	2006	In addition, we demonstrated the signal transduction pathway of mitogen-activated protein kinase (MAP kinase) in MG132-induced COX-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	prostaglandin-endoperoxide synthase 2	Mus musculus	127-132
16516846-6	2006	The p38 MAPK inhibitor (SB 203580) prevented MG132-induced COX-2 expression, whereas c-Jun N-terminal kinase (JNK) inhibitor (SP 600125) and MAPK kinase 4 (MKK4)-DN (dominant negative mutant) and MKK7-DN significantly enhanced COX-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	mitogen-activated protein kinase 14	Mus musculus	4-12
16516846-6	2006	The p38 MAPK inhibitor (SB 203580) prevented MG132-induced COX-2 expression, whereas c-Jun N-terminal kinase (JNK) inhibitor (SP 600125) and MAPK kinase 4 (MKK4)-DN (dominant negative mutant) and MKK7-DN significantly enhanced COX-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	prostaglandin-endoperoxide synthase 2	Mus musculus	59-64
16516846-6	2006	The p38 MAPK inhibitor (SB 203580) prevented MG132-induced COX-2 expression, whereas c-Jun N-terminal kinase (JNK) inhibitor (SP 600125) and MAPK kinase 4 (MKK4)-DN (dominant negative mutant) and MKK7-DN significantly enhanced COX-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	mitogen-activated protein kinase kinase 4	Mus musculus	156-160
16516846-6	2006	The p38 MAPK inhibitor (SB 203580) prevented MG132-induced COX-2 expression, whereas c-Jun N-terminal kinase (JNK) inhibitor (SP 600125) and MAPK kinase 4 (MKK4)-DN (dominant negative mutant) and MKK7-DN significantly enhanced COX-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	mitogen-activated protein kinase kinase 7	Mus musculus	196-200
16516846-6	2006	The p38 MAPK inhibitor (SB 203580) prevented MG132-induced COX-2 expression, whereas c-Jun N-terminal kinase (JNK) inhibitor (SP 600125) and MAPK kinase 4 (MKK4)-DN (dominant negative mutant) and MKK7-DN significantly enhanced COX-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	prostaglandin-endoperoxide synthase 2	Mus musculus	227-232
16516846-7	2006	These results suggest that MG132-induced COX-2 expression is associated with the activation of p38 MAPK and the inhibition of JNK signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	prostaglandin-endoperoxide synthase 2	Mus musculus	41-46
16516846-7	2006	These results suggest that MG132-induced COX-2 expression is associated with the activation of p38 MAPK and the inhibition of JNK signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	mitogen-activated protein kinase 14	Mus musculus	95-103
16516846-7	2006	These results suggest that MG132-induced COX-2 expression is associated with the activation of p38 MAPK and the inhibition of JNK signaling pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	mitogen-activated protein kinase 8	Mus musculus	126-129
16336210-2	2006	The present study shows that accumulation of aberrant proteins, caused by the proteasome inhibitor MG132 or the incorporation of the amino acid analogue AZC (L-azetidine-2-carboxylic acid), increased both clusterin protein and mRNA levels in the human glial cell line U-251 MG.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	clusterin	Homo sapiens	205-214
16673057-0	2006	MG132 induced apoptosis is associated with p53-independent induction of pro-apoptotic Noxa and transcriptional activity of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	43-46
16673057-0	2006	MG132 induced apoptosis is associated with p53-independent induction of pro-apoptotic Noxa and transcriptional activity of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	86-90
16673057-0	2006	MG132 induced apoptosis is associated with p53-independent induction of pro-apoptotic Noxa and transcriptional activity of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	catenin beta 1	Homo sapiens	123-135
16673057-3	2006	Here we demonstrate that MG132, a proteasomal inhibitor, rapidly induces Noxa mRNA and protein in two human cell lines, T/C28a and Saos2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	73-77
16673057-4	2006	The induction of Noxa is associated with a significant reduction in the number of metabolically active cells over the first 24 h of exposure to MG132 and progressive activation of caspase-3, a hallmark of caspase-dependent apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	17-21
16673057-5	2006	Partial rescue of the phenotype is observed when cells are transfected with Noxa siRNA prior to treatment with MG132, indicating functional significance of the induction of Noxa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	76-80
16673057-5	2006	Partial rescue of the phenotype is observed when cells are transfected with Noxa siRNA prior to treatment with MG132, indicating functional significance of the induction of Noxa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	173-177
16673057-8	2006	Transfection with the Tcf reporter vector pTOPFLASH confirms that treatment with MG132 leads to early increased transcriptional activity of beta-catenin in both T/C28a and Saos2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	hepatocyte nuclear factor 4 alpha	Homo sapiens	22-25
16673057-8	2006	Transfection with the Tcf reporter vector pTOPFLASH confirms that treatment with MG132 leads to early increased transcriptional activity of beta-catenin in both T/C28a and Saos2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	catenin beta 1	Homo sapiens	140-152
16564422-3	2006	A significant increase in the content of both PR isoforms, ER-beta and SRC-1 was observed after the administration of MG132 in the three studied cerebral regions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	estrogen receptor 2	Rattus norvegicus	59-66
16564422-3	2006	A significant increase in the content of both PR isoforms, ER-beta and SRC-1 was observed after the administration of MG132 in the three studied cerebral regions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	118-123	nuclear receptor coactivator 1	Rattus norvegicus	71-76
16530172-6	2006	Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibitor, which inhibits IkappaB degradation and hence prevents the activation and translocation of NF-kappaB into the nucleus) abolished the increase in NF-kappaB p65 mRNA levels after the insult, while there was no effect by helenalin (an inhibitor which inhibits NF-kappaB activity by alkylation of the p65 subunit, thereby blocking its binding to the target DNA).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	synaptotagmin 1	Rattus norvegicus	229-232
16530172-6	2006	Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibitor, which inhibits IkappaB degradation and hence prevents the activation and translocation of NF-kappaB into the nucleus) abolished the increase in NF-kappaB p65 mRNA levels after the insult, while there was no effect by helenalin (an inhibitor which inhibits NF-kappaB activity by alkylation of the p65 subunit, thereby blocking its binding to the target DNA).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	synaptotagmin 1	Rattus norvegicus	371-374
16530172-7	2006	However, MG-132 and/or helenalin significantly diminished the increase in IL-6 mRNA levels after the insult.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	interleukin 6	Rattus norvegicus	74-78
16673057-9	2006	However, although over-expression of transcriptionally active beta-catenin in T/C28a cells also induced apoptosis through a p53-independent mechanism, the levels of Noxa protein were unchanged, suggesting that beta-catenin mediated signaling and Noxa may play independent roles in MG132 induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	281-286	catenin beta 1	Homo sapiens	62-74
16673057-10	2006	In summary, our results demonstrate that MG132 induces the pro-apoptotic protein Noxa via a p53-independent mechanism that leads to caspase-dependent apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	81-85
16673057-10	2006	In summary, our results demonstrate that MG132 induces the pro-apoptotic protein Noxa via a p53-independent mechanism that leads to caspase-dependent apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	tumor protein p53	Homo sapiens	92-95
16673057-11	2006	This is the first report showing that treatment with MG132 induces Noxa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	67-71
16336210-3	2006	Consistently, MG132 treatment was capable of stimulating a 1.3 kb clusterin gene promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	clusterin	Homo sapiens	66-75
16336210-4	2006	Promoter deletion and mutation studies revealed a critical MG132-responsive region between -218 and -106 bp, which contains a particular heat-shock element, named CLE for "clusterin element".	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	clusterin	Homo sapiens	172-181
16537604-6	2006	The NF-kappaB inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	nuclear factor kappa B subunit 1	Homo sapiens	4-13
16330492-9	2006	Lactacystin and N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132), inhibitors of proteasomal proteolysis, prevented the decrease, supporting the proteasomal degradation of p53 upon APAP exposure.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	tumor protein p53	Sus scrofa	172-175
16571800-3	2006	Here we report that, in contrast to uninfected cells, mdm2 was undetectable upon treatment of infected fibroblasts with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	MDM2 proto-oncogene	Homo sapiens	54-58
16571805-6	2006	Furthermore, we detected WSSV222-mediated ubiquitination and MG132-sensitive degradation of TSL both in shrimp primary cell culture and in the TSL-expressing cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	TSL	Homo sapiens	92-95
16571805-6	2006	Furthermore, we detected WSSV222-mediated ubiquitination and MG132-sensitive degradation of TSL both in shrimp primary cell culture and in the TSL-expressing cell line.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	TSL	Homo sapiens	143-146
16537604-6	2006	The NF-kappaB inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	nuclear factor kappa B subunit 1	Homo sapiens	109-118
16431916-5	2006	Ubiquitinated proteins are degraded by the proteasome, and inhibition of the proteasome with MG132 (a proteasome inhibitor) prevented Bim degradation and blocked rapid ischemic tolerance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	BCL2 like 11	Homo sapiens	134-137
16343770-9	2006	Pre-incubation of cells with MG132 inhibited leptin-induced IkappaB-alpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	leptin	Homo sapiens	45-51
16343770-9	2006	Pre-incubation of cells with MG132 inhibited leptin-induced IkappaB-alpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	NFKB inhibitor alpha	Homo sapiens	60-73
16219794-5	2006	We evidenced down-regulation of NF-kappaB activation and induction of CTCL cell apoptosis in the presence of proteasome 26S inhibitors ALLN, MG132, and bortezomib.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	TSPY like 2	Homo sapiens	70-74
16254126-9	2006	LPS- and Pam-stimulated IL-6 expression was inhibited by the proteasome inhibitor MG-132 and the IkappaB kinase-2 (IKK2) inhibitor 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	toll-like receptor 4	Mus musculus	0-3
16254126-9	2006	LPS- and Pam-stimulated IL-6 expression was inhibited by the proteasome inhibitor MG-132 and the IkappaB kinase-2 (IKK2) inhibitor 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	peptidylglycine alpha-amidating monooxygenase	Mus musculus	9-12
16254126-9	2006	LPS- and Pam-stimulated IL-6 expression was inhibited by the proteasome inhibitor MG-132 and the IkappaB kinase-2 (IKK2) inhibitor 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	interleukin 6	Mus musculus	24-28
16520654-10	2006	Furthermore, MG132 downregulated phospho-AKT and its downstream target phospho-BAD, indicating that MG132 activated the mitochondrial apoptosis pathway by inhibiting phosphorylation of AKT and BAD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	AKT serine/threonine kinase 1	Homo sapiens	41-44
16520654-10	2006	Furthermore, MG132 downregulated phospho-AKT and its downstream target phospho-BAD, indicating that MG132 activated the mitochondrial apoptosis pathway by inhibiting phosphorylation of AKT and BAD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	AKT serine/threonine kinase 1	Homo sapiens	185-188
16520654-5	2006	Moreover, subtoxic levels of MG132 and MG115 sensitized HCC cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	TNF superfamily member 10	Homo sapiens	69-74
16520654-10	2006	Furthermore, MG132 downregulated phospho-AKT and its downstream target phospho-BAD, indicating that MG132 activated the mitochondrial apoptosis pathway by inhibiting phosphorylation of AKT and BAD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	AKT serine/threonine kinase 1	Homo sapiens	41-44
16520654-7	2006	MG132 upregulated TRAIL and its receptors (TRAIL-R1 and -R2) in SK-Hep1 and HLE, whereas MG115 upregulated them in SK-Hep1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF superfamily member 10	Homo sapiens	18-23
16520654-10	2006	Furthermore, MG132 downregulated phospho-AKT and its downstream target phospho-BAD, indicating that MG132 activated the mitochondrial apoptosis pathway by inhibiting phosphorylation of AKT and BAD.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	AKT serine/threonine kinase 1	Homo sapiens	185-188
16520654-7	2006	MG132 upregulated TRAIL and its receptors (TRAIL-R1 and -R2) in SK-Hep1 and HLE, whereas MG115 upregulated them in SK-Hep1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10a	Homo sapiens	43-59
16319082-5	2006	The H. pylori- and TLR-induced increase in syndecan-4 mRNA was blocked by the proteosome inhibitor MG-132 suggesting a role for nuclear factor kappaB (NF-kappaB) in the regulation of syndecan-4 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	syndecan 4	Homo sapiens	43-53
16520654-7	2006	MG132 upregulated TRAIL and its receptors (TRAIL-R1 and -R2) in SK-Hep1 and HLE, whereas MG115 upregulated them in SK-Hep1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNL-type zinc finger	Homo sapiens	67-71
16520654-8	2006	MG132 downregulated expression of X-linked inhibitor of apoptosis protein (XIAP) in SK-Hep1 and HLE, and of survivin in all three cell-types.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	X-linked inhibitor of apoptosis	Homo sapiens	34-73
16520654-8	2006	MG132 downregulated expression of X-linked inhibitor of apoptosis protein (XIAP) in SK-Hep1 and HLE, and of survivin in all three cell-types.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	X-linked inhibitor of apoptosis	Homo sapiens	75-79
16520654-8	2006	MG132 downregulated expression of X-linked inhibitor of apoptosis protein (XIAP) in SK-Hep1 and HLE, and of survivin in all three cell-types.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNL-type zinc finger	Homo sapiens	87-91
16319082-5	2006	The H. pylori- and TLR-induced increase in syndecan-4 mRNA was blocked by the proteosome inhibitor MG-132 suggesting a role for nuclear factor kappaB (NF-kappaB) in the regulation of syndecan-4 gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	syndecan 4	Homo sapiens	183-193
16474903-6	2006	NF-kappaB inhibitor MG132 blocked ICAM-1 expression induced by ET-1 and CGRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	intercellular adhesion molecule 1	Homo sapiens	34-40
16247459-8	2006	We also demonstrated that TRBP is ubiquitinylated and the ubiquitinylated forms of TRBP are accumulated by ectopically expressed merlin or cell confluence in the presence of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	TARBP2 pseudogene 1	Homo sapiens	26-30
16247459-8	2006	We also demonstrated that TRBP is ubiquitinylated and the ubiquitinylated forms of TRBP are accumulated by ectopically expressed merlin or cell confluence in the presence of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	TARBP2 pseudogene 1	Homo sapiens	83-87
16247459-8	2006	We also demonstrated that TRBP is ubiquitinylated and the ubiquitinylated forms of TRBP are accumulated by ectopically expressed merlin or cell confluence in the presence of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	174-179	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	129-135
16108032-10	2006	Treatment of MCF-10A and NIH 3T3 cells with the proteasome inhibitor MG-132 showed that AP-2alpha was ubiquitinated and its level significantly increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	transcription factor AP-2, alpha	Mus musculus	88-97
16474903-6	2006	NF-kappaB inhibitor MG132 blocked ICAM-1 expression induced by ET-1 and CGRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	calcitonin related polypeptide alpha	Homo sapiens	72-76
16353237-8	2006	Interestingly, TF-3-induced EGFR downregulation is inhibited by the proteasome inhibitor, MG132, but not by the EGFR-specific receptor tyrosine kinase inhibitor, AG1478.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	epidermal growth factor receptor	Mus musculus	28-32
16356934-10	2006	Upon induction of apoptosis, LZTR-1 was phosphorylated on tyrosine residues and subsequently degraded; that could be rescued partially by the addition of the caspase inhibitor Z-VAD-fmk and the proteasome inhibitors lactacystin and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	232-237	leucine zipper like transcription regulator 1	Homo sapiens	29-35
16474903-6	2006	NF-kappaB inhibitor MG132 blocked ICAM-1 expression induced by ET-1 and CGRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	endothelin 1	Homo sapiens	63-67
16192300-3	2006	Using this approach, we have demonstrated that treatment with a well-characterized proteasome inhibitor, MG-132, is sufficient to rescue the expression of dystrophin, beta-dystroglycan, and alpha-sarcoglycan in skeletal muscle explants from patients with Duchenne or Becker muscular dystrophy.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	dystrophin	Homo sapiens	155-165
16192300-4	2006	These data are consistent with our previous findings regarding systemic treatment with MG-132 in a dystrophin-deficient mdx mouse model (Bonuccelli G, Sotgia F, Schubert W, Park D, Frank PG, Woodman SE, Insabato L, Cammer M, Minetti C, and Lisanti MP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	dystrophin	Homo sapiens	99-109
16269458-9	2006	MG-132, a proteasome inhibitor that blocked degradation of the intrinsic NFkappaB inhibitor, IkappaB, and thereby prevented NFkappaB activation, was a potent inhibitor of both TNFalpha- and IL-1beta-stimulated PAPP-A mRNA and protein expression and IGF binding protein-4 protease activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor kappa B subunit 1	Homo sapiens	73-81
16269458-9	2006	MG-132, a proteasome inhibitor that blocked degradation of the intrinsic NFkappaB inhibitor, IkappaB, and thereby prevented NFkappaB activation, was a potent inhibitor of both TNFalpha- and IL-1beta-stimulated PAPP-A mRNA and protein expression and IGF binding protein-4 protease activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	nuclear factor kappa B subunit 1	Homo sapiens	124-132
16269458-9	2006	MG-132, a proteasome inhibitor that blocked degradation of the intrinsic NFkappaB inhibitor, IkappaB, and thereby prevented NFkappaB activation, was a potent inhibitor of both TNFalpha- and IL-1beta-stimulated PAPP-A mRNA and protein expression and IGF binding protein-4 protease activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	tumor necrosis factor	Homo sapiens	176-184
16269458-9	2006	MG-132, a proteasome inhibitor that blocked degradation of the intrinsic NFkappaB inhibitor, IkappaB, and thereby prevented NFkappaB activation, was a potent inhibitor of both TNFalpha- and IL-1beta-stimulated PAPP-A mRNA and protein expression and IGF binding protein-4 protease activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 1 beta	Homo sapiens	190-198
16269458-9	2006	MG-132, a proteasome inhibitor that blocked degradation of the intrinsic NFkappaB inhibitor, IkappaB, and thereby prevented NFkappaB activation, was a potent inhibitor of both TNFalpha- and IL-1beta-stimulated PAPP-A mRNA and protein expression and IGF binding protein-4 protease activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	pappalysin 1	Homo sapiens	210-216
16269458-9	2006	MG-132, a proteasome inhibitor that blocked degradation of the intrinsic NFkappaB inhibitor, IkappaB, and thereby prevented NFkappaB activation, was a potent inhibitor of both TNFalpha- and IL-1beta-stimulated PAPP-A mRNA and protein expression and IGF binding protein-4 protease activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	insulin like growth factor binding protein 4	Homo sapiens	249-270
16314411-6	2006	MG132 and lactacystin, inhibitors of the ubiquitin-proteasome pathway, prevented the calmodulin antagonist CGS9343B from reducing the amount of ER in MCF-7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	calmodulin 1	Homo sapiens	85-95
16513842-9	2006	The protease/proteasome inhibitor MG132 protected AR and p21 from the effects of trichostatin A and doxorubicin and inhibited trichostatin A-induced cell death in AR-positive prostate cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	androgen receptor	Homo sapiens	50-52
16513842-9	2006	The protease/proteasome inhibitor MG132 protected AR and p21 from the effects of trichostatin A and doxorubicin and inhibited trichostatin A-induced cell death in AR-positive prostate cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	H3 histone pseudogene 16	Homo sapiens	57-60
16513842-9	2006	The protease/proteasome inhibitor MG132 protected AR and p21 from the effects of trichostatin A and doxorubicin and inhibited trichostatin A-induced cell death in AR-positive prostate cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	androgen receptor	Homo sapiens	163-165
16338464-7	2006	Our data support an effect of p38 on PPARgamma protein stability because p38 inhibition led to reduced expression of PPARgamma protein without a significant effect on PPARgamma mRNA, and this reduction was blocked by the protease inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	mitogen-activated protein kinase 14	Homo sapiens	30-33
16338464-7	2006	Our data support an effect of p38 on PPARgamma protein stability because p38 inhibition led to reduced expression of PPARgamma protein without a significant effect on PPARgamma mRNA, and this reduction was blocked by the protease inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	peroxisome proliferator activated receptor gamma	Homo sapiens	37-46
16338464-7	2006	Our data support an effect of p38 on PPARgamma protein stability because p38 inhibition led to reduced expression of PPARgamma protein without a significant effect on PPARgamma mRNA, and this reduction was blocked by the protease inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	mitogen-activated protein kinase 14	Homo sapiens	73-76
16338464-7	2006	Our data support an effect of p38 on PPARgamma protein stability because p38 inhibition led to reduced expression of PPARgamma protein without a significant effect on PPARgamma mRNA, and this reduction was blocked by the protease inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	peroxisome proliferator activated receptor gamma	Homo sapiens	117-126
16338464-7	2006	Our data support an effect of p38 on PPARgamma protein stability because p38 inhibition led to reduced expression of PPARgamma protein without a significant effect on PPARgamma mRNA, and this reduction was blocked by the protease inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	240-246	peroxisome proliferator activated receptor gamma	Homo sapiens	117-126
16314411-6	2006	MG132 and lactacystin, inhibitors of the ubiquitin-proteasome pathway, prevented the calmodulin antagonist CGS9343B from reducing the amount of ER in MCF-7 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	estrogen receptor 1	Homo sapiens	144-146
16275144-5	2006	MG132 treatment resulted in stabilization of EGFR tyrosine phosphorylation and its association with c-Cbl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	epidermal growth factor receptor	Homo sapiens	45-49
16260777-5	2006	Metabolic labeling experiments revealed that mutant KCNQ2 subunits underwent faster degradation; 10-h treatment with the proteasomal inhibitor MG132 (20 microm) at least partially reversed such enhanced degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	potassium voltage-gated channel subfamily Q member 2	Homo sapiens	52-57
16166589-6	2006	Ectopic expression of Raf-1 or constitutively active MEK/ERK or genetic interruption of the JNK pathway significantly diminished adaphostin/MG-132-mediated lethality.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	22-27
16166589-6	2006	Ectopic expression of Raf-1 or constitutively active MEK/ERK or genetic interruption of the JNK pathway significantly diminished adaphostin/MG-132-mediated lethality.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	mitogen-activated protein kinase kinase 7	Homo sapiens	53-56
16166589-6	2006	Ectopic expression of Raf-1 or constitutively active MEK/ERK or genetic interruption of the JNK pathway significantly diminished adaphostin/MG-132-mediated lethality.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	mitogen-activated protein kinase 1	Homo sapiens	57-60
16166589-6	2006	Ectopic expression of Raf-1 or constitutively active MEK/ERK or genetic interruption of the JNK pathway significantly diminished adaphostin/MG-132-mediated lethality.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	mitogen-activated protein kinase 8	Homo sapiens	92-95
16275144-0	2006	Two different stages of epidermal growth factor (EGF) receptor endocytosis are sensitive to free ubiquitin depletion produced by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	epidermal growth factor receptor	Homo sapiens	24-62
16275144-5	2006	MG132 treatment resulted in stabilization of EGFR tyrosine phosphorylation and its association with c-Cbl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	Cbl proto-oncogene	Homo sapiens	100-105
16275144-4	2006	By subcellular fractionation, we show two MG132-sensitive steps in the EGFR degradation pathway: sorting from early (EE) to late (LE) endosomes, and late stage of LE maturation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	epidermal growth factor receptor	Homo sapiens	71-75
16275144-7	2006	Highly ubiquitinated forms of EGFR demonstrated more sensitivity to MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	epidermal growth factor receptor	Homo sapiens	30-34
16243960-6	2006	Furthermore, inhibition of Nrf2 protein degradation by carbobenzoxy-L-leucyl-L-leucyl-leucinal (MG-132), a 26S proteasome inhibitor, significantly reversed the cycloheximide-mediated inhibition of Nqo1 and Gst ya mRNAs, which coincided with an increase in the expression of Nrf2, confirming that a transcriptional mechanism is involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	nuclear factor, erythroid derived 2, like 2	Mus musculus	27-31
16687309-3	2006	Addition of MG132 or c-lact following NE stimulation causes an increase in AANAT protein level and enzyme activity without affecting the level of Aanat mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	aralkylamine N-acetyltransferase	Rattus norvegicus	75-80
16243960-6	2006	Furthermore, inhibition of Nrf2 protein degradation by carbobenzoxy-L-leucyl-L-leucyl-leucinal (MG-132), a 26S proteasome inhibitor, significantly reversed the cycloheximide-mediated inhibition of Nqo1 and Gst ya mRNAs, which coincided with an increase in the expression of Nrf2, confirming that a transcriptional mechanism is involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	nuclear factor, erythroid derived 2, like 2	Mus musculus	274-278
16243960-6	2006	Furthermore, inhibition of Nrf2 protein degradation by carbobenzoxy-L-leucyl-L-leucyl-leucinal (MG-132), a 26S proteasome inhibitor, significantly reversed the cycloheximide-mediated inhibition of Nqo1 and Gst ya mRNAs, which coincided with an increase in the expression of Nrf2, confirming that a transcriptional mechanism is involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	NAD(P)H dehydrogenase, quinone 1	Mus musculus	197-201
16337881-7	2006	Interestingly, treatment of hyperoxia-exposed CF cells with two proteasome inhibitors, MG132 and lactacystin, restored p21WAF1/CIP1 protein and was associated with an increase of caspase-3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	cyclin dependent kinase inhibitor 1A	Homo sapiens	127-131
16289033-4	2005	Treatment of cells with a proteasomal inhibitor MG132 decreased the oxidative stress-induced degradation of MKP-1, resulting in dephosphorylation of ERK1/2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	dual specificity phosphatase 1	Homo sapiens	108-113
16998592-4	2006	DNA fragmentation, mitochondrial membrane depolarization and increased caspase-3-like enzyme activity was exclusively induced only by combined treatment with proteasome inhibitors (epoxomicin, MG132, bortezomib/PS-341) and TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-198	caspase 3	Homo sapiens	71-80
16337881-7	2006	Interestingly, treatment of hyperoxia-exposed CF cells with two proteasome inhibitors, MG132 and lactacystin, restored p21WAF1/CIP1 protein and was associated with an increase of caspase-3 activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	caspase 3	Homo sapiens	179-188
16384990-7	2006	Proteasome inhibitors lactacystin and MG-132 prevented the PAF-induced depletion of PKCalpha, but the inhibitor of lysosomal proteolysis E-64d was ineffective in rescuing PKCalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	PCNA clamp associated factor	Homo sapiens	59-62
16384990-7	2006	Proteasome inhibitors lactacystin and MG-132 prevented the PAF-induced depletion of PKCalpha, but the inhibitor of lysosomal proteolysis E-64d was ineffective in rescuing PKCalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	protein kinase C alpha	Homo sapiens	84-92
16289033-4	2005	Treatment of cells with a proteasomal inhibitor MG132 decreased the oxidative stress-induced degradation of MKP-1, resulting in dephosphorylation of ERK1/2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	mitogen-activated protein kinase 3	Homo sapiens	149-155
16236257-3	2005	Expression of Rab24 mRNA was also induced in differentiated PC12 cells following proteasome inhibitor (MG132) treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	RAB24, member RAS oncogene family	Rattus norvegicus	14-19
16115879-5	2005	Pulse-chase experiments confirmed that ADRP degradation is inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	perilipin 2	Homo sapiens	39-43
16115879-7	2005	Treatment with MG132 increased the levels of ADRP associated with lipid droplets, as well as throughout the cytosol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	perilipin 2	Homo sapiens	45-49
16284183-9	2005	Pretreatment with proteasome inhibitor MG132 blocked ischemia-induced degradation of PTEN and blocked IPC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	phosphatase and tensin homolog	Rattus norvegicus	85-89
16236272-5	2005	Moreover, inhibition of proteasomes by clasto-lactacystin beta-lactone or Z-Leu-Leu-Leu-CHO (MG132) selectively increased basal and NE-stimulated phosphorylated MKK3/6 and p38MAPK levels without affecting the mRNA or protein levels of MKK3 or p38MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	mitogen activated protein kinase kinase 3	Rattus norvegicus	235-239
16236272-7	2005	Treatment with MG132 also reduced the decline in the phosphorylated levels of NE-stimulated MKK3/6 and p38MAPK that normally follows beta-adrenergic blockade.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	mitogen activated protein kinase kinase 3	Rattus norvegicus	92-96
16236272-5	2005	Moreover, inhibition of proteasomes by clasto-lactacystin beta-lactone or Z-Leu-Leu-Leu-CHO (MG132) selectively increased basal and NE-stimulated phosphorylated MKK3/6 and p38MAPK levels without affecting the mRNA or protein levels of MKK3 or p38MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-91	mitogen activated protein kinase kinase 3	Rattus norvegicus	161-165
16236272-5	2005	Moreover, inhibition of proteasomes by clasto-lactacystin beta-lactone or Z-Leu-Leu-Leu-CHO (MG132) selectively increased basal and NE-stimulated phosphorylated MKK3/6 and p38MAPK levels without affecting the mRNA or protein levels of MKK3 or p38MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-91	mitogen activated protein kinase kinase 3	Rattus norvegicus	235-239
16236272-5	2005	Moreover, inhibition of proteasomes by clasto-lactacystin beta-lactone or Z-Leu-Leu-Leu-CHO (MG132) selectively increased basal and NE-stimulated phosphorylated MKK3/6 and p38MAPK levels without affecting the mRNA or protein levels of MKK3 or p38MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-98	mitogen activated protein kinase kinase 3	Rattus norvegicus	161-165
16195339-2	2005	Here, we show that proteasome inhibitors MG132, PSI-1, and lactacystin induce COX-2 expression via enhancing gene transcription rather than preventing protein degradation in the human alveolar NCI-H292 and A549, and gastric AGS epithelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	78-83
16172035-6	2005	Proteasome inhibitors including MG132 and Z-LLF caused a rapid increase in c-Fos protein expression in these cells within several hours, but other inhibitors of cysteine protease (E-64), lysosome (chloroquine) and calpain (ALLM) did not.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	75-80
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	CCAAT enhancer binding protein delta	Homo sapiens	38-48
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 14	Homo sapiens	85-88
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	96-99
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	CCAAT enhancer binding protein delta	Homo sapiens	148-158
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	170-175
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	CCAAT enhancer binding protein delta	Homo sapiens	148-158
16195339-6	2005	MG132-induced DNA-binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38, PI3K, Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	236-241
16195339-7	2005	In addition, the generation of intracellular reactive oxygen species (ROS) in response to MG132 contributed to the activation of MAPKs and Akt.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	AKT serine/threonine kinase 1	Homo sapiens	139-142
16185657-3	2005	Interferon-induced inhibition of TRAILR4 expression was blocked by a protease inhibitor cocktail and also by MG132, suggesting that down-regulation of TRAILR4 involves the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	TNF receptor superfamily member 10d	Homo sapiens	33-40
15945097-8	2005	The effect of PS341 and MG132 on MCF7/ADR cells was associated with a significant decrease in both protein and gene levels of P-gp expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	ATP binding cassette subfamily B member 1	Homo sapiens	126-130
16288030-8	2005	These effects were prevented by pretreatment with MG132 or replacement of ATP with ATP-gamma-S, a nonhydrolyzable analogue of ATP, suggesting that ATP is required for KLF4 degradation by the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	Kruppel like factor 4	Homo sapiens	167-171
16154995-7	2005	The internalization of GH and GHR was inhibited by CIS-R107K, a dominant-negative SH2 domain mutant of CIS, and by the proteasome inhibitors MG132 and epoxomicin, which prolong GHR signaling to STAT5b.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	growth hormone receptor	Rattus norvegicus	30-33
16154995-7	2005	The internalization of GH and GHR was inhibited by CIS-R107K, a dominant-negative SH2 domain mutant of CIS, and by the proteasome inhibitors MG132 and epoxomicin, which prolong GHR signaling to STAT5b.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	growth hormone receptor	Rattus norvegicus	177-180
16185657-3	2005	Interferon-induced inhibition of TRAILR4 expression was blocked by a protease inhibitor cocktail and also by MG132, suggesting that down-regulation of TRAILR4 involves the proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	TNF receptor superfamily member 10d	Homo sapiens	151-158
16154995-7	2005	The internalization of GH and GHR was inhibited by CIS-R107K, a dominant-negative SH2 domain mutant of CIS, and by the proteasome inhibitors MG132 and epoxomicin, which prolong GHR signaling to STAT5b.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	141-146	signal transducer and activator of transcription 5B	Rattus norvegicus	194-200
16185660-4	2005	Expressed Kv1.5 had a half-life time of approximately 6.7 h, which was prolonged by the proteasome inhibitors of MG132, ALLN, proteasomal inhibitor 1, or lactacystine, but not by a lysosomal inhibitor chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	10-15
16185660-5	2005	MG132 increased the protein level of Kv1.5, as well as the level of its ubiquitinated form in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	37-42
16185660-6	2005	Similar effects of MG132 on endogenous Kv1.5 were seen in cultured rat atrial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	39-44
16185660-8	2005	MG132 increased the immunoreactivity of Kv1.5 in these compartments and also increased Ik(ur) currents through the cell-surface Kv1.5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	40-45
16185660-8	2005	MG132 increased the immunoreactivity of Kv1.5 in these compartments and also increased Ik(ur) currents through the cell-surface Kv1.5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	potassium voltage-gated channel subfamily A member 5	Rattus norvegicus	128-133
16220077-7	2005	The inhibitors of ERK 1/2 (PD98059), p38 (SB203580) MAPK, and NF-kappaB (PDTC and MG132) significantly decreased C-reactive protein-induced IL-8 secretion in human monocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	C-reactive protein	Homo sapiens	113-131
16099857-1	2005	In this study, we investigated the effect of proteasomal inhibition on the induction of arylalkylamine-N-acetyltransferase (AA-NAT) enzyme in cultured rat pinealocytes, using two proteasome inhibitors, MG132 and clastolactacystin beta-lactone (c-lact).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	202-207	aralkylamine N-acetyltransferase	Rattus norvegicus	124-130
16099857-2	2005	Addition of c-lact or MG132 3 h after norepinephrine (NE) stimulation produced a significant increase in AA-NAT protein level and enzyme activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	aralkylamine N-acetyltransferase	Rattus norvegicus	105-111
16099857-4	2005	A similar inhibitory effect of MG132 on aa-nat transcription was observed when cells were stimulated by dibutyryl cAMP, indicating an effect distal to a post-cAMP step.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	aralkylamine N-acetyltransferase	Rattus norvegicus	40-46
16099857-5	2005	The inhibitory effect of MG132 on adrenergic-induced aa-nat transcription was long lasting because it remained effective after 14 h of washout and appeared specific for aa-nat because the induction of another adrenergic-regulated gene, MAPK phosphatase-1, by NE was not affected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	aralkylamine N-acetyltransferase	Rattus norvegicus	53-59
16099857-5	2005	The inhibitory effect of MG132 on adrenergic-induced aa-nat transcription was long lasting because it remained effective after 14 h of washout and appeared specific for aa-nat because the induction of another adrenergic-regulated gene, MAPK phosphatase-1, by NE was not affected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	aralkylamine N-acetyltransferase	Rattus norvegicus	169-175
16099857-6	2005	Time-profile studies revealed that the inhibitory effect of MG132 on NE-stimulated aa-nat induction was detected after 1 h, suggesting accumulation of a protein repressor as a possible mechanism of action.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	aralkylamine N-acetyltransferase	Rattus norvegicus	83-89
16214030-5	2005	MG132 also increased HSP72 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	21-26
16214030-7	2005	Thus MG132 significantly decreased serum amylase, pancreatic weight/body weight ratio, pancreatic myeloperoxidase activity, proinflammatory cytokine concentrations, and the expression of pancreatitis-associated protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	5-10	myeloperoxidase	Rattus norvegicus	98-113
16220077-7	2005	The inhibitors of ERK 1/2 (PD98059), p38 (SB203580) MAPK, and NF-kappaB (PDTC and MG132) significantly decreased C-reactive protein-induced IL-8 secretion in human monocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	C-X-C motif chemokine ligand 8	Homo sapiens	140-144
16236153-6	2005	The enhanced degradation of FAD2-1A at high growth temperatures was partially abrogated by treating the cultures with the 26S proteasome-specific inhibitor MG132, and by expressing the FAD2-1A cDNA in yeast strains devoid of certain ubiquitin-conjugating activities, suggesting a role for ubiquitination and the 26S proteasome in protein turnover.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-161	omega-6 fatty acid desaturase	Glycine max	28-32
15894486-6	2005	Additionally, we show sensitivity of both endogenous synphilin-1 and parkin to proteolytic dysfunction and their co-localization in aggresomes formed in response to the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	synuclein alpha interacting protein	Homo sapiens	53-64
16144541-6	2005	Administration of 0.1 microM MG132 led to activation of a mitochondria-dependent apoptotic signaling cascade involving cytochrome c, caspase-9, caspase-3 and degradation of tau protein; such activation was markedly reduced with 10 microM MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	caspase 9	Mus musculus	133-142
16144541-6	2005	Administration of 0.1 microM MG132 led to activation of a mitochondria-dependent apoptotic signaling cascade involving cytochrome c, caspase-9, caspase-3 and degradation of tau protein; such activation was markedly reduced with 10 microM MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	caspase 3	Mus musculus	144-153
16144659-0	2005	Differential effect of calmodulin antagonists on MG132-induced mitochondrial dysfunction and cell death in PC12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	calmodulin 1	Rattus norvegicus	23-33
16144659-4	2005	Calmodulin antagonists (trifluoperazine, W-7 and calmidazolium) had a differential inhibitory effect on the MG132-induced cell death and GSH depletion depending on concentration with a maximal inhibitory effect at 0.5-1 microM.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	calmodulin 1	Rattus norvegicus	0-10
16144659-6	2005	Calmodulin antagonists at 5 microM exhibited a cytotoxic effect on PC12 cells but attenuated the cytotoxicity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	calmodulin 1	Rattus norvegicus	0-10
16144659-7	2005	The results suggest that the toxicity of MG132 on PC12 cells is mediated by activation of caspase-8, -9 and -3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	caspase 8	Rattus norvegicus	90-110
16144659-8	2005	Trifluoperazine and W-7 at the concentrations of 0.5-1 microM may attenuate the MG132-induced viability loss in PC12 cells by suppressing change in the mitochondrial membrane permeability and by lowering of the intracellular Ca(2+) levels as well as calmodulin inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	calmodulin 1	Rattus norvegicus	250-260
16210649-7	2005	The key role for NF-kappaB in this process was demonstrated by the ability of MG-132 or lactacystin (proteasome inhibitors) to block the enhanced production of MMP-1, COX-2, and PGE(2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	nuclear factor kappa B subunit 1	Homo sapiens	17-26
16239170-6	2005	We found that inhibition of the ubiquitin-proteasome pathway by MG-132 could partially protect Akt1 and eNOS from degradation by arsenite together with a proportional protection from the arsenite-induced cytoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	AKT serine/threonine kinase 1	Homo sapiens	95-99
16239170-6	2005	We found that inhibition of the ubiquitin-proteasome pathway by MG-132 could partially protect Akt1 and eNOS from degradation by arsenite together with a proportional protection from the arsenite-induced cytoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	nitric oxide synthase 3	Homo sapiens	104-108
16230407-6	2005	The BCR/ABL-induced decrease in expression of Bim was found to be a posttranscriptional event that depended on signaling through the mitogen-activated protein kinase pathway and was abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	220-225	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
16230407-6	2005	The BCR/ABL-induced decrease in expression of Bim was found to be a posttranscriptional event that depended on signaling through the mitogen-activated protein kinase pathway and was abrogated by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	220-225	BCL2 like 11	Homo sapiens	46-49
16230407-7	2005	Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	BCL2-like 11 (apoptosis facilitator)	Mus musculus	52-55
16230407-7	2005	Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	BCL2-like 11 (apoptosis facilitator)	Mus musculus	65-68
16230407-7	2005	Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	BCR activator of RhoGEF and GTPase	Mus musculus	139-146
16230407-7	2005	Interestingly, MG132 up-regulated the expression of bim mRNA and Bim protein and suppressed the growth of Ba/F3 cells containing wild-type BCR/ABL or imatinib-resistant mutants of BCR/ABL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	BCR activator of RhoGEF and GTPase	Mus musculus	180-187
16210649-7	2005	The key role for NF-kappaB in this process was demonstrated by the ability of MG-132 or lactacystin (proteasome inhibitors) to block the enhanced production of MMP-1, COX-2, and PGE(2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	matrix metallopeptidase 1	Homo sapiens	160-165
16210649-7	2005	The key role for NF-kappaB in this process was demonstrated by the ability of MG-132 or lactacystin (proteasome inhibitors) to block the enhanced production of MMP-1, COX-2, and PGE(2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	prostaglandin-endoperoxide synthase 2	Homo sapiens	167-172
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	nuclear factor kappa B subunit 1	Homo sapiens	298-307
16218878-4	2005	Inhibition of proteasomes by MG-132 or lactacystin led to the accumulation of intracellular Ntcp, a process dependent on de novo protein synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	solute carrier family 10 member 1	Homo sapiens	92-96
16142322-6	2005	The purpose of this study is to evaluate the potential of the proteasome inhibitor, MG-132, to improve the efficacy of radiation therapy and to determine whether its effect is linked to the suppression of the antioxidant enzyme, manganese superoxide dismutase (MnSOD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	superoxide dismutase 2	Homo sapiens	229-259
16142322-6	2005	The purpose of this study is to evaluate the potential of the proteasome inhibitor, MG-132, to improve the efficacy of radiation therapy and to determine whether its effect is linked to the suppression of the antioxidant enzyme, manganese superoxide dismutase (MnSOD).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-90	superoxide dismutase 2	Homo sapiens	261-266
16142322-10	2005	The levels of IkappaB-alpha, a NF-kappaB target gene and also an inhibitor of NF-kappaB nuclear translocation, decreased in a time-dependent manner following administration of MG-132 confirming the inhibition of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	NFKB inhibitor alpha	Homo sapiens	14-27
16142322-10	2005	The levels of IkappaB-alpha, a NF-kappaB target gene and also an inhibitor of NF-kappaB nuclear translocation, decreased in a time-dependent manner following administration of MG-132 confirming the inhibition of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	nuclear factor kappa B subunit 1	Homo sapiens	31-40
16142322-10	2005	The levels of IkappaB-alpha, a NF-kappaB target gene and also an inhibitor of NF-kappaB nuclear translocation, decreased in a time-dependent manner following administration of MG-132 confirming the inhibition of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-182	nuclear factor kappa B subunit 1	Homo sapiens	78-87
16105840-5	2005	In addition, the phospho-p65 (Ser(536)) was not associated with either IkappaBalpha or p50, and the nuclear translocation of phospho-p65 (Ser(536)), but not total p65, was unaffected by the proteosome inhibitor MG-132, which blocks IkappaB protein degradation and prevents p65/p50 dimer nuclear translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-217	RELA proto-oncogene, NF-kB subunit	Homo sapiens	25-28
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	superoxide dismutase 2	Homo sapiens	317-322
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	superoxide dismutase 2	Homo sapiens	58-63
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	nuclear factor kappa B subunit 1	Homo sapiens	298-307
16142322-12	2005	Cells treated with radiation demonstrated an induction of MnSOD; however, the administration of MG-132 suppressed this induction These results support the hypothesis that proteasome inhibitors such as MG-132 can increase the efficacy of radiation therapy, in part, by suppression of cytoprotective NF-kappaB-mediated MnSOD expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	201-207	superoxide dismutase 2	Homo sapiens	317-322
16024662-8	2005	Moreover, incubation of smooth muscle cells with the proteasome inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG132) blocked the GA-induced down-regulation of sGC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	guanylate cyclase 1 soluble subunit beta 2	Rattus norvegicus	166-169
15814588-5	2005	Run-on assay and promoter reporter study indicated that the proteasome inhibitor MG-132 repressed the rate of elastin transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-87	elastin	Homo sapiens	110-117
16112871-6	2005	Accordingly, acute exposure to MG-132 inhibited the hyperphosphorylation, loss of DNA binding, ubiquitination, and degradation of the pro-survival transcription factor MEF2D induced by removal of depolarizing medium.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	myocyte enhancer factor 2D	Rattus norvegicus	168-173
16112871-7	2005	In contrast, chronic exposure to MG-132 increased the expression and phosphorylation of c-Jun, elevated levels of the pro-apoptotic protein Bim, and triggered neuronal apoptosis, even in the presence of depolarizing medium.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	Bcl2-like 11	Rattus norvegicus	140-143
15963499-4	2005	In the stable transfectants, a proteasome inhibitor MG132 protected the poly-ubiquitinated SIM2 protein from degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	SIM bHLH transcription factor 2	Homo sapiens	91-95
16099423-8	2005	In addition, GA-induced down-regulation of Chk1 was reversed by MG132, a specific proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	checkpoint kinase 1	Homo sapiens	43-47
16046415-8	2005	In addition, the expression of phosphorylation-deficient IkappaB and pretreatment with the proteasome inhibitor MG-132 abolished Galpha13- and alpha-thrombin-induced VASP phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	G protein subunit alpha 13	Homo sapiens	129-137
16046415-8	2005	In addition, the expression of phosphorylation-deficient IkappaB and pretreatment with the proteasome inhibitor MG-132 abolished Galpha13- and alpha-thrombin-induced VASP phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	coagulation factor II, thrombin	Homo sapiens	149-157
16046415-8	2005	In addition, the expression of phosphorylation-deficient IkappaB and pretreatment with the proteasome inhibitor MG-132 abolished Galpha13- and alpha-thrombin-induced VASP phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	vasodilator stimulated phosphoprotein	Homo sapiens	166-170
16159384-7	2005	The ability of the proteasome inhibitor MG-132 to affect P-glycoprotein function was monitored by fluorescence due to accumulation of daunorubicin in P-glycoprotein overexpressing KB 8-5 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	ATP binding cassette subfamily B member 1	Homo sapiens	57-71
16159384-7	2005	The ability of the proteasome inhibitor MG-132 to affect P-glycoprotein function was monitored by fluorescence due to accumulation of daunorubicin in P-glycoprotein overexpressing KB 8-5 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	ATP binding cassette subfamily B member 1	Homo sapiens	150-164
16159384-10	2005	The proteasome inhibitor MG-132 caused a dose-dependent accumulation of daunorubicin in KB 8-5 cells that overexpress P-glycoprotein, suggesting that it blocked P-glycoprotein function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	ATP binding cassette subfamily B member 1	Homo sapiens	118-132
16159384-10	2005	The proteasome inhibitor MG-132 caused a dose-dependent accumulation of daunorubicin in KB 8-5 cells that overexpress P-glycoprotein, suggesting that it blocked P-glycoprotein function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	ATP binding cassette subfamily B member 1	Homo sapiens	161-175
15814588-6	2005	MG-132 did not affect mRNA levels of NF-kappaB and C/EBPbeta, or the nuclear presence of NF-kappaB, but markedly increased C/EBPbeta isoforms, including liver-enriched transcriptional activating protein and liver-enriched transcriptional inhibitory protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	CCAAT enhancer binding protein beta	Homo sapiens	123-132
15814588-7	2005	Addition of cycloheximide blocked these increases and the downregulation of elastin mRNA by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-98	elastin	Homo sapiens	76-83
15814588-8	2005	The MG-132-induced downregulation of elastin transcription was dependent on C/EBPbeta expression as assessed with small interfering RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-10	elastin	Homo sapiens	37-44
15814588-8	2005	The MG-132-induced downregulation of elastin transcription was dependent on C/EBPbeta expression as assessed with small interfering RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	4-10	CCAAT enhancer binding protein beta	Homo sapiens	76-85
15945068-5	2005	In the presence of the proteasome inhibitor MG-132, which blocked nuclear translocation of TonEBP, the hypertonic upregulation of BGT1 protein and transport was prevented and cell viability in hypertonic medium was impaired over 24 h. Urea also prevented the hypertonic upregulation of BGT1 protein and transport, but did not interfere with TonEBP translocation and cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	solute carrier family 6 member 12	Canis lupus familiaris	130-134
15945068-5	2005	In the presence of the proteasome inhibitor MG-132, which blocked nuclear translocation of TonEBP, the hypertonic upregulation of BGT1 protein and transport was prevented and cell viability in hypertonic medium was impaired over 24 h. Urea also prevented the hypertonic upregulation of BGT1 protein and transport, but did not interfere with TonEBP translocation and cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	solute carrier family 6 member 12	Canis lupus familiaris	286-290
15945068-7	2005	When stably transfected MDCK cells that over-expressed BGT1 were treated for 6 h with hypertonic medium containing 3 microM MG-132, there was 43% inhibition of nuclear translocation, 83% inhibition of BGT1 transport, and no change in viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	solute carrier family 6 member 12	Canis lupus familiaris	55-59
15945068-7	2005	When stably transfected MDCK cells that over-expressed BGT1 were treated for 6 h with hypertonic medium containing 3 microM MG-132, there was 43% inhibition of nuclear translocation, 83% inhibition of BGT1 transport, and no change in viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	solute carrier family 6 member 12	Canis lupus familiaris	201-205
16037944-4	2005	Pretreatment with the proteasome inhibitor MG132 and PS-341 rendered TRAIL-resistant hepatocellular carcinoma (HCC) cell lines but not primary human hepatocytes sensitive for TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	TNF superfamily member 10	Homo sapiens	69-74
16037944-4	2005	Pretreatment with the proteasome inhibitor MG132 and PS-341 rendered TRAIL-resistant hepatocellular carcinoma (HCC) cell lines but not primary human hepatocytes sensitive for TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	TNF superfamily member 10	Homo sapiens	175-180
16037944-8	2005	Compared with 5-FU pretreatment, caspase-8 was more efficiently recruited to the DISC in MG132 pretreated cells despite the presence of fewer death receptors and more cFLIP in the DISC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	caspase 8	Homo sapiens	33-42
15824729-7	2005	Moreover, dramatic Bik/NBK accumulation and apoptosis induction were observed when cells were treated with proteasome inhibitor MG132 and calpain inhibitor I (ALLN).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	BCL2 interacting killer	Homo sapiens	19-22
15941855-9	2005	The effect of DFMO on TNFalpha/MG132-induced upregulation of caspase-3 activity was reversed by the addition of 100 microM putrescine, confirming that polyamines were really involved in the apoptotic process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	tumor necrosis factor	Homo sapiens	22-30
15941855-9	2005	The effect of DFMO on TNFalpha/MG132-induced upregulation of caspase-3 activity was reversed by the addition of 100 microM putrescine, confirming that polyamines were really involved in the apoptotic process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	caspase 3	Homo sapiens	61-70
15965230-6	2005	Rather, PP2A mediated ER expression through modulation of ER mRNA stability through degradation of ER mRNA, reversible with concomitant treatment with the proteasomal inhibitor MG 132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-183	protein phosphatase 2 phosphatase activator	Homo sapiens	8-12
15964225-4	2005	In addition, the enhancement of iNOS protein degradation by TGF-beta1 treatment was almost completely blocked by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	nitric oxide synthase 2, inducible	Mus musculus	32-36
15964225-4	2005	In addition, the enhancement of iNOS protein degradation by TGF-beta1 treatment was almost completely blocked by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	transforming growth factor, beta 1	Mus musculus	60-69
15964225-7	2005	Because MG132 inhibited iNOS protein degradation and IFN-gamma plus TGF-beta1 treatment increased the trypsin-like activity of proteasomes, we hypothesized that TGF-beta1 might enhance iNOS protein degradation via the ubiquitin-proteasome pathway in the presence of IFN-gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-13	nitric oxide synthase 2, inducible	Mus musculus	24-28
15964225-7	2005	Because MG132 inhibited iNOS protein degradation and IFN-gamma plus TGF-beta1 treatment increased the trypsin-like activity of proteasomes, we hypothesized that TGF-beta1 might enhance iNOS protein degradation via the ubiquitin-proteasome pathway in the presence of IFN-gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-13	transforming growth factor, beta 1	Mus musculus	161-170
15824729-7	2005	Moreover, dramatic Bik/NBK accumulation and apoptosis induction were observed when cells were treated with proteasome inhibitor MG132 and calpain inhibitor I (ALLN).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	BCL2 interacting killer	Homo sapiens	23-26
16082182-5	2005	Subsequent studies showed that combined treatment with bortezomib or MG132 resulted in an increase of death receptor (DR) 5 and Bik at protein levels but had no effects on protein levels of DR4, Bax, Bak, Bcl-2, Bcl-XL or Flice-inhibitory protein (FLIP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	TNF receptor superfamily member 10b	Homo sapiens	102-123
15925323-4	2005	On the other hand, in A6 cells treated with carbobenzoxy-L-leucyl-leucyl-L-leucinal (MG132; 100 microM for 2 h) that inhibits endocytosis of proteins at the plasma membrane into the cytosolic space, insulin pretreatment increased the NPPB-sensitive Isc with no effects on NPPB-sensitive Gt.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	insulin	Homo sapiens	199-206
15994939-11	2005	Furthermore, CHOP small interfering RNA attenuated the DR5 up-regulation due to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	DNA damage inducible transcript 3	Homo sapiens	13-17
15994939-11	2005	Furthermore, CHOP small interfering RNA attenuated the DR5 up-regulation due to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	TNF receptor superfamily member 10b	Homo sapiens	55-58
15994939-12	2005	These results indicate that the proteasome inhibitor MG132 induces DR5 expression through CHOP up-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	TNF receptor superfamily member 10b	Homo sapiens	67-70
15994939-12	2005	These results indicate that the proteasome inhibitor MG132 induces DR5 expression through CHOP up-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	DNA damage inducible transcript 3	Homo sapiens	90-94
16001975-0	2005	The proteasome inhibitor MG-132 sensitizes PC-3 prostate cancer cells to ionizing radiation by a DNA-PK-independent mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	97-103
15994939-0	2005	Proteasome inhibitor MG132 induces death receptor 5 through CCAAT/enhancer-binding protein homologous protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF receptor superfamily member 10b	Homo sapiens	35-51
15994939-0	2005	Proteasome inhibitor MG132 induces death receptor 5 through CCAAT/enhancer-binding protein homologous protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	DNA damage inducible transcript 3	Homo sapiens	60-109
15994939-3	2005	In this study, we report that CCAAT/enhancer-binding protein homologous protein (CHOP) is a regulator of DR5 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	DNA damage inducible transcript 3	Homo sapiens	30-79
15994939-3	2005	In this study, we report that CCAAT/enhancer-binding protein homologous protein (CHOP) is a regulator of DR5 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	DNA damage inducible transcript 3	Homo sapiens	81-85
15994939-3	2005	In this study, we report that CCAAT/enhancer-binding protein homologous protein (CHOP) is a regulator of DR5 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	TNF receptor superfamily member 10b	Homo sapiens	105-108
15994939-4	2005	MG132 induced DR5 expression at a protein and mRNA level in prostate cancer DU145 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10b	Homo sapiens	14-17
16082182-5	2005	Subsequent studies showed that combined treatment with bortezomib or MG132 resulted in an increase of death receptor (DR) 5 and Bik at protein levels but had no effects on protein levels of DR4, Bax, Bak, Bcl-2, Bcl-XL or Flice-inhibitory protein (FLIP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	BCL2 interacting killer	Homo sapiens	128-131
15994939-5	2005	Furthermore, MG132 increased DR5 promoter activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	TNF receptor superfamily member 10b	Homo sapiens	29-32
15994939-6	2005	Using a series of deletion mutant plasmids containing DR5 promoters of various sizes, we found that MG132 stimulated the promoter activity via the region of -289 to -253.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	TNF receptor superfamily member 10b	Homo sapiens	54-57
15994939-9	2005	An electrophoretic mobility shift assay showed that CHOP directly bound to the MG132-responsive site on the DR5 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	DNA damage inducible transcript 3	Homo sapiens	52-56
15994939-9	2005	An electrophoretic mobility shift assay showed that CHOP directly bound to the MG132-responsive site on the DR5 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	TNF receptor superfamily member 10b	Homo sapiens	108-111
15994939-10	2005	Expression of the CHOP protein was increased with MG132 along with DR5 up-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	DNA damage inducible transcript 3	Homo sapiens	18-22
16082182-5	2005	Subsequent studies showed that combined treatment with bortezomib or MG132 resulted in an increase of death receptor (DR) 5 and Bik at protein levels but had no effects on protein levels of DR4, Bax, Bak, Bcl-2, Bcl-XL or Flice-inhibitory protein (FLIP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	BCL2 like 1	Homo sapiens	212-218
16082182-5	2005	Subsequent studies showed that combined treatment with bortezomib or MG132 resulted in an increase of death receptor (DR) 5 and Bik at protein levels but had no effects on protein levels of DR4, Bax, Bak, Bcl-2, Bcl-XL or Flice-inhibitory protein (FLIP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	CASP8 and FADD like apoptosis regulator	Homo sapiens	222-246
15882977-2	2005	When expressed in COS cells, Kir6.2 was short-lived with a half-life time of 1.9 h. The half-life time of Kir6.2 was prolonged by proteasome inhibitors MG132, ALLN, proteasome inhibitor 1, and lactacystine, but not at all by a lysosomal inhibitor chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	potassium inwardly-rectifying channel, subfamily J, member 11	Rattus norvegicus	29-35
16000563-5	2005	Deprivation of glutamine or glucose inhibited the accumulation of HIF-1alpha in the presence of MG-132, a protease inhibitor, regardless of oxygen tensions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	hypoxia inducible factor 1 subunit alpha	Homo sapiens	66-76
15966900-6	2005	Since treatment of the cells with the proteasome inhibitor MG132 or clasto-Lactacystin substantially abrogated the effects of cycloheximide and UV-C irradiation and increased the expression level of both endogenous and transfected GATA-2, the degradation of GATA-2 seems to occur through the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	GATA binding protein 2	Mus musculus	231-237
15966900-6	2005	Since treatment of the cells with the proteasome inhibitor MG132 or clasto-Lactacystin substantially abrogated the effects of cycloheximide and UV-C irradiation and increased the expression level of both endogenous and transfected GATA-2, the degradation of GATA-2 seems to occur through the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	GATA binding protein 2	Mus musculus	258-264
15800029-8	2005	The role of NF-kappaB in regulation of MMP-9 was demonstrated further by the inhibition of MMP-9 production by proteasome inhibitors, lactacystin and MG-132, which prevented the ubiquitination and dissociation of IkappaB from NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-156	nuclear factor kappa B subunit 1	Homo sapiens	12-21
15800029-8	2005	The role of NF-kappaB in regulation of MMP-9 was demonstrated further by the inhibition of MMP-9 production by proteasome inhibitors, lactacystin and MG-132, which prevented the ubiquitination and dissociation of IkappaB from NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-156	matrix metallopeptidase 9	Homo sapiens	39-44
15800029-8	2005	The role of NF-kappaB in regulation of MMP-9 was demonstrated further by the inhibition of MMP-9 production by proteasome inhibitors, lactacystin and MG-132, which prevented the ubiquitination and dissociation of IkappaB from NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-156	matrix metallopeptidase 9	Homo sapiens	91-96
15800029-8	2005	The role of NF-kappaB in regulation of MMP-9 was demonstrated further by the inhibition of MMP-9 production by proteasome inhibitors, lactacystin and MG-132, which prevented the ubiquitination and dissociation of IkappaB from NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-156	nuclear factor kappa B subunit 1	Homo sapiens	226-235
15837792-2	2005	IRF-8 induced in peritoneal macrophages by interferon-gamma and lipopolysaccharide was degraded rapidly, and degradation of IRF-8 was blocked by MG132, the proteasome inhibitor, but inhibitors of calpain and lysosomal enzymes had no effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	interferon regulatory factor 8	Mus musculus	0-5
15837792-2	2005	IRF-8 induced in peritoneal macrophages by interferon-gamma and lipopolysaccharide was degraded rapidly, and degradation of IRF-8 was blocked by MG132, the proteasome inhibitor, but inhibitors of calpain and lysosomal enzymes had no effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	interferon regulatory factor 8	Mus musculus	124-129
15882977-5	2005	Like MG132, a Na+ channel blocker aprindine prolonged the half-life time of Kir6.2 and augmented K(ATP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	5-10	potassium inwardly-rectifying channel, subfamily J, member 11	Rattus norvegicus	76-82
16181113-7	2005	Treatment of cortical astrocyte cultures with 1 microM MG-132 resulted in a rapid increase in Nrf2, to a level that was five-fold that of vehicle-treated cultures by 2 h. This was followed by a three to six-fold increase in HO-1 expression that persisted through the 16 h observation period.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	NFE2 like bZIP transcription factor 2	Homo sapiens	94-98
16181113-7	2005	Treatment of cortical astrocyte cultures with 1 microM MG-132 resulted in a rapid increase in Nrf2, to a level that was five-fold that of vehicle-treated cultures by 2 h. This was followed by a three to six-fold increase in HO-1 expression that persisted through the 16 h observation period.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-61	heme oxygenase 1	Homo sapiens	224-228
15963850-8	2005	RNA interference for SKP2 and treatment of these cells with the proteasome inhibitor MG132 restored p27 levels, corresponding with decreasing SKP2 levels after interfering in N-Ras signal transduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	interferon alpha inducible protein 27	Homo sapiens	100-103
15963850-8	2005	RNA interference for SKP2 and treatment of these cells with the proteasome inhibitor MG132 restored p27 levels, corresponding with decreasing SKP2 levels after interfering in N-Ras signal transduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	S-phase kinase associated protein 2	Homo sapiens	142-146
16026644-7	2005	Inhibition of NF(kappa)B activation by the proteasome inhibitor, MG132, enhanced the apoptotic effect of TSA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	nuclear factor kappa B subunit 1	Homo sapiens	14-24
15882977-2	2005	When expressed in COS cells, Kir6.2 was short-lived with a half-life time of 1.9 h. The half-life time of Kir6.2 was prolonged by proteasome inhibitors MG132, ALLN, proteasome inhibitor 1, and lactacystine, but not at all by a lysosomal inhibitor chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	potassium inwardly-rectifying channel, subfamily J, member 11	Rattus norvegicus	106-112
15882977-3	2005	MG132 also increased the level of ubiquitinated Kir6.2 without affecting its localization in the endoplasmic reticulum and Golgi apparatus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	potassium inwardly-rectifying channel, subfamily J, member 11	Rattus norvegicus	48-54
15882977-4	2005	In electrophysiological recordings, MG132 augmented nicorandil-activated K(ATP) currents in COS cells expressing SUR2A and Kir6.2 as well as the same currents in neonatal rat cardiomyocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	potassium inwardly-rectifying channel, subfamily J, member 11	Rattus norvegicus	123-129
15782119-4	2005	Kinetic studies revealed that a proteasome inhibitor MG132 induced p100 accumulation with reduced p52 expression in H-RS cells, suggesting proteasome-dependent processing of p100.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	98-101
15879308-10	2005	Ubiquitination inhibitors (30 micromol/L ALLN, 2 micromol/L lactacystin, or 100 nmol/L MG132) reduced the BMK1-mediated effect on HIF1alpha expression by &gt;80%, suggesting that BMK1 stimulated HIF1alpha proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	mitogen-activated protein kinase 7	Mus musculus	106-110
15879308-10	2005	Ubiquitination inhibitors (30 micromol/L ALLN, 2 micromol/L lactacystin, or 100 nmol/L MG132) reduced the BMK1-mediated effect on HIF1alpha expression by &gt;80%, suggesting that BMK1 stimulated HIF1alpha proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	hypoxia inducible factor 1, alpha subunit	Mus musculus	130-139
15879308-10	2005	Ubiquitination inhibitors (30 micromol/L ALLN, 2 micromol/L lactacystin, or 100 nmol/L MG132) reduced the BMK1-mediated effect on HIF1alpha expression by &gt;80%, suggesting that BMK1 stimulated HIF1alpha proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	mitogen-activated protein kinase 7	Mus musculus	179-183
15879308-10	2005	Ubiquitination inhibitors (30 micromol/L ALLN, 2 micromol/L lactacystin, or 100 nmol/L MG132) reduced the BMK1-mediated effect on HIF1alpha expression by &gt;80%, suggesting that BMK1 stimulated HIF1alpha proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	hypoxia inducible factor 1, alpha subunit	Mus musculus	195-204
15907785-8	2005	The enzyme activity was detected at the basic range of pH and inhibited by serine protease inhibitors, diisopropyl fluorophosphate and phenylmethylsulfonyl fluoride, but not by other protease inhibitors including a proteasome inhibitor, MG-132, and a tripeptidyl peptidase II (TPP II) inhibitor, AAF-CMK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	237-243	coagulation factor II, thrombin	Homo sapiens	75-90
15914627-7	2005	RESULTS: At the mRNA level, the proteasome inhibitor, MG132, caused a &gt;10-fold increase in HSP27 and a small increase (1.2- to 1.6-fold) in alphaB-crystallin but no change in HSP70 or -90.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	heat shock protein 1	Mus musculus	94-99
15930365-3	2005	EXPERIMENTAL DESIGN: Jurkat cells engineered to overexpress Bcl-2 were treated with proteasome inhibitors (MG132, epoxomicin, and bortezomib), anticancer drugs (etoposide and doxorubicin), TRAIL, or combinations of these compounds.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	BCL2 apoptosis regulator	Homo sapiens	60-65
15914627-7	2005	RESULTS: At the mRNA level, the proteasome inhibitor, MG132, caused a &gt;10-fold increase in HSP27 and a small increase (1.2- to 1.6-fold) in alphaB-crystallin but no change in HSP70 or -90.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	crystallin, alpha B	Mus musculus	143-160
15914627-7	2005	RESULTS: At the mRNA level, the proteasome inhibitor, MG132, caused a &gt;10-fold increase in HSP27 and a small increase (1.2- to 1.6-fold) in alphaB-crystallin but no change in HSP70 or -90.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	heat shock protein 1B	Mus musculus	178-183
15914627-10	2005	MG132 caused no significant change in heat shock factor (HSF)-1, but a more than twofold increase in HSF2 and -4 protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock factor 2	Mus musculus	101-112
15914627-11	2005	MG132 prevented the IFN-gamma-induced increase in caspase-1, -6, and -8 activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	interferon gamma	Mus musculus	20-29
15914627-11	2005	MG132 prevented the IFN-gamma-induced increase in caspase-1, -6, and -8 activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 1	Mus musculus	50-71
15914627-12	2005	Quercetin decreased MG132-induced expression of HSP27, -70, and -90 by more than 70%, and heat shock factors HSF2 and -4 by more than 65%.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	heat shock protein 1	Mus musculus	48-53
15914627-13	2005	Quercetin pretreatment significantly reversed the decrease in caspase-1, -6, and -8 activities and the antiapoptotic effect of MG132 on IFN-gamma-treated LECs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	interferon gamma	Mus musculus	136-145
15899868-4	2005	We have carried out genome array profiles from cells with decreased Rpn10/S5a levels using RNAi or from cells treated with proteasome inhibitor MG132 and have thereby identified candidate genes that are regulated as part of a metazoan proteasome network.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	Regulatory particle non-ATPase 10	Drosophila melanogaster	68-73
15605377-8	2005	Addition of a proteasome inhibitor, MG-132, into Sertoli cells cultured with db-cAMP blocked the db-cAMP-induced occludin loss in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	occludin	Homo sapiens	113-121
15605377-9	2005	Accumulations of ubiquitin-conjugated and Itch-conjugated occludin were detected in Sertoli cells cultured in the presence of both MG-132 and db-cAMP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-137	itchy E3 ubiquitin protein ligase	Homo sapiens	42-46
15605377-9	2005	Accumulations of ubiquitin-conjugated and Itch-conjugated occludin were detected in Sertoli cells cultured in the presence of both MG-132 and db-cAMP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-137	occludin	Homo sapiens	58-66
15605377-10	2005	These results suggest that MG-132 prevented db-cAMP-induced TJ disruption by altering the rate of occludin degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	occludin	Homo sapiens	98-106
15899868-4	2005	We have carried out genome array profiles from cells with decreased Rpn10/S5a levels using RNAi or from cells treated with proteasome inhibitor MG132 and have thereby identified candidate genes that are regulated as part of a metazoan proteasome network.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-149	Regulatory particle non-ATPase 10	Drosophila melanogaster	74-77
15845394-3	2005	In vitro studies identified those proteins in the ubiquitin- and alpha-synuclein (known as the major component of LB)-positive LB-like inclusions generated in dopaminergic SH-SY5Y cells treated with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	199-204	synuclein alpha	Homo sapiens	65-80
15845394-4	2005	Intriguingly, IkappaBalpha migration into such ubiquitinated inclusions in cells treated with MG132 was inhibited by a cell-permeable peptide known to block phosphorylation of IkappaBalpha, although this peptide did not influence cell viability under proteasomal inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	NFKB inhibitor alpha	Homo sapiens	14-26
15845394-4	2005	Intriguingly, IkappaBalpha migration into such ubiquitinated inclusions in cells treated with MG132 was inhibited by a cell-permeable peptide known to block phosphorylation of IkappaBalpha, although this peptide did not influence cell viability under proteasomal inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	NFKB inhibitor alpha	Homo sapiens	176-188
15823586-2	2005	The effects of proteasome inhibitor MG132 on p14(ARF) protein stabilization were detectable using our experimental procedure.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	cyclin dependent kinase inhibitor 2A	Homo sapiens	45-48
15753096-7	2005	The rapid degradation of PDGFRbeta in the LRP1-deficient fibroblasts was prevented by MG132 and chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	platelet derived growth factor receptor, beta polypeptide	Mus musculus	25-34
16117894-1	2005	OBJECTIVE: To investigate the reversing effect of NF-kappaB inhibitor MG-132 on chemoresistance of gastric cancer cells to vincristine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	nuclear factor kappa B subunit 1	Homo sapiens	50-59
16117894-6	2005	Pretreatment with MG-132, the NF-kappaB inhibitor, for 30 minutes remarkably reduced the NF-kappaB activation, IkappaB-alpha degradation and nuclear translocation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-24	nuclear factor kappa B subunit 1	Homo sapiens	30-39
16117894-6	2005	Pretreatment with MG-132, the NF-kappaB inhibitor, for 30 minutes remarkably reduced the NF-kappaB activation, IkappaB-alpha degradation and nuclear translocation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-24	nuclear factor kappa B subunit 1	Homo sapiens	89-98
16117894-6	2005	Pretreatment with MG-132, the NF-kappaB inhibitor, for 30 minutes remarkably reduced the NF-kappaB activation, IkappaB-alpha degradation and nuclear translocation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-24	NFKB inhibitor alpha	Homo sapiens	111-124
16117894-6	2005	Pretreatment with MG-132, the NF-kappaB inhibitor, for 30 minutes remarkably reduced the NF-kappaB activation, IkappaB-alpha degradation and nuclear translocation of p65.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-24	RELA proto-oncogene, NF-kB subunit	Homo sapiens	166-169
15741163-8	2005	4) Treatment of Caco-2/15 cells with MG132 (a proteasome inhibitor) and (R)-roscovitine (a specific Cdk2 inhibitor) induced an increase in CDX2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	cyclin dependent kinase 2	Homo sapiens	100-104
15741163-8	2005	4) Treatment of Caco-2/15 cells with MG132 (a proteasome inhibitor) and (R)-roscovitine (a specific Cdk2 inhibitor) induced an increase in CDX2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	caudal type homeobox 2	Homo sapiens	139-143
15753096-7	2005	The rapid degradation of PDGFRbeta in the LRP1-deficient fibroblasts was prevented by MG132 and chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	low density lipoprotein receptor-related protein 1	Mus musculus	42-46
15854272-4	2005	Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	cyclin dependent kinase inhibitor 1A	Homo sapiens	73-76
15867377-9	2005	Treatment of cells with MG132, a proteasome inhibitor, inhibited eEF-2 kinase degradation and induced the accumulation of polyubiquitinated forms of the enzyme, resulting in an increase in its half-life.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	eukaryotic elongation factor 2 kinase	Oryctolagus cuniculus	65-77
15778120-6	2005	Meanwhile, blockade of the NF-kappa B signaling pathway using MG132 inhibited cellular growth without impacting cytolytic capability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	nuclear factor kappa B subunit 1	Homo sapiens	27-37
15886795-9	2005	Intracellular FVIII was degraded through both lysosomal and proteasomal pathways as evidenced by inhibitor treatments (e.g. NH(4)Cl, leupeptin, clasto-Lactacystin beta-lactone and MG-132), pulse-chase analysis and confocal observations.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	180-186	coagulation factor VIII	Homo sapiens	14-19
15653552-6	2005	Our data indicate that troglitazone- and Delta2-TG-induced cyclin D1 repression is mediated via proteasome-facilitated proteolysis because it is inhibited by different proteasome inhibitors, including N-carbobenzoxy-l-leucinyl-l-leucinyl-l-norleucinal (MG132), lactacystin, and epoxomicin, and is preceded by increased ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	253-258	cyclin D1	Homo sapiens	59-68
15737467-4	2005	In contrast, treatment with the proteasome inhibitors lactacystin or MG132 repressed GLUT4 mRNA level to 35% (10 microM lactacystin) and 12% (10 microM MG132) of control levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	solute carrier family 2 member 4	Homo sapiens	85-90
15737467-4	2005	In contrast, treatment with the proteasome inhibitors lactacystin or MG132 repressed GLUT4 mRNA level to 35% (10 microM lactacystin) and 12% (10 microM MG132) of control levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	solute carrier family 2 member 4	Homo sapiens	85-90
15782132-8	2005	Treatment of JN-DSRCT-1 cells with MG-132, a proteasome specific inhibitor, also resulted in the induction of apoptosis through a similar increase in the Bax : Bcl-xL ratio specifically caused by inhibiting Bax degradation and turnover.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	BCL2 associated X, apoptosis regulator	Homo sapiens	154-157
15782132-8	2005	Treatment of JN-DSRCT-1 cells with MG-132, a proteasome specific inhibitor, also resulted in the induction of apoptosis through a similar increase in the Bax : Bcl-xL ratio specifically caused by inhibiting Bax degradation and turnover.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	BCL2 like 1	Homo sapiens	160-166
15782132-8	2005	Treatment of JN-DSRCT-1 cells with MG-132, a proteasome specific inhibitor, also resulted in the induction of apoptosis through a similar increase in the Bax : Bcl-xL ratio specifically caused by inhibiting Bax degradation and turnover.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	BCL2 associated X, apoptosis regulator	Homo sapiens	207-210
15616827-7	2005	Treatment with MG-132, a proteasome inhibitor, inhibited translocation of NF-kappaB p65, and abrogated TNF-alpha induction induced by Tipalpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	tumor necrosis factor	Mus musculus	103-112
15752769-10	2005	However, effects of diazoxide on SNAP-25 protein were nullified by proteasome inhibitors (ALLN, MG-132, and epoxomicin) but not by lysosomal inhibition (NH(4)Cl).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-102	synaptosome associated protein 25	Rattus norvegicus	33-40
15795279-6	2005	Inhibition of NF-kappaB activity by different pharmacological inhibitors (i.e., parthenolide, MG132 and BAY 11-7082) and by overexpressed mutated IkappaBalpha prevented the activation of STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	NFKB inhibitor alpha	Homo sapiens	146-158
15795279-6	2005	Inhibition of NF-kappaB activity by different pharmacological inhibitors (i.e., parthenolide, MG132 and BAY 11-7082) and by overexpressed mutated IkappaBalpha prevented the activation of STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	signal transducer and activator of transcription 1	Homo sapiens	187-192
15781656-5	2005	Proteosomal inhibition by MG132 reversed antisense-mediated decrease of S6K1 and 4E-BP1 protein expression, but failed to affect the effect of ezrin on phosphorylation of S6K1 and 4E-BP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	72-87
15854272-4	2005	Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	cyclin dependent kinase inhibitor 1A	Homo sapiens	77-81
15854272-4	2005	Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	cyclin dependent kinase inhibitor 1A	Homo sapiens	82-87
15854272-4	2005	Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	cyclin dependent kinase inhibitor 1A	Homo sapiens	171-174
15854272-4	2005	Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	cyclin dependent kinase inhibitor 1A	Homo sapiens	175-179
15854272-4	2005	Meanwhile, the proteasome inhibitor MG-132 could inhibit the decrease of p21(WAF1/Cip-1) at the early stage of apoptosis, which showed that proteasome pathway involved in p21(WAF1/Cip-1) degradation during the TSA induced G(2)/M arrest and apoptosis responses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-42	cyclin dependent kinase inhibitor 1A	Homo sapiens	180-185
15854272-6	2005	Compared to cells treated by TSA only, exposure MOLT-4 cells to TSA meanwhile treatment with MG-132 increased the protein level of p21(WAF1/Cip-1) and increased the numbers of cell in G(2)/M-phase, whereas the cell apoptosis were delayed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	cyclin dependent kinase inhibitor 1A	Homo sapiens	131-134
15854272-6	2005	Compared to cells treated by TSA only, exposure MOLT-4 cells to TSA meanwhile treatment with MG-132 increased the protein level of p21(WAF1/Cip-1) and increased the numbers of cell in G(2)/M-phase, whereas the cell apoptosis were delayed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	cyclin dependent kinase inhibitor 1A	Homo sapiens	135-139
15854272-6	2005	Compared to cells treated by TSA only, exposure MOLT-4 cells to TSA meanwhile treatment with MG-132 increased the protein level of p21(WAF1/Cip-1) and increased the numbers of cell in G(2)/M-phase, whereas the cell apoptosis were delayed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	93-99	cyclin dependent kinase inhibitor 1A	Homo sapiens	140-145
15668958-7	2005	We found that the proteasome inhibitors, lactacystin and MG132 increased the cellular GAP-43 level, leading to the accumulation of polyubiquitinated forms of this protein in transfected cells and that the Ub-proteasome pathway is also involved in the turnover of this protein in neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	growth associated protein 43	Mus musculus	86-92
15670752-9	2005	Importantly, TPA-induced TLR2 expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including MG132 and BAY11-7085.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	toll like receptor 2	Homo sapiens	25-29
15670752-9	2005	Importantly, TPA-induced TLR2 expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including MG132 and BAY11-7085.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	nuclear factor kappa B subunit 1	Homo sapiens	70-79
15725397-2	2005	Treatment of PC12 cells with MG132 resulted in the nuclear damage, decrease in the mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c, activation of caspase-3, increase in the formation of reactive oxygen species (ROS), and depletion of GSH.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	caspase 3	Rattus norvegicus	176-185
15857753-2	2005	Progesterone induced CAT and HSD11beta2 transcription while co-treatment with the proteasome inhibitor, MG132, blocked PR-induced transcription in a time-dependent fashion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	progesterone receptor	Homo sapiens	119-121
15764834-5	2005	Co-administration of PSI, lactacystin, or MG-132 significantly prevented the nigral degeneration and apomorphine-induced rotational asymmetry of the model with increased appearance of alpha-syn- and Ub-positive inclusions in the substantia nigra.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	synuclein alpha	Homo sapiens	184-193
15731265-8	2005	In cells carrying an EBV mutant with the BFRF1 gene deleted (293-BFRF1-KO cells) BFLF2 expression was low, and it was restored to wild-type levels upon treatment of the cells with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	205-210	nuclear egress membrane protein	Human gammaherpesvirus 4	41-46
15857753-5	2005	Surprisingly, progesterone-mediated acetylation of histone H4 was inhibited by MG132 with the concomitant recruitment of HDAC3, NCoR, and SMRT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	histone deacetylase 3	Homo sapiens	121-126
15857753-3	2005	MG132 treatment also inhibited transcription of beta-actin and cyclophilin, but not two proteasome subunit genes, PSMA1 and PSMC1, indicating that proteasome inhibition affects a subset of RNA polymerase II (RNAP(II))-regulated genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	POTE ankyrin domain family member F	Homo sapiens	48-58
15857753-5	2005	Surprisingly, progesterone-mediated acetylation of histone H4 was inhibited by MG132 with the concomitant recruitment of HDAC3, NCoR, and SMRT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	nuclear receptor corepressor 1	Homo sapiens	128-132
15550677-3	2005	Down-regulation of SMA protein by MG132 or LC occurred at the level of SMA transcription and via the inhibition of SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	serum response factor	Homo sapiens	115-118
15857753-5	2005	Surprisingly, progesterone-mediated acetylation of histone H4 was inhibited by MG132 with the concomitant recruitment of HDAC3, NCoR, and SMRT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	nuclear receptor corepressor 2	Homo sapiens	138-142
15857753-6	2005	We demonstrate that the steady-state protein levels of SMRT and NCoR are higher in the presence of MG132 in CAT0 cells, consistent with other reports that SMRT and NCoR are targets of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear receptor corepressor 2	Homo sapiens	55-59
15857753-6	2005	We demonstrate that the steady-state protein levels of SMRT and NCoR are higher in the presence of MG132 in CAT0 cells, consistent with other reports that SMRT and NCoR are targets of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear receptor corepressor 1	Homo sapiens	64-68
15857753-6	2005	We demonstrate that the steady-state protein levels of SMRT and NCoR are higher in the presence of MG132 in CAT0 cells, consistent with other reports that SMRT and NCoR are targets of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear receptor corepressor 2	Homo sapiens	155-159
15857753-6	2005	We demonstrate that the steady-state protein levels of SMRT and NCoR are higher in the presence of MG132 in CAT0 cells, consistent with other reports that SMRT and NCoR are targets of the 26S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear receptor corepressor 1	Homo sapiens	164-168
15550677-4	2005	By contrast, MG132 and LC potentiated the activity of activator protein-1 transcription factor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-73
15550677-5	2005	Regulation of SRF by MG132 was not related to inhibition of nuclear factor-kappaB, an established target of proteasome inhibitors, and was not mediated by protein kinase A, a powerful regulator of SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	serum response factor	Homo sapiens	14-17
15550677-6	2005	Signaling studies indicate that inhibition of ET1-induced SRF activity by MG132 occurs at the level downstream of heterotrimeric G proteins Gq/11 and G13, of small GTPase RhoA, and of actin dynamics but at the level of SRF-DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	endothelin 1	Homo sapiens	46-49
15737734-2	2005	Axons protected by MG132 displayed persistent phosphorylation of Erk1/2, and pharmacological inhibition of MEK activity with U0126 (50 microM) restored rapid axonal degeneration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	mitogen activated protein kinase 3	Rattus norvegicus	65-71
15550677-6	2005	Signaling studies indicate that inhibition of ET1-induced SRF activity by MG132 occurs at the level downstream of heterotrimeric G proteins Gq/11 and G13, of small GTPase RhoA, and of actin dynamics but at the level of SRF-DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	serum response factor	Homo sapiens	58-61
15550677-6	2005	Signaling studies indicate that inhibition of ET1-induced SRF activity by MG132 occurs at the level downstream of heterotrimeric G proteins Gq/11 and G13, of small GTPase RhoA, and of actin dynamics but at the level of SRF-DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	G protein subunit alpha 13	Homo sapiens	114-153
15550677-6	2005	Signaling studies indicate that inhibition of ET1-induced SRF activity by MG132 occurs at the level downstream of heterotrimeric G proteins Gq/11 and G13, of small GTPase RhoA, and of actin dynamics but at the level of SRF-DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	ras homolog family member A	Homo sapiens	171-175
15550677-6	2005	Signaling studies indicate that inhibition of ET1-induced SRF activity by MG132 occurs at the level downstream of heterotrimeric G proteins Gq/11 and G13, of small GTPase RhoA, and of actin dynamics but at the level of SRF-DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	serum response factor	Homo sapiens	219-222
15550677-8	2005	By contrast, the levels of c-Jun were rapidly increased upon incubation of cells with MG132, and ectopic overexpression of c-Jun mimicked the effect of MG132 on SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
15550677-8	2005	By contrast, the levels of c-Jun were rapidly increased upon incubation of cells with MG132, and ectopic overexpression of c-Jun mimicked the effect of MG132 on SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	86-91	serum response factor	Homo sapiens	161-164
15550677-8	2005	By contrast, the levels of c-Jun were rapidly increased upon incubation of cells with MG132, and ectopic overexpression of c-Jun mimicked the effect of MG132 on SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
15550677-8	2005	By contrast, the levels of c-Jun were rapidly increased upon incubation of cells with MG132, and ectopic overexpression of c-Jun mimicked the effect of MG132 on SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	123-128
15550677-8	2005	By contrast, the levels of c-Jun were rapidly increased upon incubation of cells with MG132, and ectopic overexpression of c-Jun mimicked the effect of MG132 on SRF activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	serum response factor	Homo sapiens	161-164
15749954-4	2005	MVP was identified by matrix-assisted laser-desorption ionization-time-of-flight (MALDI-TOF) peptide sequencing and Western blotting as a protein accumulating in porcine zygotes cultured in the presence of specific proteasomal inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	237-242	major vault protein	Homo sapiens	0-3
15710413-3	2005	The inhibition of tyrosine hydroxylase (TH) by alpha-methyltyrosine dramatically decreased MG132-induced aggregate formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	tyrosine hydroxylase	Rattus norvegicus	18-38
15629152-3	2005	Here we show that E1AF protein is stabilized by treatment with the 26S protease inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	ETS variant transcription factor 4	Homo sapiens	18-22
15494213-4	2005	In addition, ICP0 interacted specifically with IkappaBalpha and its activating effect was attenuated by Ubch5A(C85A) and MG132, but not by IkappaBalpha(S32A/S36A).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	NFKB inhibitor alpha	Homo sapiens	47-59
15710384-6	2005	This Smurf1-dependent reduction in RhoA protein levels was abrogated using the general proteasome inhibitor MG132, suggesting that RhoA is targeted for ubiquitination and degradation via Smurf1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	SMAD specific E3 ubiquitin protein ligase 1	Mus musculus	5-11
15710384-6	2005	This Smurf1-dependent reduction in RhoA protein levels was abrogated using the general proteasome inhibitor MG132, suggesting that RhoA is targeted for ubiquitination and degradation via Smurf1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	ras homolog family member A	Mus musculus	35-39
15710384-6	2005	This Smurf1-dependent reduction in RhoA protein levels was abrogated using the general proteasome inhibitor MG132, suggesting that RhoA is targeted for ubiquitination and degradation via Smurf1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	ras homolog family member A	Mus musculus	131-135
15710384-6	2005	This Smurf1-dependent reduction in RhoA protein levels was abrogated using the general proteasome inhibitor MG132, suggesting that RhoA is targeted for ubiquitination and degradation via Smurf1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	SMAD specific E3 ubiquitin protein ligase 1	Mus musculus	187-193
16301819-0	2005	Osmotic regulation of MG-132-induced MAP-kinase phosphatase MKP-1 expression in H4IIE rat hepatoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	dual specificity phosphatase 1	Rattus norvegicus	60-65
15486049-6	2005	The presence of the proteasome inhibitor MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leuleucinal] increased the stability not only of immunodetectable CYP1B1, but also--unexpectedly given the size of the proteasome access channel--increased the stability of enzymatically active CYP1B1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	143-149
15486049-6	2005	The presence of the proteasome inhibitor MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leuleucinal] increased the stability not only of immunodetectable CYP1B1, but also--unexpectedly given the size of the proteasome access channel--increased the stability of enzymatically active CYP1B1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	271-277
15695611-11	2005	When rat oocytes were treated with MG132, a proteasome inhibitor, delayed inactivation of the p34cdc2 kinase was observed in the MG132-treated oocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	cyclin dependent kinase 1	Homo sapiens	94-101
15695611-11	2005	When rat oocytes were treated with MG132, a proteasome inhibitor, delayed inactivation of the p34cdc2 kinase was observed in the MG132-treated oocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	cyclin dependent kinase 1	Homo sapiens	94-101
15695611-14	2005	These results suggest that the decreased level of p34cdc2 kinase activity in aged or enucleated rat oocytes is responsible for their inability to support PCC of microinjected donor cell nuclei and that inhibition of p34cdc2 kinase inactivation by chemicals such as MG132 is in part effective for rat oocytes to promote PCC and further development.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	265-270	cyclin dependent kinase 1	Homo sapiens	50-57
15695611-14	2005	These results suggest that the decreased level of p34cdc2 kinase activity in aged or enucleated rat oocytes is responsible for their inability to support PCC of microinjected donor cell nuclei and that inhibition of p34cdc2 kinase inactivation by chemicals such as MG132 is in part effective for rat oocytes to promote PCC and further development.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	265-270	cyclin dependent kinase 1	Homo sapiens	216-223
15531915-4	2005	Pulse-chase experiments and treatment with proteasome inhibitor MG-132 revealed that siPalpha interferes with both Ets1 protein synthesis and stability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	ETS proto-oncogene 1, transcription factor	Homo sapiens	115-119
15567145-5	2005	The ubiquitination and destabilization of p53 is observed in cells treated with the protease inhibitor MG132, implying that the HECT domain of hUREB1 suppresses the transcriptional activity of p53 through a ubiquitin-dependent degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	tumor protein p53	Homo sapiens	42-45
15567145-5	2005	The ubiquitination and destabilization of p53 is observed in cells treated with the protease inhibitor MG132, implying that the HECT domain of hUREB1 suppresses the transcriptional activity of p53 through a ubiquitin-dependent degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	HECT, UBA and WWE domain containing E3 ubiquitin protein ligase 1	Homo sapiens	143-149
15567145-5	2005	The ubiquitination and destabilization of p53 is observed in cells treated with the protease inhibitor MG132, implying that the HECT domain of hUREB1 suppresses the transcriptional activity of p53 through a ubiquitin-dependent degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	tumor protein p53	Homo sapiens	193-196
15862952-2	2005	All hsp90 ligands induced an E(2)- and MG132-inhibited decrease of both ER cell content.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	heat shock protein 90 alpha family class A member 1	Homo sapiens	4-9
15580311-9	2005	Furthermore, through the use of proteasome inhibitors, such as MG-132, in vivo and proteasome degradation assays in vitro, we found that Tax destabilizes the hypo-phosphorylated (active) form of Rb via the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-69	RB transcriptional corepressor 1	Homo sapiens	195-197
16301819-3	2005	Here the effect of cell hydration on MG-132-induced MKP-1 expression was investigated in H4IIE rat hepatoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	dual specificity phosphatase 1	Rattus norvegicus	52-57
16301819-4	2005	RESULTS: Hyperosmolarity (405mosmol/l) increased MKP-1 expression by MG-132, which was accompanied by an induction of c-Fos, c-Jun, cJun Ser73 phosphorylation, and AP-1 DNA binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	dual specificity phosphatase 1	Rattus norvegicus	49-54
16301819-5	2005	MKP-1 induction by MG-132 plus hyperosmolarity was sensitive to inhibition of p38(MAPK) and c-Jun-N-terminal kinases (JNKs) but not extracellular signal-regulated kinases Erk-1/Erk-2, and was accompanied by a decline of MAP-kinase activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	dual specificity phosphatase 1	Rattus norvegicus	0-5
16301819-5	2005	MKP-1 induction by MG-132 plus hyperosmolarity was sensitive to inhibition of p38(MAPK) and c-Jun-N-terminal kinases (JNKs) but not extracellular signal-regulated kinases Erk-1/Erk-2, and was accompanied by a decline of MAP-kinase activities.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	mitogen activated protein kinase 14	Rattus norvegicus	78-81
16301819-7	2005	Hyperosmolarity also enabled MG-132 to induce poly-ADP-ribose polymerase (PARP) cleavage which was sensitive to inhibition of p38(MAPK) and JNKs but not Erk-1/Erk-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	poly (ADP-ribose) polymerase 1	Rattus norvegicus	46-72
16301819-7	2005	Hyperosmolarity also enabled MG-132 to induce poly-ADP-ribose polymerase (PARP) cleavage which was sensitive to inhibition of p38(MAPK) and JNKs but not Erk-1/Erk-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	poly (ADP-ribose) polymerase 1	Rattus norvegicus	74-78
16301819-7	2005	Hyperosmolarity also enabled MG-132 to induce poly-ADP-ribose polymerase (PARP) cleavage which was sensitive to inhibition of p38(MAPK) and JNKs but not Erk-1/Erk-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	mitogen activated protein kinase 14	Rattus norvegicus	126-129
16301819-7	2005	Hyperosmolarity also enabled MG-132 to induce poly-ADP-ribose polymerase (PARP) cleavage which was sensitive to inhibition of p38(MAPK) and JNKs but not Erk-1/Erk-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-35	mitogen activated protein kinase 1	Rattus norvegicus	159-164
16301819-8	2005	PARP cleavage and caspase-3 activation in H4IIE cells treated with hyperosmolarity plus MG-132 was further increased by vanadate, consistent with a contribution of MKP-1 to counterbalance proapoptotic MAP-kinase signals.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-4
16301819-8	2005	PARP cleavage and caspase-3 activation in H4IIE cells treated with hyperosmolarity plus MG-132 was further increased by vanadate, consistent with a contribution of MKP-1 to counterbalance proapoptotic MAP-kinase signals.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	caspase 3	Rattus norvegicus	18-27
16301819-8	2005	PARP cleavage and caspase-3 activation in H4IIE cells treated with hyperosmolarity plus MG-132 was further increased by vanadate, consistent with a contribution of MKP-1 to counterbalance proapoptotic MAP-kinase signals.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	dual specificity phosphatase 1	Rattus norvegicus	164-169
15516986-4	2004	Two proteasome inhibitors, MG-132 and lactacystin, blocked the RA-mediated degradation of IRS-1, and RA increased ubiquitination of IRS-1 in the RA-sensitive breast cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	insulin receptor substrate 1	Homo sapiens	90-95
15583047-9	2005	Because the proteasome inhibitor MG-132 blocked activation of caspase-3, these results functionally locate the proteasome pathway upstream of the caspase pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	caspase 3	Bos taurus	62-71
15547920-8	2005	Moreover, the UV-induced recruitment of repair factor xeroderma pigmentosum protein C (XPC) to damage sites was negatively affected by treatment of repair competent cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	54-85
15547920-8	2005	Moreover, the UV-induced recruitment of repair factor xeroderma pigmentosum protein C (XPC) to damage sites was negatively affected by treatment of repair competent cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	87-90
15623602-10	2004	Interestingly, the selective proteasome inhibitor MG-132 completely reversed the reduction of HIF-1alpha protein in the PAB-treated MDA-MB-468 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	hypoxia inducible factor 1 subunit alpha	Homo sapiens	94-104
15265789-3	2004	In PPAR-gamma-null NK cells, 15-deoxy-Delta(12,14) prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, reduces IFN-gamma production that can be reversed by MG132 and/or chloroquine, and it inhibits cytolytic activity of NK cells through reduction of both conjugate formation and CD69 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-171	interferon gamma	Homo sapiens	121-130
15498507-5	2004	Of interest, catalase-induced iNOS protein expression was abrogated through inactivation of NF-kappaB pathway by MG132 or BAY 11-7085 and PI3K pathway by LY294002 or wortmannin, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	catalase	Mus musculus	13-21
15498507-5	2004	Of interest, catalase-induced iNOS protein expression was abrogated through inactivation of NF-kappaB pathway by MG132 or BAY 11-7085 and PI3K pathway by LY294002 or wortmannin, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	nitric oxide synthase 2, inducible	Mus musculus	30-34
15528042-4	2004	In both cell types, proteasome activities were required for the spontaneous degradation of iNOS protein, and the inhibition of proteasome activity by MG132 after maximum increase of iNOS protein levels further enhanced iNOS protein induction by LPS/IFN, suggesting the involvement of proteasome in iNOS degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	nitric oxide synthase 2	Homo sapiens	182-186
15528042-4	2004	In both cell types, proteasome activities were required for the spontaneous degradation of iNOS protein, and the inhibition of proteasome activity by MG132 after maximum increase of iNOS protein levels further enhanced iNOS protein induction by LPS/IFN, suggesting the involvement of proteasome in iNOS degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	nitric oxide synthase 2	Homo sapiens	182-186
15528042-4	2004	In both cell types, proteasome activities were required for the spontaneous degradation of iNOS protein, and the inhibition of proteasome activity by MG132 after maximum increase of iNOS protein levels further enhanced iNOS protein induction by LPS/IFN, suggesting the involvement of proteasome in iNOS degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	interferon alpha 1	Homo sapiens	249-252
15528042-4	2004	In both cell types, proteasome activities were required for the spontaneous degradation of iNOS protein, and the inhibition of proteasome activity by MG132 after maximum increase of iNOS protein levels further enhanced iNOS protein induction by LPS/IFN, suggesting the involvement of proteasome in iNOS degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	nitric oxide synthase 2	Homo sapiens	182-186
15528042-5	2004	More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	nitric oxide synthase 2	Homo sapiens	22-26
15528042-5	2004	More importantly, the iNOS protein levels were equalized by the MG132 posttreatment in macrophages treated with LPS/IFN alone and along with FSK, and ubiquitinated iNOS protein levels were reduced by FSK posttreatment, suggesting that the FSK-mediated inhibition of ubiquitination of iNOS protein and the following increased stability of iNOS protein are one of the mechanisms of cAMP-pathway-mediated enhancement of iNOS gene expression in macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	interferon alpha 1	Homo sapiens	116-119
15282190-9	2004	LPS stimulated the expression of an NF-kappabeta reporter plasmid, and this was inhibited by the proteasomal inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-125	toll-like receptor 4	Mus musculus	0-3
15329330-8	2004	The 26 S proteasome inhibitor, MG-132, selectively abrogated IL-1beta-driven NFkappaB activation and COX-2 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	interleukin 1 beta	Homo sapiens	61-69
15329330-8	2004	The 26 S proteasome inhibitor, MG-132, selectively abrogated IL-1beta-driven NFkappaB activation and COX-2 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	nuclear factor kappa B subunit 1	Homo sapiens	77-85
15329330-8	2004	The 26 S proteasome inhibitor, MG-132, selectively abrogated IL-1beta-driven NFkappaB activation and COX-2 mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	101-106
15347661-6	2004	The proteasome inhibitors MG132 and lactacystin abolished the PKA-mediated degradation of GRIP1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	glutamate receptor interacting protein 1	Mus musculus	90-95
15390118-7	2004	TNF induced a time-dependent degradation of IkappaB-alpha in microglial cells that was reverted by two inhibitors of nuclear factor kappaB activation, N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and N-CBZ-Leu-Leu-Leu-al (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	228-233	tumor necrosis factor-like	Rattus norvegicus	0-3
15390118-7	2004	TNF induced a time-dependent degradation of IkappaB-alpha in microglial cells that was reverted by two inhibitors of nuclear factor kappaB activation, N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and N-CBZ-Leu-Leu-Leu-al (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	228-233	NFKB inhibitor alpha	Rattus norvegicus	44-57
15492836-3	2004	Addition of MG132 or lactacystin, 1 h prior to the addition of the CDK-inhibitor roscovitine to the cell cultures inhibited apoptosis significantly, as measured by PS exposure, cytokeratin 18 cleavage and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	keratin 18	Homo sapiens	177-191
15492836-3	2004	Addition of MG132 or lactacystin, 1 h prior to the addition of the CDK-inhibitor roscovitine to the cell cultures inhibited apoptosis significantly, as measured by PS exposure, cytokeratin 18 cleavage and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-17	caspase 3	Homo sapiens	205-214
15492836-5	2004	In addition we found that MG132 and lactacystin prevent release of cytochrome c from the mitochondrion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	cytochrome c, somatic	Homo sapiens	67-79
15473924-9	2004	Expression of cyclin-dependent kinase inhibitor p21waf/cip1 up-regulated after treated with MG132 for 3 h, but no p53 or p27 detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	cyclin dependent kinase inhibitor 1A	Homo sapiens	55-59
15304498-5	2004	Treatment with MG-132, a proteasome inhibitor, causes time-dependent increased ASBT levels and increased intracellular accumulation of ASBT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	solute carrier family 10 member 2	Homo sapiens	79-83
15304498-5	2004	Treatment with MG-132, a proteasome inhibitor, causes time-dependent increased ASBT levels and increased intracellular accumulation of ASBT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	solute carrier family 10 member 2	Homo sapiens	135-139
15351720-4	2004	NF-kappaB blocking agents (MG-132, PGA1) prevented elastase-induced TNF-alpha secretion from THP-1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	nuclear factor kappa B subunit 1	Homo sapiens	0-9
15351720-4	2004	NF-kappaB blocking agents (MG-132, PGA1) prevented elastase-induced TNF-alpha secretion from THP-1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	tumor necrosis factor	Homo sapiens	68-77
15351720-4	2004	NF-kappaB blocking agents (MG-132, PGA1) prevented elastase-induced TNF-alpha secretion from THP-1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-33	GLI family zinc finger 2	Homo sapiens	93-98
15473924-11	2004	The obvious up-regulation of p21 indicated that it is p21(waf/cip1), but not p53 or p53-related proteins,that involved in the regulation of G(2)/M arrest and subsequent apoptosis induced by MG132 in HL-60 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	cyclin dependent kinase inhibitor 1A	Homo sapiens	29-32
15473924-11	2004	The obvious up-regulation of p21 indicated that it is p21(waf/cip1), but not p53 or p53-related proteins,that involved in the regulation of G(2)/M arrest and subsequent apoptosis induced by MG132 in HL-60 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	cyclin dependent kinase inhibitor 1A	Homo sapiens	54-57
15473924-11	2004	The obvious up-regulation of p21 indicated that it is p21(waf/cip1), but not p53 or p53-related proteins,that involved in the regulation of G(2)/M arrest and subsequent apoptosis induced by MG132 in HL-60 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	cyclin dependent kinase inhibitor 1A	Homo sapiens	62-66
15247282-5	2004	The down-regulation of cyclin D1 protein was suppressed by a proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	cyclin D1	Homo sapiens	23-32
15175222-6	2004	Monolayers pretreated with NF-kappaB inhibitors (MG-132, lactacystin) were protected against oxidation, showing decreases in all measures of the NF-kappaB --&gt; iNOS --&gt; NO pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	nuclear factor kappa B subunit 1	Homo sapiens	27-36
15175222-6	2004	Monolayers pretreated with NF-kappaB inhibitors (MG-132, lactacystin) were protected against oxidation, showing decreases in all measures of the NF-kappaB --&gt; iNOS --&gt; NO pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	nuclear factor kappa B subunit 1	Homo sapiens	145-154
15175222-6	2004	Monolayers pretreated with NF-kappaB inhibitors (MG-132, lactacystin) were protected against oxidation, showing decreases in all measures of the NF-kappaB --&gt; iNOS --&gt; NO pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	nitric oxide synthase 2	Homo sapiens	162-166
15504253-7	2004	Treatments with NF-kappaB inhibitors, such as LLnL, MG132, and SN50, significantly increased the sensitivity of glioma cells to TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	TNF superfamily member 10	Homo sapiens	128-133
15385644-10	2004	Cotreatment with N-benzoyloxycarbonyl-(Z)-Leu-Leu-leucinal (MG132) but not leptomycin B suppressed AhR loss.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	aryl hydrocarbon receptor	Homo sapiens	99-102
15355857-8	2004	Also, the proteasomal inhibitors lactacystin and MG132 partially restored MKP-1 protein levels in GK diabetic VSMCs and inhibited their migration.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	dual specificity phosphatase 1	Rattus norvegicus	74-79
15327787-8	2004	The expression of cyclin B1 and the phosphorylation of MAPK/p90rsk could still be detected in ALLN or MG-132-treated oocytes even at 8 h after parthenogenetic activation or insemination, which may account for the inhibition of PB2 emission and pronuclear formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	cyclin B1	Mus musculus	18-27
15327787-8	2004	The expression of cyclin B1 and the phosphorylation of MAPK/p90rsk could still be detected in ALLN or MG-132-treated oocytes even at 8 h after parthenogenetic activation or insemination, which may account for the inhibition of PB2 emission and pronuclear formation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-108	ribosomal protein S6 kinase, polypeptide 2	Mus musculus	60-66
15334669-16	2004	In addition, the positive signals of p27(kip1) were located in cytoplasm and nuclei in MG-132 group in contrast to cytoplasm staining in control group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	zinc ribbon domain containing 2	Homo sapiens	37-40
15334669-16	2004	In addition, the positive signals of p27(kip1) were located in cytoplasm and nuclei in MG-132 group in contrast to cytoplasm staining in control group.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-93	cyclin dependent kinase inhibitor 1B	Homo sapiens	41-45
15364548-3	2004	In contrast, NADPH cytochrome P450 reductase which is constitutively expressed in Tc-HeLa cells had a half-life of about 30 h. Lactacystin and other selective proteasome inhibitors including N-benzyloxycarbonyl-leucyl-leucyl-leucinal (MG132) and N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-norvalinal (MG115) significantly inhibited both CYP2E1 and CYP2B1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	235-240	cytochrome p450 oxidoreductase	Homo sapiens	13-44
15289872-9	2004	MG132 induced the phosphorylation of ERK at 4 h and thereafter persisted for 8 to 16 h. In contrast, JNK and p38 activation persisted for longer periods and remained enhanced until 24 h. The concomitant activation of effector caspases, caspase-3 and caspase-7 was observed in 786-O cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 7	Homo sapiens	250-259
15208331-14	2004	Furthermore, the inhibition of Skp-2 expression by dominant negative FAK was reversed by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	S-phase kinase associated protein 2	Rattus norvegicus	31-36
15208331-14	2004	Furthermore, the inhibition of Skp-2 expression by dominant negative FAK was reversed by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	protein tyrosine kinase 2	Rattus norvegicus	69-72
15317596-0	2004	The proteasome inhibitor, MG132, promotes the reprogramming of translation in C2C12 myoblasts and facilitates the association of hsp25 with the eIF4F complex.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	heat shock protein family B (small) member 1	Homo sapiens	129-134
15317596-0	2004	The proteasome inhibitor, MG132, promotes the reprogramming of translation in C2C12 myoblasts and facilitates the association of hsp25 with the eIF4F complex.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	144-149
15317596-5	2004	Prolonged incubation with MG132 resulted in the increased expression of heat shock protein (hsp)25, alphaB-crystallin and hsp70, with a population of hsp25 associating with the eIF4F complex in a p38 mitogen-activated protein kinase-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	heat shock protein family B (small) member 1	Homo sapiens	92-98
15317596-5	2004	Prolonged incubation with MG132 resulted in the increased expression of heat shock protein (hsp)25, alphaB-crystallin and hsp70, with a population of hsp25 associating with the eIF4F complex in a p38 mitogen-activated protein kinase-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	heat shock protein family A (Hsp70) member 4	Homo sapiens	122-127
15317596-5	2004	Prolonged incubation with MG132 resulted in the increased expression of heat shock protein (hsp)25, alphaB-crystallin and hsp70, with a population of hsp25 associating with the eIF4F complex in a p38 mitogen-activated protein kinase-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	heat shock protein family B (small) member 1	Homo sapiens	150-155
15317596-5	2004	Prolonged incubation with MG132 resulted in the increased expression of heat shock protein (hsp)25, alphaB-crystallin and hsp70, with a population of hsp25 associating with the eIF4F complex in a p38 mitogen-activated protein kinase-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	177-182
15317596-7	2004	Although MG132 had little effect on the colocalization of eIF4E and eIF4GI, it promoted the SB203580-sensitive association of eIF4GI and hsp25, an effect not observed with alphaB-crystallin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	126-132
15317596-7	2004	Although MG132 had little effect on the colocalization of eIF4E and eIF4GI, it promoted the SB203580-sensitive association of eIF4GI and hsp25, an effect not observed with alphaB-crystallin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	heat shock protein family B (small) member 1	Homo sapiens	137-142
15289872-9	2004	MG132 induced the phosphorylation of ERK at 4 h and thereafter persisted for 8 to 16 h. In contrast, JNK and p38 activation persisted for longer periods and remained enhanced until 24 h. The concomitant activation of effector caspases, caspase-3 and caspase-7 was observed in 786-O cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	236-245
15289872-11	2004	The persistence of JNK and p38 activation may therefore be a unique mechanism underlying MG132 induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	mitogen-activated protein kinase 8	Homo sapiens	19-22
15289872-11	2004	The persistence of JNK and p38 activation may therefore be a unique mechanism underlying MG132 induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	mitogen-activated protein kinase 14	Homo sapiens	27-30
15229225-6	2004	MG-132, a proteasome inhibitor, stabilized the expression of NPDC-1 and allowed detection of ubiquitinated NPDC-1 in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	neural proliferation, differentiation and control 1	Homo sapiens	61-67
15229225-6	2004	MG-132, a proteasome inhibitor, stabilized the expression of NPDC-1 and allowed detection of ubiquitinated NPDC-1 in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	neural proliferation, differentiation and control 1	Homo sapiens	107-113
15276073-2	2004	Viability loss and decrease in GSH contents in small cell lung cancer (SCLC) cells treated with MG132 was attenuated by caspase inhibitors (z-IETD.fmk, z-LEHD.fmk and z-DQMD.fmk).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	caspase 8	Homo sapiens	120-127
15276073-4	2004	Antioxidants, including N-acetylcysteine, inhibited the MG132-induced nuclear damage, loss in mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	cytochrome c, somatic	Homo sapiens	159-171
15276073-4	2004	Antioxidants, including N-acetylcysteine, inhibited the MG132-induced nuclear damage, loss in mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	caspase 3	Homo sapiens	176-185
15276073-7	2004	The results suggest that the toxicity of MG132 on SCLC cells is mediated by activation of caspase-8, -9 and -3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	caspase 8	Homo sapiens	90-110
15136564-6	2004	The proteasomal inhibitor MG132 and Proteasome Inhibitor I extended the time course of c-Fos protein elevation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-92
15166223-3	2004	We demonstrate here that treatment with the 26 S proteosome inhibitors, MG132 and ALLN, leads to detection of ubiquitinated HDAC7 and causes accumulation of cytoplasmic HDAC7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	histone deacetylase 7	Homo sapiens	124-129
15166223-3	2004	We demonstrate here that treatment with the 26 S proteosome inhibitors, MG132 and ALLN, leads to detection of ubiquitinated HDAC7 and causes accumulation of cytoplasmic HDAC7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	histone deacetylase 7	Homo sapiens	169-174
15136564-8	2004	Interestingly, treating the whole cell lysates with PP2A, but not calcineurin (i.e. PP2B), resulted in disappearance of c-Fos protein and MG132 was able to prevent this loss.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	protein phosphatase 2 phosphatase activator	Homo sapiens	52-56
15240151-7	2004	Importantly, IL-1beta-induced HBD-2 mRNA expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including pyrrolidine dithiocarbamate and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	interleukin 1 beta	Homo sapiens	13-21
15265881-5	2004	The NF-kappa B inhibitors MG132 and pyrrolidinedithiocarbamate efficiently inhibited the induction of IRF-7 by HSV or LPS, and also down-regulated the constitutive expression of IRF-7 in PDC and blocked the HSV-induced production of IFN-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	nuclear factor kappa B subunit 1	Homo sapiens	4-14
15265881-5	2004	The NF-kappa B inhibitors MG132 and pyrrolidinedithiocarbamate efficiently inhibited the induction of IRF-7 by HSV or LPS, and also down-regulated the constitutive expression of IRF-7 in PDC and blocked the HSV-induced production of IFN-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	interferon regulatory factor 7	Homo sapiens	102-107
15265881-5	2004	The NF-kappa B inhibitors MG132 and pyrrolidinedithiocarbamate efficiently inhibited the induction of IRF-7 by HSV or LPS, and also down-regulated the constitutive expression of IRF-7 in PDC and blocked the HSV-induced production of IFN-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	interferon regulatory factor 7	Homo sapiens	178-183
15265881-5	2004	The NF-kappa B inhibitors MG132 and pyrrolidinedithiocarbamate efficiently inhibited the induction of IRF-7 by HSV or LPS, and also down-regulated the constitutive expression of IRF-7 in PDC and blocked the HSV-induced production of IFN-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	interferon alpha 1	Homo sapiens	233-242
15280488-1	2004	The Sendai virus C protein acts to dismantle the interferon-induced cellular antiviral state in an MG132-sensitive manner, in part by inducing STAT1 instability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	signal transducer and activator of transcription 1	Homo sapiens	143-148
15299081-7	2004	In an attempt to reverse NF-kappaB activity, cells were treated either with vehicle alone (DMSO) or with a proteasome inhibitor Z-Leu-Leu-Leu-H (MG132; 10 micromol/L for 2 hours prior to irradiation) that inhibited both constitutive and radiation-induced NF-kappaB activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-143	nuclear factor kappa B subunit 1	Homo sapiens	25-34
15270727-4	2004	GFP-TRP-2 expressed in COS-7 cells was rapidly degradated in vitro and the degradation was almost completely prevented by adding a proteasome inhibitor, MG-132, in the culture.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-159	tRNA proline 2	Mus musculus	4-9
15240151-7	2004	Importantly, IL-1beta-induced HBD-2 mRNA expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including pyrrolidine dithiocarbamate and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	defensin beta 4A	Homo sapiens	30-35
15240151-7	2004	Importantly, IL-1beta-induced HBD-2 mRNA expression was inhibited by blockage of NF-kappaB activation using NF-kappaB inhibitors, including pyrrolidine dithiocarbamate and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	nuclear factor kappa B subunit 1	Homo sapiens	81-90
15469741-6	2004	Inhibitors of NF-kappaB activation, such as PDTC and MG132, suppressed the gamma-IR-mediated CD23 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	nuclear factor kappa B subunit 1	Homo sapiens	14-23
15218360-12	2004	Interestingly, MG-132 alone produced an ER-independent increase of PgR expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-21	progesterone receptor	Homo sapiens	67-70
15469741-6	2004	Inhibitors of NF-kappaB activation, such as PDTC and MG132, suppressed the gamma-IR-mediated CD23 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	Fc epsilon receptor II	Homo sapiens	93-97
15219840-5	2004	We then found that M26I and L166P, both of which are derived from homozygous mutations of the DJ-1 gene, were unstable and that their stabilities were recovered, in part, in the presence of proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	212-217	Parkinsonism associated deglycase	Homo sapiens	94-98
15184053-7	2004	Intriguingly, the proteasome-mediated proteolysis is responsible for 14-3-3sigma reduction in DU145 and PC3 cells, as 14-3-3sigma protein expression was increased by treatment with a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	204-209	stratifin	Homo sapiens	69-80
15184053-7	2004	Intriguingly, the proteasome-mediated proteolysis is responsible for 14-3-3sigma reduction in DU145 and PC3 cells, as 14-3-3sigma protein expression was increased by treatment with a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	204-209	chromobox 8	Homo sapiens	104-107
15184053-7	2004	Intriguingly, the proteasome-mediated proteolysis is responsible for 14-3-3sigma reduction in DU145 and PC3 cells, as 14-3-3sigma protein expression was increased by treatment with a proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	204-209	stratifin	Homo sapiens	118-129
15102855-7	2004	Treatment with MG132, a proteasome inhibitor, inhibited the degradation of Cdt1 and resulted in the accumulation of the phosphorylated form of Cdt1 after UV treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	chromatin licensing and DNA replication factor 1	Homo sapiens	75-79
15211107-8	2004	However, in the presence of MG132 or IkappaBalphaM, which blocks the nuclear localization of NF-kappaB, both were significantly suppressed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	nuclear factor kappa B subunit 1	Homo sapiens	93-102
15158159-4	2004	To study the role of p62 in the formation of protein aggregates in PC12 cells, we monitored the intracellular localizations of p62 and ubiquitinated proteins and the levels of both components during treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	21-24
15158159-7	2004	After the treatment of the cells with MG132, we found that the expression level of p62 increased due to the transcriptional activation of the gene and that higher molecular sizes of p62, corresponding to mono- and di-ubiquitinated formes, were also formed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	83-86
15123628-4	2004	Consistently, the half-life of the protein decreased from 2.3 to 1.9 h. The proteasome inhibitors MG132 and lactacystin prevented the loss of Cx43 induced by high glucose and extended Cx43 half-life.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	gap junction protein alpha 1	Bos taurus	142-146
15102855-7	2004	Treatment with MG132, a proteasome inhibitor, inhibited the degradation of Cdt1 and resulted in the accumulation of the phosphorylated form of Cdt1 after UV treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	chromatin licensing and DNA replication factor 1	Homo sapiens	143-147
15123628-4	2004	Consistently, the half-life of the protein decreased from 2.3 to 1.9 h. The proteasome inhibitors MG132 and lactacystin prevented the loss of Cx43 induced by high glucose and extended Cx43 half-life.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	gap junction protein alpha 1	Bos taurus	184-188
15158159-7	2004	After the treatment of the cells with MG132, we found that the expression level of p62 increased due to the transcriptional activation of the gene and that higher molecular sizes of p62, corresponding to mono- and di-ubiquitinated formes, were also formed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	182-185
15158159-8	2004	Both the transcriptional inhibitor actinomycin D and an antisense oligonucleotide of p62 inhibited the MG132-mediated increase of p62, the sequestration of ubiquitinated proteins, and the enlargement of the aggregates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	85-88
15060076-6	2004	First, we show that proteasome inhibition by MG132 induces an increase in VEGF-R2 amount, and that VEGF-R2 is ubiquitinated in response to VEGF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	kinase insert domain receptor	Homo sapiens	74-81
15158159-8	2004	Both the transcriptional inhibitor actinomycin D and an antisense oligonucleotide of p62 inhibited the MG132-mediated increase of p62, the sequestration of ubiquitinated proteins, and the enlargement of the aggregates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	130-133
15060076-6	2004	First, we show that proteasome inhibition by MG132 induces an increase in VEGF-R2 amount, and that VEGF-R2 is ubiquitinated in response to VEGF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	vascular endothelial growth factor A	Homo sapiens	74-78
15147952-7	2004	However, MG132-induced repression of E2F1 and E2F2 is not associated with ROS generation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	E2F transcription factor 1	Homo sapiens	37-41
15018608-7	2004	Furthermore, treatment of mIMCD3 cells with MAPK (mitogen-activated protein kinase) inhibitors (SB203580, PD98059, U0126 and SP600125) and a proteasome inhibitor (MG132) suppressed the increase in Osp94 gene expression caused by hypertonic NaCl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	heat shock protein 4 like	Mus musculus	197-202
15147952-4	2004	Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	tumor protein p53	Homo sapiens	82-85
15122333-3	2004	Inhibition of the proteasome complex with MG-132 increased p21 protein levels in TGCT cells but much more in A2780 cells, whereas cisplatin had no additional effect on p21 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	H3 histone pseudogene 16	Homo sapiens	59-62
15205349-6	2004	The decrease in DHFR protein was abolished when the cells were treated with the proteasome inhibitor MG132, demonstrating that p14(ARF) augments proteasomal degradation of the protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	dihydrofolate reductase	Homo sapiens	16-20
15205349-6	2004	The decrease in DHFR protein was abolished when the cells were treated with the proteasome inhibitor MG132, demonstrating that p14(ARF) augments proteasomal degradation of the protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	cyclin dependent kinase inhibitor 2A	Homo sapiens	127-130
15147952-4	2004	Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	H3 histone pseudogene 16	Homo sapiens	106-109
15147952-7	2004	However, MG132-induced repression of E2F1 and E2F2 is not associated with ROS generation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	E2F transcription factor 2	Homo sapiens	46-50
15147952-4	2004	Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	interferon alpha inducible protein 27	Homo sapiens	114-117
15147952-4	2004	Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	cyclin A2	Homo sapiens	123-131
15044435-12	2004	The curcumin-dependent suppression of C/EBP factor level is inhibited by treatment with the proteasome inhibitor MG132, suggesting that the proteasome function is required for curcumin action.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	CCAAT enhancer binding protein alpha	Homo sapiens	38-43
15147830-7	2004	BAY11-7082, an inhibitor of nuclear factor kappaB (NF-kappaB) activation, and MG132, a 26S proteasome inhibitor, reduced the TPA-induced ICAM-1 expression but not the IFN-gamma-induced one.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	intercellular adhesion molecule 1	Homo sapiens	137-143
15155840-8	2004	Immunoprecipitation and immunoblot analyses showed that C2 decreased the level of ubiquitinated HNF1, which was reversed by treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	complement C2	Rattus norvegicus	56-58
14993243-4	2004	We found that proteasome inhibitors MG132 and lactacystin blocked the degradation of the LDLR mutants, but not that of the wild-type LDLR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	low-density lipoprotein receptor	Cricetulus griseus	89-93
14978197-7	2004	When SP600125 was added simultaneously, MG132 completely inhibited TNF-alpha-induced CCL2/MCP-1 production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	tumor necrosis factor	Rattus norvegicus	67-76
14978197-7	2004	When SP600125 was added simultaneously, MG132 completely inhibited TNF-alpha-induced CCL2/MCP-1 production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	C-C motif chemokine ligand 2	Rattus norvegicus	85-89
14978197-7	2004	When SP600125 was added simultaneously, MG132 completely inhibited TNF-alpha-induced CCL2/MCP-1 production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	C-C motif chemokine ligand 2	Rattus norvegicus	90-95
14726307-7	2004	Functional impact of NF-kappa B activation was determined by blocking the proteasome activity with MG132 or by preventing IKK activity with a dominant-negative IKK beta delivered by adenoviral dominant-negative (dn) IKK beta (Ad5dnIKK beta).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear factor kappa B subunit 1	Homo sapiens	21-31
15173011-8	2004	Additionally, resistant cells displayed heightened sensitivity to the proteasome inhibitor MG132, which induced p27(kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	dynactin subunit 6	Homo sapiens	112-115
15173011-8	2004	Additionally, resistant cells displayed heightened sensitivity to the proteasome inhibitor MG132, which induced p27(kip1) expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	cyclin dependent kinase inhibitor 1B	Homo sapiens	116-120
14978197-6	2004	The NF-kappaB inhibitor carbobenzoxy-l-leucyl-l-leucyl-l-leucinal (MG132) attenuated TNF-alpha-induced CCL2/MCP-1 production in the presence of increased phospho-JNK and phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	tumor necrosis factor	Rattus norvegicus	85-94
14978197-6	2004	The NF-kappaB inhibitor carbobenzoxy-l-leucyl-l-leucyl-l-leucinal (MG132) attenuated TNF-alpha-induced CCL2/MCP-1 production in the presence of increased phospho-JNK and phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	C-C motif chemokine ligand 2	Rattus norvegicus	103-107
14978197-6	2004	The NF-kappaB inhibitor carbobenzoxy-l-leucyl-l-leucyl-l-leucinal (MG132) attenuated TNF-alpha-induced CCL2/MCP-1 production in the presence of increased phospho-JNK and phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	C-C motif chemokine ligand 2	Rattus norvegicus	108-113
14978197-6	2004	The NF-kappaB inhibitor carbobenzoxy-l-leucyl-l-leucyl-l-leucinal (MG132) attenuated TNF-alpha-induced CCL2/MCP-1 production in the presence of increased phospho-JNK and phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	mitogen-activated protein kinase 8	Rattus norvegicus	162-165
15163746-3	2004	In this study, we showed that in contrast to herpes simplex virus type 1 (HSV-1) IE110 (ICP0), the loss of sumoylated forms of PML by cotransfected IE1 was resistant to the proteasome inhibitor MG132 and that IE1 did not reduce the level of unmodified PML.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	194-199	PML nuclear body scaffold	Homo sapiens	127-130
15155840-8	2004	Immunoprecipitation and immunoblot analyses showed that C2 decreased the level of ubiquitinated HNF1, which was reversed by treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	HNF1 homeobox A	Rattus norvegicus	96-100
14731112-3	2004	In the present study, we found a novel action of proteasome inhibitors MG132 and MG262 on HO-1 induction, and characterized the underlying mechanisms.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	heme oxygenase 1	Homo sapiens	90-94
14731112-4	2004	MG132 (&gt; or =0.1 microM) treatment resulted in a marked time- and concentration-dependent induction of the steady-state level of HO-1 mRNA in RAW264.7 macrophages, followed by a corresponding increase in HO-1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heme oxygenase 1	Homo sapiens	132-136
14731112-9	2004	The half-life of HO-1 protein was prolonged by MG132, indicating that the upregulation of HO-1 by proteasome inhibitor is partially attributable to the inhibition of protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	heme oxygenase 1	Homo sapiens	90-94
14731112-4	2004	MG132 (&gt; or =0.1 microM) treatment resulted in a marked time- and concentration-dependent induction of the steady-state level of HO-1 mRNA in RAW264.7 macrophages, followed by a corresponding increase in HO-1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heme oxygenase 1	Homo sapiens	207-211
14731112-10	2004	MG132 can ablate IkappaBalpha degradation and NF-kappaB (nuclear factor kappaB) activation induced by lipopolysaccharide, similar to the effect of another NF-kappaB inhibitor pyrrolidine dithiocarbamate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	NFKB inhibitor alpha	Homo sapiens	17-29
14731112-5	2004	Actinomycin D and cycloheximide inhibited MG132-responsive HO-1 protein expression, indicating a requirement for transcription and de novo protein synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	heme oxygenase 1	Homo sapiens	59-63
14731112-10	2004	MG132 can ablate IkappaBalpha degradation and NF-kappaB (nuclear factor kappaB) activation induced by lipopolysaccharide, similar to the effect of another NF-kappaB inhibitor pyrrolidine dithiocarbamate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	46-55
14731112-10	2004	MG132 can ablate IkappaBalpha degradation and NF-kappaB (nuclear factor kappaB) activation induced by lipopolysaccharide, similar to the effect of another NF-kappaB inhibitor pyrrolidine dithiocarbamate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	57-78
14731112-6	2004	The involvement of signal pathways in MG132-induced HO-1 gene expression was examined using chemical inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	heme oxygenase 1	Homo sapiens	52-56
14731112-10	2004	MG132 can ablate IkappaBalpha degradation and NF-kappaB (nuclear factor kappaB) activation induced by lipopolysaccharide, similar to the effect of another NF-kappaB inhibitor pyrrolidine dithiocarbamate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	155-164
14731112-7	2004	Antioxidant N -acetylcysteine and SB203580, an antioxidant and inhibitor of p38 MAPK (mitogen-activated protein kinase), abolished MG132-inducible HO-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	mitogen-activated protein kinase 14	Homo sapiens	76-79
14731112-11	2004	We found HO-1 upregulation by MG132 and pyrrolidine dithiocarbamate is unrelated to their inhibition of NF-kappaB, since leptomycin B, another NF-kappaB inhibitor, did not elicit similar induction of HO-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-35	heme oxygenase 1	Homo sapiens	9-13
14731112-7	2004	Antioxidant N -acetylcysteine and SB203580, an antioxidant and inhibitor of p38 MAPK (mitogen-activated protein kinase), abolished MG132-inducible HO-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	heme oxygenase 1	Homo sapiens	147-151
14731112-8	2004	Furthermore, MG132 activated the p38 MAPK pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	mitogen-activated protein kinase 14	Homo sapiens	33-36
14731112-9	2004	The half-life of HO-1 protein was prolonged by MG132, indicating that the upregulation of HO-1 by proteasome inhibitor is partially attributable to the inhibition of protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	heme oxygenase 1	Homo sapiens	17-21
15102941-13	2004	Moreover, ECs either over-expressed ATF3 or, when treated with an ATF3 activator (MG-132; carbobenzoxy-l-leucyl-l-leucyl-l-leucinal), resulted in a repression of MMP-2 promoter activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	activating transcription factor 3	Homo sapiens	36-40
15102941-13	2004	Moreover, ECs either over-expressed ATF3 or, when treated with an ATF3 activator (MG-132; carbobenzoxy-l-leucyl-l-leucyl-l-leucinal), resulted in a repression of MMP-2 promoter activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	activating transcription factor 3	Homo sapiens	66-70
15102941-13	2004	Moreover, ECs either over-expressed ATF3 or, when treated with an ATF3 activator (MG-132; carbobenzoxy-l-leucyl-l-leucyl-l-leucinal), resulted in a repression of MMP-2 promoter activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-88	matrix metallopeptidase 2	Homo sapiens	162-167
15020231-6	2004	Catalase-induced COX-2 expression was abrogated by treatment of MG-132 (a NF-kappaB inhibitor) or LY294002 (a PI3K inhibitor), but not by treatment of PD98059 (an ERK inhibitor), SB203580 (a p38 inhibitor), or SP600125 (a JNK inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	catalase	Homo sapiens	0-8
15067380-0	2004	Induction of apoptosis by the proteasome inhibitor MG132 in human HCC cells: Possible correlation with specific caspase-dependent cleavage of beta-catenin and inhibition of beta-catenin-mediated transactivation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	catenin beta 1	Homo sapiens	142-154
15067380-0	2004	Induction of apoptosis by the proteasome inhibitor MG132 in human HCC cells: Possible correlation with specific caspase-dependent cleavage of beta-catenin and inhibition of beta-catenin-mediated transactivation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	catenin beta 1	Homo sapiens	173-185
15067380-8	2004	Analyses through the reporter plasmid pTOPflash showed that MG132 significantly reduces Tcf transcriptional activity in the cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	hepatocyte nuclear factor 4 alpha	Homo sapiens	88-91
15125768-6	2004	In both sucrose-starved and exponentially growing cells, CYCD3;1 protein abundance increases in response to treatment with MG132 (carbobenzoxyl-leucinyl-leucinyl-leucinal), a reversible proteasome inhibitor, but not in response to the cysteine protease inhibitor E-64 or the calpain inhibitor ALLN (N-acetyl-leucyl-leucyl-norleucinal).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	CYCLIN D3;1	Arabidopsis thaliana	57-62
15125768-7	2004	The increase on MG132 treatment is because of de novo protein synthesis coupled with the blocking of CYCD3;1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	CYCLIN D3;1	Arabidopsis thaliana	101-106
15125768-8	2004	Longer MG132 treatment leads to C-terminal cleavage of CYCD3;1, accumulation of a hyperphosphorylated form and its subsequent disappearance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	7-12	CYCLIN D3;1	Arabidopsis thaliana	55-62
15020231-6	2004	Catalase-induced COX-2 expression was abrogated by treatment of MG-132 (a NF-kappaB inhibitor) or LY294002 (a PI3K inhibitor), but not by treatment of PD98059 (an ERK inhibitor), SB203580 (a p38 inhibitor), or SP600125 (a JNK inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	17-22
15020231-6	2004	Catalase-induced COX-2 expression was abrogated by treatment of MG-132 (a NF-kappaB inhibitor) or LY294002 (a PI3K inhibitor), but not by treatment of PD98059 (an ERK inhibitor), SB203580 (a p38 inhibitor), or SP600125 (a JNK inhibitor).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	nuclear factor kappa B subunit 1	Homo sapiens	74-83
15010833-5	2004	MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	94-97
15023536-8	2004	The mammalian counterpart mouse HSF2 (mHSF2) also exhibited changes in intracellular distribution upon MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	heat shock factor 2	Mus musculus	32-36
15023536-8	2004	The mammalian counterpart mouse HSF2 (mHSF2) also exhibited changes in intracellular distribution upon MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	heat shock factor 2	Mus musculus	38-43
15010833-5	2004	MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin A2	Homo sapiens	199-207
15010833-5	2004	MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1A	Homo sapiens	212-215
15010833-5	2004	MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	130-133
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	151-154
15035668-9	2004	Accordingly, the proteosome inhibitor, MG132 [5 microM], blocked RAR degradation, quelled RAR trans-activation and enhanced RAR trans-repression of NFkappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	retinoic acid receptor, alpha	Mus musculus	65-68
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cyclin dependent kinase inhibitor 1A	Homo sapiens	159-162
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	tumor protein p53	Homo sapiens	100-103
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	tumor protein p53	Homo sapiens	100-103
15118249-7	2004	Furthermore, when ESC were incubated with MG132 (3 microM), which inhibits NF-kappaB activation, during EP-withdrawal, MG132 blocked the increases in PGF2alpha production and COX-2 mRNA expression caused by EP-withdrawal.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	prostaglandin-endoperoxide synthase 2	Homo sapiens	175-180
15118249-7	2004	Furthermore, when ESC were incubated with MG132 (3 microM), which inhibits NF-kappaB activation, during EP-withdrawal, MG132 blocked the increases in PGF2alpha production and COX-2 mRNA expression caused by EP-withdrawal.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	prostaglandin-endoperoxide synthase 2	Homo sapiens	175-180
14691451-5	2004	Here, we report that proteasome inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -deficient HCT116 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	TNF receptor superfamily member 10b	Homo sapiens	72-88
14691451-5	2004	Here, we report that proteasome inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -deficient HCT116 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	BCL2 associated X, apoptosis regulator	Homo sapiens	108-111
14691451-6	2004	MG132 effectively cooperated with Apo2L/TRAIL to induce apoptosis in both Bax-proficient and -deficient cells that was coupled with caspases-8 and -3 activation and Bid cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BCL2 associated X, apoptosis regulator	Homo sapiens	74-77
14691451-6	2004	MG132 effectively cooperated with Apo2L/TRAIL to induce apoptosis in both Bax-proficient and -deficient cells that was coupled with caspases-8 and -3 activation and Bid cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 8	Homo sapiens	132-149
14691451-6	2004	MG132 effectively cooperated with Apo2L/TRAIL to induce apoptosis in both Bax-proficient and -deficient cells that was coupled with caspases-8 and -3 activation and Bid cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	BH3 interacting domain death agonist	Homo sapiens	165-168
14691451-8	2004	These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	TNF receptor superfamily member 10b	Homo sapiens	133-136
14691451-8	2004	These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	TNF superfamily member 10	Homo sapiens	171-176
14691451-8	2004	These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	BCL2 associated X, apoptosis regulator	Homo sapiens	189-192
14691451-8	2004	These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	TNF superfamily member 10	Homo sapiens	226-231
14691451-8	2004	These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	TNF superfamily member 10	Homo sapiens	232-237
14691451-0	2004	Proteasome inhibitor MG132 upregulates death receptor 5 and cooperates with Apo2L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF receptor superfamily member 10b	Homo sapiens	39-55
14691451-0	2004	Proteasome inhibitor MG132 upregulates death receptor 5 and cooperates with Apo2L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF superfamily member 10	Homo sapiens	76-81
14691451-0	2004	Proteasome inhibitor MG132 upregulates death receptor 5 and cooperates with Apo2L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF superfamily member 10	Homo sapiens	82-87
14691451-0	2004	Proteasome inhibitor MG132 upregulates death receptor 5 and cooperates with Apo2L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	BCL2 associated X, apoptosis regulator	Homo sapiens	111-114
14691451-5	2004	Here, we report that proteasome inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -deficient HCT116 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	TNF superfamily member 10	Homo sapiens	60-65
14691451-5	2004	Here, we report that proteasome inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -deficient HCT116 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	TNF superfamily member 10	Homo sapiens	66-71
15035668-9	2004	Accordingly, the proteosome inhibitor, MG132 [5 microM], blocked RAR degradation, quelled RAR trans-activation and enhanced RAR trans-repression of NFkappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	retinoic acid receptor, alpha	Mus musculus	90-93
15035668-9	2004	Accordingly, the proteosome inhibitor, MG132 [5 microM], blocked RAR degradation, quelled RAR trans-activation and enhanced RAR trans-repression of NFkappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	retinoic acid receptor, alpha	Mus musculus	90-93
15035668-9	2004	Accordingly, the proteosome inhibitor, MG132 [5 microM], blocked RAR degradation, quelled RAR trans-activation and enhanced RAR trans-repression of NFkappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	148-156
15036402-2	2004	The transient exposure to the specific and reversible proteasome inhibitor MG132 during a mild heat shock induced late passage HDF to synthesize and accumulate high levels of HSP72.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	heat shock protein family A (Hsp70) member 1A	Homo sapiens	175-180
15036402-4	2004	The level of HuR, a stabilizing mRNA-binding protein, increased following the MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	ELAV like RNA binding protein 1	Homo sapiens	13-16
14970263-8	2004	The EGF-induced destruction of Cx43 was proteasome-dependent, because the loss of Cx43 protein was counteracted by the proteasome inhibitor MG132 but not the lysosomal inhibitor leupeptin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	epidermal growth factor like 1	Rattus norvegicus	4-7
14970263-8	2004	The EGF-induced destruction of Cx43 was proteasome-dependent, because the loss of Cx43 protein was counteracted by the proteasome inhibitor MG132 but not the lysosomal inhibitor leupeptin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	gap junction protein, alpha 1	Rattus norvegicus	31-35
14970263-8	2004	The EGF-induced destruction of Cx43 was proteasome-dependent, because the loss of Cx43 protein was counteracted by the proteasome inhibitor MG132 but not the lysosomal inhibitor leupeptin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-145	gap junction protein, alpha 1	Rattus norvegicus	82-86
14607841-7	2004	Proteasomal degradation was not the major pathway of DJ-1 breakdown because treatment with the proteasome inhibitor MG-132 caused only minimal accumulation of DJ-1, even of the very unstable [L166P]DJ-1 mutant.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-122	Parkinsonism associated deglycase	Homo sapiens	159-163
14607841-7	2004	Proteasomal degradation was not the major pathway of DJ-1 breakdown because treatment with the proteasome inhibitor MG-132 caused only minimal accumulation of DJ-1, even of the very unstable [L166P]DJ-1 mutant.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-122	Parkinsonism associated deglycase	Homo sapiens	159-163
14769821-5	2004	MG132 (50-250 nmol/L) dose-dependently increased mRNA and protein levels of eNOS.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nitric oxide synthase 3	Bos taurus	76-80
15135296-6	2004	Proteasome inhibition with either lactacystin or MG-132 attenuated LPS-induced IRAK degradation, and enhanced activation of JNK/SAPK, ERK 1/2, and p38.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	interleukin 1 receptor associated kinase 1	Homo sapiens	79-83
15135296-6	2004	Proteasome inhibition with either lactacystin or MG-132 attenuated LPS-induced IRAK degradation, and enhanced activation of JNK/SAPK, ERK 1/2, and p38.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	mitogen-activated protein kinase 3	Homo sapiens	134-141
15135296-6	2004	Proteasome inhibition with either lactacystin or MG-132 attenuated LPS-induced IRAK degradation, and enhanced activation of JNK/SAPK, ERK 1/2, and p38.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	mitogen-activated protein kinase 1	Homo sapiens	147-150
14769821-9	2004	eNOS activity was increased up to 2.8-fold (MG132 100 nmol/L, 48 h).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	nitric oxide synthase 3	Bos taurus	0-4
14769821-11	2004	Single MG132 treatment (100 nmol/L) induced long-term effects in CPAE cells, with increases of eNOS protein and activity for up to 10 days.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	7-12	nitric oxide synthase 3	Bos taurus	95-99
15005272-4	2004	Shear stress-induced iNOS expression was inhibited by pyrrolidine dithiocarbamate (PDTC), an antioxidant and nuclear factor kappaB (NF-kappaB) blocker, and by MG132, an aldehyde peptide proteasome inhibitor that antagonizes I kappaB-kinase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	nitric oxide synthase 2	Homo sapiens	21-25
14700734-3	2004	The proteasome inhibitor, MG132, induced the accumulation of p53 in human dopaminergic neuroblastoma SH-SY5Y cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	tumor protein p53	Homo sapiens	61-64
29350818-7	2004	IkappaBalpha was markedly degraded at 1 h, and NF-kappaB-DNA-binding activity markedly increased 2 h after beta2 integrin aggregation, which activated IkappaB kinase activity at 1 h. beta2 Integrin-induced cytokine production was suppressed by MG132 or SN50 pretreatment, which blocked the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	NFKB inhibitor alpha	Homo sapiens	0-12
29350818-7	2004	IkappaBalpha was markedly degraded at 1 h, and NF-kappaB-DNA-binding activity markedly increased 2 h after beta2 integrin aggregation, which activated IkappaB kinase activity at 1 h. beta2 Integrin-induced cytokine production was suppressed by MG132 or SN50 pretreatment, which blocked the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	nuclear factor kappa B subunit 1	Homo sapiens	47-56
29350818-7	2004	IkappaBalpha was markedly degraded at 1 h, and NF-kappaB-DNA-binding activity markedly increased 2 h after beta2 integrin aggregation, which activated IkappaB kinase activity at 1 h. beta2 Integrin-induced cytokine production was suppressed by MG132 or SN50 pretreatment, which blocked the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	107-112
29350818-7	2004	IkappaBalpha was markedly degraded at 1 h, and NF-kappaB-DNA-binding activity markedly increased 2 h after beta2 integrin aggregation, which activated IkappaB kinase activity at 1 h. beta2 Integrin-induced cytokine production was suppressed by MG132 or SN50 pretreatment, which blocked the activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	244-249	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	183-188
14747572-3	2004	We now report that HIV-1 Vif could induce rapid degradation of human APOBEC3G that was blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	Vif	Human immunodeficiency virus 1	25-28
14747572-3	2004	We now report that HIV-1 Vif could induce rapid degradation of human APOBEC3G that was blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	69-77
14747572-7	2004	In the presence of the proteasome inhibitor MG132, virion-associated Vif increased dramatically.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	Vif	Human immunodeficiency virus 1	69-72
14573621-8	2004	H. pylori HSP60-induced IL-6 mRNA expression, and NF-kappaB activation in RAW 264.7 cells was abrogated in the presence of MG-132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	interleukin 6	Mus musculus	24-28
14712236-5	2004	Similar to the dispersal of PML NBs in response to some viral infections, PML redistribution after DNA damage was inhibited by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	PML nuclear body scaffold	Homo sapiens	28-31
14712236-5	2004	Similar to the dispersal of PML NBs in response to some viral infections, PML redistribution after DNA damage was inhibited by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	PML nuclear body scaffold	Homo sapiens	74-77
14691177-13	2004	Proteasome inhibitors MG132 and lactacystin protected the cells against IFN-gamma-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	interferon gamma	Mus musculus	72-81
14510636-6	2004	Moreover, blocking Nrf2 degradation with proteasome inhibitor MG132 increases the amount of Nrf2 and superinduces NQO1 in the presence of TCDD or tBHQ.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	nuclear factor, erythroid derived 2, like 2	Mus musculus	19-23
14510636-6	2004	Moreover, blocking Nrf2 degradation with proteasome inhibitor MG132 increases the amount of Nrf2 and superinduces NQO1 in the presence of TCDD or tBHQ.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	nuclear factor, erythroid derived 2, like 2	Mus musculus	92-96
14510636-6	2004	Moreover, blocking Nrf2 degradation with proteasome inhibitor MG132 increases the amount of Nrf2 and superinduces NQO1 in the presence of TCDD or tBHQ.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	NAD(P)H dehydrogenase, quinone 1	Mus musculus	114-118
14739600-8	2004	Both the caspase inhibitor zVAD and calpain inhibitors blocked PABP cleavage in vivo, while the proteosome inhibitor MG132 induced PABP degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	poly(A) binding protein cytoplasmic 1	Homo sapiens	131-135
15299283-0	2004	Induction of heat shock protein 70 (Hsp70) by proteasome inhibitor MG 132 protects articular chondrocytes from cellular death in vitro and in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-73	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	13-34
15299283-0	2004	Induction of heat shock protein 70 (Hsp70) by proteasome inhibitor MG 132 protects articular chondrocytes from cellular death in vitro and in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-73	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	36-41
15299283-1	2004	The aim of this work was to determine whether Hsp70 overexpression via proteasome inhibitor MG132 was able to protect chondrocytes towards mono-iodoacetate (MIA) cytotoxicity both in vitro and in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	46-51
15299283-2	2004	In vitro, overexpression of Hsp70 via MG132 was significantly able to protect chondrocytes from MIA toxicity (MTT/LDH analyses).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	28-33
15299283-4	2004	In vivo, chondrocytic overexpression of Hsp70, after a preventive intra-articular injection of MG132 in rat knee, was sufficient to decrease the severity of OA-induced MIA lesions, as demonstrated histologically and biochemically.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	40-45
14691177-14	2004	A positive control treatment with staurosporine (STP) caused increased caspase-3 activity, which was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	caspase 3	Mus musculus	71-80
15507280-9	2004	There is also indication of activation of nuclear factor kappa B (NFkappaB), increase in phosphorylation of p38MAPK in ECs by aPL antibodies that can be reversed by specific inhibitors MG132 and SB203580, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	42-64
15507280-9	2004	There is also indication of activation of nuclear factor kappa B (NFkappaB), increase in phosphorylation of p38MAPK in ECs by aPL antibodies that can be reversed by specific inhibitors MG132 and SB203580, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	66-74
15507280-9	2004	There is also indication of activation of nuclear factor kappa B (NFkappaB), increase in phosphorylation of p38MAPK in ECs by aPL antibodies that can be reversed by specific inhibitors MG132 and SB203580, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-190	mitogen-activated protein kinase 14	Mus musculus	108-115
14760889-5	2003	Here, proteasome inhibitors like MG132, PSI, II and III (MG262) have been shown to block both TNF-alpha-associated up-regulation of the HCMV IE1/2 enhancer/promoter in monocytic cells in an in vitro transient transfection system and HCMV replication in permissive embryonal fibroblasts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	olfactory receptor family 13 subfamily A member 20	Mus musculus	141-146
15033727-4	2003	Pretreatment of cells with NF-kappaB inhibitors (PDTC, MG132, or SN50) strongly enhanced CH11-induced apoptosis in HuT78 and Hut78G9 cells, while only MG132 showed a similar potentiating effect in HuT78B1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	nuclear factor kappa B subunit 1	Homo sapiens	27-36
14633995-4	2003	This decrease was reversed by the proteasome inhibitors MG132 and lactacystin, by p19(arf), and by small interfering RNA (siRNA) against MDM2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	MDM2 proto-oncogene	Homo sapiens	137-141
14527959-8	2003	Treatment with the proteasome inhibitor, MG132 or inhibitors of NF-kappa B (e.g. PDTC and gliotoxin), decreased PMA-induced up-regulation of cIAP-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	baculoviral IAP repeat containing 3	Homo sapiens	141-147
14527959-9	2003	PMA-induced NF-kappa B activation was blocked by either GF109203x, MG132, PDTC, or gliotoxin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	nuclear factor kappa B subunit 1	Homo sapiens	12-22
15033727-4	2003	Pretreatment of cells with NF-kappaB inhibitors (PDTC, MG132, or SN50) strongly enhanced CH11-induced apoptosis in HuT78 and Hut78G9 cells, while only MG132 showed a similar potentiating effect in HuT78B1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	nuclear factor kappa B subunit 1	Homo sapiens	27-36
14760889-11	2003	MG132 also reduced the immune modulatory activity of the virus by abrogating virus-induced up-regulation of cellular ICAM-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	intercellular adhesion molecule 1	Homo sapiens	117-123
14624462-8	2003	The SHP-1 accelerated degradation of JAK1 kinase in HTB26 cells was blocked with the treatment of MG132, a specific inhibitor for proteasome-mediated proteolysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	nuclear receptor subfamily 0 group B member 2	Homo sapiens	4-9
14520698-7	2003	The expression of hHb1-DeltaN protein was detectable by immunofluorescence and Western blotting in EBV-positive but not in EBV-negative NU-GC-3 clones after proteasome inhibitor (MG132) treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	179-184	histocompatibility minor HB-1	Homo sapiens	18-22
12958217-5	2003	During phase I, which normally lasts for the first approximately 2 h following import, StAR is rapidly degraded by a protease, or proteases, that can be arrested by a nonclassical action of proteasome inhibitors such as MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	220-225	steroidogenic acute regulatory protein	Homo sapiens	87-91
12958217-6	2003	StAR molecules that evade phase I are subjected to a second class of protease(s), which is slower and MG132 resistant.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-107	steroidogenic acute regulatory protein	Homo sapiens	0-4
12958217-9	2003	Degradation of C-28 StAR, probably by an intermembrane space protease, is extremely rapid and MG132 insensitive.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	steroidogenic acute regulatory protein	Homo sapiens	20-24
14605272-15	2003	This cytokine- and growth factor-stimulated CX3CL1/fractalkine expression could be abolished by the nuclear factor-kappaB inhibitors, curcumin and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	C-X3-C motif chemokine ligand 1	Rattus norvegicus	44-50
14605272-15	2003	This cytokine- and growth factor-stimulated CX3CL1/fractalkine expression could be abolished by the nuclear factor-kappaB inhibitors, curcumin and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	C-X3-C motif chemokine ligand 1	Rattus norvegicus	51-62
14581000-10	2003	We conclude that MG132 upregulates GRO-alpha expression in vascular endothelial cells, at least in part, through the activation of p38 MAPK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	C-X-C motif chemokine ligand 1	Homo sapiens	35-44
12842862-14	2003	SP-600125 and the proteasomal inhibitor MG-132 blocked LPS-induced degradation of IkappaB-alpha/epsilon and LPS-stimulated expression of IkappaB-alpha mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	toll-like receptor 4	Mus musculus	55-58
14581000-6	2003	MG132 alone increased the levels of GRO-alpha mRNA and protein; however, it did not affect the GRO-alpha mRNA induced by lipopolysaccharide (LPS) and inhibited the LPS-induced decrease in IkappaB levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	C-X-C motif chemokine ligand 1	Homo sapiens	36-45
14581000-8	2003	MG132 induced the phosphorylation of p38 MAPK, MEK and JNK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase kinase 7	Homo sapiens	47-50
14581000-8	2003	MG132 induced the phosphorylation of p38 MAPK, MEK and JNK.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen-activated protein kinase 8	Homo sapiens	55-58
14581000-9	2003	Pretreatment of the cells with SB203580, an inhibitor of p38 MAPK, suppressed the MG132-induced GRO-alpha expression, but pretreatment of the cells with U0126, PD98059 or SP600125, inhibitors of MEK1/2 or JNK, did not influence the effect of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	C-X-C motif chemokine ligand 1	Homo sapiens	96-105
14581000-9	2003	Pretreatment of the cells with SB203580, an inhibitor of p38 MAPK, suppressed the MG132-induced GRO-alpha expression, but pretreatment of the cells with U0126, PD98059 or SP600125, inhibitors of MEK1/2 or JNK, did not influence the effect of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	mitogen-activated protein kinase kinase 1	Homo sapiens	195-201
14581000-9	2003	Pretreatment of the cells with SB203580, an inhibitor of p38 MAPK, suppressed the MG132-induced GRO-alpha expression, but pretreatment of the cells with U0126, PD98059 or SP600125, inhibitors of MEK1/2 or JNK, did not influence the effect of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	mitogen-activated protein kinase 8	Homo sapiens	205-208
14596918-4	2003	The downregulation of Akt was abrogated by MG-132, a proteasome inhibitor, but not by inhibitors of calpain or cathepsins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-49	AKT serine/threonine kinase 1	Homo sapiens	22-25
12871860-4	2003	Semiquantitative RT-PCR and immunoblotting experiments demonstrate decreased COX-2 expression following treatment with the p38 MAPK inhibitor SB-203580 (25 microM) or the proteosome inhibitor MG-132 (1 microM).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-198	prostaglandin-endoperoxide synthase 2	Homo sapiens	77-82
12842862-14	2003	SP-600125 and the proteasomal inhibitor MG-132 blocked LPS-induced degradation of IkappaB-alpha/epsilon and LPS-stimulated expression of IkappaB-alpha mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	82-95
12842862-14	2003	SP-600125 and the proteasomal inhibitor MG-132 blocked LPS-induced degradation of IkappaB-alpha/epsilon and LPS-stimulated expression of IkappaB-alpha mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	toll-like receptor 4	Mus musculus	108-111
12842862-14	2003	SP-600125 and the proteasomal inhibitor MG-132 blocked LPS-induced degradation of IkappaB-alpha/epsilon and LPS-stimulated expression of IkappaB-alpha mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-46	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	137-150
14576821-9	2003	We further showed that the reducing effect of BCSG1 on BubR1 protein expression could be prevented by treating BCSG1-transfected cells with MG-132, a selective 26S proteasome inhibitor, implying that the proteasome machinery may be involved in the BCSG1-induced reduction of the BubR1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	synuclein gamma	Homo sapiens	46-51
14695066-3	2003	Blocking NF-kappaB DNA-binding activity by the proteasome inhibitor MG-132 results in decrease of C. pneumoniae-induced c-IAP2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-74	baculoviral IAP repeat containing 3	Homo sapiens	120-126
12960060-11	2003	Proteosome inhibitors MG132 and ALLnL were able to reverse AR degradation induced by prostatic lysates from adult intact and castrate rats as well as from developing and estrogenized prostates, indicating that AR degradation was mediated through the proteosome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	androgen receptor	Rattus norvegicus	59-61
12960060-11	2003	Proteosome inhibitors MG132 and ALLnL were able to reverse AR degradation induced by prostatic lysates from adult intact and castrate rats as well as from developing and estrogenized prostates, indicating that AR degradation was mediated through the proteosome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	androgen receptor	Rattus norvegicus	210-212
14572618-5	2003	In contrast, either the proteasome inhibitor carbobenzoxy-L-leucy-L-leucy-L-leucinal (MG 132) or the IkappaBalpha inhibitor BAY 11-7082 ablated TNFalpha-induced ICAM-1 gene expression and MG132 inhibited TNFalpha-induced NFkappaB complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	188-193	tumor necrosis factor	Homo sapiens	144-152
14615419-8	2003	The nuclear translocation and increased binding of NF-kappaB by lipopolysaccharide were blocked by addition of MG132, an inhibitor of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	nuclear factor kappa B subunit 1	Homo sapiens	51-60
14615419-8	2003	The nuclear translocation and increased binding of NF-kappaB by lipopolysaccharide were blocked by addition of MG132, an inhibitor of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	nuclear factor kappa B subunit 1	Homo sapiens	134-143
14576821-9	2003	We further showed that the reducing effect of BCSG1 on BubR1 protein expression could be prevented by treating BCSG1-transfected cells with MG-132, a selective 26S proteasome inhibitor, implying that the proteasome machinery may be involved in the BCSG1-induced reduction of the BubR1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	BUB1 mitotic checkpoint serine/threonine kinase B	Homo sapiens	55-60
14576821-9	2003	We further showed that the reducing effect of BCSG1 on BubR1 protein expression could be prevented by treating BCSG1-transfected cells with MG-132, a selective 26S proteasome inhibitor, implying that the proteasome machinery may be involved in the BCSG1-induced reduction of the BubR1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	synuclein gamma	Homo sapiens	111-116
14576821-9	2003	We further showed that the reducing effect of BCSG1 on BubR1 protein expression could be prevented by treating BCSG1-transfected cells with MG-132, a selective 26S proteasome inhibitor, implying that the proteasome machinery may be involved in the BCSG1-induced reduction of the BubR1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	synuclein gamma	Homo sapiens	111-116
14576821-9	2003	We further showed that the reducing effect of BCSG1 on BubR1 protein expression could be prevented by treating BCSG1-transfected cells with MG-132, a selective 26S proteasome inhibitor, implying that the proteasome machinery may be involved in the BCSG1-induced reduction of the BubR1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	BUB1 mitotic checkpoint serine/threonine kinase B	Homo sapiens	279-284
12909627-6	2003	Furthermore, the 26 S proteasome inhibitor MG132 blocks the decrease in ORC1, suggesting that the ORC1 cycle is mainly due to 26 S proteasome-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	origin recognition complex subunit 1	Homo sapiens	72-76
12909627-6	2003	Furthermore, the 26 S proteasome inhibitor MG132 blocks the decrease in ORC1, suggesting that the ORC1 cycle is mainly due to 26 S proteasome-dependent degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	origin recognition complex subunit 1	Homo sapiens	98-102
14530354-7	2003	In the same manner, agonist-specific activation of TLR4 efficiently mediated macrophage apoptosis in the presence of the proteasome inhibitor MG-132, an effect that was less pronounced for activation through TLR2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-148	toll-like receptor 4	Mus musculus	51-55
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	X-linked inhibitor of apoptosis	Homo sapiens	214-218
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	223-228
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	mitogen-activated protein kinase 8	Homo sapiens	244-247
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	alpha and gamma adaptin binding protein	Homo sapiens	252-255
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	cyclin dependent kinase 1	Homo sapiens	256-260
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	cyclin dependent kinase inhibitor 1A	Homo sapiens	292-295
14562039-4	2003	In U937 cells, synergistic interactions between MG-132 and flavopiridol were associated with multiple perturbations in expression/activation of signaling- and survival-related proteins, including downregulation of XIAP and Mcl-1, activation of JNK and p34(cdc2), and diminished expression of p21(CIP1).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-54	cyclin dependent kinase inhibitor 1A	Homo sapiens	296-300
14562039-5	2003	The lethal effects of MG-132/flavopiridol were not reduced in leukemic cells ectopically expressing Bcl-2, but were partially attenuated in cells ectopically expressing dominant-negative caspase-8 or CrmA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	caspase 8	Homo sapiens	187-196
14529614-6	2003	Treatment with the proteasome inhibitor MG132 increased endogenous Sp1 phosphorylation and its DNA-binding activity to the ARNT promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	aryl hydrocarbon receptor nuclear translocator	Mus musculus	123-127
12942543-7	2003	MCP-1 upregulation in RPE cells on plastic was attenuated by the addition of MG-132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-83	chemokine (C-C motif) ligand 2	Mus musculus	0-5
14507673-0	2003	Proteasome inhibitor (MG-132) treatment of mdx mice rescues the expression and membrane localization of dystrophin and dystrophin-associated proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	dystrophin, muscular dystrophy	Mus musculus	104-114
14507673-0	2003	Proteasome inhibitor (MG-132) treatment of mdx mice rescues the expression and membrane localization of dystrophin and dystrophin-associated proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-28	dystrophin, muscular dystrophy	Mus musculus	119-129
14507673-8	2003	By immunofluorescence and Western blot analysis, we show that administration of the proteasomal inhibitor MG-132 effectively rescues the expression levels and plasma membrane localization of dystrophin, beta-dystroglycan, alpha-dystroglycan, and alpha-sarcoglycan in skeletal muscle fibers from mdx mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	dystrophin, muscular dystrophy	Mus musculus	191-201
14507673-8	2003	By immunofluorescence and Western blot analysis, we show that administration of the proteasomal inhibitor MG-132 effectively rescues the expression levels and plasma membrane localization of dystrophin, beta-dystroglycan, alpha-dystroglycan, and alpha-sarcoglycan in skeletal muscle fibers from mdx mice.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-112	sarcoglycan, alpha (dystrophin-associated glycoprotein)	Mus musculus	246-263
12871956-9	2003	Indeed, PBX-2 level drastically decreased after 3 h of cycloheximide treatment in control but not in PREP-1-overexpressing cells and the proteasome inhibitor MG132 prevented PBX-2 decay in control cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	PBX homeobox 2	Homo sapiens	8-13
12871956-9	2003	Indeed, PBX-2 level drastically decreased after 3 h of cycloheximide treatment in control but not in PREP-1-overexpressing cells and the proteasome inhibitor MG132 prevented PBX-2 decay in control cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-163	PBX homeobox 2	Homo sapiens	174-179
14513055-2	2003	Sequential (but not simultaneous) exposure of MM.1S cells to bortezomib or MG-132 (10 h) followed by HA14-1 (8 h) resulted in a marked increase in mitochondrial injury (loss of DeltaPsim, cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), activation of procaspases-3, -8, and -9, and Bid, induction of apoptosis, and loss of clonogenicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	cytochrome c, somatic	Homo sapiens	188-200
14523089-8	2003	Incubation with MG-132 alone inhibited tau proteolysis and led to the induction of HSPs, including alphaB-crystallin and to its translocation to the perinuclear region, but did not induce the formation of thioflavin-S-positive aggregates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	microtubule associated protein tau	Homo sapiens	39-42
14513055-2	2003	Sequential (but not simultaneous) exposure of MM.1S cells to bortezomib or MG-132 (10 h) followed by HA14-1 (8 h) resulted in a marked increase in mitochondrial injury (loss of DeltaPsim, cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), activation of procaspases-3, -8, and -9, and Bid, induction of apoptosis, and loss of clonogenicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	diablo IAP-binding mitochondrial protein	Homo sapiens	202-206
12946329-7	2003	Pretreatment of the BEAS-2B cells with the NF-kappa B inhibitors pyrrolidine dithiocarbamate (PDTC), MG-132, and SN50 resulted in a marked decrease in B. pertussis-induced ICAM-1 expression, implying the involvement of NF-kappa B in ICAM-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-107	nuclear factor kappa B subunit 1	Homo sapiens	43-53
14513055-2	2003	Sequential (but not simultaneous) exposure of MM.1S cells to bortezomib or MG-132 (10 h) followed by HA14-1 (8 h) resulted in a marked increase in mitochondrial injury (loss of DeltaPsim, cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), activation of procaspases-3, -8, and -9, and Bid, induction of apoptosis, and loss of clonogenicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	diablo IAP-binding mitochondrial protein	Homo sapiens	207-213
12946329-7	2003	Pretreatment of the BEAS-2B cells with the NF-kappa B inhibitors pyrrolidine dithiocarbamate (PDTC), MG-132, and SN50 resulted in a marked decrease in B. pertussis-induced ICAM-1 expression, implying the involvement of NF-kappa B in ICAM-1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-107	nuclear factor kappa B subunit 1	Homo sapiens	219-229
14513055-2	2003	Sequential (but not simultaneous) exposure of MM.1S cells to bortezomib or MG-132 (10 h) followed by HA14-1 (8 h) resulted in a marked increase in mitochondrial injury (loss of DeltaPsim, cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), activation of procaspases-3, -8, and -9, and Bid, induction of apoptosis, and loss of clonogenicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	caspase 3	Homo sapiens	269-294
14513055-2	2003	Sequential (but not simultaneous) exposure of MM.1S cells to bortezomib or MG-132 (10 h) followed by HA14-1 (8 h) resulted in a marked increase in mitochondrial injury (loss of DeltaPsim, cytochrome c, Smac/DIABLO, and apoptosis-inducing factor release), activation of procaspases-3, -8, and -9, and Bid, induction of apoptosis, and loss of clonogenicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	BH3 interacting domain death agonist	Homo sapiens	300-303
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	proliferating cell nuclear antigen	Mus musculus	92-98
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	224-228
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase 4	Mus musculus	99-103
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1B	Mus musculus	123-131
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	137-140
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	141-145
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	proliferating cell nuclear antigen	Mus musculus	194-200
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase 4	Mus musculus	201-205
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1B	Mus musculus	123-126
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1B	Mus musculus	127-131
14517297-4	2003	However, as determined by treatment of wild-type MEFs with MG132, maximal accumulation of D cyclin-cdk4 complexes required p27(Kip1) and p21(Cip1) and coincided with the formation of inactive D cyclin-cdk4-p27(Kip1) or -p21(Cip1) complexes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	220-223
12832419-7	2003	Switching cells from copper-deficient to copper-rich medium promoted the rapid degradation of CCS, which could be blocked by the proteosome inhibitors MG132 and lactacystin but not a cysteine protease inhibitor or inhibitors of the lysosomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	copper chaperone for superoxide dismutase	Rattus norvegicus	94-97
12941295-4	2003	The caspase inhibitor Z-VAD.fmk and the proteasome inhibitor MG132 partially protected Mcl-1 from decay, indicating that both caspase-dependent and proteasome pathways are involved during apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	87-92
14575542-7	2003	In conclusion, the combination of Z-LLL-CHO and VP16 enhanced their individual cytotoxic effect by inducing apoptosis, in which increase of S + G2/M fraction in cell cycle as well as the enhanced cleavage of Bcl-2 are the possible mechanism of the additive effect on leukemic cells by Z-LLL-CHO and VP16.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-43	BCL2 apoptosis regulator	Homo sapiens	208-213
12970875-10	2003	When cells were pre-incubated with proteasome inhibitor MG132 for 3 hrs, followed by TPA for another 12 hrs, TPA-induced RXRalpha degradation was inhibited.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	retinoid X receptor alpha	Homo sapiens	121-129
12927592-5	2003	Surprisingly, agonist-induced increases in eNOS activity were reduced to 42 and 50% in the presence of the proteasome inhibiting drugs MG132 and clasto-lactacystin-beta-lactone, respectively (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	135-140	nitric oxide synthase 3	Homo sapiens	43-47
12805411-4	2003	MG-132 caused an increase in newly synthesized receptors, detected by microscopy using a TRHR coupled to Timer, a DsRed that undergoes a spontaneous time-dependent color change.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	thyrotropin releasing hormone receptor	Mus musculus	89-93
14555707-7	2003	Inhibition of proteasome activity with MG-132 partially blocked the ability of sulindac sulfide and sulindac sulfone to inhibit beta-catenin protein expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	catenin beta 1	Homo sapiens	128-140
12958623-7	2003	The oxidative stress-dependent MMP-9 induction was accompanied by a significant increase in the NF-kappaB localized in the nuclei and these responses were blunted with a proteasome inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	matrix metallopeptidase 9	Homo sapiens	31-36
12958623-7	2003	The oxidative stress-dependent MMP-9 induction was accompanied by a significant increase in the NF-kappaB localized in the nuclei and these responses were blunted with a proteasome inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	192-197	nuclear factor kappa B subunit 1	Homo sapiens	96-105
12970875-11	2003	Further observation of RXRalpha translocation in the presence of MG132 showed that MG-132 could block TPA-induced RXRalpha redistribution.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-89	retinoid X receptor alpha	Homo sapiens	23-31
12970875-11	2003	Further observation of RXRalpha translocation in the presence of MG132 showed that MG-132 could block TPA-induced RXRalpha redistribution.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-89	retinoid X receptor alpha	Homo sapiens	114-122
12807762-7	2003	Co-treatment of IAR20 cells with TPA and the proteasomal inhibitor MG132 suppressed down-regulation of PKCalpha, delta and epsilon and caused prolonged PKC activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	protein kinase C, alpha	Rattus norvegicus	103-111
12646415-9	2003	The peptide aldehyde Cbz-Leu-Leu-leucinal (LLL-CHO or MG132) potently inhibited z-LLL-AMC hydrolysis in cell extracts as well as increasing p27KIP1 and decreasing cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	cyclin dependent kinase inhibitor 1B	Homo sapiens	140-147
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	NFKB inhibitor alpha	Homo sapiens	146-158
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	cyclin dependent kinase inhibitor 1B	Homo sapiens	163-170
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	ring finger protein 7	Homo sapiens	255-265
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	casein kinase 2 alpha 1	Homo sapiens	276-280
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	ring finger protein 7	Homo sapiens	255-261
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	NFKB inhibitor alpha	Homo sapiens	354-366
12748192-7	2003	Experiments using proteasome inhibitor MG132 and CKII inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole suggest that the accumulation of IkappaBalpha and p27Kip1 results primarily from the reduction of proteasomal degradation in cells expressing CKBBP1T10A, and that CKII-mediated CKBBP1 phosphorylation is required for efficient degradation of IkappaBalpha and p27Kip1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	cyclin dependent kinase inhibitor 1B	Homo sapiens	371-378
12660150-7	2003	The intracellular degradation of TC II expressed by these constructs was inhibited by lactacystin or MG-132 but not by the lysosomal degradation inhibitors ammonium chloride or chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-107	transcobalamin 2	Homo sapiens	33-38
12839933-9	2003	Treatment with the proteasome inhibitor, MG-132, blocked BBS-stimulated NF kappa B DNA binding, and IL-8 and VEGF expression and secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	gastrin releasing peptide	Homo sapiens	57-60
12839933-9	2003	Treatment with the proteasome inhibitor, MG-132, blocked BBS-stimulated NF kappa B DNA binding, and IL-8 and VEGF expression and secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	nuclear factor kappa B subunit 1	Homo sapiens	72-82
12839933-9	2003	Treatment with the proteasome inhibitor, MG-132, blocked BBS-stimulated NF kappa B DNA binding, and IL-8 and VEGF expression and secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	C-X-C motif chemokine ligand 8	Homo sapiens	100-104
12839933-9	2003	Treatment with the proteasome inhibitor, MG-132, blocked BBS-stimulated NF kappa B DNA binding, and IL-8 and VEGF expression and secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	vascular endothelial growth factor A	Homo sapiens	109-113
12904574-5	2003	Treatment with the 26S-proteasome inhibitor MG132 restores the UL9 protein to normal levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	DNA replication origin-binding helicase	Human alphaherpesvirus 1	63-66
12906869-6	2003	The p38 kinase inhibitor, SB 203580, and the NF-kappaB inhibitor, MG-132, inhibited the induction of mob-1 mRNA and the effects were not additive.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-72	sphingomyelin synthase 1	Rattus norvegicus	101-106
12885939-6	2003	The key role of NF-kappaB in mediating the biological effects of TNF-alpha and TRAIL was demonstrated by the ability of unrelated pharmacological inhibitors of the NF-kappaB pathway (parthenolide and MG-132) to abrogate TNF-alpha- and TRAIL-induced monocytic maturation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	200-206	tumor necrosis factor	Homo sapiens	65-74
12885939-6	2003	The key role of NF-kappaB in mediating the biological effects of TNF-alpha and TRAIL was demonstrated by the ability of unrelated pharmacological inhibitors of the NF-kappaB pathway (parthenolide and MG-132) to abrogate TNF-alpha- and TRAIL-induced monocytic maturation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	200-206	TNF superfamily member 10	Homo sapiens	79-84
12885939-6	2003	The key role of NF-kappaB in mediating the biological effects of TNF-alpha and TRAIL was demonstrated by the ability of unrelated pharmacological inhibitors of the NF-kappaB pathway (parthenolide and MG-132) to abrogate TNF-alpha- and TRAIL-induced monocytic maturation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	200-206	tumor necrosis factor	Homo sapiens	220-229
12885939-6	2003	The key role of NF-kappaB in mediating the biological effects of TNF-alpha and TRAIL was demonstrated by the ability of unrelated pharmacological inhibitors of the NF-kappaB pathway (parthenolide and MG-132) to abrogate TNF-alpha- and TRAIL-induced monocytic maturation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	200-206	TNF superfamily member 10	Homo sapiens	235-240
12897156-7	2003	The protein synthesis inhibitor cycloheximide and the proteasome inhibitor MG132 block E2-mediated decrease in GR protein levels, suggesting that estrogen agonists down regulate the GR via the proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	nuclear receptor subfamily 3 group C member 1	Homo sapiens	111-113
12897156-7	2003	The protein synthesis inhibitor cycloheximide and the proteasome inhibitor MG132 block E2-mediated decrease in GR protein levels, suggesting that estrogen agonists down regulate the GR via the proteasomal degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	nuclear receptor subfamily 3 group C member 1	Homo sapiens	182-184
12600815-6	2003	Either SB 203580 or MG-132 was able to offset the cytokine-induced expression of ICAM-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-26	intercellular adhesion molecule 1	Homo sapiens	81-87
12807762-7	2003	Co-treatment of IAR20 cells with TPA and the proteasomal inhibitor MG132 suppressed down-regulation of PKCalpha, delta and epsilon and caused prolonged PKC activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	protein kinase C, alpha	Rattus norvegicus	103-106
12807762-9	2003	The general PKC inhibitor GF109203X reversed the effect of MG132, indicating that the prolonged TPA-induced inhibition of GJIC caused by MG132 was due to the prolonged PKC activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	protein kinase C, alpha	Rattus norvegicus	12-15
12807762-9	2003	The general PKC inhibitor GF109203X reversed the effect of MG132, indicating that the prolonged TPA-induced inhibition of GJIC caused by MG132 was due to the prolonged PKC activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	protein kinase C, alpha	Rattus norvegicus	168-171
12761567-7	2003	TNF-induced Tsg-5 expression is NF-kappa B-dependent as it was inhibited by MG132, lactacystin, Bay 11-7083, and Bay 11-7085.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	tumor necrosis factor	Mus musculus	0-3
12815011-9	2003	I-kappaBalpha stabilizers and NF-kappaB inhibitors [e.g., carbobenzyloxy-leuleu-leucinol (MG-132), lactacystin] suppressed oxidants injurious effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-96	NFKB inhibitor alpha	Homo sapiens	0-13
12827204-5	2003	In transgenic plants, inducible COP1 overexpression leads to a decrease in LAF1 concentrations, but is blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	139-144	COP1 E3 ubiquitin ligase	Homo sapiens	32-36
12805415-5	2003	The repression of HBx by HBc was relieved by treating cells with the proteasome inhibitor MG132, indicating that HBc acts by stimulating the proteasome-mediated degradation of HBx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	X protein	Hepatitis B virus	18-21
12805415-5	2003	The repression of HBx by HBc was relieved by treating cells with the proteasome inhibitor MG132, indicating that HBc acts by stimulating the proteasome-mediated degradation of HBx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	keratin 88, pseudogene	Homo sapiens	25-28
12805415-5	2003	The repression of HBx by HBc was relieved by treating cells with the proteasome inhibitor MG132, indicating that HBc acts by stimulating the proteasome-mediated degradation of HBx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	keratin 88, pseudogene	Homo sapiens	113-116
12805415-5	2003	The repression of HBx by HBc was relieved by treating cells with the proteasome inhibitor MG132, indicating that HBc acts by stimulating the proteasome-mediated degradation of HBx.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-95	X protein	Hepatitis B virus	176-179
12584114-4	2003	Indeed, treatment of hepatocytes with MG-132, a proteasomal inhibitor shown to prevent GR degradation by cortisol, abolished cortisol-mediated GR mRNA upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	glucocorticoid receptor	Oncorhynchus mykiss	87-89
12584114-4	2003	Indeed, treatment of hepatocytes with MG-132, a proteasomal inhibitor shown to prevent GR degradation by cortisol, abolished cortisol-mediated GR mRNA upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	glucocorticoid receptor	Oncorhynchus mykiss	143-145
12761567-7	2003	TNF-induced Tsg-5 expression is NF-kappa B-dependent as it was inhibited by MG132, lactacystin, Bay 11-7083, and Bay 11-7085.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	32-42
12668682-3	2003	In cycloheximide-treated BALB/MK2 keratinocytes we found that C/EBPalpha is a short-lived protein with a half-life of approximately 1 h. Treatment with proteasome inhibitors, MG-132 or lactacystin, blocked the degradation of the C/EBPalpha protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	175-181	CCAAT/enhancer binding protein (C/EBP), alpha	Mus musculus	62-72
12800089-7	2003	When L6 cells were pretreated with Na(3)VO(4) plus the proteasome inhibitor MG-132 or the mTOR inhibitor rapamycin prior to insulin addition, IRS-1 mass loss as well as IRS-1/PI-3 kinase complex decay was blocked at 2 hours and PI 3-kinase activity was increased 2.5-fold and 4-fold, respectively, over insulin alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-82	insulin receptor substrate 1	Homo sapiens	142-147
12787065-8	2003	Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	apolipoprotein E	Rattus norvegicus	82-86
12787065-8	2003	Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	clusterin	Rattus norvegicus	91-95
12787065-8	2003	Two NF-kappa B inhibitors, aspirin (10 mM) and MG-132 (0.1 microM), blocked basal apoE and apoJ secretion as well as LPS-induced apoJ secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-53	clusterin	Rattus norvegicus	129-133
12833516-6	2003	We also observed that a specific pattern of PCNA proteolysis occurred during isoelectric focusing in spite of high urea (8 M) and detergent (2% 3-[(3-cholamidopropyl)dimethylamino]-1-propane sulfonate), which was largely inhibited by the proteosome inhibitor MG132 or boiling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	259-264	proliferating cell nuclear antigen	Homo sapiens	44-48
12615917-5	2003	The commonly used proteasome inhibitors, MG132 and lactacystin but not N-acetyl-Leu-Leu-norleucinal, suppressed the TNFalpha-induced response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	tumor necrosis factor	Homo sapiens	116-124
12761494-8	2003	In addition, NF-kappaB inhibition by MG132, sulfasalazine or the IkappaBalpha super-repressor strongly diminished the resistance against gemcitabine (0.04-20 micro M).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	nuclear factor kappa B subunit 1	Homo sapiens	13-22
12714616-14	2003	The NFkappaB inhibitors pyrrolidinedithiocarbamate (PDTC; 100 microM), caffeic acid phenethyl ester (CAPE; 90 microM), and MG-132 (25 microM), blocked IL-1beta-stimulated expression of hBD-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	interleukin 1 beta	Homo sapiens	151-159
12540365-8	2003	Moreover, proteosome inhibitors (MG-132 and lactacystin) reversed PKC effects on this protected pool of gamma-ENaC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	sodium channel epithelial 1 subunit gamma	Homo sapiens	104-114
12750770-6	2003	Yet, lactacystin and MG132, two unrelated proteasome inhibitors, prevented IRS1 degradation induced by prolonged insulin but not by oxidative stress.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	insulin receptor substrate 1	Rattus norvegicus	75-79
12714616-14	2003	The NFkappaB inhibitors pyrrolidinedithiocarbamate (PDTC; 100 microM), caffeic acid phenethyl ester (CAPE; 90 microM), and MG-132 (25 microM), blocked IL-1beta-stimulated expression of hBD-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-129	defensin beta 4A	Homo sapiens	185-190
12642397-6	2003	(3) The ubiquitin/proteosome inhibitors, MG132 (10 micro M) and pyrrolidine dithiocarbamate (200 micro M), suppressed activation of NF-kappaB as well as stimulation of fractalkine mRNA and protein expression by TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	C-X3-C motif chemokine ligand 1	Rattus norvegicus	168-179
12697834-12	2003	The IGF-IR is stabilized following treatment with both MG132 and chloroquine, indicating that both the proteasome and lysosomal pathways mediate degradation of the receptor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	insulin-like growth factor I receptor	Mus musculus	4-10
12711254-10	2003	Treatment of cells with MG-132, an inhibitor of NF-kappaB activation, resulted in a dramatic decrease in basal PDGF-B transcript levels, and essentially abrogated the response to IL-1beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	platelet derived growth factor subunit B	Bos taurus	111-117
12711254-10	2003	Treatment of cells with MG-132, an inhibitor of NF-kappaB activation, resulted in a dramatic decrease in basal PDGF-B transcript levels, and essentially abrogated the response to IL-1beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	interleukin 1 beta	Bos taurus	179-187
12655090-7	2003	Both HTLV-I Tax and the proteasome-specific inhibitor MG132 inhibited p53-mediated TRX protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	tumor protein p53	Homo sapiens	70-73
12655090-7	2003	Both HTLV-I Tax and the proteasome-specific inhibitor MG132 inhibited p53-mediated TRX protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	VAC14 component of PIKFYVE complex	Homo sapiens	83-86
12640129-6	2003	Treatment of MCF10A cells with MG132, a 26S proteasome inhibitor, effectively stabilized monoubiquitinated p53 and rescued ADR-induced downregulation of Hdm2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	tumor protein p53	Homo sapiens	107-110
12640129-6	2003	Treatment of MCF10A cells with MG132, a 26S proteasome inhibitor, effectively stabilized monoubiquitinated p53 and rescued ADR-induced downregulation of Hdm2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	MDM2 proto-oncogene	Homo sapiens	153-157
12715098-4	2003	The effects of NF-kappaB inhibitor MG-132 on ICAM-1 expression were also observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	intercellular adhesion molecule 1	Homo sapiens	45-51
12715098-6	2003	MG-132 blocked ICAM-1 expression induced by O(3), ET-1 and CGRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	intercellular adhesion molecule 1	Homo sapiens	15-21
12715098-6	2003	MG-132 blocked ICAM-1 expression induced by O(3), ET-1 and CGRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	endothelin 1	Homo sapiens	50-54
12715098-6	2003	MG-132 blocked ICAM-1 expression induced by O(3), ET-1 and CGRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	calcitonin related polypeptide alpha	Homo sapiens	59-63
12682256-6	2003	In addition, a mutation of the NF-kappaB site at -200 (pkappaB1 site) completely abolished this IL-1beta- and TNF-alpha-induced hBD-2 promoter activation, whereas NF-kappaB inhibitors (MG-132 and helenalin) strongly suppressed it.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	nuclear factor kappa B subunit 1	Homo sapiens	31-40
12682256-6	2003	In addition, a mutation of the NF-kappaB site at -200 (pkappaB1 site) completely abolished this IL-1beta- and TNF-alpha-induced hBD-2 promoter activation, whereas NF-kappaB inhibitors (MG-132 and helenalin) strongly suppressed it.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	tumor necrosis factor	Homo sapiens	110-119
12682256-6	2003	In addition, a mutation of the NF-kappaB site at -200 (pkappaB1 site) completely abolished this IL-1beta- and TNF-alpha-induced hBD-2 promoter activation, whereas NF-kappaB inhibitors (MG-132 and helenalin) strongly suppressed it.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	defensin beta 4A	Homo sapiens	128-133
12682256-6	2003	In addition, a mutation of the NF-kappaB site at -200 (pkappaB1 site) completely abolished this IL-1beta- and TNF-alpha-induced hBD-2 promoter activation, whereas NF-kappaB inhibitors (MG-132 and helenalin) strongly suppressed it.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	185-191	nuclear factor kappa B subunit 1	Homo sapiens	163-172
12615709-2	2003	Down-regulation of cyclin D1 and ER alpha by PPARgamma agonists was inhibited in cells cotreated with the proteasome inhibitors MG132 and PSII, but not in cells cotreated with the protease inhibitors calpain II and calpeptin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	cyclin D1	Homo sapiens	19-28
12615709-2	2003	Down-regulation of cyclin D1 and ER alpha by PPARgamma agonists was inhibited in cells cotreated with the proteasome inhibitors MG132 and PSII, but not in cells cotreated with the protease inhibitors calpain II and calpeptin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	estrogen receptor 1	Homo sapiens	33-41
12615709-2	2003	Down-regulation of cyclin D1 and ER alpha by PPARgamma agonists was inhibited in cells cotreated with the proteasome inhibitors MG132 and PSII, but not in cells cotreated with the protease inhibitors calpain II and calpeptin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-133	peroxisome proliferator activated receptor gamma	Homo sapiens	45-54
12642397-6	2003	(3) The ubiquitin/proteosome inhibitors, MG132 (10 micro M) and pyrrolidine dithiocarbamate (200 micro M), suppressed activation of NF-kappaB as well as stimulation of fractalkine mRNA and protein expression by TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	tumor necrosis factor	Rattus norvegicus	211-220
12603864-8	2003	MG132 only partially blocked tumor necrosis factor-alpha-induced tissue factor protein expression, despite an almost complete inhibition of tumor necrosis factor-alpha-induced E-selectin expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Homo sapiens	29-56
12700629-4	2003	p27(Kip1)-expressing K562 cells, however, become resistant to apoptosis induction by the proteasome inhibitors PSI, MG132 and epoxomicin, in contrast to wild-type K562 cells that are efficiently killed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	zinc ribbon domain containing 2	Homo sapiens	0-3
12700629-4	2003	p27(Kip1)-expressing K562 cells, however, become resistant to apoptosis induction by the proteasome inhibitors PSI, MG132 and epoxomicin, in contrast to wild-type K562 cells that are efficiently killed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	cyclin dependent kinase inhibitor 1B	Homo sapiens	4-8
12603864-8	2003	MG132 only partially blocked tumor necrosis factor-alpha-induced tissue factor protein expression, despite an almost complete inhibition of tumor necrosis factor-alpha-induced E-selectin expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	coagulation factor III, tissue factor	Homo sapiens	65-78
12603864-10	2003	Both SB203580 and MG132 treatment inhibited tumor necrosis factor-alpha-mediated increases in tissue factor mRNA and tissue factor gene transcription as measured by expression of tissue factor heterogeneous nuclear RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	tumor necrosis factor	Homo sapiens	44-71
12603864-10	2003	Both SB203580 and MG132 treatment inhibited tumor necrosis factor-alpha-mediated increases in tissue factor mRNA and tissue factor gene transcription as measured by expression of tissue factor heterogeneous nuclear RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	coagulation factor III, tissue factor	Homo sapiens	94-107
12603864-10	2003	Both SB203580 and MG132 treatment inhibited tumor necrosis factor-alpha-mediated increases in tissue factor mRNA and tissue factor gene transcription as measured by expression of tissue factor heterogeneous nuclear RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	coagulation factor III, tissue factor	Homo sapiens	117-130
12603864-10	2003	Both SB203580 and MG132 treatment inhibited tumor necrosis factor-alpha-mediated increases in tissue factor mRNA and tissue factor gene transcription as measured by expression of tissue factor heterogeneous nuclear RNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	coagulation factor III, tissue factor	Homo sapiens	117-130
12581860-4	2003	Inhibitors of I-kappaB degradation, MG132 and N(alpha)-p-tosyl-L-lysine chloromethyl ketone (TLCK), suppressed the further increase by gamma-irradiation in IFN-gamma-induced NO production, showing that gamma-irradiation induced NO production via NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	interferon gamma	Mus musculus	156-165
12610816-10	2003	The expression of the p53 response proteins, MDM2 and p21, was elevated in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	tumor protein p53	Homo sapiens	22-25
12610816-10	2003	The expression of the p53 response proteins, MDM2 and p21, was elevated in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	MDM2 proto-oncogene	Homo sapiens	45-49
12610816-10	2003	The expression of the p53 response proteins, MDM2 and p21, was elevated in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	H3 histone pseudogene 16	Homo sapiens	54-57
12581860-4	2003	Inhibitors of I-kappaB degradation, MG132 and N(alpha)-p-tosyl-L-lysine chloromethyl ketone (TLCK), suppressed the further increase by gamma-irradiation in IFN-gamma-induced NO production, showing that gamma-irradiation induced NO production via NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	246-255
12580918-8	2003	A specific proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132), but not a p38 MAPK inhibitor (SB 203580), was found to suppress the TNF-alpha-induced expression of ICAM-1 on EoL-1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-62	tumor necrosis factor	Homo sapiens	133-142
12446695-6	2003	By contrast, treatment with the proteasome inhibitors (lactacystin or MG-132) caused an accumulation of Nrf2 as well as an induction of reporter gene activity in cells transfected with the GSTA2 antioxidant response element-chloramphenicol acetyl transferase construct.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	NFE2 like bZIP transcription factor 2	Homo sapiens	104-108
12446695-6	2003	By contrast, treatment with the proteasome inhibitors (lactacystin or MG-132) caused an accumulation of Nrf2 as well as an induction of reporter gene activity in cells transfected with the GSTA2 antioxidant response element-chloramphenicol acetyl transferase construct.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	glutathione S-transferase alpha 2	Homo sapiens	189-194
12554628-5	2003	The proteasome inhibitor MG-132, which blocks NF-kappaB activation, also inhibited CD86 upregulation, but not endocytosis downregulation by reactive oxygen species.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	CD86 molecule	Homo sapiens	83-87
12580918-8	2003	A specific proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132), but not a p38 MAPK inhibitor (SB 203580), was found to suppress the TNF-alpha-induced expression of ICAM-1 on EoL-1 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-62	intercellular adhesion molecule 1	Homo sapiens	165-171
12556975-5	2003	Exposure of the cells to TRAIL led to a rapid, transient activation of NF-kappaB, a process that was suppressed by cell pretreatment with alpha-TOS or MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	TNF superfamily member 10	Homo sapiens	25-30
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	nuclear factor kappa B subunit 1	Homo sapiens	36-45
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	tumor necrosis factor	Homo sapiens	67-76
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	nuclear factor kappa B subunit 1	Homo sapiens	122-131
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	NFKB inhibitor alpha	Homo sapiens	133-147
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	nuclear factor kappa B subunit 1	Homo sapiens	122-131
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	C-X3-C motif chemokine ligand 1	Homo sapiens	189-200
12631113-13	2003	The incubation of MCs with MG132, a NF-kappaB inhibitor, abolished TNF-alpha-induced degradation of inhibitory protein of NF-kappaB (I-kappaB)alpha, nuclear translocation of NF-kappaB, and fractalkine expression, without affecting phospho-c-Jun levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	239-244
12556975-5	2003	Exposure of the cells to TRAIL led to a rapid, transient activation of NF-kappaB, a process that was suppressed by cell pretreatment with alpha-TOS or MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	nuclear factor kappa B subunit 1	Homo sapiens	71-80
12461787-7	2003	Use of the proteasome inhibitor, MG132, abolished all effects on ERalpha by TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	estrogen receptor 1	Homo sapiens	65-72
12461787-7	2003	Use of the proteasome inhibitor, MG132, abolished all effects on ERalpha by TGF-beta1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	transforming growth factor beta 1	Homo sapiens	76-85
12529444-4	2003	The ER clusters can be maintained by inhibiting the decrease in cdk1-cyclin B activity by using the proteasome inhibitor MG132, or by microinjecting excess cyclin B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-126	cyclin-dependent kinase 1	Mus musculus	64-68
12539000-9	2003	Monocyte nuclear factor kappaB activation, monocyte tissue factor expression, thrombin generation, and the procoagulant activity of blood in extracorporeal circulation were all blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	213-218	coagulation factor III, tissue factor	Homo sapiens	52-65
12539000-9	2003	Monocyte nuclear factor kappaB activation, monocyte tissue factor expression, thrombin generation, and the procoagulant activity of blood in extracorporeal circulation were all blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	213-218	coagulation factor II, thrombin	Homo sapiens	78-86
12481256-6	2003	Some of these latter changes (reduction of c-myc and cyclin D expression) were not accompanied by corresponding reduction of mRNAs and were abrogated by a proteosome inhibitor (MG132), suggesting that their loss was associated with their increased degradation rather than through transcriptional controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-182	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	43-48
12397080-7	2002	In addition, treatment with the proteasome inhibitor MG132 resulted in accumulation of this initially processed form of DRONC, but not full-length DRONC, in non-apoptotic cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	Death regulator Nedd2-like caspase	Drosophila melanogaster	120-125
15080267-10	2003	ActD, CHX, and MG132 rendered cultured synovial fibroblasts susceptible to TRAIL-induced apoptosis by a caspase-dependent mechanism.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	TNF superfamily member 10	Homo sapiens	75-80
12526088-5	2002	Pretreatment with MG132 which is a well-known NF-kappaB inhibitor by blocking degradation of IkappaBalpha also greatly sensitized lung cancer cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	NFKB inhibitor alpha	Homo sapiens	93-105
12526088-5	2002	Pretreatment with MG132 which is a well-known NF-kappaB inhibitor by blocking degradation of IkappaBalpha also greatly sensitized lung cancer cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	TNF superfamily member 10	Homo sapiens	151-156
14989173-2	2003	Here it is shown that treatment of A431 carcinoma cells with proteasome inhibitors Mg132 and lactacystin results in increasing the PLC gamma 1 intracellular level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	phospholipase C gamma 1	Homo sapiens	131-142
12397080-7	2002	In addition, treatment with the proteasome inhibitor MG132 resulted in accumulation of this initially processed form of DRONC, but not full-length DRONC, in non-apoptotic cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	Death regulator Nedd2-like caspase	Drosophila melanogaster	147-152
12202477-6	2002	p21 protein levels increased in cultured primary hepatocytes treated with the proteasome inhibitor MG132 and cycloheximide, indicating that p21 expression is regulated at the level of protein stability in liver cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	0-3
12438594-8	2002	STAT-1 production was restored and detectable in FLMT cells treated with a proteosome inhibitor, such as MG132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	signal transducer and activator of transcription 1	Homo sapiens	0-6
12438594-9	2002	In the presence of MG132, ubiquitination of STAT-1 and the interaction of MuV-V with STAT-1 were demonstrated in FLMT cells by immunoprecipitation with anti-STAT-1 antibody.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	signal transducer and activator of transcription 1	Homo sapiens	85-91
12438594-9	2002	In the presence of MG132, ubiquitination of STAT-1 and the interaction of MuV-V with STAT-1 were demonstrated in FLMT cells by immunoprecipitation with anti-STAT-1 antibody.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	signal transducer and activator of transcription 1	Homo sapiens	85-91
12456802-6	2002	Treatment with the proteasome inhibitor MG132 restored both the level of p300 protein and the transcriptional response to steroid over 20 h of treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	E1A binding protein p300	Homo sapiens	73-77
12392815-7	2002	Exisulind-induced beta-catenin reduction was blocked by the proteasomal inhibitor MG132 (Z-leu-Leu-Leu-CHO), indicating that the effect of exisulind involved ubiquitin-proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	catenin beta 1	Homo sapiens	18-30
12392815-7	2002	Exisulind-induced beta-catenin reduction was blocked by the proteasomal inhibitor MG132 (Z-leu-Leu-Leu-CHO), indicating that the effect of exisulind involved ubiquitin-proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-106	catenin beta 1	Homo sapiens	18-30
12376534-6	2002	Proteasome is involved in the regulation of AR-dependent transcription, as a proteasome inhibitor, MG-132, prevents the release of the receptor from the PSA promoter, and it also blocks the androgen-induced PSA mRNA accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	androgen receptor	Homo sapiens	44-46
12376534-6	2002	Proteasome is involved in the regulation of AR-dependent transcription, as a proteasome inhibitor, MG-132, prevents the release of the receptor from the PSA promoter, and it also blocks the androgen-induced PSA mRNA accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	kallikrein related peptidase 3	Homo sapiens	153-156
12376534-6	2002	Proteasome is involved in the regulation of AR-dependent transcription, as a proteasome inhibitor, MG-132, prevents the release of the receptor from the PSA promoter, and it also blocks the androgen-induced PSA mRNA accumulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	kallikrein related peptidase 3	Homo sapiens	207-210
12202477-6	2002	p21 protein levels increased in cultured primary hepatocytes treated with the proteasome inhibitor MG132 and cycloheximide, indicating that p21 expression is regulated at the level of protein stability in liver cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	140-143
12507320-5	2002	Inhibition of NF-kappaB action by MG132 and NF-kappaB inhibitory peptide suppressed the cell-protective effect of PAC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	nuclear factor kappa B subunit 1	Homo sapiens	14-23
12372430-2	2002	In this report, upon exposure of cells to ultraviolet (UV) or proteasome inhibitor MG132, ATF3 protein was induced more efficiently in cells with intact p53 allele than in those with null mutant p53 allele.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	activating transcription factor 3	Homo sapiens	90-94
12361713-5	2002	Similar concentrations of MG-132, a membrane-permeable proteasome inhibitor, prevented the vanadate-induced decrease in both intracellular leptin content and leptin secretion, suggesting the involvement of the proteasome in the vanadate action.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	leptin	Mus musculus	139-145
12361713-5	2002	Similar concentrations of MG-132, a membrane-permeable proteasome inhibitor, prevented the vanadate-induced decrease in both intracellular leptin content and leptin secretion, suggesting the involvement of the proteasome in the vanadate action.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	leptin	Mus musculus	158-164
12370803-9	2002	Treatment of 32Dp210 Bcr-Abl cells with both the proteasome inhibitor MG132 and AG490 blocked the reduction of the c-Myc protein observed by AG490 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-28
12370803-9	2002	Treatment of 32Dp210 Bcr-Abl cells with both the proteasome inhibitor MG132 and AG490 blocked the reduction of the c-Myc protein observed by AG490 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	115-120
12372430-2	2002	In this report, upon exposure of cells to ultraviolet (UV) or proteasome inhibitor MG132, ATF3 protein was induced more efficiently in cells with intact p53 allele than in those with null mutant p53 allele.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	tumor protein p53	Homo sapiens	153-156
12372430-2	2002	In this report, upon exposure of cells to ultraviolet (UV) or proteasome inhibitor MG132, ATF3 protein was induced more efficiently in cells with intact p53 allele than in those with null mutant p53 allele.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	tumor protein p53	Homo sapiens	195-198
12408953-6	2002	The increased E-selectin antigen levels induced by BLM were abrogated by pretreatment with MG132 (10 microM) or PDTC (100 microM), in parallel with inhibition of the NF-kappaB/Rel activation and nuclear translocation, although no inhibition of the AP-1 activation was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	selectin E	Homo sapiens	14-24
12408953-6	2002	The increased E-selectin antigen levels induced by BLM were abrogated by pretreatment with MG132 (10 microM) or PDTC (100 microM), in parallel with inhibition of the NF-kappaB/Rel activation and nuclear translocation, although no inhibition of the AP-1 activation was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	nuclear factor kappa B subunit 1	Homo sapiens	166-175
12239627-0	2002	Apoptosis induced in hepatoblastoma HepG2 cells by the proteasome inhibitor MG132 is associated with hydrogen peroxide production, expression of Bcl-XS and activation of caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	caspase 3	Homo sapiens	170-179
12118000-8	2002	In addition, treatment with MG132, a selective proteasome inhibitor, increases the level of ubiquitinated PPARalpha and inhibits its degradation in transfected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	peroxisome proliferator activated receptor alpha	Homo sapiens	106-115
12118000-9	2002	Furthermore, MG132 treatment enhances the level of endogenous PPARalpha in HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	peroxisome proliferator activated receptor alpha	Homo sapiens	62-71
12296854-7	2002	Moreover, blocking the activation of NF-kappaB by MG-132 or antisense p50 oligonucleotide transfection resulted in down-regulated expression of chemokines such as CXCL1, CXCL8, and CCL2 in BFT-stimulated HT-29 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	C-X-C motif chemokine ligand 1	Homo sapiens	163-168
12296854-7	2002	Moreover, blocking the activation of NF-kappaB by MG-132 or antisense p50 oligonucleotide transfection resulted in down-regulated expression of chemokines such as CXCL1, CXCL8, and CCL2 in BFT-stimulated HT-29 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	C-X-C motif chemokine ligand 8	Homo sapiens	170-175
12296854-7	2002	Moreover, blocking the activation of NF-kappaB by MG-132 or antisense p50 oligonucleotide transfection resulted in down-regulated expression of chemokines such as CXCL1, CXCL8, and CCL2 in BFT-stimulated HT-29 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-56	C-C motif chemokine ligand 2	Homo sapiens	181-185
12354109-4	2002	Incorporation of 32P into a 53-kDa protein, which was judged to be TPH based on autoradiography and Western blot analysis using anti-TPH serum and purified TPH as the size marker, was observed in FMA3 cells only in the presence of both okadaic acid and MG132, inhibitors of protein phosphatase and proteasome, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	253-258	tryptophan hydroxylase 1	Mus musculus	67-70
12239627-7	2002	When the cells were exposed to MG132 the level of Bcl-XL diminished, while a new band, corresponding to the expression of the proapoptotic protein Bcl-XS was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	BCL2 like 1	Homo sapiens	50-56
12239627-8	2002	MG132 also caused the release of cytochrome c from mitochondria and the activation of caspase-3 with the consequent degradation of poly-ADP ribose polymerase (PARP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cytochrome c, somatic	Homo sapiens	33-45
12239627-8	2002	MG132 also caused the release of cytochrome c from mitochondria and the activation of caspase-3 with the consequent degradation of poly-ADP ribose polymerase (PARP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	86-95
12239627-8	2002	MG132 also caused the release of cytochrome c from mitochondria and the activation of caspase-3 with the consequent degradation of poly-ADP ribose polymerase (PARP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	poly(ADP-ribose) polymerase 1	Homo sapiens	131-157
12239627-8	2002	MG132 also caused the release of cytochrome c from mitochondria and the activation of caspase-3 with the consequent degradation of poly-ADP ribose polymerase (PARP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	poly(ADP-ribose) polymerase 1	Homo sapiens	159-163
12388747-4	2002	However, treatment with the proteosome inhibitor MG-132 inhibited NF-kappaB activation induced by IR, suggesting that I(kappa)B(alpha) degradation was a critical event in this process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	NFKB inhibitor alpha	Homo sapiens	118-133
12237327-3	2002	The findings indicate that treatment of cells with geldanamycin (GA) or MG-132 (an inhibitor of the 26S proteasome) results in nuclear translocation of the endogenous AHR in both human HepG2 and murine Hepa-1 cells without induction of endogenous CYP1A1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	aryl hydrocarbon receptor	Homo sapiens	167-170
12388747-4	2002	However, treatment with the proteosome inhibitor MG-132 inhibited NF-kappaB activation induced by IR, suggesting that I(kappa)B(alpha) degradation was a critical event in this process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	nuclear factor kappa B subunit 1	Homo sapiens	66-75
12237327-3	2002	The findings indicate that treatment of cells with geldanamycin (GA) or MG-132 (an inhibitor of the 26S proteasome) results in nuclear translocation of the endogenous AHR in both human HepG2 and murine Hepa-1 cells without induction of endogenous CYP1A1 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	247-253
12105203-1	2002	The heat shock protein 90 (Hsp-90) inhibitor, geldanamycin, and the proteasome inhibitor, MG-132, both inhibited tumor necrosis factor receptor 1 (TNF-R1)- but not TRAIL-induced apoptosis in Kym-1 cells, suggesting that TNF-R1-induced cell death is dependent on NF-kappaB activation in this model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-96	TNF receptor superfamily member 1A	Homo sapiens	113-145
12127413-8	2002	This nuclear localization of NF kappa B as well as iNOS activity was completely inhibited by pretreatment of macrophages with 50 micro M MG132, a proteosome inhibitor, both in K and GB2 macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	137-142	nitric oxide synthase 2	Gallus gallus	51-55
12351689-2	2002	ZR-75 breast cancer cells were grown under conditions of normoxia (21% O(2)) or hypoxia (1% O(2) or cobaltous chloride), and hypoxia significantly increased hypoxia-inducible factor 1alpha protein within 3 h after treatment, whereas ERalpha protein levels were dramatically decreased within 6-12 h, and this response was blocked by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	357-363	hypoxia inducible factor 1 subunit alpha	Homo sapiens	157-188
12119296-2	2002	Here we have shown that MG132, a 26 S proteasome inhibitor, suppressed AR transactivation in an androgen-dependent manner in prostate cancer LNCaP and PC-3 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	androgen receptor	Homo sapiens	71-73
12119296-5	2002	The suppression of AR transactivation by MG132 may then result in the suppression of prostate-specific antigen, a well known marker used to monitor the progress of prostate cancer.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	androgen receptor	Homo sapiens	19-21
12119296-5	2002	The suppression of AR transactivation by MG132 may then result in the suppression of prostate-specific antigen, a well known marker used to monitor the progress of prostate cancer.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	kallikrein related peptidase 3	Homo sapiens	85-110
12119296-6	2002	Further mechanistic studies indicated that MG132 may suppress AR transactivation via inhibition of AR nuclear translocation and/or inhibition of interactions between AR and its coregulators, such as ARA70 or TIF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	androgen receptor	Homo sapiens	62-64
12119296-6	2002	Further mechanistic studies indicated that MG132 may suppress AR transactivation via inhibition of AR nuclear translocation and/or inhibition of interactions between AR and its coregulators, such as ARA70 or TIF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	androgen receptor	Homo sapiens	99-101
12119296-6	2002	Further mechanistic studies indicated that MG132 may suppress AR transactivation via inhibition of AR nuclear translocation and/or inhibition of interactions between AR and its coregulators, such as ARA70 or TIF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	androgen receptor	Homo sapiens	99-101
12119296-6	2002	Further mechanistic studies indicated that MG132 may suppress AR transactivation via inhibition of AR nuclear translocation and/or inhibition of interactions between AR and its coregulators, such as ARA70 or TIF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	nuclear receptor coactivator 4	Homo sapiens	199-204
12119296-6	2002	Further mechanistic studies indicated that MG132 may suppress AR transactivation via inhibition of AR nuclear translocation and/or inhibition of interactions between AR and its coregulators, such as ARA70 or TIF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	nuclear receptor coactivator 2	Homo sapiens	208-212
12105203-1	2002	The heat shock protein 90 (Hsp-90) inhibitor, geldanamycin, and the proteasome inhibitor, MG-132, both inhibited tumor necrosis factor receptor 1 (TNF-R1)- but not TRAIL-induced apoptosis in Kym-1 cells, suggesting that TNF-R1-induced cell death is dependent on NF-kappaB activation in this model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-96	TNF receptor superfamily member 1A	Homo sapiens	147-153
12105203-1	2002	The heat shock protein 90 (Hsp-90) inhibitor, geldanamycin, and the proteasome inhibitor, MG-132, both inhibited tumor necrosis factor receptor 1 (TNF-R1)- but not TRAIL-induced apoptosis in Kym-1 cells, suggesting that TNF-R1-induced cell death is dependent on NF-kappaB activation in this model.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-96	TNF receptor superfamily member 1A	Homo sapiens	220-226
12207909-3	2002	We report here that the insulin-induced IRS-1 tyrosine phosphorylation and PI 3-kinase association to IRS-1 were strongly sustained by the proteasome inhibitors, MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	162-167	insulin receptor substrate 1	Homo sapiens	40-45
12209009-6	2002	The SNP-mediated increase of ferritin synthesis could be blocked by MG132, an inhibitor of proteasome-dependent protein degradation, which also prevented the degradation of IRP2 caused by SNP treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	iron responsive element binding protein 2	Mus musculus	173-177
12207909-3	2002	We report here that the insulin-induced IRS-1 tyrosine phosphorylation and PI 3-kinase association to IRS-1 were strongly sustained by the proteasome inhibitors, MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	162-167	insulin receptor substrate 1	Homo sapiens	102-107
12207909-3	2002	We report here that the insulin-induced IRS-1 tyrosine phosphorylation and PI 3-kinase association to IRS-1 were strongly sustained by the proteasome inhibitors, MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	162-167	insulin	Homo sapiens	24-31
12147270-9	2002	Finally, inhibition of the 26S proteasomes by MG132 superinduces TiPARP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	TCDD-inducible poly(ADP-ribose) polymerase	Mus musculus	65-71
12185005-7	2002	In contrast, the proteasomal inhibitor MG-132 blocked TNF-alpha mRNA expression but not IL-6.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	tumor necrosis factor	Mus musculus	54-63
12203103-6	2002	The role of NF-kappaB in enhancement of TNF-alpha production was confirmed in experiments in which MG132, an inhibitor of NF-kappaB activation, reversed the effect of AdAMP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	12-21
12203103-6	2002	The role of NF-kappaB in enhancement of TNF-alpha production was confirmed in experiments in which MG132, an inhibitor of NF-kappaB activation, reversed the effect of AdAMP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	tumor necrosis factor	Mus musculus	40-49
12203103-6	2002	The role of NF-kappaB in enhancement of TNF-alpha production was confirmed in experiments in which MG132, an inhibitor of NF-kappaB activation, reversed the effect of AdAMP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	122-131
12193734-10	2002	In addition, the proteasome inhibitor MG132, which blocks NF-kappaB induction, blocked TNF-alpha-induced Bf promoter activity and the synergistic induction of Bf promoter activity by TNF-alpha and IFN-gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	tumor necrosis factor	Mus musculus	87-96
12193734-10	2002	In addition, the proteasome inhibitor MG132, which blocks NF-kappaB induction, blocked TNF-alpha-induced Bf promoter activity and the synergistic induction of Bf promoter activity by TNF-alpha and IFN-gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	tumor necrosis factor	Mus musculus	183-192
12193734-10	2002	In addition, the proteasome inhibitor MG132, which blocks NF-kappaB induction, blocked TNF-alpha-induced Bf promoter activity and the synergistic induction of Bf promoter activity by TNF-alpha and IFN-gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	interferon gamma	Mus musculus	197-206
12221136-4	2002	By examining both endogenous full-length and a minireceptor form of LRP, we found that proteasomal inhibitors, MG132 and lactacystin, prolong the cellular half-life of LRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	LDL receptor related protein 1	Homo sapiens	68-71
12221136-4	2002	By examining both endogenous full-length and a minireceptor form of LRP, we found that proteasomal inhibitors, MG132 and lactacystin, prolong the cellular half-life of LRP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	LDL receptor related protein 1	Homo sapiens	168-171
12208513-1	2002	In this report we explored the effects of proteasome inhibitors (MG132, aLLN, lactacystin and MG262) on interleukin-8 (IL-8) induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	C-X-C motif chemokine ligand 8	Homo sapiens	104-117
12193575-8	2002	Cellular pretreatment with the proteosomal inhibitor MG132 reversed the effect of c-Cbl overexpression with prolonged duration of GH-stimulated STAT5 tyrosine phosphorylation and restoration of STAT5-mediated transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	Casitas B-lineage lymphoma	Mus musculus	82-87
12193575-8	2002	Cellular pretreatment with the proteosomal inhibitor MG132 reversed the effect of c-Cbl overexpression with prolonged duration of GH-stimulated STAT5 tyrosine phosphorylation and restoration of STAT5-mediated transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	signal transducer and activator of transcription 5A	Mus musculus	144-149
12193575-8	2002	Cellular pretreatment with the proteosomal inhibitor MG132 reversed the effect of c-Cbl overexpression with prolonged duration of GH-stimulated STAT5 tyrosine phosphorylation and restoration of STAT5-mediated transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	signal transducer and activator of transcription 5A	Mus musculus	194-199
12396717-5	2002	Pretreatment of GM00637 cells with the proteasome inhibitors, lactacystin or MG132, completely blocked H(2)O(2)-induced p21 downregulation, suggesting that H(2)O(2) treatment accelerated p21 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	cyclin dependent kinase inhibitor 1A	Homo sapiens	120-123
12396717-5	2002	Pretreatment of GM00637 cells with the proteasome inhibitors, lactacystin or MG132, completely blocked H(2)O(2)-induced p21 downregulation, suggesting that H(2)O(2) treatment accelerated p21 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	cyclin dependent kinase inhibitor 1A	Homo sapiens	187-190
12151316-1	2002	In this study, we investigated the effects of proteasome inhibibors (MG132 and lactacystin) on interleukin (IL)-8 induction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	C-X-C motif chemokine ligand 8	Homo sapiens	95-113
12146975-8	2002	The nonproteasomal apoB100 degradative pathway was nonlysosomal and resistant to E64d, DTT, and peptide aldehydes such as MG132 or ALLN but was partially sensitive to the serine protease inhibitor APMSF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	apolipoprotein B	Homo sapiens	19-26
12151316-2	2002	In human epithelial A549 cells, MG132 and lactacystin induced IL-8 release within the range of 0.1-30 microM.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	C-X-C motif chemokine ligand 8	Homo sapiens	62-66
12151316-3	2002	The effect of MG132 resulted from IL-8 gene transcription and was blocked by PD 98059, but was unaffected by GF109203X, Ro 31-8220, or SB 203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	C-X-C motif chemokine ligand 8	Homo sapiens	34-38
12151316-4	2002	Mutational analysis of the 5" flanking region of the IL-8 gene revealed that activator protein (AP)-1-binding element, but not that element responsive to nuclear factor (NF)-IL-6 or NF-kappaB, was necessary for MG132 stimulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-216	C-X-C motif chemokine ligand 8	Homo sapiens	53-57
12151316-7	2002	In addition, activations of the IL-8 gene and AP-1 by MG132 and lactacystin were inhibited by GSH and NAC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	C-X-C motif chemokine ligand 8	Homo sapiens	32-36
12151316-7	2002	In addition, activations of the IL-8 gene and AP-1 by MG132 and lactacystin were inhibited by GSH and NAC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	X-linked Kx blood group	Homo sapiens	102-105
12209633-4	2002	Inhibition of the proteasome by MG-132 or lactacystin completely blocked TNF-alpha-induced IkappaBalpha degradation as well as NF-kappaB activity in human arterial endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-38	tumor necrosis factor	Homo sapiens	73-82
12145100-6	2002	HPMEC pre-treatment with MG-132, a proteasome inhibitor, prevented NF-kappaB activation as well as more distal signalling response, indicating that NF-kappaB activation is required but not sufficient for PGHS-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	nuclear factor kappa B subunit 1	Homo sapiens	67-76
12145100-6	2002	HPMEC pre-treatment with MG-132, a proteasome inhibitor, prevented NF-kappaB activation as well as more distal signalling response, indicating that NF-kappaB activation is required but not sufficient for PGHS-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	nuclear factor kappa B subunit 1	Homo sapiens	148-157
12145100-6	2002	HPMEC pre-treatment with MG-132, a proteasome inhibitor, prevented NF-kappaB activation as well as more distal signalling response, indicating that NF-kappaB activation is required but not sufficient for PGHS-2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	prostaglandin-endoperoxide synthase 2	Homo sapiens	204-210
12209633-4	2002	Inhibition of the proteasome by MG-132 or lactacystin completely blocked TNF-alpha-induced IkappaBalpha degradation as well as NF-kappaB activity in human arterial endothelial cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-38	NFKB inhibitor alpha	Homo sapiens	91-103
12209633-8	2002	With DNA binding assays we found a seven- to eightfold induction of phosphorylated c-Jun and hence JNK kinase activity under MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-131	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	83-88
12209633-8	2002	With DNA binding assays we found a seven- to eightfold induction of phosphorylated c-Jun and hence JNK kinase activity under MG-132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-131	mitogen-activated protein kinase 8	Homo sapiens	99-102
12160329-7	2002	In MDA-MB-231 cells, inhibition of NF-KB by adenovirus-mediated expression of a dominant negative NF-kappaB or by a proteasome inhibitor, MG132, decreased the VEGF mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	138-143	vascular endothelial growth factor A	Homo sapiens	159-163
12135659-5	2002	RESULTS: Treatment of EPO-stimulated FVA cells with lactacystin or MG132 at later periods of culture increased accumulations of nuclear and cytosolic ubiquitinated proteins and decreased nuclear extrusion to less than 40% of controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	erythropoietin	Homo sapiens	22-25
12168659-8	2002	NFKB activation was found to be dependent upon proteasome activity, since administration of MG 132, a proteasome inhibitor, blocked NFkappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-98	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	132-140
12161520-4	2002	Secondly, ESC were incubated with MG132 (proteasome inhibitor) or SN50 (inhibitor of translocation of NF-kappa B into the nucleus) in the presence of TNF alpha or TPA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	plasminogen activator, tissue type	Homo sapiens	163-166
12161520-5	2002	TNF alpha and TPA significantly increased Mn-SOD activities and Mn-SOD mRNA levels, and those effects were completely inhibited by MG132 and SN50.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	tumor necrosis factor	Homo sapiens	0-9
12161520-5	2002	TNF alpha and TPA significantly increased Mn-SOD activities and Mn-SOD mRNA levels, and those effects were completely inhibited by MG132 and SN50.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	plasminogen activator, tissue type	Homo sapiens	14-17
12161520-5	2002	TNF alpha and TPA significantly increased Mn-SOD activities and Mn-SOD mRNA levels, and those effects were completely inhibited by MG132 and SN50.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	superoxide dismutase 2	Homo sapiens	42-48
12161520-5	2002	TNF alpha and TPA significantly increased Mn-SOD activities and Mn-SOD mRNA levels, and those effects were completely inhibited by MG132 and SN50.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	131-136	superoxide dismutase 2	Homo sapiens	64-70
12161520-6	2002	TNF alpha alone caused no effect on cell viability, but in the presence of MG132, TNF alpha significantly decreased cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	tumor necrosis factor	Homo sapiens	82-91
12127985-0	2002	TNF-alpha-mediated apoptosis in chondrocytes sensitized by MG132 or actinomycin D.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	tumor necrosis factor	Homo sapiens	0-9
12127985-6	2002	MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	61-64
12127985-6	2002	MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	tumor protein p53	Homo sapiens	93-96
12127985-8	2002	MG132, but not actinomycin D, inhibited the chondrocyte IkappaB degradation induced by TNF-alpha and NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor necrosis factor	Homo sapiens	87-96
12127985-9	2002	Our results suggest that MG132 and actinomycin D exert different influences upon TNF-alpha-mediated chondrocyte apoptotic signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor necrosis factor	Homo sapiens	81-90
12114546-5	2002	Experiments using a proteasome inhibitor, MG132, suggest that phosphorylation of BZR1 increases its degradation by the proteasome machinery.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	Brassinosteroid signaling positive regulator (BZR1) family protein	Arabidopsis thaliana	81-85
11884387-6	2002	Relieving the inhibition of the proteasome by chasing MG132-treated cells in medium without the inhibitor led to the rapid disappearance of the accumulated prepro-PTH, and the rate of PTH secretion was restored to levels comparable to those in mock-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	parathyroid hormone	Bos taurus	163-166
12067303-11	2002	TNF-induced IkappaBalpha degradation was inhibited by the proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132) and a non-steroidal anti-inflammatory drug sodium salicylate (NaSal).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-109	tumor necrosis factor	Homo sapiens	0-3
12067303-11	2002	TNF-induced IkappaBalpha degradation was inhibited by the proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132) and a non-steroidal anti-inflammatory drug sodium salicylate (NaSal).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-109	NFKB inhibitor alpha	Homo sapiens	12-24
12067303-12	2002	Using EMSA, both MG-132 and NaSal were found to suppress the TNF-induced NF-kappaB activation in eosinophils.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-23	tumor necrosis factor	Homo sapiens	61-64
12067303-12	2002	Using EMSA, both MG-132 and NaSal were found to suppress the TNF-induced NF-kappaB activation in eosinophils.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-23	nuclear factor kappa B subunit 1	Homo sapiens	73-82
12032842-5	2002	Furthermore, inhibition of NF-kappaB transcriptional activity by the use of the proteasome inhibitor MG132 totally precluded differentiation by insulin+PD98059, demonstrating a direct role for NF-kappaB on C2Ras myogenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	nuclear factor kappa B subunit 1	Homo sapiens	27-36
12032842-5	2002	Furthermore, inhibition of NF-kappaB transcriptional activity by the use of the proteasome inhibitor MG132 totally precluded differentiation by insulin+PD98059, demonstrating a direct role for NF-kappaB on C2Ras myogenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	insulin	Homo sapiens	144-151
12032842-5	2002	Furthermore, inhibition of NF-kappaB transcriptional activity by the use of the proteasome inhibitor MG132 totally precluded differentiation by insulin+PD98059, demonstrating a direct role for NF-kappaB on C2Ras myogenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	nuclear factor kappa B subunit 1	Homo sapiens	193-202
12060613-6	2002	Cells treated with the proteasome inhibitor MG132 showed strong perinuclear staining with a decorin-specific monoclonal antibody by immunohistochemistry.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	decorin	Homo sapiens	92-99
12060613-7	2002	Also, Western blot analysis showed the presence of a ladder of decorin-specific bands that were intensified by treatment with MG132, suggesting that de novo synthesized decorin was degraded by the ubiquitination pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	decorin	Homo sapiens	63-70
12060613-7	2002	Also, Western blot analysis showed the presence of a ladder of decorin-specific bands that were intensified by treatment with MG132, suggesting that de novo synthesized decorin was degraded by the ubiquitination pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	decorin	Homo sapiens	169-176
12067409-0	2002	Proteasome inhibitor MG-132 enhances the expression of interleukin-6 in human umbilical vein endothelial cells: Involvement of MAP/ERK kinase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	interleukin 6	Homo sapiens	55-68
12067409-4	2002	MG-132 increased the expression of IL-6 mRNA and protein;and this effect was abolished by the pretreatment of the cells with U0126, an inhibitor of MAP or ERK kinases (MEK 1/2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 6	Homo sapiens	35-39
12067409-4	2002	MG-132 increased the expression of IL-6 mRNA and protein;and this effect was abolished by the pretreatment of the cells with U0126, an inhibitor of MAP or ERK kinases (MEK 1/2).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	mitogen-activated protein kinase kinase 1	Homo sapiens	168-175
12067409-5	2002	MG-132 treatment was also found to enhance the level of phosphorylated MEK 1/2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	mitogen-activated protein kinase kinase 1	Homo sapiens	71-78
12067409-7	2002	We conclude that a protease inhibitor MG-132 upregulates IL-6 expression in vascular endothelial cells, at least in part, through the activation of MEK 1/2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	interleukin 6	Homo sapiens	57-61
12067409-7	2002	We conclude that a protease inhibitor MG-132 upregulates IL-6 expression in vascular endothelial cells, at least in part, through the activation of MEK 1/2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	mitogen-activated protein kinase kinase 1	Homo sapiens	148-155
12024025-3	2002	We show here that proteasome inhibition with MG132 results in increased accumulation of the glucocorticoid receptor (GR), confirming that it is likewise a substrate for the ubiquitin-proteasome degradative pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	nuclear receptor subfamily 3 group C member 1	Homo sapiens	92-115
12024025-3	2002	We show here that proteasome inhibition with MG132 results in increased accumulation of the glucocorticoid receptor (GR), confirming that it is likewise a substrate for the ubiquitin-proteasome degradative pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	nuclear receptor subfamily 3 group C member 1	Homo sapiens	117-119
11884387-6	2002	Relieving the inhibition of the proteasome by chasing MG132-treated cells in medium without the inhibitor led to the rapid disappearance of the accumulated prepro-PTH, and the rate of PTH secretion was restored to levels comparable to those in mock-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	parathyroid hormone	Bos taurus	184-187
11980636-8	2002	The geldanamycin-induced degradation of HIF-1alpha was reversed by proteosome inhibitors lactacystin and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	hypoxia inducible factor 1 subunit alpha	Homo sapiens	40-50
11864973-8	2002	In contrast, proteasome inhibitor MG-132 and lactacystin blocked both TNF-induced degradation of IkappaBalpha and down-regulation of D-type cyclins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	tumor necrosis factor	Homo sapiens	70-73
11864973-8	2002	In contrast, proteasome inhibitor MG-132 and lactacystin blocked both TNF-induced degradation of IkappaBalpha and down-regulation of D-type cyclins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-40	NFKB inhibitor alpha	Homo sapiens	97-109
11973430-7	2002	Conversely, BB3103 (0.1 micromol/L) caused apoptosis after glutamate exposure as shown by annexin and Hoechst 33342 staining and caspase-3 activity, an effect mimicked by the proteasome inhibitor MG-132 (caspase activity: glutamate: 5.1 +/- 0.1; glutamate + BB: 7.8 +/- 0.8; glutamate + MG: 11.9 +/- 0.5 pmol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-202	caspase 3	Rattus norvegicus	129-138
11981032-6	2002	Treatment with inhibitors of proteasomal degradation (lactacystin and MG132) selectively enhanced GFP-VDR and YFP-RXR expression and also increased the endogenous levels of VDR and RXR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	vitamin D receptor	Rattus norvegicus	102-105
11940670-8	2002	The proteasome inhibitor MG132 reversed the Notch1-induced degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	notch receptor 1	Homo sapiens	44-50
11981032-6	2002	Treatment with inhibitors of proteasomal degradation (lactacystin and MG132) selectively enhanced GFP-VDR and YFP-RXR expression and also increased the endogenous levels of VDR and RXR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	vitamin D receptor	Rattus norvegicus	173-176
11812794-4	2002	Here we report that only inhibitors of the proteasome have a significant effect on preventing the degradation of CFTR, whereas cell-permeable inhibitors of lysosomal degradation, autophagy, and several classes of protease had no measurable effect on CFTR degradation, when used either alone or in combination with the specific proteasome inhibitor carbobenzoxy-l-leucyl-leucyl-l-leucinal (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	389-394	CF transmembrane conductance regulator	Homo sapiens	113-117
12033784-8	2002	We have also shown that the proteasomal inhibitor MG132 can prevent the C protein-induced dismantling of the antiviral (VSV) state in murine cells; thus, the turnover of Stat1 correlates with the C protein-mediated counteraction of the antiviral (VSV) state.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	signal transducer and activator of transcription 1	Mus musculus	170-175
12062370-1	2002	OBJECTIVE: In several cell types, proteasome inhibitors like carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132) induce the 72 kDa heat shock protein (Hsp72) and exert cell protective effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	selenoprotein K	Rattus norvegicus	128-146
11893605-5	2002	Treatment of Caco-2 cells with one of the proteasome inhibitors MG-132 or lactacystin activated the transcription factor heat shock factors (HSF)-1 and -2 and upregulated cellular levels of the 72-kDa heat shock protein HSP-72.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	heat shock transcription factor 1	Homo sapiens	121-154
11893605-5	2002	Treatment of Caco-2 cells with one of the proteasome inhibitors MG-132 or lactacystin activated the transcription factor heat shock factors (HSF)-1 and -2 and upregulated cellular levels of the 72-kDa heat shock protein HSP-72.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	heat shock protein family A (Hsp70) member 1A	Homo sapiens	220-226
12062370-1	2002	OBJECTIVE: In several cell types, proteasome inhibitors like carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132) induce the 72 kDa heat shock protein (Hsp72) and exert cell protective effects.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	148-153
12062370-4	2002	MG132 time- and concentration-dependently induced Hsp72 and Hsp32 at mRNA and protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	50-55
12062370-4	2002	MG132 time- and concentration-dependently induced Hsp72 and Hsp32 at mRNA and protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	heme oxygenase 1	Rattus norvegicus	60-65
12062370-6	2002	MG132 activated p38 MAP kinase already after 0.5 h. Hsp mRNA induction started after 2 h of MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	mitogen activated protein kinase 14	Rattus norvegicus	16-19
12062370-7	2002	Subsequently, Hsp72 and Hsp32 protein levels were increased after 4 h. SB202190, an inhibitor of p38 MAP kinase, concentration-dependently attenuated MG132-induced Hsp72-and Hsp32-elevations (by 59% and 41%, respectively, at 1 microM SB202190).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	14-19
12062370-7	2002	Subsequently, Hsp72 and Hsp32 protein levels were increased after 4 h. SB202190, an inhibitor of p38 MAP kinase, concentration-dependently attenuated MG132-induced Hsp72-and Hsp32-elevations (by 59% and 41%, respectively, at 1 microM SB202190).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	heme oxygenase 1	Rattus norvegicus	24-29
12062370-7	2002	Subsequently, Hsp72 and Hsp32 protein levels were increased after 4 h. SB202190, an inhibitor of p38 MAP kinase, concentration-dependently attenuated MG132-induced Hsp72-and Hsp32-elevations (by 59% and 41%, respectively, at 1 microM SB202190).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	mitogen activated protein kinase 14	Rattus norvegicus	97-100
12062370-7	2002	Subsequently, Hsp72 and Hsp32 protein levels were increased after 4 h. SB202190, an inhibitor of p38 MAP kinase, concentration-dependently attenuated MG132-induced Hsp72-and Hsp32-elevations (by 59% and 41%, respectively, at 1 microM SB202190).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	164-169
12062370-7	2002	Subsequently, Hsp72 and Hsp32 protein levels were increased after 4 h. SB202190, an inhibitor of p38 MAP kinase, concentration-dependently attenuated MG132-induced Hsp72-and Hsp32-elevations (by 59% and 41%, respectively, at 1 microM SB202190).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	150-155	heme oxygenase 1	Rattus norvegicus	174-179
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	47-52
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	99-104
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	heme oxygenase 1	Rattus norvegicus	109-114
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	99-104
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	heme oxygenase 1	Rattus norvegicus	201-206
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	241-246	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	99-104
12062370-8	2002	In contrast, herbimycin A, a known inductor of Hsp72 in cardiomyocytes, enhanced the MG132-induced Hsp72 and Hsp32 expression even further: additionally applied 2 microM herbimycin A induced Hsp72 and Hsp32 about 2-fold higher than 1 microM MG132 alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	241-246	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	99-104
11926998-3	2002	HSP27 and alphaB-crystallin accumulated in both soluble and, more prominently, insoluble fractions after exposure to MG-132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-123	heat shock protein family B (small) member 1	Homo sapiens	0-5
11926998-5	2002	Phosphorylation of HSP27 and alphaB-crystallin in cells treated with MG-132 was enhanced concomitantly with activation of p38 and p44/42 MAP kinase pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	heat shock protein family B (small) member 1	Homo sapiens	19-24
11926998-5	2002	Phosphorylation of HSP27 and alphaB-crystallin in cells treated with MG-132 was enhanced concomitantly with activation of p38 and p44/42 MAP kinase pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	mitogen-activated protein kinase 14	Homo sapiens	122-125
11926998-5	2002	Phosphorylation of HSP27 and alphaB-crystallin in cells treated with MG-132 was enhanced concomitantly with activation of p38 and p44/42 MAP kinase pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-75	interferon induced protein 44	Homo sapiens	130-133
11818334-9	2002	The 26S proteasome inhibitors lactacystin and MG132 reduced the degradation rate of Smad4 protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	SMAD family member 4	Homo sapiens	84-89
12086154-7	2002	Pretreatment of the cells with MG132, which inhibits the proteasomal degradation of HIF-1alpha, increased the production of PAI-1 under both normoxia and hypoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	hypoxia inducible factor 1 subunit alpha	Homo sapiens	84-94
12086154-7	2002	Pretreatment of the cells with MG132, which inhibits the proteasomal degradation of HIF-1alpha, increased the production of PAI-1 under both normoxia and hypoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	serpin family E member 1	Homo sapiens	124-129
11855864-6	2002	Furthermore, MG132 potentiated retinoid-induced receptor activity, as assessed by expression of the retinoid-regulated CRABP-II gene in HaCaT cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	cellular retinoic acid binding protein 2	Homo sapiens	119-127
11861830-3	2002	Here we show that the budding of equine infectious anemia virus (EIAV) from infected equine cells is largely unaffected by these drugs, although use of one inhibitor (MG-132) resulted in a dramatic block to proteolytic processing of Gag.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	167-173	Pr76 polyprotein precursor	Rous sarcoma virus	233-236
11853686-6	2002	Although incubation of drug-treated cells with carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132), a potent proteasome inhibitor, increased cellular apoB (70%), it failed to increase apoB secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	apolipoprotein B	Homo sapiens	147-151
11853686-6	2002	Although incubation of drug-treated cells with carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132), a potent proteasome inhibitor, increased cellular apoB (70%), it failed to increase apoB secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-94	apolipoprotein B	Homo sapiens	181-185
11834481-5	2002	Furthermore, inhibitors of NF-kappaB activation, such as lactacystin, MG132, and pyrrolidine dithiocarbamate, were found to completely block the production of TNF-alpha in response to LPS stimulation, indicating a requirement of NF-kappaB for TNF-alpha expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	tumor necrosis factor	Homo sapiens	159-168
11834481-5	2002	Furthermore, inhibitors of NF-kappaB activation, such as lactacystin, MG132, and pyrrolidine dithiocarbamate, were found to completely block the production of TNF-alpha in response to LPS stimulation, indicating a requirement of NF-kappaB for TNF-alpha expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	tumor necrosis factor	Homo sapiens	243-252
11726647-2	2002	ERK-1/2 is also activated in HT22 cells that undergo caspase-dependent cell death upon inhibition of proteasome-dependent protein degradation brought about by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	159-164	mitogen-activated protein kinase 3	Mus musculus	0-7
11726647-3	2002	As in glutamate-treated HT22 cells and primary neurons, inhibition of MEK-1, an upstream activator of ERK-1/2 protects against MG132-induced toxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	mitogen-activated protein kinase kinase 1	Mus musculus	70-75
11726647-3	2002	As in glutamate-treated HT22 cells and primary neurons, inhibition of MEK-1, an upstream activator of ERK-1/2 protects against MG132-induced toxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	mitogen-activated protein kinase 3	Mus musculus	102-109
11726647-4	2002	Furthermore, activated ERK-1/2 is retained within the nucleus in glutamate- and MG132-treated HT22 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	mitogen-activated protein kinase 3	Mus musculus	23-30
11726647-5	2002	Although previous studies suggested that ERK-1/2 activation was downstream of many cell death-inducing signals in HT22 cells, we show here that cycloheximide, the Z-vad caspase inhibitor, and a nonlethal heat shock protect against glutamate- and MG132-induced toxicity without diminishing ERK-1/2 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	246-251	mitogen-activated protein kinase 3	Mus musculus	41-48
11830551-8	2002	Blockade of NF-kappaB activation by MG132, sulfasalazine, or an IkappaBalpha superrepressor disrupted the IL-1beta-mediated amplification loop and the accompanying chemoresistance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	nuclear factor kappa B subunit 1	Homo sapiens	12-21
11830551-8	2002	Blockade of NF-kappaB activation by MG132, sulfasalazine, or an IkappaBalpha superrepressor disrupted the IL-1beta-mediated amplification loop and the accompanying chemoresistance.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	interleukin 1 beta	Homo sapiens	106-114
11813164-4	2002	Inhibition of TNF-alpha-mediated IkappaBalpha degradation and NF-kappaB activation by gliotoxin or the proteasome inhibitor MG-132 un-masks the caspase-dependent pro-apoptotic properties of TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	tumor necrosis factor	Homo sapiens	14-23
11813164-4	2002	Inhibition of TNF-alpha-mediated IkappaBalpha degradation and NF-kappaB activation by gliotoxin or the proteasome inhibitor MG-132 un-masks the caspase-dependent pro-apoptotic properties of TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	nuclear factor kappa B subunit 1	Homo sapiens	62-71
11840331-4	2002	This p53wt diminution was dependent on proteasome activity, as inhibited by MG-132 inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-82	tumor protein p53	Homo sapiens	5-8
11813164-4	2002	Inhibition of TNF-alpha-mediated IkappaBalpha degradation and NF-kappaB activation by gliotoxin or the proteasome inhibitor MG-132 un-masks the caspase-dependent pro-apoptotic properties of TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	tumor necrosis factor	Homo sapiens	190-199
11803460-8	2002	CD95-resistant HPV-positive cells underwent apoptosis within 3-5 h upon co-incubation with MG132 and agonistic antibodies or CD95 ligand, which was preceded by a strong re-expression of p53 and c-Myc, but not of other half-life controlled proteins such as Bax or IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	Fas cell surface death receptor	Homo sapiens	0-4
11777344-8	2002	The importance of XIAP in mediating apoptosis resistance was illustrated in cells transiently transfected with XIAP, which conferred on THP-1 cells the ability to resist Z-LLL-CHO-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	X-linked inhibitor of apoptosis	Homo sapiens	18-22
11777344-8	2002	The importance of XIAP in mediating apoptosis resistance was illustrated in cells transiently transfected with XIAP, which conferred on THP-1 cells the ability to resist Z-LLL-CHO-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	170-175	X-linked inhibitor of apoptosis	Homo sapiens	111-115
11803460-8	2002	CD95-resistant HPV-positive cells underwent apoptosis within 3-5 h upon co-incubation with MG132 and agonistic antibodies or CD95 ligand, which was preceded by a strong re-expression of p53 and c-Myc, but not of other half-life controlled proteins such as Bax or IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	tumor protein p53	Homo sapiens	186-189
11803460-8	2002	CD95-resistant HPV-positive cells underwent apoptosis within 3-5 h upon co-incubation with MG132 and agonistic antibodies or CD95 ligand, which was preceded by a strong re-expression of p53 and c-Myc, but not of other half-life controlled proteins such as Bax or IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	194-199
11803460-8	2002	CD95-resistant HPV-positive cells underwent apoptosis within 3-5 h upon co-incubation with MG132 and agonistic antibodies or CD95 ligand, which was preceded by a strong re-expression of p53 and c-Myc, but not of other half-life controlled proteins such as Bax or IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	BCL2 associated X, apoptosis regulator	Homo sapiens	256-259
11803460-8	2002	CD95-resistant HPV-positive cells underwent apoptosis within 3-5 h upon co-incubation with MG132 and agonistic antibodies or CD95 ligand, which was preceded by a strong re-expression of p53 and c-Myc, but not of other half-life controlled proteins such as Bax or IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	NFKB inhibitor alpha	Homo sapiens	263-275
11967994-4	2002	Early G1-phase activation of cdk3 was downregulated by treatment of cells with MG132, an inhibitor of the proteasome, and by the protein synthesis inhibitor cycloheximide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	cyclin-dependent kinase 3	Cricetulus griseus	29-33
11555652-4	2001	Pretreatment of COS-1 cells expressing mouse glucocorticoid receptor with the proteasome inhibitor MG-132 effectively blocks glucocorticoid receptor protein down-regulation by the glucocorticoid dexamethasone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	nuclear receptor subfamily 3, group C, member 1	Mus musculus	45-68
11585836-6	2001	We found that proteasome inhibitors (lactacystin and MG132) increased Rac1(V12) protein level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	immunoglobulin lambda variable 2-8	Homo sapiens	70-78
11716468-5	2001	Addition of the proteosome inhibitor MG-132 sustained the level of ubiquitin-LRP for longer time intervals in macrophages treated with either alpha2M* or Pseudomonas exotoxin A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	LDL receptor related protein 1	Homo sapiens	77-80
11716468-5	2001	Addition of the proteosome inhibitor MG-132 sustained the level of ubiquitin-LRP for longer time intervals in macrophages treated with either alpha2M* or Pseudomonas exotoxin A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-43	alpha-2-macroglobulin	Homo sapiens	142-149
11555652-4	2001	Pretreatment of COS-1 cells expressing mouse glucocorticoid receptor with the proteasome inhibitor MG-132 effectively blocks glucocorticoid receptor protein down-regulation by the glucocorticoid dexamethasone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-105	nuclear receptor subfamily 3 group C member 1	Homo sapiens	125-148
11555652-5	2001	Interestingly, both MG-132 and a second proteasome inhibitor beta-lactone significantly enhanced hormone response of transfected mouse glucocorticoid receptor toward transcriptional activation of glucocorticoid receptor-mediated reporter gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-26	nuclear receptor subfamily 3, group C, member 1	Mus musculus	135-158
11555652-5	2001	Interestingly, both MG-132 and a second proteasome inhibitor beta-lactone significantly enhanced hormone response of transfected mouse glucocorticoid receptor toward transcriptional activation of glucocorticoid receptor-mediated reporter gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-26	nuclear receptor subfamily 3, group C, member 1	Mus musculus	196-219
11555652-6	2001	The transcriptional activity of the endogenous human glucocorticoid receptor in HeLa cells was also enhanced by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	nuclear receptor subfamily 3 group C member 1	Homo sapiens	53-76
11860188-8	2001	When NBP2-PN25 cells were treated with a proteasome inhibitor, lactacystin or MG132, a dose-dependent increase in the constitutive levels of d2EGFP expression was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	NUBP iron-sulfur cluster assembly factor 2, cytosolic	Homo sapiens	5-9
11597920-7	2001	Finally, the selective NF-kappa B inhibitor MG-132 dose dependently reduced NF-kappa B binding and beta(2)-AR promoter activity but increased AP-1 binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	nuclear factor kappa B subunit 1	Homo sapiens	23-33
11597920-7	2001	Finally, the selective NF-kappa B inhibitor MG-132 dose dependently reduced NF-kappa B binding and beta(2)-AR promoter activity but increased AP-1 binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	nuclear factor kappa B subunit 1	Homo sapiens	76-86
11597920-7	2001	Finally, the selective NF-kappa B inhibitor MG-132 dose dependently reduced NF-kappa B binding and beta(2)-AR promoter activity but increased AP-1 binding.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	adrenoceptor beta 2	Homo sapiens	99-109
11911275-6	2001	MG-132 was found to be more effective in combination with drugs such as doxorubicin and etoposide that act in the S/G2-phase of the cell cycle via a mechanism that involves stabilization of cyclin B1 and increased expression of Bax.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	cyclin B1	Homo sapiens	190-199
11911275-6	2001	MG-132 was found to be more effective in combination with drugs such as doxorubicin and etoposide that act in the S/G2-phase of the cell cycle via a mechanism that involves stabilization of cyclin B1 and increased expression of Bax.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	BCL2 associated X, apoptosis regulator	Homo sapiens	228-231
11911275-7	2001	Further, MG-132 inhibits CFU-GM colony formation of the CD34+ enriched PBSC population and this inhibition correlates with release of cyt C into the cytosol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	CD34 molecule	Homo sapiens	56-60
11679969-8	2001	This IL-1 beta-induced decrease was likely caused by degradation via the proteasome, because it was prevented by the addition of the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	155-160	interleukin 1 beta	Rattus norvegicus	5-14
11588023-7	2001	Given the expression of NF-kappaB in leukemic, but not normal primitive cells, the hypothesis that inhibition of NF-kappaB might induce leukemia-specific apoptosis was tested by treating primary cells with the proteasome inhibitor MG-132, a well-known inhibitor of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	231-237	nuclear factor kappa B subunit 1	Homo sapiens	113-122
11588023-7	2001	Given the expression of NF-kappaB in leukemic, but not normal primitive cells, the hypothesis that inhibition of NF-kappaB might induce leukemia-specific apoptosis was tested by treating primary cells with the proteasome inhibitor MG-132, a well-known inhibitor of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	231-237	nuclear factor kappa B subunit 1	Homo sapiens	113-122
11588023-8	2001	Leukemic CD34(+)/CD38(-) cells displayed a rapid induction of cell death in response to MG-132, whereas normal CD34(+)/CD38(-) cells showed little if any effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	CD34 molecule	Homo sapiens	9-13
11588023-8	2001	Leukemic CD34(+)/CD38(-) cells displayed a rapid induction of cell death in response to MG-132, whereas normal CD34(+)/CD38(-) cells showed little if any effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-94	CD38 molecule	Homo sapiens	17-21
11703322-6	2001	Inhibition of constitutively active NF-kappa B, by either proteasome inhibitors (MG132, gliotoxin) or inhibitors of I kappa B phosphorylation (Bay117082, and Bay117085), induced apoptosis as demonstrated by both flow cytometric analysis and light microscopic morphological evaluation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	nuclear factor kappa B subunit 1	Homo sapiens	36-46
11598079-9	2001	In the complete absence of activated NF-kappaB, when Mono Mac 6 cells were pretreated with the more potent NF-kappaB inhibitors MG-132 and parthenolide a C. pneumoniae-mediated rescue of cells from induced apoptosis could not be achieved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	128-134	nuclear factor kappa B subunit 1	Homo sapiens	107-116
11585899-5	2001	Above a low basal activity of both HSFs, heat shock preferentially activates HSF1, whereas the amino acid analogue azetidine or the proteasome inhibitor MG132 coactivates both HSFs to different levels and hemin preferentially induces HSF2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	153-158	heat shock transcription factor 2	Homo sapiens	234-238
11546773-4	2001	MG132 or lactacystin, specific inhibitors of 26S proteasome, blocked insulin/IGF-1-induced degradation of IRS-2 and enhanced the detection of ubiquitinated IRS-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	insulin	Cricetulus griseus	69-76
11546773-4	2001	MG132 or lactacystin, specific inhibitors of 26S proteasome, blocked insulin/IGF-1-induced degradation of IRS-2 and enhanced the detection of ubiquitinated IRS-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	insulin-like growth factor 1	Mus musculus	77-82
11546773-4	2001	MG132 or lactacystin, specific inhibitors of 26S proteasome, blocked insulin/IGF-1-induced degradation of IRS-2 and enhanced the detection of ubiquitinated IRS-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	insulin receptor substrate 2	Mus musculus	106-111
11546773-4	2001	MG132 or lactacystin, specific inhibitors of 26S proteasome, blocked insulin/IGF-1-induced degradation of IRS-2 and enhanced the detection of ubiquitinated IRS-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	insulin receptor substrate 2	Mus musculus	156-161
11593412-4	2001	Also both NF-kappaB and Ku activities were activated or inhibited by treatment with etoposide (VP-16) or MG-132 (a proteasome inhibitor), respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	nuclear factor kappa B subunit 1	Homo sapiens	10-19
11562742-3	2001	The levels of BRCA1 protein were up-regulated by proteasome inhibitors, such as MG-132 and ALLnL, suggesting rapid degradation via the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-86	BRCA1 DNA repair associated	Homo sapiens	14-19
11585641-4	2001	Both IL-1beta- mRNAs and proteins hypoxia-induced NF-kappaB activation were blocked by the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	interleukin 1 beta	Homo sapiens	5-13
11585641-5	2001	MG-132 inhibited IL-1beta-induced up-regulation of IL-1beta and IL-8 mRNA and protein but increased hypoxia-stimulated expression/release of IL-1beta and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 1 beta	Homo sapiens	17-25
11585641-5	2001	MG-132 inhibited IL-1beta-induced up-regulation of IL-1beta and IL-8 mRNA and protein but increased hypoxia-stimulated expression/release of IL-1beta and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 1 beta	Homo sapiens	51-59
11585641-5	2001	MG-132 inhibited IL-1beta-induced up-regulation of IL-1beta and IL-8 mRNA and protein but increased hypoxia-stimulated expression/release of IL-1beta and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	C-X-C motif chemokine ligand 8	Homo sapiens	64-68
11585641-5	2001	MG-132 inhibited IL-1beta-induced up-regulation of IL-1beta and IL-8 mRNA and protein but increased hypoxia-stimulated expression/release of IL-1beta and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	interleukin 1 beta	Homo sapiens	51-59
11585641-5	2001	MG-132 inhibited IL-1beta-induced up-regulation of IL-1beta and IL-8 mRNA and protein but increased hypoxia-stimulated expression/release of IL-1beta and IL-8.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	C-X-C motif chemokine ligand 8	Homo sapiens	154-158
11582519-5	2001	In in vitro studies using protease inhibitors, IkappaBalpha proteolysis in ts1-infected astrocytes was significantly blocked by a specific calpain inhibitor calpeptin but not by MG-132, a specific proteasome inhibitor, whereas rapid IkappaBbeta proteolysis was blocked by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	272-278	NFKB inhibitor alpha	Homo sapiens	47-59
11582519-5	2001	In in vitro studies using protease inhibitors, IkappaBalpha proteolysis in ts1-infected astrocytes was significantly blocked by a specific calpain inhibitor calpeptin but not by MG-132, a specific proteasome inhibitor, whereas rapid IkappaBbeta proteolysis was blocked by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	272-278	Trichinella spiralis resistance 1	Mus musculus	75-78
11582519-6	2001	Furthermore, treatment with MG-132 increased levels of multiubiquitinated IkappaBbeta protein in ts1-infected astrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	NFKB inhibitor beta	Homo sapiens	74-85
11582519-6	2001	Furthermore, treatment with MG-132 increased levels of multiubiquitinated IkappaBbeta protein in ts1-infected astrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	Trichinella spiralis resistance 1	Mus musculus	97-100
11585620-5	2001	The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	nitric oxide synthase 2	Rattus norvegicus	17-21
11585620-5	2001	The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	interleukin 17A	Rattus norvegicus	30-35
11585620-5	2001	The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	172-177	interferon gamma	Rattus norvegicus	39-48
11461910-5	2001	In the presence of the proteasome inhibitor MG132, the amount of Notch 1 IC and its level of ubiquitination are increased.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	notch receptor 1	Homo sapiens	65-72
11461910-6	2001	Interestingly, this accumulation of Notch 1 IC in the presence of MG132 is accompanied by decreased activation of the HES 1 promoter, suggesting that ubiquitinated Notch 1 IC is a less potent transactivator.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	notch receptor 1	Homo sapiens	36-43
11461910-6	2001	Interestingly, this accumulation of Notch 1 IC in the presence of MG132 is accompanied by decreased activation of the HES 1 promoter, suggesting that ubiquitinated Notch 1 IC is a less potent transactivator.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	notch receptor 1	Homo sapiens	164-171
11517161-7	2001	In addition, MG-132 and epoxomicin, inhibitors of proteasomal protease activity, inhibited the E2-induced decrease in uterine insulin receptor substrate-2 protein levels, and this correlated to an increase in uterine protein ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	insulin receptor	Mus musculus	126-142
11522450-4	2001	Lens epithelial cells treated with H(2)O(2) demonstrated at 1 h a strong activation of NF-kappa B which returned to basal levels by 2 h. Under proteasome inhibition using both MG132 and lactacystin, H(2)O(2)-mediated activation of NF-kappa B was prevented, implicating the involvement of proteasome degradation of I kappa B proteins as being necessary for this activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	176-181	nuclear factor kappa B subunit 1	Homo sapiens	87-97
11494409-4	2001	The activation of transcription factor NF-kappaB was apparently required for AMB-induced iNOS mRNA expression, as the latter was abolished by NF-kappaB inhibitors: pyrrolidine dithiocarbamate and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	196-201	nitric oxide synthase 2	Rattus norvegicus	89-93
11513883-3	2001	Using wild-type Jurkat T cells, we show that the proteasome inhibitors MG132 and lactacystin promote the cleavage of eIF4G, activate caspase-8 and caspase-3-like activities and decrease cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	117-122
11514050-5	2001	The proteasome inhibitors MG-132 and clasto-lactacystin beta-lactone also increased hGH-BP release from Ba/F3-hGHR cells, and MG-132 and PDBu synergistically increased hGH-BP release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	growth hormone receptor	Homo sapiens	84-90
11514050-5	2001	The proteasome inhibitors MG-132 and clasto-lactacystin beta-lactone also increased hGH-BP release from Ba/F3-hGHR cells, and MG-132 and PDBu synergistically increased hGH-BP release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	growth hormone receptor	Homo sapiens	110-114
11514050-5	2001	The proteasome inhibitors MG-132 and clasto-lactacystin beta-lactone also increased hGH-BP release from Ba/F3-hGHR cells, and MG-132 and PDBu synergistically increased hGH-BP release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	growth hormone receptor	Homo sapiens	168-174
11514050-5	2001	The proteasome inhibitors MG-132 and clasto-lactacystin beta-lactone also increased hGH-BP release from Ba/F3-hGHR cells, and MG-132 and PDBu synergistically increased hGH-BP release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	growth hormone receptor	Homo sapiens	168-174
11514050-6	2001	The results obtained by using three PKC inhibitors Go 6976, GF 109203X and Go 6983 suggest that the enhancement of hGH-BP release by MG-132 and PDBu is mediated by different mechanisms probably involving different PKC isozymes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-139	growth hormone receptor	Homo sapiens	115-121
11513883-3	2001	Using wild-type Jurkat T cells, we show that the proteasome inhibitors MG132 and lactacystin promote the cleavage of eIF4G, activate caspase-8 and caspase-3-like activities and decrease cell viability.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	caspase 8	Homo sapiens	133-142
11513883-4	2001	Furthermore, MG132 also promotes the cleavage of eIF4G and the activation of caspase-3-like activity in a caspase-8-deficient Jurkat cell line which is resistant to anti-Fas-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	49-54
11513883-4	2001	Furthermore, MG132 also promotes the cleavage of eIF4G and the activation of caspase-3-like activity in a caspase-8-deficient Jurkat cell line which is resistant to anti-Fas-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	caspase 8	Homo sapiens	106-115
11513883-5	2001	Using specific anti-peptide antisera, we show that both eIF4GI and eIF4GII are cleaved in either cell line in response to MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	56-62
11513883-5	2001	Using specific anti-peptide antisera, we show that both eIF4GI and eIF4GII are cleaved in either cell line in response to MG132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	eukaryotic translation initiation factor 4 gamma 3	Homo sapiens	67-74
11406522-3	2001	Apoptosis of cultured synovial cells was induced by inhibition of NF-kappaB nuclear translocation by Z-Leu-Leu-Leu-aldehyde (LLL-CHO).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-123	nuclear factor kappa B subunit 1	Homo sapiens	66-75
11477551-4	2001	Gastric cancer cell lines AGS (p53 wild-type) and MKN-28 (p53 mutant) were treated with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	tumor protein p53	Homo sapiens	58-61
11477551-11	2001	Although z-DEVD-fmk, a specific caspase-3 inhibitor, suppressed MG132-induced apoptosis in MKN28 cells, it only partially rescued the apoptotic effect in AGS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	caspase 3	Homo sapiens	32-41
11490372-6	2001	MG132 inhibited NF-kappa B binding and enhanced gemcitabine hydrochloride"s inhibition of DNA synthesis (gemcitabine hydrochloride = 73% +/- 1.4% vs gemcitabine hydrochloride + MG132 = 6% +/- 0.4%, P &lt;.05), cell killing (gemcitabine hydrochloride = 87% +/- 2.0 vs gemcitabine hydrochloride + MG132 = 25% +/- 1.3%, P &lt;.05), and caspase-3 activity (gemcitabine hydrochloride = 870 +/- 17.4 vs gemcitabine hydrochloride + MG132 = 1075 +/- 20.4, P &lt;.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	nuclear factor kappa B subunit 1	Homo sapiens	16-26
11490372-6	2001	MG132 inhibited NF-kappa B binding and enhanced gemcitabine hydrochloride"s inhibition of DNA synthesis (gemcitabine hydrochloride = 73% +/- 1.4% vs gemcitabine hydrochloride + MG132 = 6% +/- 0.4%, P &lt;.05), cell killing (gemcitabine hydrochloride = 87% +/- 2.0 vs gemcitabine hydrochloride + MG132 = 25% +/- 1.3%, P &lt;.05), and caspase-3 activity (gemcitabine hydrochloride = 870 +/- 17.4 vs gemcitabine hydrochloride + MG132 = 1075 +/- 20.4, P &lt;.05).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	333-342
11453641-4	2001	Furthermore, both lactacystin and MG132 prevented the decrease in ADH caused by DHT.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	aldo-keto reductase family 1 member A1	Rattus norvegicus	66-69
11453641-7	2001	Ubiquitinated ADH was also demonstrated in hepatocytes exposed to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	aldo-keto reductase family 1 member A1	Rattus norvegicus	14-17
11453641-8	2001	The combination of DHT and MG132 resulted in more ubiquitinated ADH than exposure to either compound alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	aldo-keto reductase family 1 member A1	Rattus norvegicus	64-67
11526482-10	2001	In addition we show that like p14ARF, the proteasome inhibitor MG132 can promote the accumulation of Mdm2 in the nucleolus and that this can occur in the absence of p14ARF expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	cyclin dependent kinase inhibitor 2A	Homo sapiens	30-36
11526482-10	2001	In addition we show that like p14ARF, the proteasome inhibitor MG132 can promote the accumulation of Mdm2 in the nucleolus and that this can occur in the absence of p14ARF expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	MDM2 proto-oncogene	Homo sapiens	101-105
11425850-8	2001	MG132 or lactacystin (10 microm), inhibitors of the proteasome pathway by which D2 is degraded, increase both D2 activity and (75)Se-p31 3-4-fold and prevent the loss of D2 activity during cycloheximide or substrate (T(4)) exposure.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	iodothyronine deiodinase 2	Homo sapiens	80-82
11425850-8	2001	MG132 or lactacystin (10 microm), inhibitors of the proteasome pathway by which D2 is degraded, increase both D2 activity and (75)Se-p31 3-4-fold and prevent the loss of D2 activity during cycloheximide or substrate (T(4)) exposure.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	iodothyronine deiodinase 2	Homo sapiens	110-112
11425850-8	2001	MG132 or lactacystin (10 microm), inhibitors of the proteasome pathway by which D2 is degraded, increase both D2 activity and (75)Se-p31 3-4-fold and prevent the loss of D2 activity during cycloheximide or substrate (T(4)) exposure.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	iodothyronine deiodinase 2	Homo sapiens	110-112
11505050-9	2001	Experiments using the proteasome inhibitor, MG132, revealed that augmentation of NF-kappaB by ethanol and IFNalpha is mediated via the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	interferon alpha 1	Homo sapiens	106-114
11454583-5	2001	To examine whether NF-kappaB contributed to leukocyte recruitment 4 h post thrombin stimulation, we treated HUVEC with the NF-kappaB inhibitor MG-132 for 1 h before thrombin stimulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	nuclear factor kappa B subunit 1	Homo sapiens	19-28
11454583-5	2001	To examine whether NF-kappaB contributed to leukocyte recruitment 4 h post thrombin stimulation, we treated HUVEC with the NF-kappaB inhibitor MG-132 for 1 h before thrombin stimulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	coagulation factor II, thrombin	Homo sapiens	75-83
11454583-5	2001	To examine whether NF-kappaB contributed to leukocyte recruitment 4 h post thrombin stimulation, we treated HUVEC with the NF-kappaB inhibitor MG-132 for 1 h before thrombin stimulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-149	nuclear factor kappa B subunit 1	Homo sapiens	123-132
11454583-6	2001	MG-132 significantly reduced the number of rolling (77.1%) and adherent (79.9%) leukocytes compared with thrombin stimulation alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	coagulation factor II, thrombin	Homo sapiens	105-113
11454583-8	2001	Tumor necrosis factor-alpha- and MG-132-treated HUVEC displayed no inhibition of leukocyte recruitment despite a decrease in NF-kappaB activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	nuclear factor kappa B subunit 1	Homo sapiens	125-134
11466328-4	2001	We found that proteasome inhibitor MG132 dose-dependently induced expression of MCP-1 at the transcriptional level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	chemokine (C-C motif) ligand 2	Mus musculus	80-85
11466328-8	2001	Northern blot analysis showed that MG132 rapidly induced the expression of c-jun, but not c-fos.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	jun proto-oncogene	Mus musculus	75-80
11466328-9	2001	Immunoblot analysis showed that MG132 prevented degradation of c-Jun protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	jun proto-oncogene	Mus musculus	63-68
11466328-10	2001	Kinase assay revealed that c-Jun N-terminal kinase (JNK) was rapidly activated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	mitogen-activated protein kinase 8	Mus musculus	27-50
11466328-10	2001	Kinase assay revealed that c-Jun N-terminal kinase (JNK) was rapidly activated by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	mitogen-activated protein kinase 8	Mus musculus	52-55
11466328-12	2001	Curcumin, a pharmacological inhibitor of the JNK-AP-1 pathway, abrogated the induction of MCP-1 by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	mitogen-activated protein kinase 8	Mus musculus	45-48
11466328-12	2001	Curcumin, a pharmacological inhibitor of the JNK-AP-1 pathway, abrogated the induction of MCP-1 by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	chemokine (C-C motif) ligand 2	Mus musculus	90-95
11466328-13	2001	Similarly, stable transfection with a dominant-negative mutant of c-Jun attenuated both MG132-induced activation of AP-1 and expression of MCP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	jun proto-oncogene	Mus musculus	66-71
11466328-13	2001	Similarly, stable transfection with a dominant-negative mutant of c-Jun attenuated both MG132-induced activation of AP-1 and expression of MCP-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	chemokine (C-C motif) ligand 2	Mus musculus	139-144
11453641-3	2001	Exposure of hepatocytes in culture to lactacystin or to MG132, which are inhibitors of the ubiquitin-proteasome pathway of protein degradation, resulted in higher ADH.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	aldo-keto reductase family 1 member A1	Rattus norvegicus	163-166
11426935-10	2001	Addition of the specific proteasome inhibitor MG132 blocked a decrease in HSF1 during heat shock, maintaining levels observed in late passage cells and HSF1 activity comparable to that of early passage HF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	heat shock transcription factor 1	Homo sapiens	74-78
11426935-10	2001	Addition of the specific proteasome inhibitor MG132 blocked a decrease in HSF1 during heat shock, maintaining levels observed in late passage cells and HSF1 activity comparable to that of early passage HF.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	heat shock transcription factor 1	Homo sapiens	152-156
11426935-11	2001	The recovery of the level and activity of HSF1 observed in late passage HF incubated in the presence of MG132 suggests that heat shock unmasks a latent proteasome activity responsible for HSF1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	heat shock transcription factor 1	Homo sapiens	42-46
11426935-11	2001	The recovery of the level and activity of HSF1 observed in late passage HF incubated in the presence of MG132 suggests that heat shock unmasks a latent proteasome activity responsible for HSF1 degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	heat shock transcription factor 1	Homo sapiens	188-192
11478501-6	2001	The down-regulation of PKC-alpha from the membrane was prevented by either calpain inhibitor I or MG-132 and resulted in a sustained permeability increase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	protein kinase C alpha	Homo sapiens	23-32
11465715-7	2001	CD95 antibody-induced apoptosis was potentiated by the proteasome inhibitors MG-132 and PS1, and this was associated with a reduced nuclear translocation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-83	Fas cell surface death receptor	Homo sapiens	0-4
11465715-9	2001	Procaspase 3 processing was enhanced by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-71	caspase 3	Homo sapiens	0-12
11368167-4	2001	Exposure of HO-1-expressing hepatocytes to cycloheximide unraveled a hyperosmotic acceleration of HO-1 degradation which was counteracted by betaine and the proteolysis inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	179-185	heme oxygenase 1	Rattus norvegicus	12-16
11331270-6	2001	ET1 potently stimulated the nuclear factor-kappaB pathway, and this effect was inhibited by overexpression of the inhibitor of kappaB dominant negative mutant (IkappaBalpham) and by treatment with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	222-228	endothelin 1	Homo sapiens	0-3
11331270-7	2001	Importantly, IkappaBalpham and MG-132 had similar inhibitory effects on ET1-induced activation of PKA without affecting G(s)-mediated activation of PKA or ET1-induced phosphorylation of mitogen-activated protein kinase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-37	endothelin 1	Homo sapiens	72-75
11368525-5	2001	MG132 caused glycosylated Bbeta to accumulate on Sec61beta in COS cells expressing Bbeta and acted similarly with all three fibrinogen chains in HepG2 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	SEC61 translocon subunit beta	Homo sapiens	49-58
11444925-5	2001	Addition of proteasome inhibitor MG132 or adenoviral expression of a truncated I kappa B alpha (I kappa B Delta N) inhibited TNF-alpha-induced NF-kappa B nuclear translocation in a dose-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	tumor necrosis factor	Rattus norvegicus	125-134
12578613-6	2001	A highly sensitive colorimetric assay was employed and the elevation of caspase-3 activity was detected in both cell lines after treatment with Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-153	caspase 3	Homo sapiens	72-81
12578613-7	2001	By comparison, these results showed that the leukemic cell line M-07e and KG-1a, which both express bcl-2 at a relative high level, had different susceptibility to undergo apoptosis induced by Z-LLL-CHO, which possibly due to their different levels of expression and activation of caspase-3 precursor, as well as their different degree of bcl-2 cleavage after treated by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-202	BCL2 apoptosis regulator	Homo sapiens	100-105
12578613-7	2001	By comparison, these results showed that the leukemic cell line M-07e and KG-1a, which both express bcl-2 at a relative high level, had different susceptibility to undergo apoptosis induced by Z-LLL-CHO, which possibly due to their different levels of expression and activation of caspase-3 precursor, as well as their different degree of bcl-2 cleavage after treated by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-202	caspase 3	Homo sapiens	281-290
12578613-7	2001	By comparison, these results showed that the leukemic cell line M-07e and KG-1a, which both express bcl-2 at a relative high level, had different susceptibility to undergo apoptosis induced by Z-LLL-CHO, which possibly due to their different levels of expression and activation of caspase-3 precursor, as well as their different degree of bcl-2 cleavage after treated by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-202	BCL2 apoptosis regulator	Homo sapiens	339-344
12578613-7	2001	By comparison, these results showed that the leukemic cell line M-07e and KG-1a, which both express bcl-2 at a relative high level, had different susceptibility to undergo apoptosis induced by Z-LLL-CHO, which possibly due to their different levels of expression and activation of caspase-3 precursor, as well as their different degree of bcl-2 cleavage after treated by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	371-380	BCL2 apoptosis regulator	Homo sapiens	100-105
11422196-5	2001	Inhibition of endothelial NF-kappaB activation using the proteosome inhibitors MG-132 and BAY 11-7082 resulted in a significant decrease of ICAM-1 expression, indicating an important role for NF-kappaB in this response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	nuclear factor kappa B subunit 1	Homo sapiens	26-35
11422196-5	2001	Inhibition of endothelial NF-kappaB activation using the proteosome inhibitors MG-132 and BAY 11-7082 resulted in a significant decrease of ICAM-1 expression, indicating an important role for NF-kappaB in this response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	intercellular adhesion molecule 1	Homo sapiens	140-146
11422196-5	2001	Inhibition of endothelial NF-kappaB activation using the proteosome inhibitors MG-132 and BAY 11-7082 resulted in a significant decrease of ICAM-1 expression, indicating an important role for NF-kappaB in this response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	nuclear factor kappa B subunit 1	Homo sapiens	192-201
11329373-4	2001	Immunocytochemistry of fixed human fibroblasts treated with either UV light, the kinase and transcription inhibitor DRB or the proteasome inhibitor MG132 revealed abundant p53 localized to the nucleus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	148-153	tumor protein p53	Homo sapiens	172-175
11329373-6	2001	However, in cells treated with MG132, residual p53 localized to distinct large foci.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	tumor protein p53	Homo sapiens	47-50
11312270-3	2001	Treatment with the proteasomal inhibitors lactacystin, MG132, and N-acetyl-l-leucinyl-l-leucinyl-l-norleucinal resulted in the accumulation of iNOS, indicating that these inhibitors blocked its degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	nitric oxide synthase 2	Homo sapiens	143-147
11359904-3	2001	Treatment of SV80 cells with the proteasome inhibitor N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal (MG-132) or geldanamycin, a drug interfering with tumor necrosis factor (TNF)-induced NF-kappaB activation, inhibited TNF-induced upregulation of cFLIP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-103	tumor necrosis factor	Homo sapiens	146-167
11350057-6	2001	The TNF-alpha-induced increase in transgenic I(kappa)B-alpha appeared to result from the stabilization of newly synthesized I(kappa)B-alpha, since this increase was effectively preempted by a proteasome inhibitor (MG132) or by I(kappa)B-alpha stabilization through the deletion C-terminal destabilizing elements (without additive or synergistic effects).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-219	tumor necrosis factor	Homo sapiens	4-13
11292609-7	2001	Inhibition of NF-kappaB binding activity by sulfasalazine or MG-132 not only prevented the increased susceptibility to STS-induced apoptosis but also blocked the resistance to cell death induced by TNF-alpha in combination with cycloheximide in polyamine-deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-67	tumor necrosis factor	Rattus norvegicus	198-207
11309196-3	2001	Induction of apoptosis by staurosporine or MG132 and oxidative stress by H(2)O(2) or FeCN enhanced the nuclear translocation of endogenous GAPDH in all cell types, as detected by immunocytochemistry.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	139-144
11368167-4	2001	Exposure of HO-1-expressing hepatocytes to cycloheximide unraveled a hyperosmotic acceleration of HO-1 degradation which was counteracted by betaine and the proteolysis inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	179-185	heme oxygenase 1	Rattus norvegicus	98-102
11264351-12	2001	Treatment of HCMV-infected cells with MG132, an inhibitor of proteasome-mediated proteolysis, provided substantial protection of p21cip1 in mock-infected cells, but MG132 was much less effective in protecting p21cip1 in HCMV-infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	cyclin dependent kinase inhibitor 1A	Homo sapiens	129-136
11152671-3	2001	Here, we present evidence that the proteasomal inhibitor MG132 prolongs the GH-induced activity of both GHR and JAK2, presumably through stabilization of GHR and JAK2 tyrosine phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	growth hormone receptor	Homo sapiens	104-107
11152671-3	2001	Here, we present evidence that the proteasomal inhibitor MG132 prolongs the GH-induced activity of both GHR and JAK2, presumably through stabilization of GHR and JAK2 tyrosine phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	Janus kinase 2	Homo sapiens	112-116
11152671-3	2001	Here, we present evidence that the proteasomal inhibitor MG132 prolongs the GH-induced activity of both GHR and JAK2, presumably through stabilization of GHR and JAK2 tyrosine phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	growth hormone receptor	Homo sapiens	154-157
11152671-3	2001	Here, we present evidence that the proteasomal inhibitor MG132 prolongs the GH-induced activity of both GHR and JAK2, presumably through stabilization of GHR and JAK2 tyrosine phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	Janus kinase 2	Homo sapiens	162-166
11264351-12	2001	Treatment of HCMV-infected cells with MG132, an inhibitor of proteasome-mediated proteolysis, provided substantial protection of p21cip1 in mock-infected cells, but MG132 was much less effective in protecting p21cip1 in HCMV-infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	cyclin dependent kinase inhibitor 1A	Homo sapiens	209-216
11237715-5	2001	Treatment with MG132, a potent proteasome inhibitor, resulted in the accumulation of ubiquitinated Dorfin and Dorfin-associated cellular proteins in cultured cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	ring finger protein 19A, RBR E3 ubiquitin protein ligase	Homo sapiens	99-105
11115510-3	2001	Inhibiting the degradation of IkappaBalpha by pretreatment with the proteasome inhibitor MG-132 significantly inhibited NF-kappaB activation and apoptosis but not DNA damage induced by SN-38 or VP-16.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-95	NFKB inhibitor alpha	Homo sapiens	30-42
11115510-3	2001	Inhibiting the degradation of IkappaBalpha by pretreatment with the proteasome inhibitor MG-132 significantly inhibited NF-kappaB activation and apoptosis but not DNA damage induced by SN-38 or VP-16.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	89-95	host cell factor C1	Homo sapiens	194-199
11115510-6	2001	In contrast to pretreatment with MG-132, exposure to MG-132 after SN-38 or VP-16 treatment of neo or mIkappaBalpha cells decreased cell cycle arrest in the S/G2 + M fraction and enhanced apoptosis compared with drug alone.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	host cell factor C1	Homo sapiens	75-80
11237715-5	2001	Treatment with MG132, a potent proteasome inhibitor, resulted in the accumulation of ubiquitinated Dorfin and Dorfin-associated cellular proteins in cultured cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	15-20	ring finger protein 19A, RBR E3 ubiquitin protein ligase	Homo sapiens	110-116
11179729-7	2001	With proteasome inhibitor MG-132 formation of Sug-1-RXRbeta-VDR-VDRE complex was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	proteasome 26S subunit, ATPase 5	Homo sapiens	46-51
11319608-8	2001	However, in the presence of the proteasome inhibitors MG-132, lactacystin or ALLN we found that cells overexpressing pro-caspase-3 are rapidly targeted for apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-60	caspase 3	Homo sapiens	117-130
11179729-7	2001	With proteasome inhibitor MG-132 formation of Sug-1-RXRbeta-VDR-VDRE complex was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	retinoid X receptor beta	Homo sapiens	52-59
11179729-7	2001	With proteasome inhibitor MG-132 formation of Sug-1-RXRbeta-VDR-VDRE complex was detected.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	vitamin D receptor	Homo sapiens	60-63
11172811-0	2001	The proteasome inhibitor MG132 promotes accumulation of the steroidogenic acute regulatory protein (StAR) and steroidogenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	steroidogenic acute regulatory protein	Homo sapiens	60-98
11226337-6	2001	Immunoblots demonstrated ubiquitination of AQP1 under control conditions that increased after treatment with proteasome inhibitors (MG132, lactacystin).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	132-137	aquaporin 1 (Colton blood group)	Homo sapiens	43-47
11314019-4	2001	Treatment with various NF-kappaB inhibitors (Gliotoxin, MG132 and Sulfasalazine), or transfection with the IkappaBalpha super-repressor, strongly enhanced the apoptotic effects of VP16 or doxorubicin on resistant Capan-1 and 818-4 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	nuclear factor kappa B subunit 1	Homo sapiens	23-32
11172811-0	2001	The proteasome inhibitor MG132 promotes accumulation of the steroidogenic acute regulatory protein (StAR) and steroidogenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	steroidogenic acute regulatory protein	Homo sapiens	100-104
11172811-8	2001	The increase of the 37 kDa StAR protein was evident after 15 min and 30 min of incubation with MG132 (143% and 187% of control values, respectively) with no significant elevation of the 30 kDa protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	steroidogenic acute regulatory protein	Homo sapiens	27-31
11172811-12	2001	Moreover, it seems that the cytosolic 37 kDa protein, which is responsible for the steroidogenic activity of StAR, is the primary proteasomal substrate and that the inhibition of its degradation by MG132 causes the up-regulation of progesterone production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	198-203	steroidogenic acute regulatory protein	Homo sapiens	109-113
11161273-12	2001	EBNA-5 also enhanced the nucleolar translocation of a mutant p53 in a colon cancer line, SW480, treated with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	tumor protein p53	Homo sapiens	61-64
11161273-13	2001	The coordinated changes in EBNA-5 and Hsp70 localization and the effect of EBNA-5 on mutant p53 distribution upon MG132 treatment might reflect the involvement of EBNA-5 in the regulation of intracellular protein trafficking associated with the proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	tumor protein p53	Homo sapiens	92-95
11160671-12	2001	Finally, we demonstrate that the presence of the proteasome inhibitor MG-132 inhibits the induction of NF-kappa B binding, as well as IL-8 expression, supporting the role of NF-kappa B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	nuclear factor kappa B subunit 1	Homo sapiens	103-113
11160671-12	2001	Finally, we demonstrate that the presence of the proteasome inhibitor MG-132 inhibits the induction of NF-kappa B binding, as well as IL-8 expression, supporting the role of NF-kappa B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	C-X-C motif chemokine ligand 8	Homo sapiens	134-138
11160671-12	2001	Finally, we demonstrate that the presence of the proteasome inhibitor MG-132 inhibits the induction of NF-kappa B binding, as well as IL-8 expression, supporting the role of NF-kappa B.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	nuclear factor kappa B subunit 1	Homo sapiens	174-184
11527157-2	2001	We showed that treatment of HeLa cells with MG132, a proteasome inhibitor and known INK activator, caused the transcriptional activation domain of HSF1 to be targeted and phosphorylated by JNK2 in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	heat shock transcription factor 1	Homo sapiens	147-151
11272138-6	2001	Inhibitors of NF-kappaB activation-the proteasome inhibitor MG-132 and the antioxidant pyrrolidine-dithiocarbamate (PDTC)-prevented poly IC + IFN-gamma-induced iNOS expression and nitric oxide production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-66	interferon gamma	Rattus norvegicus	142-151
11272138-6	2001	Inhibitors of NF-kappaB activation-the proteasome inhibitor MG-132 and the antioxidant pyrrolidine-dithiocarbamate (PDTC)-prevented poly IC + IFN-gamma-induced iNOS expression and nitric oxide production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-66	nitric oxide synthase 2	Rattus norvegicus	160-164
11272138-7	2001	Incubation of rat islets for 3 h or human islets for 2 h with poly IC alone or poly IC + IFN-gamma resulted in NF-kappaB nuclear translocation and degradation of the NF-kappaB inhibitor protein, IkappaB, events that are prevented by MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	233-239	interferon gamma	Homo sapiens	89-98
11160862-8	2001	Mutant NQO1 incubated in rabbit reticulocyte lysate with MG132 resulted in the accumulation of proteins with increased molecular masses that were immunoreactive for both NQO1 and ubiquitin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	NAD(P)H dehydrogenase [quinone] 1	Oryctolagus cuniculus	7-11
11160862-8	2001	Mutant NQO1 incubated in rabbit reticulocyte lysate with MG132 resulted in the accumulation of proteins with increased molecular masses that were immunoreactive for both NQO1 and ubiquitin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	NAD(P)H dehydrogenase [quinone] 1	Oryctolagus cuniculus	170-174
11158586-3	2001	We used high-resolution microscopy to study the distribution of PML protein and other POD-associated proteins along with the proteasomes themselves under normal conditions and in cells treated with the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	PML nuclear body scaffold	Homo sapiens	64-67
11158586-5	2001	After 6-10 h of MG132 treatment, PML, Sp100, and SUMO-1 were no longer detectable in the PODs and accumulated mainly in the nucleolus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	PML nuclear body scaffold	Homo sapiens	33-36
11158586-5	2001	After 6-10 h of MG132 treatment, PML, Sp100, and SUMO-1 were no longer detectable in the PODs and accumulated mainly in the nucleolus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	SP100 nuclear antigen	Homo sapiens	38-43
11158586-5	2001	After 6-10 h of MG132 treatment, PML, Sp100, and SUMO-1 were no longer detectable in the PODs and accumulated mainly in the nucleolus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-21	small ubiquitin like modifier 1	Homo sapiens	49-55
11158615-6	2001	This reduction was prevented by the proteasome inhibitors MG132 and lactacystin, suggesting enhanced p53 degradation in the presence of dicoumarol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	tumor protein p53	Homo sapiens	101-104
11162503-6	2001	Accordingly, we show that proteasomal inhibitors MG-132, lactacystin, and PSI caused a prominent upregulation of p62 mRNA and protein expression, with a concomitant increase in ubiquitinated proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-55	nucleoporin 62	Mus musculus	113-116
11527157-2	2001	We showed that treatment of HeLa cells with MG132, a proteasome inhibitor and known INK activator, caused the transcriptional activation domain of HSF1 to be targeted and phosphorylated by JNK2 in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	mitogen-activated protein kinase 9	Homo sapiens	189-193
10991939-5	2000	The proteasome inhibitor MG132 blocked this protein degradation and also blocked the inhibitory action of CIS, but not that of SOCS-1 or SOCS-3, on STAT5b signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cytokine inducible SH2-containing protein	Rattus norvegicus	106-109
11311545-6	2001	Neuronal injury-induced glial apoE secretion is attenuated by the nuclear factor kappaB inhibitors, aspirin, Bay 11-7082 and MG-132, suggesting that this transcription factor is involved in both constitutive and induced glial apoE expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	125-131	apolipoprotein E	Homo sapiens	30-34
11162356-6	2001	In addition, the inhibitor of NF-kappaB, IkappaB-alpha, became phosphorylated and was rapidly degraded in cytokine-treated cells; this process was abolished by co-incubation with the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	205-211	nuclear factor kappa B subunit 1	Homo sapiens	30-39
11162356-6	2001	In addition, the inhibitor of NF-kappaB, IkappaB-alpha, became phosphorylated and was rapidly degraded in cytokine-treated cells; this process was abolished by co-incubation with the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	205-211	NFKB inhibitor alpha	Homo sapiens	41-54
11162356-7	2001	Finally, when cells were pre-incubated with MG-132 and then challenged with TNF-alpha, PG formation was attenuated in a concentration-dependent manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	tumor necrosis factor	Homo sapiens	76-85
11104703-5	2000	However, pretreatment with the proteasome inhibitor MG132 under conditions that prevented the IL-1beta-dependent activation of the nuclear factor NF-kappaB also blocked the inhibitory effect of IL-1beta on IL-6-activated STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	interleukin 1 beta	Homo sapiens	94-102
11104703-5	2000	However, pretreatment with the proteasome inhibitor MG132 under conditions that prevented the IL-1beta-dependent activation of the nuclear factor NF-kappaB also blocked the inhibitory effect of IL-1beta on IL-6-activated STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	nuclear factor kappa B subunit 1	Homo sapiens	146-155
11104703-5	2000	However, pretreatment with the proteasome inhibitor MG132 under conditions that prevented the IL-1beta-dependent activation of the nuclear factor NF-kappaB also blocked the inhibitory effect of IL-1beta on IL-6-activated STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	interleukin 1 beta	Homo sapiens	194-202
11104703-5	2000	However, pretreatment with the proteasome inhibitor MG132 under conditions that prevented the IL-1beta-dependent activation of the nuclear factor NF-kappaB also blocked the inhibitory effect of IL-1beta on IL-6-activated STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	interleukin 6	Homo sapiens	206-210
11104703-5	2000	However, pretreatment with the proteasome inhibitor MG132 under conditions that prevented the IL-1beta-dependent activation of the nuclear factor NF-kappaB also blocked the inhibitory effect of IL-1beta on IL-6-activated STAT1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	signal transducer and activator of transcription 1	Homo sapiens	221-226
10991939-5	2000	The proteasome inhibitor MG132 blocked this protein degradation and also blocked the inhibitory action of CIS, but not that of SOCS-1 or SOCS-3, on STAT5b signaling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	signal transducer and activator of transcription 5B	Rattus norvegicus	148-154
10991939-7	2000	Finally, the down-regulation of GHR-JAK2 signaling to STAT5b seen in continuous GH-treated cells could be prevented by treatment of cells with the proteasome inhibitor MG132 or by expression of CIS-R107K, a selective, dominant-negative inhibitor of CIS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	growth hormone receptor	Rattus norvegicus	32-35
10991939-7	2000	Finally, the down-regulation of GHR-JAK2 signaling to STAT5b seen in continuous GH-treated cells could be prevented by treatment of cells with the proteasome inhibitor MG132 or by expression of CIS-R107K, a selective, dominant-negative inhibitor of CIS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	Janus kinase 2	Rattus norvegicus	36-40
10991939-7	2000	Finally, the down-regulation of GHR-JAK2 signaling to STAT5b seen in continuous GH-treated cells could be prevented by treatment of cells with the proteasome inhibitor MG132 or by expression of CIS-R107K, a selective, dominant-negative inhibitor of CIS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	signal transducer and activator of transcription 5B	Rattus norvegicus	54-60
10991939-7	2000	Finally, the down-regulation of GHR-JAK2 signaling to STAT5b seen in continuous GH-treated cells could be prevented by treatment of cells with the proteasome inhibitor MG132 or by expression of CIS-R107K, a selective, dominant-negative inhibitor of CIS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	gonadotropin releasing hormone receptor	Rattus norvegicus	32-34
10991939-7	2000	Finally, the down-regulation of GHR-JAK2 signaling to STAT5b seen in continuous GH-treated cells could be prevented by treatment of cells with the proteasome inhibitor MG132 or by expression of CIS-R107K, a selective, dominant-negative inhibitor of CIS activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	168-173	cytokine inducible SH2-containing protein	Rattus norvegicus	249-252
11073163-5	2000	Induction of apoptosis by lactacystin or ZLLLal was accompanied by cell cycle arrest at G2/M phase and by accumulation and stabilization of cyclin-dependent kinase inhibitor p21WAF1/Cip and tumor suppressor protein p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	muscular LMNA interacting protein	Homo sapiens	182-185
10938272-8	2000	The proteasome inhibitors MG-132 and lactacystin completely protected HDAC1 from the action of quinidine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	histone deacetylase 1	Homo sapiens	70-75
11004677-11	2000	However, the proteasome inhibitor MG132 sensitised to TRAIL in resistant cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	TNF superfamily member 10	Homo sapiens	54-59
10973975-7	2000	Treatment with proteasomal inhibitors (MG-132, MG-115, lactacystin, or proteasome inhibitor I), but not lysosomal inhibitors, prevented degradation of LGMD-1C caveolin-3 mutants.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	caveolin 3	Homo sapiens	159-169
10934190-9	2000	Using the proteasome inhibitor MG132, we show that when degradation of I kappa B alpha is inhibited, A238Lp binding to NF-kappa B p65 is reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	NFKB inhibitor alpha	Homo sapiens	71-86
10934190-9	2000	Using the proteasome inhibitor MG132, we show that when degradation of I kappa B alpha is inhibited, A238Lp binding to NF-kappa B p65 is reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	nuclear factor kappa B subunit 1	Homo sapiens	119-129
10934190-9	2000	Using the proteasome inhibitor MG132, we show that when degradation of I kappa B alpha is inhibited, A238Lp binding to NF-kappa B p65 is reduced.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	RELA proto-oncogene, NF-kB subunit	Homo sapiens	130-133
11073163-5	2000	Induction of apoptosis by lactacystin or ZLLLal was accompanied by cell cycle arrest at G2/M phase and by accumulation and stabilization of cyclin-dependent kinase inhibitor p21WAF1/Cip and tumor suppressor protein p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	tumor protein p53	Homo sapiens	215-218
10930537-5	2000	Pretreatment of U937 cells with MG132 or LLnL inhibited etoposide-induced morphological apoptosis and caspase-3 activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	caspase 3	Homo sapiens	102-111
11006097-1	2000	Treating HepG2 cells with MG132 for 4 h to inhibit proteasomal activity increased androgen receptor immunoreactivity in two major bands with molecular weights of 102 and 110 kDa by 77% each (P &lt; 0.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	androgen receptor	Homo sapiens	82-99
11006097-4	2000	Antiubiquitin immunoreactivity comigrating with the androgen receptor bands was also increased by MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	androgen receptor	Homo sapiens	52-69
10930537-6	2000	Furthermore, MG132 or LLnL prevented NF-kappaB activation and IkappaBalpha degradation, but not IkappaBalpha phosphorylation at Ser32.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	nuclear factor kappa B subunit 1	Homo sapiens	37-46
10930537-6	2000	Furthermore, MG132 or LLnL prevented NF-kappaB activation and IkappaBalpha degradation, but not IkappaBalpha phosphorylation at Ser32.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	NFKB inhibitor alpha	Homo sapiens	62-74
10942602-5	2000	Inhibition of the ubiquitin-dependent proteasome pathway by MG132 results in stabilization of MyoD-wt, with little effect on a MyoD mutant where serine 200 is replaced by an alanine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	myogenic differentiation 1	Homo sapiens	94-98
10956637-6	2000	Gel shift and Western blot analyses confirmed that TNF-alpha activated NF-kappaB and depleted IkappaB in this system and that these effects were prevented by MG-132 and pyrrolidine dithiocarbamate.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	158-164	tumor necrosis factor	Rattus norvegicus	51-60
10965915-10	2000	When cells were coincubated with progesterone and the proteasome inhibitor, MG132 (1 microM), the expected decrease in PR protein was abrogated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	progesterone receptor	Rattus norvegicus	119-121
11005380-3	2000	Here, we show that although stress caused by the proteasome inhibitors MG132 and clasto-lactacystine beta-lactone induces the expression of Hsp70, the formation of HSF1 granules is affected differently in comparison to heat shock.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	heat shock protein family A (Hsp70) member 4	Homo sapiens	140-145
10969781-2	2000	We demonstrated that treatment of THP-1 human monocytic leukemia cells with Z-LLL-CHO, a reversible proteasome inhibitor, induced cell death through an apoptotic pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-85	GLI family zinc finger 2	Homo sapiens	34-39
10969781-3	2000	Apoptosis in THP-1 cells induced by Z-LLL-CHO involved a cytochrome c-dependent pathway, which included the release of mitochondrial cytochrome c, activation of caspase-9 and -3, and cleavage of Bcl-2 into a shortened 22-kDa fragment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-45	GLI family zinc finger 2	Homo sapiens	13-18
10969781-3	2000	Apoptosis in THP-1 cells induced by Z-LLL-CHO involved a cytochrome c-dependent pathway, which included the release of mitochondrial cytochrome c, activation of caspase-9 and -3, and cleavage of Bcl-2 into a shortened 22-kDa fragment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-45	cytochrome c, somatic	Homo sapiens	57-69
10969781-3	2000	Apoptosis in THP-1 cells induced by Z-LLL-CHO involved a cytochrome c-dependent pathway, which included the release of mitochondrial cytochrome c, activation of caspase-9 and -3, and cleavage of Bcl-2 into a shortened 22-kDa fragment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-45	cytochrome c, somatic	Homo sapiens	133-145
10969781-3	2000	Apoptosis in THP-1 cells induced by Z-LLL-CHO involved a cytochrome c-dependent pathway, which included the release of mitochondrial cytochrome c, activation of caspase-9 and -3, and cleavage of Bcl-2 into a shortened 22-kDa fragment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-45	caspase 9	Homo sapiens	161-177
10969781-3	2000	Apoptosis in THP-1 cells induced by Z-LLL-CHO involved a cytochrome c-dependent pathway, which included the release of mitochondrial cytochrome c, activation of caspase-9 and -3, and cleavage of Bcl-2 into a shortened 22-kDa fragment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-45	BCL2 apoptosis regulator	Homo sapiens	195-200
10969781-6	2000	Interestingly, when THP-1 cells were induced to undergo monocytic differentiation by bryostatin 1, a naturally occurring protein kinase C activator, they were no longer susceptible to apoptosis induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	205-214	GLI family zinc finger 2	Homo sapiens	20-25
10969781-8	2000	Likewise, differentiated THP-1 cells were refractory to Z-LLL-CHO-induced cytochrome c release, caspase activation, and Bcl-2 cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	GLI family zinc finger 2	Homo sapiens	25-30
10969781-8	2000	Likewise, differentiated THP-1 cells were refractory to Z-LLL-CHO-induced cytochrome c release, caspase activation, and Bcl-2 cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	cytochrome c, somatic	Homo sapiens	74-86
10969781-8	2000	Likewise, differentiated THP-1 cells were refractory to Z-LLL-CHO-induced cytochrome c release, caspase activation, and Bcl-2 cleavage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	BCL2 apoptosis regulator	Homo sapiens	120-125
10969781-9	2000	Resistance to Z-LLL-CHO-induced apoptosis in differentiated THP-1 cells was not due to cell cycle arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-23	GLI family zinc finger 2	Homo sapiens	60-65
10891461-8	2000	In contrast, p53 was stabilized by MG132 or LLnL in malignant and normal cells undergoing apoptosis, indicating that in normal lymphocytes p53 is regulated mainly by calpains and not by the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	tumor protein p53	Homo sapiens	13-16
11005380-3	2000	Here, we show that although stress caused by the proteasome inhibitors MG132 and clasto-lactacystine beta-lactone induces the expression of Hsp70, the formation of HSF1 granules is affected differently in comparison to heat shock.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	71-76	heat shock transcription factor 1	Homo sapiens	164-168
10694430-7	2000	MITF protein was stabilized by the proteasome inhibitor MG132, indicating the role of the ubiquitin-proteasome system in MITF degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	melanocyte inducing transcription factor	Homo sapiens	0-4
10873576-5	2000	NF-kappaB activation was blocked by either adenovirus-mediated overexpression of IkappaBalpha superrepressor or pretreatment with proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	152-157	nuclear factor kappa B subunit 1	Homo sapiens	0-9
10837373-8	2000	With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	H3 histone pseudogene 16	Homo sapiens	87-90
10837373-8	2000	With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	tumor protein p53	Homo sapiens	95-98
10837373-8	2000	With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	H3 histone pseudogene 16	Homo sapiens	155-158
10837373-8	2000	With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	tumor protein p53	Homo sapiens	220-223
10748190-6	2000	UV-induced IL-6 release is mediated via NFkappaB since the NFkappaB inhibitor MG132 or transfection of cells with a super-repressor form of the NFkappaB inhibitor IkappaB reduced IL-6 release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	interleukin 6	Homo sapiens	11-15
10748190-6	2000	UV-induced IL-6 release is mediated via NFkappaB since the NFkappaB inhibitor MG132 or transfection of cells with a super-repressor form of the NFkappaB inhibitor IkappaB reduced IL-6 release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	nuclear factor kappa B subunit 1	Homo sapiens	40-48
10748190-6	2000	UV-induced IL-6 release is mediated via NFkappaB since the NFkappaB inhibitor MG132 or transfection of cells with a super-repressor form of the NFkappaB inhibitor IkappaB reduced IL-6 release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	nuclear factor kappa B subunit 1	Homo sapiens	59-67
10748190-6	2000	UV-induced IL-6 release is mediated via NFkappaB since the NFkappaB inhibitor MG132 or transfection of cells with a super-repressor form of the NFkappaB inhibitor IkappaB reduced IL-6 release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	nuclear factor kappa B subunit 1	Homo sapiens	59-67
10748190-6	2000	UV-induced IL-6 release is mediated via NFkappaB since the NFkappaB inhibitor MG132 or transfection of cells with a super-repressor form of the NFkappaB inhibitor IkappaB reduced IL-6 release.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	interleukin 6	Homo sapiens	179-183
10800947-8	2000	Glutamate-dependent iNOS expression was concentration-dependent and was blocked by EGTA and by the inhibitors of nuclear factor kappaB (NF-kappaB) activation pyrrolidine dithiocarbamate and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	nitric oxide synthase 2	Rattus norvegicus	20-24
10786691-6	2000	The addition of proteasome inhibitors MG132 and LLvL, but not the lysosomal inhibitor E64, prevented loss of RARgamma and RXRalpha proteins after exposure of keratinocytes to either UV radiation or cycloheximide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	retinoic acid receptor gamma	Homo sapiens	109-117
10786691-6	2000	The addition of proteasome inhibitors MG132 and LLvL, but not the lysosomal inhibitor E64, prevented loss of RARgamma and RXRalpha proteins after exposure of keratinocytes to either UV radiation or cycloheximide.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	retinoid X receptor alpha	Homo sapiens	122-130
10744744-6	2000	MG-132, a specific proteasome inhibitor, abrogated GA-induced degradation of RIP but failed to restore the activation of IkappaB kinase by TNF, perhaps because, in the presence of GA and MG-132, RIP accumulated in a detergent-insoluble subcellular fraction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	receptor interacting serine/threonine kinase 1	Homo sapiens	77-80
10744744-6	2000	MG-132, a specific proteasome inhibitor, abrogated GA-induced degradation of RIP but failed to restore the activation of IkappaB kinase by TNF, perhaps because, in the presence of GA and MG-132, RIP accumulated in a detergent-insoluble subcellular fraction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	receptor interacting serine/threonine kinase 1	Homo sapiens	195-198
10744744-6	2000	MG-132, a specific proteasome inhibitor, abrogated GA-induced degradation of RIP but failed to restore the activation of IkappaB kinase by TNF, perhaps because, in the presence of GA and MG-132, RIP accumulated in a detergent-insoluble subcellular fraction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	187-193	receptor interacting serine/threonine kinase 1	Homo sapiens	195-198
10716728-10	2000	Last, PKCtheta-mediated activation of the same reporter was inhibited by the proteasome inhibitor MG132 (which blocks IkappaB degradation) and was found to involve IkappaB-kinase beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	protein kinase C theta	Homo sapiens	6-14
19002827-6	2000	Both RANKL- andIL-1beta-induced OCL formation from pOCs wasinhibited by ZLLL-H, a peptide inhibitor ofproteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	TNF superfamily member 11	Homo sapiens	5-10
10856232-6	2000	Extracts of sugar-starved (but not sugar-fed) Arabidopsis cells contained an ATP-independent, MG132-sensitive, neutral protease that cleaved Arabidopsis SPS, and the mammalian 14-3-3-regulated transcription factor, FKHR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	94-99	forkhead box O1	Homo sapiens	215-219
10766806-5	2000	The proteasome inhibitor (MG-132) and a dominant-negative mutant of nuclear factor-kappaB-inducing kinase also promoted TNFalpha- and Fas-mediated apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	tumor necrosis factor	Mus musculus	120-128
10736180-4	2000	Transient expression of wild-type CFTR in the presence of submicromolar concentrations of MG-132 blocks maturation of the protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	90-96	CF transmembrane conductance regulator	Homo sapiens	34-38
10736180-5	2000	We found that expression of CFTR in the presence of MG-132 trapped the protein in a trypsin-sensitive conformation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-58	CF transmembrane conductance regulator	Homo sapiens	28-32
10736180-8	2000	These results show that expression of CFTR in the presence of MG-132 traps the protein in an altered conformation that may be inactive.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	CF transmembrane conductance regulator	Homo sapiens	38-42
10722677-5	2000	Inhibitors of the 26 S proteasome, lactacystin and MG132, block the TCDD-induced turnover of AhR.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-56	aryl-hydrocarbon receptor	Mus musculus	93-96
10694430-7	2000	MITF protein was stabilized by the proteasome inhibitor MG132, indicating the role of the ubiquitin-proteasome system in MITF degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-61	melanocyte inducing transcription factor	Homo sapiens	121-125
10669726-9	2000	Inhibition of 26S proteasome activity by the use of lactacystin or MG132 completely blocked IGF-mediated degradation of IRS-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	insulin receptor substrate 1	Homo sapiens	120-125
10691992-10	2000	The use of the inhibitors MG-132 and lactacystine significantly inhibited the degradation of 1-512 HDC, suggesting that a ubiquitin-dependent, proteasome 26S proteolytic pathway is involved.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	histidine decarboxylase	Rattus norvegicus	99-102
10654938-3	2000	Among a variety of inhibitors examined, the proteasome inhibitors MG132 and lactacystin affected Stat4, Stat5 and Stat6 turnover by significantly stabilizing the tyrosine-phosphorylated form.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	signal transducer and activator of transcription 4	Homo sapiens	97-102
10654938-3	2000	Among a variety of inhibitors examined, the proteasome inhibitors MG132 and lactacystin affected Stat4, Stat5 and Stat6 turnover by significantly stabilizing the tyrosine-phosphorylated form.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	signal transducer and activator of transcription 5A	Homo sapiens	104-109
10654938-3	2000	Among a variety of inhibitors examined, the proteasome inhibitors MG132 and lactacystin affected Stat4, Stat5 and Stat6 turnover by significantly stabilizing the tyrosine-phosphorylated form.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	signal transducer and activator of transcription 6	Homo sapiens	114-119
10637303-2	2000	Here we show that the peptide aldehydes MG132 and PS1 and the specific proteasome inhibitor lactacystin effectively increased the half-life of kappa(NS1), arguing for a proteasome-mediated degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	influenza virus NS1A binding protein	Mus musculus	143-152
10731674-5	2000	Among various protease inhibitors tested, proteasome inhibitors MG115, MG101, MG132, and lactacystin effectively inhibited the intracellular degradation of TPH.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	tryptophan hydroxylase 1	Rattus norvegicus	156-159
10653974-5	2000	Inhibition of proteasome activity by the inhibitor MG-132 resulted in a marked increase in the VDR levels in cells treated with the vehicle or GS 1558 (2.5-fold and 2.7-fold, respectively), more than twice the levels observed in the presence of calcitriol or EB 1089 (1.2-fold and 1.1-fold, respectively).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	51-57	vitamin D receptor	Homo sapiens	95-98
10653974-7	2000	The electrophoretic mobility shift assay (EMSA) with nuclear extracts from MG-132-treated cells revealed formation of a high-molecular-weight RXRbeta-VDR-VDRE complex, which also contained Sug1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	vitamin D receptor	Homo sapiens	150-153
10653974-7	2000	The electrophoretic mobility shift assay (EMSA) with nuclear extracts from MG-132-treated cells revealed formation of a high-molecular-weight RXRbeta-VDR-VDRE complex, which also contained Sug1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-81	proteasome 26S subunit, ATPase 5	Homo sapiens	189-193
10667916-8	2000	Since treatment with proteasome inhibitors (MG-132, lactacystin) increased only the intracellular level of nascent, mutant P-gp, the decreased incorporation of (35)S-methionine/cysteine in Gly(-) P-gp appears to be due to degradation of improperly folded mutant protein by the proteasome and endoplasmic reticulum-associated proteases.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	ATP binding cassette subfamily B member 1	Homo sapiens	123-127
10667916-8	2000	Since treatment with proteasome inhibitors (MG-132, lactacystin) increased only the intracellular level of nascent, mutant P-gp, the decreased incorporation of (35)S-methionine/cysteine in Gly(-) P-gp appears to be due to degradation of improperly folded mutant protein by the proteasome and endoplasmic reticulum-associated proteases.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-50	ATP binding cassette subfamily B member 1	Homo sapiens	196-200
10551872-6	1999	The SNP-mediated degradation of IRP-2 in RAW 264.7 cells could be prevented by MG-132 or lactacystin, known inhibitors of proteasome-dependent protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	iron responsive element binding protein 2	Mus musculus	32-37
10611258-6	2000	The proteasome inhibitor MG132 (0.3 and 3 micromol/l) also caused a dose-dependent decrease in IL-1alpha and TNFalpha-stimulated IL-6 (P &lt; 0.001 and P &lt; 0.001 respectively) and leukaemia inhibitory factor (LIF) (P &lt; 0.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	interleukin 1 alpha	Homo sapiens	95-104
10611258-6	2000	The proteasome inhibitor MG132 (0.3 and 3 micromol/l) also caused a dose-dependent decrease in IL-1alpha and TNFalpha-stimulated IL-6 (P &lt; 0.001 and P &lt; 0.001 respectively) and leukaemia inhibitory factor (LIF) (P &lt; 0.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	tumor necrosis factor	Homo sapiens	109-117
10611258-6	2000	The proteasome inhibitor MG132 (0.3 and 3 micromol/l) also caused a dose-dependent decrease in IL-1alpha and TNFalpha-stimulated IL-6 (P &lt; 0.001 and P &lt; 0.001 respectively) and leukaemia inhibitory factor (LIF) (P &lt; 0.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	interleukin 6	Homo sapiens	129-133
10611258-6	2000	The proteasome inhibitor MG132 (0.3 and 3 micromol/l) also caused a dose-dependent decrease in IL-1alpha and TNFalpha-stimulated IL-6 (P &lt; 0.001 and P &lt; 0.001 respectively) and leukaemia inhibitory factor (LIF) (P &lt; 0.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	LIF interleukin 6 family cytokine	Homo sapiens	183-210
10611258-6	2000	The proteasome inhibitor MG132 (0.3 and 3 micromol/l) also caused a dose-dependent decrease in IL-1alpha and TNFalpha-stimulated IL-6 (P &lt; 0.001 and P &lt; 0.001 respectively) and leukaemia inhibitory factor (LIF) (P &lt; 0.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	LIF interleukin 6 family cytokine	Homo sapiens	212-215
10567231-6	1999	At 24 h after treatment with 500 nM MG132, apoptosis in bcl-x(L) cells (22%) was less than that observed in control cells (34%).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	BCL2-like 1	Mus musculus	56-64
10567231-8	1999	By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	BCL2-like 1	Mus musculus	65-73
10567231-8	1999	By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	heat shock protein 1B	Mus musculus	183-188
10567231-8	1999	By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	BCL2-like 1	Mus musculus	219-227
10567231-8	1999	By 48 h after MG132 treatment, apoptosis and caspase activity in bcl-x(L) cells were similar to those observed in control cells at 24 h. Proteasome inhibition stimulated increases in hsp70 protein levels in control and bcl-x(L) cells by 12 h, although the maximal increases found in bcl-x(L) cells were less.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	BCL2-like 1	Mus musculus	219-227
10567231-9	1999	Blocking this induction with hsp70 antisense oligonucleotides potentiated apoptosis after treatment with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-110	heat shock protein 1B	Mus musculus	29-34
10608813-13	1999	Inhibiting protein degradation with MG132 caused the constitutive activation of SAPK2/p38, which was blocked by a pretreatment with either cycloheximide or heat shock.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	mitogen-activated protein kinase 11	Homo sapiens	80-85
10608813-13	1999	Inhibiting protein degradation with MG132 caused the constitutive activation of SAPK2/p38, which was blocked by a pretreatment with either cycloheximide or heat shock.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	mitogen-activated protein kinase 14	Homo sapiens	86-89
10551872-8	1999	Importantly, the proteasome inhibitor MG-132 prevented the SNP-mediated decrease in TfR mRNA levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-44	transferrin receptor	Mus musculus	84-87
10531416-7	1999	The proteasome inhibitor MG132 (30 and 100 nM) and the calpain I inhibitor N-acetyl-Leu-Leu-leucinal (10 microM) attenuated the reduction in thrombin-stimulated cyclin D1 levels in ASM exposed to albuterol (100 nM), 8-bromo-cAMP (300 microM), or the phosphodiesterase inhibitor isobutylmethylxanthine (100 microM).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	coagulation factor II, thrombin	Homo sapiens	141-149
10554039-11	1999	MG132 also favored the release of cytochrome c from the mitochondria and increased the activity of caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	cytochrome c, somatic	Homo sapiens	34-46
10554039-11	1999	MG132 also favored the release of cytochrome c from the mitochondria and increased the activity of caspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	99-108
10554039-12	1999	When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	tumor protein p53	Homo sapiens	171-174
10554039-12	1999	When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	176-181
10554039-12	1999	When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	NFKB inhibitor alpha	Homo sapiens	187-199
10554039-14	1999	Clear synergistic effects concerning the activation of both caspase-3 and apoptosis were induced by a combination of suboptimal doses of sodium butyrate and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	157-162	caspase 3	Homo sapiens	60-69
10592469-9	1999	IL-8 production was significantly inhibited by N-acetyl-L-cysteine, FK506 and MG-132, inhibitors of NF-kappaB activation and translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
10592469-9	1999	IL-8 production was significantly inhibited by N-acetyl-L-cysteine, FK506 and MG-132, inhibitors of NF-kappaB activation and translocation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-84	nuclear factor kappa B subunit 1	Homo sapiens	100-109
10541287-7	1999	NF-kappaB inhibitor MG132 diminished the IL-1-induced expression of MCP-1 in mesangial cells and isolated glomeruli, whereas c-Jun/AP-1 inhibitor curcumin did not affect this process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	0-9
10541287-7	1999	NF-kappaB inhibitor MG132 diminished the IL-1-induced expression of MCP-1 in mesangial cells and isolated glomeruli, whereas c-Jun/AP-1 inhibitor curcumin did not affect this process.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-25	chemokine (C-C motif) ligand 2	Mus musculus	68-73
10531416-7	1999	The proteasome inhibitor MG132 (30 and 100 nM) and the calpain I inhibitor N-acetyl-Leu-Leu-leucinal (10 microM) attenuated the reduction in thrombin-stimulated cyclin D1 levels in ASM exposed to albuterol (100 nM), 8-bromo-cAMP (300 microM), or the phosphodiesterase inhibitor isobutylmethylxanthine (100 microM).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cyclin D1	Homo sapiens	161-170
10531416-7	1999	The proteasome inhibitor MG132 (30 and 100 nM) and the calpain I inhibitor N-acetyl-Leu-Leu-leucinal (10 microM) attenuated the reduction in thrombin-stimulated cyclin D1 levels in ASM exposed to albuterol (100 nM), 8-bromo-cAMP (300 microM), or the phosphodiesterase inhibitor isobutylmethylxanthine (100 microM).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	cathelicidin antimicrobial peptide	Homo sapiens	224-228
10544244-4	1999	TNF-induced upregulation of TRAF1 could be prevented by pretreatment of the cells with the proteasome inhibitor MG-132, whereas the PKC inhibitor Ro31-8220 was without effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	tumor necrosis factor	Homo sapiens	0-3
10531381-7	1999	MG132, a proteasome inhibitor, significantly prolonged the ligand-induced phosphorylation of both the EGFR and c-Cbl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	epidermal growth factor receptor	Homo sapiens	102-106
10531381-7	1999	MG132, a proteasome inhibitor, significantly prolonged the ligand-induced phosphorylation of both the EGFR and c-Cbl.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	Cbl proto-oncogene	Homo sapiens	111-116
10544244-4	1999	TNF-induced upregulation of TRAF1 could be prevented by pretreatment of the cells with the proteasome inhibitor MG-132, whereas the PKC inhibitor Ro31-8220 was without effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-118	TNF receptor associated factor 1	Homo sapiens	28-33
10529368-0	1999	Proteasome inhibitors lactacystin and MG132 inhibit the dephosphorylation of HSF1 after heat shock and suppress thermal induction of heat shock gene expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	heat shock transcription factor 1	Homo sapiens	77-81
10471409-5	1999	Furthermore, we show that Bcl-2 is degraded in mitosis by the proteasome-dependent pathway since Bcl-2 down-regulation is inhibited by proteasome inhibitors such as MG132, Lactacystin and LLnL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	165-170	BCL2 apoptosis regulator	Homo sapiens	26-31
10506575-3	1999	Here we report that immature, core-glycosylated P-gp that is prevented from reaching the cell surface by processing mutations or by proteasome inhibitors such as lactacystin or MG-132 exhibited no detectable drug-stimulated ATPase activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	177-183	ATP binding cassette subfamily B member 1	Homo sapiens	48-52
10493941-4	1999	The simultaneous apoptosis with Bcl2 phosphorylation was evident in cancer cells challenged with the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	123-128	BCL2 apoptosis regulator	Homo sapiens	32-36
10493941-5	1999	Our studies suggest that the proteasome inhibitor MG132 induced tumor cell killing is mediated through Bcl2 phosphorylation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	BCL2 apoptosis regulator	Homo sapiens	103-107
10504293-7	1999	Furthermore, the proteasome inhibitor MG132 induced an association between centromeres and ND10 proteins PML and Sp100 in a significant number of cells in the G(2) phase of the cell cycle.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	PML nuclear body scaffold	Homo sapiens	105-108
10504293-7	1999	Furthermore, the proteasome inhibitor MG132 induced an association between centromeres and ND10 proteins PML and Sp100 in a significant number of cells in the G(2) phase of the cell cycle.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	SP100 nuclear antigen	Homo sapiens	113-118
10471329-7	1999	In addition, treatment with the proteasome inhibitor MG132 increased the endogenous level of E2F1 protein in neurons.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	E2F transcription factor 1	Mus musculus	93-97
10471409-5	1999	Furthermore, we show that Bcl-2 is degraded in mitosis by the proteasome-dependent pathway since Bcl-2 down-regulation is inhibited by proteasome inhibitors such as MG132, Lactacystin and LLnL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	165-170	BCL2 apoptosis regulator	Homo sapiens	97-102
10455122-2	1999	Here we show that cell-cell dissociation during scattering induced by hepatocyte growth factor (HGF) or activation of the temperature-sensitive v-Src tyrosine kinase in MDCK cells can be blocked by inhibiting the proteasome with lactacystin and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-250	hepatocyte growth factor	Canis lupus familiaris	70-94
10455122-2	1999	Here we show that cell-cell dissociation during scattering induced by hepatocyte growth factor (HGF) or activation of the temperature-sensitive v-Src tyrosine kinase in MDCK cells can be blocked by inhibiting the proteasome with lactacystin and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	245-250	hepatocyte growth factor	Canis lupus familiaris	96-99
10347228-10	1999	Inhibition of IRP inactivation by cycloheximide or by the specific proteasome inhibitor MG132 correlated with the stabilization of TfR mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	Wnt family member 2	Homo sapiens	14-17
10441471-3	1999	In transfected COS cells, the degradation of fibrinogen Bbeta and gamma chain was markedly inhibited by the proteasome inhibitors lactacystin and MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	fibrinogen beta chain	Homo sapiens	45-55
10441471-5	1999	In HepG2 cells, which synthesize and secrete fibrinogen, the degradation of intracellular free gamma chain was also inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	fibrinogen beta chain	Homo sapiens	45-55
10433212-7	1999	Different types of NF-kappaB inhibitors, pyrrolidine dithiocarbamate and MG132, which specifically abolished IkappaB degradation and subsequent NF-kappaB activation by LPS, suppressed TNF alpha secretion from VSMC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	tumor necrosis factor	Rattus norvegicus	184-193
10433212-10	1999	TNF alpha messenger RNA expression induced by LPS was inhibited by pyrrolidine dithiocarbamate, MG132, and SB203580, but not by PD98059.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	96-101	tumor necrosis factor	Rattus norvegicus	0-9
10454636-7	1999	Consistent with the role of NF-kappaB in mediating dopamine responsiveness, the proteasome inhibitor MG132 abolished dopamine-induced transcriptional activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	nuclear factor kappa B subunit 1	Homo sapiens	28-37
10347228-10	1999	Inhibition of IRP inactivation by cycloheximide or by the specific proteasome inhibitor MG132 correlated with the stabilization of TfR mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	transferrin receptor	Homo sapiens	131-134
10415162-9	1999	Direct evidence that loss of NF-kappaB activity can sensitize brain cells to TNF cytotoxicity was obtained in vitro by co-administration of MG-132, an inhibitor of NF-kappaB activation, and TNF to neuronal-like and glial-like cell cultures.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	140-146	tumor necrosis factor-like	Rattus norvegicus	77-80
10075698-9	1999	Inhibitors of NF-kappaB signaling, lactacystin, and MG132 abolished the AR promoter response to TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	aldo-keto reductase family 1 member B	Homo sapiens	72-74
10229667-4	1999	Treatment of M-07e cells with benzyloxycarbonyl-Leu-Leu-l-leucinal (Z-LLL-CHO; MG-132), a reversible ubiquitin-proteasome inhibitor, markedly accelerated the cleavage of Bcl-2 and promoted cell death through the apoptotic pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	BCL2 apoptosis regulator	Homo sapiens	170-175
10075698-9	1999	Inhibitors of NF-kappaB signaling, lactacystin, and MG132 abolished the AR promoter response to TNF-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	tumor necrosis factor	Homo sapiens	96-105
10229667-6	1999	The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-160	colony stimulating factor 2	Homo sapiens	47-53
10229667-6	1999	The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-160	caspase 3	Homo sapiens	109-118
10229667-6	1999	The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-160	BCL2 apoptosis regulator	Homo sapiens	123-128
10229667-6	1999	The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-160	colony stimulating factor 2	Homo sapiens	57-63
10229667-6	1999	The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	278-287	colony stimulating factor 2	Homo sapiens	47-53
10229667-6	1999	The simultaneous addition of recombinant human GM-CSF (rhGM-CSF) to M-07e cultures delayed the activation of caspase 3 and Bcl-2 cleavage triggered by Z-LLL-CHO, suggesting that the activation of the GM-CSF signalling pathway can partly overcome the apoptotic effect induced by Z-LLL-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	278-287	colony stimulating factor 2	Homo sapiens	57-63
10226064-4	1999	In addition, the proteosome inhibitor MG132 did not affect activation of NF-kappaB by ROS/RNS, whereas it abolished the TNF response.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	tumor necrosis factor-like	Rattus norvegicus	120-123
10212182-7	1999	The decrease in p57 was inhibited by treating the cells with proteasome inhibitors, Z-Leu-Leu-Leu-aldehyde or lactacystin, but not with Z-Leu-Leu-aldehyde, which is an inhibitor of calpain, indicating that p57 is degraded through the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-106	cyclin-dependent kinase inhibitor 1C	Rattus norvegicus	16-19
10095055-7	1999	A similar induction is seen in cells treated with the proteosome inhibitor MG132 suggesting that elevated Hsc70 expression may be coupled to protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	heat shock protein 8	Mus musculus	106-111
10051559-4	1999	The treatment of mammalian cells with the proteasome inhibitor MG132 inhibits activity of the proteasome and blocks ER degradation, suggesting that ER protein is turned over through the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	estrogen receptor 1	Homo sapiens	116-118
10096573-8	1999	Pretreatment of Hs294T or RPE cells with proteasome inhibitors MG115 or MG132 captures the slower migrating, constitutively phosphorylated form of IkappaB-alpha in Hs294T melanoma cells, but not in RPE cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	NFKB inhibitor alpha	Homo sapiens	147-160
10051559-4	1999	The treatment of mammalian cells with the proteasome inhibitor MG132 inhibits activity of the proteasome and blocks ER degradation, suggesting that ER protein is turned over through the ubiquitin-proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	estrogen receptor 1	Homo sapiens	148-150
10051559-5	1999	In addition, we show that in vitro ER degradation depends on ubiquitin-activating E1 enzyme (UBA) and ubiquitin-conjugating E2 enzymes (UBCs), and the proteasome inhibitors MG132 and lactacystin block ER protein degradation in vitro.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-178	estrogen receptor 1	Homo sapiens	35-37
10209066-4	1999	The decline in STAT3 was inhibited by treatment with MG132, an inhibitor of proteasome-dependent protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	signal transducer and activator of transcription 3	Homo sapiens	15-20
10209066-6	1999	Loss of tyrosine phosphorylated STAT3 was inhibited by MG132 but did not require protein kinase C activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	signal transducer and activator of transcription 3	Homo sapiens	32-37
10037479-4	1999	Induction of neurite outgrowth with PSI, CI, or its close analogue, carbobenzoxy-Leu-Leu-leucinal (MG132), was associated with stress-activated protein kinase (SAPK) activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-97	mitogen-activated protein kinase 9	Rattus norvegicus	127-158
10037479-4	1999	Induction of neurite outgrowth with PSI, CI, or its close analogue, carbobenzoxy-Leu-Leu-leucinal (MG132), was associated with stress-activated protein kinase (SAPK) activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-97	mitogen-activated protein kinase 9	Rattus norvegicus	160-164
10037479-4	1999	Induction of neurite outgrowth with PSI, CI, or its close analogue, carbobenzoxy-Leu-Leu-leucinal (MG132), was associated with stress-activated protein kinase (SAPK) activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	mitogen-activated protein kinase 9	Rattus norvegicus	127-158
10037479-4	1999	Induction of neurite outgrowth with PSI, CI, or its close analogue, carbobenzoxy-Leu-Leu-leucinal (MG132), was associated with stress-activated protein kinase (SAPK) activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	99-104	mitogen-activated protein kinase 9	Rattus norvegicus	160-164
9973252-4	1999	Increased STAT5b DNA-binding activity was observed in cells treated with the proteasome inhibitor MG132, suggesting that at least one component of the GH receptor (GHR)-JAK2-STAT5b signaling pathway becomes labile in response to continuous GH treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	signal transducer and activator of transcription 5B	Rattus norvegicus	10-16
10229115-5	1999	In addition, we performed electrophoretic mobility shift analysis and determined that in microglia, the p50/p65 heterodimer of NF-kappaB is activated by LPS stimulation, and is inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	nuclear factor kappa B subunit 1	Homo sapiens	104-107
10229115-5	1999	In addition, we performed electrophoretic mobility shift analysis and determined that in microglia, the p50/p65 heterodimer of NF-kappaB is activated by LPS stimulation, and is inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	RELA proto-oncogene, NF-kB subunit	Homo sapiens	108-111
10229115-5	1999	In addition, we performed electrophoretic mobility shift analysis and determined that in microglia, the p50/p65 heterodimer of NF-kappaB is activated by LPS stimulation, and is inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-195	nuclear factor kappa B subunit 1	Homo sapiens	127-136
9950608-9	1999	RESULTS: TNF-alpha, IL-1beta, and TII but not IFN-gamma alone caused degradation of I kappaB, Rel A nuclear translocation, and increased NF-kappaB DNA binding activity, effects that were blocked by pretreatment with MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-222	tumor necrosis factor	Homo sapiens	9-18
9950608-9	1999	RESULTS: TNF-alpha, IL-1beta, and TII but not IFN-gamma alone caused degradation of I kappaB, Rel A nuclear translocation, and increased NF-kappaB DNA binding activity, effects that were blocked by pretreatment with MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-222	interleukin 1 beta	Homo sapiens	20-28
9950608-9	1999	RESULTS: TNF-alpha, IL-1beta, and TII but not IFN-gamma alone caused degradation of I kappaB, Rel A nuclear translocation, and increased NF-kappaB DNA binding activity, effects that were blocked by pretreatment with MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	216-222	nuclear factor kappa B subunit 1	Homo sapiens	137-146
9933632-3	1999	This induction of apoptosis was abolished by the caspase inhibitor zVAD-fmk, correlated with the inhibition of nuclear factor-kappa B (NF-kappaB), and was mimicked by a cell permeable inhibitory peptide of NF-kappaB, SN-50; other NF-kappaB inhibitors, curcumin and pyrrolidine dithiocarbamate; and the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	324-330	nuclear factor kappa B subunit 1	Homo sapiens	135-144
9933632-3	1999	This induction of apoptosis was abolished by the caspase inhibitor zVAD-fmk, correlated with the inhibition of nuclear factor-kappa B (NF-kappaB), and was mimicked by a cell permeable inhibitory peptide of NF-kappaB, SN-50; other NF-kappaB inhibitors, curcumin and pyrrolidine dithiocarbamate; and the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	324-330	nuclear factor kappa B subunit 1	Homo sapiens	206-215
9933632-3	1999	This induction of apoptosis was abolished by the caspase inhibitor zVAD-fmk, correlated with the inhibition of nuclear factor-kappa B (NF-kappaB), and was mimicked by a cell permeable inhibitory peptide of NF-kappaB, SN-50; other NF-kappaB inhibitors, curcumin and pyrrolidine dithiocarbamate; and the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	324-330	nuclear factor kappa B subunit 1	Homo sapiens	206-215
9973252-4	1999	Increased STAT5b DNA-binding activity was observed in cells treated with the proteasome inhibitor MG132, suggesting that at least one component of the GH receptor (GHR)-JAK2-STAT5b signaling pathway becomes labile in response to continuous GH treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	growth hormone receptor	Rattus norvegicus	151-162
9973252-4	1999	Increased STAT5b DNA-binding activity was observed in cells treated with the proteasome inhibitor MG132, suggesting that at least one component of the GH receptor (GHR)-JAK2-STAT5b signaling pathway becomes labile in response to continuous GH treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	growth hormone receptor	Rattus norvegicus	164-167
9973252-4	1999	Increased STAT5b DNA-binding activity was observed in cells treated with the proteasome inhibitor MG132, suggesting that at least one component of the GH receptor (GHR)-JAK2-STAT5b signaling pathway becomes labile in response to continuous GH treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	Janus kinase 2	Rattus norvegicus	169-173
9973252-4	1999	Increased STAT5b DNA-binding activity was observed in cells treated with the proteasome inhibitor MG132, suggesting that at least one component of the GH receptor (GHR)-JAK2-STAT5b signaling pathway becomes labile in response to continuous GH treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	signal transducer and activator of transcription 5B	Rattus norvegicus	174-180
9836745-1	1998	Identification Of the destruction box pathway and metaphase arrest produced by the proteasome inhibitor mg132 It is widely assumed that mitotic cyclins are rapidly degraded during anaphase, leading to the inactivation of the cell cycle-dependent protein kinase Cdc2 and allowing exit from mitosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	104-109	cell division control protein 2 homolog A	Nicotiana tabacum	262-266
9931444-5	1999	ApoB degradation was decreased to 50% when potent proteasome inhibitors, clasto-lactacystin beta-lactone (10 microM) or MG-132 (50 microM), were added to the reaction mixture, but was not affected by the cysteine protease inhibitor, E-64, or the serine protease inhibitor, phenylmethylsulfonyl fluoride.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	120-126	apolipoprotein B	Homo sapiens	0-4
9887050-5	1999	Pyrrolidinedithiocarbamate and the proteasome inhibitor MG-132 blocked TNF- and LPS-stimulated U-937 cell adhesion to HUVECs.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	56-62	tumor necrosis factor	Homo sapiens	71-74
10023669-10	1999	The proteasome inhibitor MG132 abrogated the HSV-1-induced PML and Sp100 degradation and partially restored their NB-localization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	PML nuclear body scaffold	Homo sapiens	59-62
10023669-10	1999	The proteasome inhibitor MG132 abrogated the HSV-1-induced PML and Sp100 degradation and partially restored their NB-localization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	SP100 nuclear antigen	Homo sapiens	67-72
9920768-0	1999	Proteasome inhibitors MG132 and lactacystin hyperphosphorylate HSF1 and induce hsp70 and hsp27 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	heat shock transcription factor 1	Homo sapiens	63-67
9920768-0	1999	Proteasome inhibitors MG132 and lactacystin hyperphosphorylate HSF1 and induce hsp70 and hsp27 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	heat shock protein family A (Hsp70) member 4	Homo sapiens	79-84
9920768-0	1999	Proteasome inhibitors MG132 and lactacystin hyperphosphorylate HSF1 and induce hsp70 and hsp27 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	heat shock protein family B (small) member 1	Homo sapiens	89-94
9920768-3	1999	Since trimerization of HSF1 is known to precede the acquisition of HSF1-DNA binding activity, it seems that MG132- and lactacystin-induced hyperphosphorylation of HSF1 causes conformational changes of HSF1 molecules at 37 degreesC and subsequently triggers its trimerization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	heat shock transcription factor 1	Homo sapiens	23-27
9920768-3	1999	Since trimerization of HSF1 is known to precede the acquisition of HSF1-DNA binding activity, it seems that MG132- and lactacystin-induced hyperphosphorylation of HSF1 causes conformational changes of HSF1 molecules at 37 degreesC and subsequently triggers its trimerization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	heat shock transcription factor 1	Homo sapiens	67-71
9920768-3	1999	Since trimerization of HSF1 is known to precede the acquisition of HSF1-DNA binding activity, it seems that MG132- and lactacystin-induced hyperphosphorylation of HSF1 causes conformational changes of HSF1 molecules at 37 degreesC and subsequently triggers its trimerization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	heat shock transcription factor 1	Homo sapiens	67-71
9920768-3	1999	Since trimerization of HSF1 is known to precede the acquisition of HSF1-DNA binding activity, it seems that MG132- and lactacystin-induced hyperphosphorylation of HSF1 causes conformational changes of HSF1 molecules at 37 degreesC and subsequently triggers its trimerization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	heat shock transcription factor 1	Homo sapiens	67-71
9920768-4	1999	Inhibition of protein synthesis by cycloheximide abolished the MG132- or lactacystin-induced hyperphosphorylation and DNA-binding activity of HSF1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	heat shock transcription factor 1	Homo sapiens	142-146
9920768-5	1999	These data suggest that the activity of a putative kinase(s) targeting HSF1 is upregulated in the presence of MG132 or lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	110-115	heat shock transcription factor 1	Homo sapiens	71-75
9892011-4	1999	JAK2 signaling to STAT5b at the conclusion of a GH pulse could be sustained by the protein synthesis inhibitor cycloheximide or by the proteasome inhibitor MG132, indicating that termination of this JAK2-catalyzed STAT activation loop requires synthesis of a labile or GH-inducible protein factor and is facilitated by the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-161	Janus kinase 2	Rattus norvegicus	0-4
9892011-4	1999	JAK2 signaling to STAT5b at the conclusion of a GH pulse could be sustained by the protein synthesis inhibitor cycloheximide or by the proteasome inhibitor MG132, indicating that termination of this JAK2-catalyzed STAT activation loop requires synthesis of a labile or GH-inducible protein factor and is facilitated by the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-161	signal transducer and activator of transcription 5B	Rattus norvegicus	18-24
9892011-4	1999	JAK2 signaling to STAT5b at the conclusion of a GH pulse could be sustained by the protein synthesis inhibitor cycloheximide or by the proteasome inhibitor MG132, indicating that termination of this JAK2-catalyzed STAT activation loop requires synthesis of a labile or GH-inducible protein factor and is facilitated by the proteasome pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	156-161	Janus kinase 2	Rattus norvegicus	199-203
9831079-4	1998	Furthermore, treatment of ROS 17/2.8 osteosarcoma cells with the proteasome inhibitors MG132 or beta-lactone increased steady-state levels of the VDR protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	87-92	vitamin D receptor	Rattus norvegicus	146-149
9831079-5	1998	In the presence cycloheximide (10 microg/ml), the liganded VDR protein was degraded with a half-life of approximately 8 h, and this rate of degradation was completely blocked by 0.05 mM MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	186-191	vitamin D receptor	Rattus norvegicus	59-62
9737957-4	1998	The degradation of c-Fos preceded caspase-3 activation and apoptotic nuclear chromatin condensation and was inhibited by the proteasome inhibitors MG132, N-acetyl-leucyl-leucyl-norleucinal, and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	FBJ osteosarcoma oncogene	Mus musculus	19-24
9786937-7	1998	Moreover, the proteasome inhibitor MG132, which inhibits IL-1-induced NFkappaB activation, completely prevented the protective effect of IL-1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	nuclear factor kappa B subunit 1	Homo sapiens	70-78
9737957-4	1998	The degradation of c-Fos preceded caspase-3 activation and apoptotic nuclear chromatin condensation and was inhibited by the proteasome inhibitors MG132, N-acetyl-leucyl-leucyl-norleucinal, and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-152	caspase 3	Mus musculus	34-43
9698598-0	1998	Inhibition of TNF-alpha-induced NF-kappaB activation and IL-8 release in A549 cells with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	tumor necrosis factor	Homo sapiens	14-23
9710593-5	1998	HSF2 DNA-binding activity is induced upon exposure of mammalian cells to the proteasome inhibitors hemin, MG132, and lactacystin, and in the mouse ts85 cell line, which carries a temperature sensitivity mutation in the ubiquitin-activating enzyme (E1) upon shift to the nonpermissive temperature.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	heat shock transcription factor 2	Homo sapiens	0-4
9698598-7	1998	MG-132 also reversed the increase in NF-kappaB binding in nuclear extracts from TNF-alpha-treated cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	tumor necrosis factor	Homo sapiens	80-89
9722548-6	1998	Activation of NF-kappaB and degradation of IkappaB-alpha were prevented by the NF-kappaB inhibitors sodium salicylate and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	nuclear factor kappa B subunit 1	Homo sapiens	14-23
9722548-6	1998	Activation of NF-kappaB and degradation of IkappaB-alpha were prevented by the NF-kappaB inhibitors sodium salicylate and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	NFKB inhibitor alpha	Homo sapiens	43-56
9722548-6	1998	Activation of NF-kappaB and degradation of IkappaB-alpha were prevented by the NF-kappaB inhibitors sodium salicylate and MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	nuclear factor kappa B subunit 1	Homo sapiens	79-88
9722548-9	1998	Induction of COX-2 and stimulation of COX activity by ET-1 and TNF-alpha were prevented by sodium salicylate and MG-132, suggesting that activation of NF-kappaB by either factor is needed for stimulation of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	13-18
9722548-9	1998	Induction of COX-2 and stimulation of COX activity by ET-1 and TNF-alpha were prevented by sodium salicylate and MG-132, suggesting that activation of NF-kappaB by either factor is needed for stimulation of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	endothelin 1	Homo sapiens	54-58
9722548-9	1998	Induction of COX-2 and stimulation of COX activity by ET-1 and TNF-alpha were prevented by sodium salicylate and MG-132, suggesting that activation of NF-kappaB by either factor is needed for stimulation of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	tumor necrosis factor	Homo sapiens	63-72
9722548-9	1998	Induction of COX-2 and stimulation of COX activity by ET-1 and TNF-alpha were prevented by sodium salicylate and MG-132, suggesting that activation of NF-kappaB by either factor is needed for stimulation of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	nuclear factor kappa B subunit 1	Homo sapiens	151-160
9722548-9	1998	Induction of COX-2 and stimulation of COX activity by ET-1 and TNF-alpha were prevented by sodium salicylate and MG-132, suggesting that activation of NF-kappaB by either factor is needed for stimulation of COX-2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-119	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	207-212
9698598-0	1998	Inhibition of TNF-alpha-induced NF-kappaB activation and IL-8 release in A549 cells with the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-120	C-X-C motif chemokine ligand 8	Homo sapiens	57-61
9698598-5	1998	MG-132 reversed the effects of TNF-alpha on IkappaB degradation as determined by Western blot analysis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	tumor necrosis factor	Homo sapiens	31-40
9679971-8	1998	Furthermore, we demonstrate that treatment with the proteasome inhibitor MG-132 blocks the activation of NF-kappaB and prevents the development of resistance to VM26 induced by brefeldin A.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-79	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	105-114
9535733-1	1998	Inhibitors of proteasomal functions Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132) and Carbobenzoxy-L-isoleucyl-gamma-t-butyl-L-alanyl-L-leucinal (PSI) were found to inhibit the conversion of the Insulin proreceptor to its mature alpha and beta subunits.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-77	insulin	Homo sapiens	199-206
9657527-6	1998	TNF-alpha stimulated total ubiquitin conjugation whereas a 26S proteasome inhibitor (MG132 10-40 microM) blocked TNF-alpha activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	tumor necrosis factor	Mus musculus	113-122
9657527-6	1998	TNF-alpha stimulated total ubiquitin conjugation whereas a 26S proteasome inhibitor (MG132 10-40 microM) blocked TNF-alpha activation of NF-kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-90	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	137-146
9620666-6	1998	The 26S proteasome inhibitor MG132 prevented the degradation of phosphorylated IkappaB-alpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	NFKB inhibitor alpha	Homo sapiens	79-92
9598838-12	1998	The stimulated degradation of apoB in atorvastatin-treated cells was sensitive to MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	apolipoprotein B	Homo sapiens	30-34
9653139-3	1998	Here we report that the degradation of the myc proteins in cells is inhibited by lactacystin and MG132, two inhibitors of the 20S proteasome.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	43-46
9573251-8	1998	IkappaBalpha proteolysis induced by TNF-alpha occurred through the 26S proteasome, as both 26S proteasome activity and IkappaBalpha proteolysis were blocked by specific inhibitors lactacystin, MG-132, and ZLLF-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-199	NFKB inhibitor alpha	Homo sapiens	0-12
9573251-8	1998	IkappaBalpha proteolysis induced by TNF-alpha occurred through the 26S proteasome, as both 26S proteasome activity and IkappaBalpha proteolysis were blocked by specific inhibitors lactacystin, MG-132, and ZLLF-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-199	tumor necrosis factor	Homo sapiens	36-45
9573251-8	1998	IkappaBalpha proteolysis induced by TNF-alpha occurred through the 26S proteasome, as both 26S proteasome activity and IkappaBalpha proteolysis were blocked by specific inhibitors lactacystin, MG-132, and ZLLF-CHO.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	193-199	NFKB inhibitor alpha	Homo sapiens	119-131
9572490-6	1998	Treatment of cells with a proteasome inhibitor, such as ALLN or MG132, blocks EGF-mediated NF-kappaB activation, indicating that EGF-induced NF-kappa-B activation requires proteasome-dependent IkappaB degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	epidermal growth factor	Mus musculus	78-81
9572490-6	1998	Treatment of cells with a proteasome inhibitor, such as ALLN or MG132, blocks EGF-mediated NF-kappaB activation, indicating that EGF-induced NF-kappa-B activation requires proteasome-dependent IkappaB degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	epidermal growth factor	Mus musculus	129-132
9572490-6	1998	Treatment of cells with a proteasome inhibitor, such as ALLN or MG132, blocks EGF-mediated NF-kappaB activation, indicating that EGF-induced NF-kappa-B activation requires proteasome-dependent IkappaB degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	141-151
9529323-5	1998	When NF-kappaB activation was prevented by the proteasome inhibitor MG-132, nonvirulent yersiniae as well as LPS became able to trigger J774A.1 cell apoptosis and inhibition of the TNF-alpha secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-74	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	5-14
9529323-5	1998	When NF-kappaB activation was prevented by the proteasome inhibitor MG-132, nonvirulent yersiniae as well as LPS became able to trigger J774A.1 cell apoptosis and inhibition of the TNF-alpha secretion.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-74	tumor necrosis factor	Mus musculus	181-190
9529323-7	1998	Although neither Y. enterocolitica nor TNF-alpha could induce HeLa cell apoptosis alone, TNF-alpha provoked apoptosis when activation of NF-kappaB was inhibited by Yersinia infection or by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-220	tumor necrosis factor	Homo sapiens	89-98
9529323-7	1998	Although neither Y. enterocolitica nor TNF-alpha could induce HeLa cell apoptosis alone, TNF-alpha provoked apoptosis when activation of NF-kappaB was inhibited by Yersinia infection or by the proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	214-220	nuclear factor kappa B subunit 1	Homo sapiens	137-146
9568691-9	1998	In human islets, the proteasome inhibitor MG 132 also inhibited the formation of the products of iNOS and COX-2 enzyme activity, nitrite, and PGE2, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	nitric oxide synthase 2	Homo sapiens	97-101
9568691-9	1998	In human islets, the proteasome inhibitor MG 132 also inhibited the formation of the products of iNOS and COX-2 enzyme activity, nitrite, and PGE2, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-48	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	106-111
9568691-10	1998	These findings suggest that the inhibitory action of TLCK and MG 132 on iNOS and COX-2 expression precedes transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	nitric oxide synthase 2	Rattus norvegicus	72-76
9568691-10	1998	These findings suggest that the inhibitory action of TLCK and MG 132 on iNOS and COX-2 expression precedes transcription.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	81-86
9497367-4	1998	Treatment with peptidyl aldehyde MG132 and other proteasome inhibitors led to a steady increase in activity of c-Jun N-terminal kinase, JNK1, which is known to initiate the apoptotic program in response to certain stresses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	mitogen-activated protein kinase 8	Homo sapiens	136-140
9506962-8	1998	Treatment with the proteasome inhibitors MG132 and lactacystin resulted in the stabilization of YY1 protein, which is consistent with the finding that YY1 is readily polyubiquitinated in reticulocyte lysates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	YY1 transcription factor	Homo sapiens	96-99
9506962-8	1998	Treatment with the proteasome inhibitors MG132 and lactacystin resulted in the stabilization of YY1 protein, which is consistent with the finding that YY1 is readily polyubiquitinated in reticulocyte lysates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	YY1 transcription factor	Homo sapiens	151-154
9497367-5	1998	Dose dependence of MG132-induced JNK activation was parallel with that of apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	mitogen-activated protein kinase 8	Homo sapiens	33-36
9497367-6	1998	Furthermore, inhibition of the JNK signaling pathway strongly suppressed MG132-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	73-78	mitogen-activated protein kinase 8	Homo sapiens	31-34
9497367-10	1998	Accordingly, pretreatment with MG132 reduced JNK-dependent apoptosis caused by heat shock or ethanol, but it was unable to block JNK-independent apoptosis induced by TNFalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	mitogen-activated protein kinase 8	Homo sapiens	45-48
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	E2F transcription factor 1	Homo sapiens	347-352
9438391-2	1998	Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	tumor protein p53	Homo sapiens	131-134
9438391-2	1998	Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	BCL2 associated X, apoptosis regulator	Homo sapiens	154-157
9438391-2	1998	Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	MDM2 proto-oncogene	Homo sapiens	162-166
9438391-2	1998	Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	H3 histone pseudogene 16	Homo sapiens	178-181
9438391-3	1998	MG132 also increased expression of the three proteins in cells that lack p53, showing that stabilization of the p53 response proteins is not due to increased levels of p53 itself.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	73-76
9438391-3	1998	MG132 also increased expression of the three proteins in cells that lack p53, showing that stabilization of the p53 response proteins is not due to increased levels of p53 itself.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	112-115
9438391-3	1998	MG132 also increased expression of the three proteins in cells that lack p53, showing that stabilization of the p53 response proteins is not due to increased levels of p53 itself.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	tumor protein p53	Homo sapiens	112-115
9438391-4	1998	Increases in mdm2 protein levels by MG132 was accompanied by increases in polyubiquitinated forms of the proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	MDM2 proto-oncogene	Homo sapiens	13-17
9266962-0	1997	Transcriptional squelching by ectopic expression of E2F-1 and p53 is alleviated by proteasome inhibitors MG-132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	E2F transcription factor 1	Homo sapiens	52-57
9266962-0	1997	Transcriptional squelching by ectopic expression of E2F-1 and p53 is alleviated by proteasome inhibitors MG-132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	tumor protein p53	Homo sapiens	62-65
9266962-3	1997	Although the proteasome inhibitors MG-132 and lactacystin markedly increased the level of expression of E2F-1 and p53, these inhibitors completely alleviated squelching by both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	E2F transcription factor 1	Homo sapiens	104-109
9367633-3	1997	After treatment of BWEM cells with Brefeldin A to prevent transport of newly synthesized connexin43 polypeptides to the plasma membrane, quantitative confocal microscopy showed the disappearance of immunoreactive connexin43 from the cell surface with a half-life of approximately 1 h. This loss of connexin43 immunoreactivity was inhibited by cotreatment with proteasomal inhibitors (ALLN, MG132, or lactacystin) or lysosomal inhibitors (leupeptin or E-64).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	390-395	gap junction protein, alpha 1	Rattus norvegicus	213-223
9367633-3	1997	After treatment of BWEM cells with Brefeldin A to prevent transport of newly synthesized connexin43 polypeptides to the plasma membrane, quantitative confocal microscopy showed the disappearance of immunoreactive connexin43 from the cell surface with a half-life of approximately 1 h. This loss of connexin43 immunoreactivity was inhibited by cotreatment with proteasomal inhibitors (ALLN, MG132, or lactacystin) or lysosomal inhibitors (leupeptin or E-64).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	390-395	gap junction protein, alpha 1	Rattus norvegicus	213-223
9278421-6	1997	Lactacystin and MG-132 were found to protect the degradation of the HIF-1 complex in cells transferred from hypoxia to normoxia.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	16-22	hypoxia inducible factor 1 subunit alpha	Homo sapiens	68-73
9286755-9	1997	In the thyroparathyriodectomized rat model, Cbz-Leu-Leu-Leu-H inhibited the increase in blood ionized calcium induced by a 6 h infusion of PTH.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-61	parathyroid hormone	Rattus norvegicus	139-142
9266962-3	1997	Although the proteasome inhibitors MG-132 and lactacystin markedly increased the level of expression of E2F-1 and p53, these inhibitors completely alleviated squelching by both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	tumor protein p53	Homo sapiens	114-117
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	RB transcriptional corepressor like 1	Homo sapiens	381-385
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	tumor protein p53	Homo sapiens	112-115
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	E2F transcription factor 1	Homo sapiens	120-125
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	heat shock protein family A (Hsp70) member 4	Homo sapiens	283-288
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	tumor protein p53	Homo sapiens	112-115
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	E2F transcription factor 1	Homo sapiens	120-125
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	heat shock protein family A (Hsp70) member 4	Homo sapiens	283-288
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	tumor protein p53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	E2F transcription factor 1	Homo sapiens	347-352
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	RB transcriptional corepressor like 1	Homo sapiens	381-385
9266962-6	1997	Because MG-132 and lactacycstin are highly specific inhibitors of the proteasome protease, our results suggest that the proteasome influences post-translational processes involved in proper folding and cytoplasmic clearing of E2F-1 and p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-14	E2F transcription factor 1	Homo sapiens	226-231
9266962-6	1997	Because MG-132 and lactacycstin are highly specific inhibitors of the proteasome protease, our results suggest that the proteasome influences post-translational processes involved in proper folding and cytoplasmic clearing of E2F-1 and p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-14	tumor protein p53	Homo sapiens	236-239
9133543-9	1997	Exposure of IFN-gamma-treated beta-cells to a peptide aldehyde inhibitor of the proteasome (MG132) significantly attenuated MHC class I cell-surface expression but did not prevent the negative effects of IFN-gamma on glucose responsiveness.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	interferon gamma	Mus musculus	12-21
9162019-3	1997	We report here that IL-2-induced DNA-binding activity and tyrosine phosphorylation of STAT5 are stabilized by a proteasome inhibitor MG132; however, no detectable ubiquitination of the STAT proteins is observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	interleukin 2	Homo sapiens	20-24
9162019-3	1997	We report here that IL-2-induced DNA-binding activity and tyrosine phosphorylation of STAT5 are stabilized by a proteasome inhibitor MG132; however, no detectable ubiquitination of the STAT proteins is observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	signal transducer and activator of transcription 5A	Homo sapiens	86-91
9186501-2	1997	In this report, we demonstrate that MG132, a relatively specific proteasome inhibitor, is capable of suppressing LPS-induced I kappa B alpha degradation and NF-kappa B activation in mouse macrophage line RAW 264.7 cells, but is unable to influence the same induction produced by silica.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	125-140
9186501-2	1997	In this report, we demonstrate that MG132, a relatively specific proteasome inhibitor, is capable of suppressing LPS-induced I kappa B alpha degradation and NF-kappa B activation in mouse macrophage line RAW 264.7 cells, but is unable to influence the same induction produced by silica.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	157-167
9030516-6	1997	The loss of STAT3 and STAT5 immunostaining was transient (lasted 120 min) and tyrosine kinase-dependent, and even though the loss was blocked by the proteasome inhibitors MG132 and lactacystin it was not accompanied by changes in cellular levels of STAT3 and STAT5 proteins suggesting that IL-6 triggered a rapid masking but not degradation of these transcription factors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	171-176	signal transducer and activator of transcription 3	Homo sapiens	12-17
9030516-6	1997	The loss of STAT3 and STAT5 immunostaining was transient (lasted 120 min) and tyrosine kinase-dependent, and even though the loss was blocked by the proteasome inhibitors MG132 and lactacystin it was not accompanied by changes in cellular levels of STAT3 and STAT5 proteins suggesting that IL-6 triggered a rapid masking but not degradation of these transcription factors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	171-176	signal transducer and activator of transcription 5A	Homo sapiens	22-27
8694836-3	1996	Unexpectedly, proteasome inhibitors (at 5 microM) such as Z-LLnV, Z-LLL, and lactacystin enhanced CPP32-like activity, Ac-DEVD-MCA degrading activity, in the TNF-treated U937 cells in 3 hr, but E64d, cysteine protease inhibitor, did not.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	caspase 3	Homo sapiens	98-103
8694836-3	1996	Unexpectedly, proteasome inhibitors (at 5 microM) such as Z-LLnV, Z-LLL, and lactacystin enhanced CPP32-like activity, Ac-DEVD-MCA degrading activity, in the TNF-treated U937 cells in 3 hr, but E64d, cysteine protease inhibitor, did not.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	tumor necrosis factor	Homo sapiens	158-161
8694836-3	1996	Unexpectedly, proteasome inhibitors (at 5 microM) such as Z-LLnV, Z-LLL, and lactacystin enhanced CPP32-like activity, Ac-DEVD-MCA degrading activity, in the TNF-treated U937 cells in 3 hr, but E64d, cysteine protease inhibitor, did not.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	66-71	cathepsin B	Homo sapiens	200-217
33824292-10	2021	The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	ring finger protein 31	Homo sapiens	65-70
33812054-8	2021	Utilising BAY11-7082 and MG-132, inhibitors of the respective ubiquitin and proteasome pathways essential for NF-kappaB activation, suggested a prospective role for NF-kappaB, or more specifically signalling via IKKalpha/beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	110-119
33812054-8	2021	Utilising BAY11-7082 and MG-132, inhibitors of the respective ubiquitin and proteasome pathways essential for NF-kappaB activation, suggested a prospective role for NF-kappaB, or more specifically signalling via IKKalpha/beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	165-174
33812054-8	2021	Utilising BAY11-7082 and MG-132, inhibitors of the respective ubiquitin and proteasome pathways essential for NF-kappaB activation, suggested a prospective role for NF-kappaB, or more specifically signalling via IKKalpha/beta.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	conserved helix-loop-helix ubiquitous kinase	Mus musculus	212-225
33824292-10	2021	The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	tumor protein p53	Homo sapiens	82-85
33767588-6	2021	Delivery of the proteasome inhibitor, MG132, reversed the inhibitory effect of miR-26b on the level of p53 following doxorubicin treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	microRNA 26b	Homo sapiens	79-86
33803345-5	2021	Treatment with cycloheximide and MG132 revealed that both endogenous CREB3 and CREB3L2 are proteasome substrates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	cAMP responsive element binding protein 3	Homo sapiens	69-74
33803345-5	2021	Treatment with cycloheximide and MG132 revealed that both endogenous CREB3 and CREB3L2 are proteasome substrates.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-38	cAMP responsive element binding protein 3 like 2	Homo sapiens	79-86
33234350-7	2021	The use of proteasome inhibitor MG132 showed that CUR-mediated loss of IRS-1 involved proteasomal degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	insulin receptor substrate 1	Homo sapiens	71-76
33810320-6	2021	In addition, treatment with MG-132 (a proteasome inhibitor) could partially restore the levels of PML and SP100, suggesting that a cellular proteasome dependent degradation pathway is involved in MDV US3 induced disruption of PML and SP100.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	PML nuclear body scaffold	Homo sapiens	98-101
33810320-6	2021	In addition, treatment with MG-132 (a proteasome inhibitor) could partially restore the levels of PML and SP100, suggesting that a cellular proteasome dependent degradation pathway is involved in MDV US3 induced disruption of PML and SP100.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	SP100 nuclear antigen	Homo sapiens	106-111
33810320-6	2021	In addition, treatment with MG-132 (a proteasome inhibitor) could partially restore the levels of PML and SP100, suggesting that a cellular proteasome dependent degradation pathway is involved in MDV US3 induced disruption of PML and SP100.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	PML nuclear body scaffold	Homo sapiens	226-229
33810320-6	2021	In addition, treatment with MG-132 (a proteasome inhibitor) could partially restore the levels of PML and SP100, suggesting that a cellular proteasome dependent degradation pathway is involved in MDV US3 induced disruption of PML and SP100.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-34	SP100 nuclear antigen	Homo sapiens	234-239
33767588-6	2021	Delivery of the proteasome inhibitor, MG132, reversed the inhibitory effect of miR-26b on the level of p53 following doxorubicin treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	tumor protein p53	Homo sapiens	103-106
26323600-8	2015	Additionally, we found that MG132 and PMSF, which are inhibitors of proteasomes and serine proteases, respectively, increased the Sit1 protein level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	siderophore transporter	Saccharomyces cerevisiae S288C	130-134
27746171-7	2017	In some cells treated with cadmium chloride or the proteasomal inhibitor, MG132, large BiP complexes were observed that co-localized with aggregated protein or aggresome-like structures.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	74-79	heat shock protein family A (Hsp70) member 5 L homeolog	Xenopus laevis	87-90
16287099-6	2006	MG132 massively induced TRAIL receptor DR4 and DR5 membrane expression in HeLa, whereas in SiHa only DR5 membrane expression was upregulated from almost undetectable to high levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10a	Homo sapiens	39-42
25771395-5	2015	However, allocortical neurons exhibited higher MG132-induced increases in Hsp70 and heat shock cognate 70 (Hsc70).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	heat shock protein family A (Hsp70) member 4	Homo sapiens	74-79
25771395-5	2015	However, allocortical neurons exhibited higher MG132-induced increases in Hsp70 and heat shock cognate 70 (Hsc70).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	heat shock protein family A (Hsp70) member 8	Homo sapiens	84-105
25771395-5	2015	However, allocortical neurons exhibited higher MG132-induced increases in Hsp70 and heat shock cognate 70 (Hsc70).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	heat shock protein family A (Hsp70) member 8	Homo sapiens	107-112
25771395-7	2015	Inhibition of Hsp70/Hsc70 activity synergistically exacerbated MG132 toxicity in allocortical neurons more than neocortical neurons, suggesting that the allocortex is more reliant on these Hsp defenses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	heat shock protein family A (Hsp70) member 4	Homo sapiens	14-19
25771395-7	2015	Inhibition of Hsp70/Hsc70 activity synergistically exacerbated MG132 toxicity in allocortical neurons more than neocortical neurons, suggesting that the allocortex is more reliant on these Hsp defenses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	heat shock protein family A (Hsp70) member 8	Homo sapiens	20-25
25771395-7	2015	Inhibition of Hsp70/Hsc70 activity synergistically exacerbated MG132 toxicity in allocortical neurons more than neocortical neurons, suggesting that the allocortex is more reliant on these Hsp defenses.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	63-68	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	14-17
21150308-8	2011	Pharmacological inhibition of the proteasome signaling pathway with the inhibitor MG132 blocks degradation of DNMT1 and alters BaP-mediated histone epigenetic modifications.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	DNA methyltransferase 1	Homo sapiens	110-115
16879986-6	2006	Further, exposure of amelanotic melanoma cells with proteasome-specific inhibitor MG132 resulted in an increased Tyr activity, increased levels of Tyr and Trp1, leading to increased melanin synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	tyrosinase	Mus musculus	113-116
16879986-6	2006	Further, exposure of amelanotic melanoma cells with proteasome-specific inhibitor MG132 resulted in an increased Tyr activity, increased levels of Tyr and Trp1, leading to increased melanin synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	tyrosinase	Mus musculus	147-150
16879986-6	2006	Further, exposure of amelanotic melanoma cells with proteasome-specific inhibitor MG132 resulted in an increased Tyr activity, increased levels of Tyr and Trp1, leading to increased melanin synthesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	tyrosinase-related protein 1	Mus musculus	155-159
16287099-10	2006	MG132 plus rhTRAIL enhanced caspase 8 and caspase 3 activation and concomitant cleavage of X-linked inhibitor of apoptosis (XIAP), particularly in HeLa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	X-linked inhibitor of apoptosis	Homo sapiens	124-128
16287099-14	2006	Our results indicate that not only DR4 and DR5 upregulation but also XIAP inactivation contribute to rhTRAIL sensitization by MG132 in cervical cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	TNF receptor superfamily member 10a	Homo sapiens	35-38
16287099-14	2006	Our results indicate that not only DR4 and DR5 upregulation but also XIAP inactivation contribute to rhTRAIL sensitization by MG132 in cervical cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	TNF receptor superfamily member 10b	Homo sapiens	43-46
16287099-14	2006	Our results indicate that not only DR4 and DR5 upregulation but also XIAP inactivation contribute to rhTRAIL sensitization by MG132 in cervical cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	X-linked inhibitor of apoptosis	Homo sapiens	69-73
16287099-6	2006	MG132 massively induced TRAIL receptor DR4 and DR5 membrane expression in HeLa, whereas in SiHa only DR5 membrane expression was upregulated from almost undetectable to high levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10b	Homo sapiens	47-50
16287099-7	2006	Antagonistic DR4 antibody partially inhibited apoptosis induction by rhTRAIL and MG132 in HeLa but had no effect on apoptosis in SiHa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	81-86	TNF receptor superfamily member 10a	Homo sapiens	13-16
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	26-29
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	101-104
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	tumor protein p53	Homo sapiens	101-104
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	H3 histone pseudogene 16	Homo sapiens	168-171
16287099-9	2006	Although p53 siRNA partially inhibited MG132-induced DR5 upregulation in HeLa and SiHa, no effect on rhTRAIL-induced apoptosis was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	tumor protein p53	Homo sapiens	9-12
16287099-9	2006	Although p53 siRNA partially inhibited MG132-induced DR5 upregulation in HeLa and SiHa, no effect on rhTRAIL-induced apoptosis was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	TNF receptor superfamily member 10b	Homo sapiens	53-56
16287099-10	2006	MG132 plus rhTRAIL enhanced caspase 8 and caspase 3 activation and concomitant cleavage of X-linked inhibitor of apoptosis (XIAP), particularly in HeLa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 8	Homo sapiens	28-37
16287099-10	2006	MG132 plus rhTRAIL enhanced caspase 8 and caspase 3 activation and concomitant cleavage of X-linked inhibitor of apoptosis (XIAP), particularly in HeLa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	caspase 3	Homo sapiens	42-51
16287099-10	2006	MG132 plus rhTRAIL enhanced caspase 8 and caspase 3 activation and concomitant cleavage of X-linked inhibitor of apoptosis (XIAP), particularly in HeLa.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	X-linked inhibitor of apoptosis	Homo sapiens	91-122
34915026-12	2022	Inhibitors of ER-associated degradation (ERAD) (eeyarestatin I) and the proteasome (MG132, bortezomib) prevented ABCB1 loss induced by CerS2/6 downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	ATP binding cassette subfamily B member 1	Homo sapiens	113-118
34086898-7	2021	Moreover, alphaB-crystallin-mediated reduction of Nav1.5 expression was rescued in the presence of a proteasome inhibitor MG-132, suggesting the importance of the alphaB-crystallin-modulated ubiquitin-proteasome system for the stability of Nav1.5 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	sodium voltage-gated channel alpha subunit 5	Homo sapiens	50-56
34086898-7	2021	Moreover, alphaB-crystallin-mediated reduction of Nav1.5 expression was rescued in the presence of a proteasome inhibitor MG-132, suggesting the importance of the alphaB-crystallin-modulated ubiquitin-proteasome system for the stability of Nav1.5 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-128	sodium voltage-gated channel alpha subunit 5	Homo sapiens	240-246
34715142-10	2021	MG132 treatment prevented TGF-beta-induced pJNK in HK-11 cells and in type 1 diabetic OVE26 mouse kidneys, demonstrating that TGF-beta- and diabetes-induced pJNK occurs downstream of proteasome activation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	transforming growth factor alpha	Mus musculus	126-134
34921974-13	2022	Hyperphosphatemia in vitro increased insoluble TFEB and decreased soluble TFEB in VSMCs, both of which were abrogated by the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-153	transcription factor EB	Rattus norvegicus	47-51
34921974-13	2022	Hyperphosphatemia in vitro increased insoluble TFEB and decreased soluble TFEB in VSMCs, both of which were abrogated by the proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	147-153	transcription factor EB	Rattus norvegicus	74-78
34872023-14	2022	Mechanistically, USP13 knockdown promoted Snail degradation, which could be blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	ubiquitin specific peptidase 13	Homo sapiens	17-22
34872023-14	2022	Mechanistically, USP13 knockdown promoted Snail degradation, which could be blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	112-117	snail family transcriptional repressor 1	Homo sapiens	42-47
34952616-13	2021	RESULTS: Following treatment with MG132, the levels of Rap1GAP were increased in the HR HPV-positive HeLa and SiHa cells, but not in the HPV-negative C33A cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	RAP1 GTPase activating protein	Homo sapiens	55-62
34975472-10	2021	The proteasome inhibitor MG132 antagonized the effect of UDCA on HIF-1alpha degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	hypoxia inducible factor 1 subunit alpha	Homo sapiens	65-75
34915026-12	2022	Inhibitors of ER-associated degradation (ERAD) (eeyarestatin I) and the proteasome (MG132, bortezomib) prevented ABCB1 loss induced by CerS2/6 downregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	84-89	ceramide synthase 2	Homo sapiens	135-140
34851506-7	2022	TRbeta protein stability was evaluated by ubiquitination assay with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	68-73	T cell receptor alpha locus	Homo sapiens	0-6
34848256-6	2021	Following DQ treatment, SH-SY5Y cells were found to have induced phosphorylated and detergent-insoluble alpha-synuclein deposits, and MG132, a proteasome inhibitor, effectively potentiated both CMA and macroautophagy for preventing alpha-synuclein aggregation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	134-139	synuclein alpha	Homo sapiens	232-247
34882921-8	2022	E6/E7 knockdown mediated PGK1 downregulation could be blocked by adding MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	protein E6*;transforming protein E6	Human papillomavirus type 16	0-5
34882921-8	2022	E6/E7 knockdown mediated PGK1 downregulation could be blocked by adding MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	phosphoglycerate kinase 1	Homo sapiens	25-29
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	activating transcription factor 4	Rattus norvegicus	107-140
34837126-8	2022	The proteasome inhibitor MG-132 significantly reverses the LPS-induced decrease in FTL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-31	ferritin light polypeptide 1	Mus musculus	83-86
34429248-4	2021	TDP-43 transgenic human iPS cells were constructed, differentiated into motor neurons, and then treated with MG-132 and sodium arsenite (stressors) to induce nuclear to cytoplasmic localization of TDP-43.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-115	TAR DNA binding protein	Homo sapiens	0-6
34429248-4	2021	TDP-43 transgenic human iPS cells were constructed, differentiated into motor neurons, and then treated with MG-132 and sodium arsenite (stressors) to induce nuclear to cytoplasmic localization of TDP-43.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-115	TAR DNA binding protein	Homo sapiens	197-203
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	41-69
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	71-77
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	activating transcription factor 4	Rattus norvegicus	142-146
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	activating transcription factor 6	Rattus norvegicus	149-182
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	activating transcription factor 6	Rattus norvegicus	184-188
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	DNA-damage inducible transcript 3	Rattus norvegicus	194-218
34809635-11	2021	We found that the proteins expression of glucose-regulated protein 78 (GRP-78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), as well as AECII apoptosis were increased following MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	279-284	DNA-damage inducible transcript 3	Rattus norvegicus	220-224
34916189-9	2021	Treatment of the cells with 0.2 mumol/L MG132 significantly aggravated alpha-Syn-induced increase of IRF-1 protein expression (P < 0.01) while 30 mumol/L chloroquine produced no significant changes in IRF-1 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	synuclein alpha	Homo sapiens	71-80
34916189-9	2021	Treatment of the cells with 0.2 mumol/L MG132 significantly aggravated alpha-Syn-induced increase of IRF-1 protein expression (P < 0.01) while 30 mumol/L chloroquine produced no significant changes in IRF-1 level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	40-45	interferon regulatory factor 1	Homo sapiens	101-106
34711178-14	2021	The proteasome inhibitor MG132 activated the Nrf2/ARE signalling pathway, thereby reversing the promoting effect of CYLD knockdown on oxidative stress.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	NFE2 like bZIP transcription factor 2	Homo sapiens	45-49
34739170-10	2022	Using high resolution three-dimensional immuno-FISH and ChIP-qPCR we showed an association between the alpha-Satellite upregulation and the recruitment of the transcription factor NFY-A to the centromere upon MG132-induced proteasome inhibition.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	209-214	nuclear transcription factor Y subunit alpha	Homo sapiens	180-185
34260096-5	2021	The degradation of gB by Nedd4 was inhibited by proteasome inhibitor MG132, lysosome inhibitor chloroquine, and the co-expression of UL42 proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	NEDD4 E3 ubiquitin protein ligase	Homo sapiens	25-30
34769210-0	2021	Structural and Biochemical Analysis of the Dual Inhibition of MG-132 against SARS-CoV-2 Main Protease (Mpro/3CLpro) and Human Cathepsin-L.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	cathepsin L	Homo sapiens	126-137
34769210-4	2021	Here we present a structural and biochemical characterization of the binding mode of MG-132 to both the main protease of SARS-CoV-2, and to the human Cathepsin-L, suggesting thus an interesting scaffold for the development of double-inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-91	cathepsin L	Homo sapiens	150-161
34769210-5	2021	X-ray diffraction data show that MG-132 well fits into the Mpro active site, forming a covalent bond with Cys145 independently from reducing agents and crystallization conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	59-63
34769210-6	2021	Docking of MG-132 into Cathepsin-L well-matches with a covalent binding to the catalytic cysteine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-17	cathepsin L	Homo sapiens	23-34
34769210-7	2021	Accordingly, MG-132 inhibits Cathepsin-L with nanomolar potency and reversibly inhibits Mpro with micromolar potency, but with a prolonged residency time.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	cathepsin L	Homo sapiens	29-40
34769210-7	2021	Accordingly, MG-132 inhibits Cathepsin-L with nanomolar potency and reversibly inhibits Mpro with micromolar potency, but with a prolonged residency time.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-19	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	88-92
34769210-8	2021	We compared the apo and MG-132-inhibited structures of Mpro solved in different space groups and we identified a new apo structure that features several similarities with the inhibited ones, offering interesting perspectives for future drug design and in silico efforts.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	55-59
34711178-14	2021	The proteasome inhibitor MG132 activated the Nrf2/ARE signalling pathway, thereby reversing the promoting effect of CYLD knockdown on oxidative stress.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	CYLD lysine 63 deubiquitinase	Homo sapiens	116-120
34516972-5	2021	MTTP was synergistically accumulated after Cd exposure or treated with proteasome inhibitor MG132 and lysosome inhibitor chloroquine (CQ), which suggested the Cd increased MTTP protein stability by inhibiting both the proteasome and the lysosomal protein degradation pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	microsomal triglyceride transfer protein	Homo sapiens	0-4
34606682-7	2022	Importantly, we found that ubiquitinated MCL1 was accumulated upon depletion of USP9X and/or DDX3 in MG132-treated cells, suggesting that USP9X and DDX3 play a role in regulating MCL1 protein stability and anti-apoptotic function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	41-45
34606682-7	2022	Importantly, we found that ubiquitinated MCL1 was accumulated upon depletion of USP9X and/or DDX3 in MG132-treated cells, suggesting that USP9X and DDX3 play a role in regulating MCL1 protein stability and anti-apoptotic function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	ubiquitin specific peptidase 9 X-linked	Homo sapiens	138-143
34606682-7	2022	Importantly, we found that ubiquitinated MCL1 was accumulated upon depletion of USP9X and/or DDX3 in MG132-treated cells, suggesting that USP9X and DDX3 play a role in regulating MCL1 protein stability and anti-apoptotic function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	DEAD-box helicase 3 X-linked	Homo sapiens	148-152
34606682-7	2022	Importantly, we found that ubiquitinated MCL1 was accumulated upon depletion of USP9X and/or DDX3 in MG132-treated cells, suggesting that USP9X and DDX3 play a role in regulating MCL1 protein stability and anti-apoptotic function.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	179-183
34696420-6	2021	Treatment with a proteasome inhibitor MG132 effectively blocked MAVS degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	mitochondrial antiviral-signaling protein	Chlorocebus sabaeus	64-68
34696420-7	2021	Moreover, we demonstrated that MAVS mainly underwent K48-linked ubiquitination in the presence of MG132 in aMPV/C-infected cells, with amino acids 363, 462, and 501 of MAVS being pivotal sites in the formation of polyubiquitin chains.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	mitochondrial antiviral-signaling protein	Chlorocebus sabaeus	31-35
34696420-7	2021	Moreover, we demonstrated that MAVS mainly underwent K48-linked ubiquitination in the presence of MG132 in aMPV/C-infected cells, with amino acids 363, 462, and 501 of MAVS being pivotal sites in the formation of polyubiquitin chains.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	mitochondrial antiviral-signaling protein	Chlorocebus sabaeus	168-172
34516972-5	2021	MTTP was synergistically accumulated after Cd exposure or treated with proteasome inhibitor MG132 and lysosome inhibitor chloroquine (CQ), which suggested the Cd increased MTTP protein stability by inhibiting both the proteasome and the lysosomal protein degradation pathways.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	92-97	microsomal triglyceride transfer protein	Homo sapiens	172-176
34611473-8	2021	Proteasome inhibitor MG-132 partially rescued HIF-1alpha expression when Smurf2 was overexpressed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	hypoxia inducible factor 1 subunit alpha	Homo sapiens	46-56
34331380-6	2021	Of note, the protein stability of Prickle1, a binding factor of Rictor, was reduced by morin, and MG132 but not Baf A1 showed a repressive effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	prickle planar cell polarity protein 1	Rattus norvegicus	34-70
34611473-8	2021	Proteasome inhibitor MG-132 partially rescued HIF-1alpha expression when Smurf2 was overexpressed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	SMAD specific E3 ubiquitin protein ligase 2	Homo sapiens	73-79
34575794-8	2021	Mac1 was downregulated dramatically under nitrogen starvation, and treatment with MG132, which is an inhibitor of proteasome-dependent protein degradation, partially attenuated the downregulation of Mac1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	Mac1p	Saccharomyces cerevisiae S288C	0-4
34552711-9	2021	Furthermore, pre-treatment of cells with proteasome inhibitor MG-132 also abolished PDGF-induced FoxO4 reduction, CyclinD1 elevation and cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	forkhead box O4	Mus musculus	97-102
34552711-9	2021	Furthermore, pre-treatment of cells with proteasome inhibitor MG-132 also abolished PDGF-induced FoxO4 reduction, CyclinD1 elevation and cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-68	cyclin D1	Mus musculus	114-122
34685531-4	2021	In macrophage-like RAW264.7 cells, bortezomib as well as MG132, a well-known proteasome inhibitor, caused HMGB1 release, an effect inhibited by caspase inhibitors but not inhibitors of NF-kappaB and p38 MAP kinase, known to mediate paclitaxel-induced HMGB1 release from macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	high mobility group box 1	Mus musculus	106-111
34685531-4	2021	In macrophage-like RAW264.7 cells, bortezomib as well as MG132, a well-known proteasome inhibitor, caused HMGB1 release, an effect inhibited by caspase inhibitors but not inhibitors of NF-kappaB and p38 MAP kinase, known to mediate paclitaxel-induced HMGB1 release from macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	caspase 8	Mus musculus	144-151
34685531-4	2021	In macrophage-like RAW264.7 cells, bortezomib as well as MG132, a well-known proteasome inhibitor, caused HMGB1 release, an effect inhibited by caspase inhibitors but not inhibitors of NF-kappaB and p38 MAP kinase, known to mediate paclitaxel-induced HMGB1 release from macrophages.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	high mobility group box 1	Mus musculus	251-256
34575794-8	2021	Mac1 was downregulated dramatically under nitrogen starvation, and treatment with MG132, which is an inhibitor of proteasome-dependent protein degradation, partially attenuated the downregulation of Mac1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	Mac1p	Saccharomyces cerevisiae S288C	199-203
34566695-7	2021	The proteasome inhibitor MG132 significantly increased the expression level of S157/161A telethonin protein in myocytes from Tcap S157/161A mice, but not telethonin protein in myocytes from WT mice, indicating a role for the ubiquitin-proteasome system in the regulation of telethonin protein expression level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	titin-cap	Mus musculus	274-284
34572355-5	2021	Inhibition of RhoGDI1 degradation via MG132 reversed the decrease in VSMC phenotypic transformation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	Rho GDP dissociation inhibitor alpha	Homo sapiens	14-21
34343822-9	2021	We also found that MG132, an inhibitor of the proteasome that results in proteotoxic stress, prominently enhances Hpa2 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	heparanase 2	Mus musculus	114-118
34414662-9	2021	The NF-kappaB inhibitor MG-132 indeed altered NMDA-mediated transcriptional changes, revealing components of opposing expression signatures that converge on the single response element.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-30	nuclear factor kappa B subunit 1	Homo sapiens	4-13
34278473-11	2021	Moreover, MG132 alleviated the decrease in MAD2L2 expression, while reducing siMAD2L2-induced cell apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	mitotic arrest deficient 2 like 2	Homo sapiens	43-49
34158350-7	2021	MSU38225 strikingly decreases the protein level of Nrf2, which can be blocked by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	NFE2 like bZIP transcription factor 2	Homo sapiens	51-55
34343822-10	2021	Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	heparanase 2	Mus musculus	9-13
34343822-10	2021	Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	60-64
34343822-10	2021	Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	heparanase 2	Mus musculus	168-172
34343822-10	2021	Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	182-186
34343822-10	2021	Notably, Hpa2 induction by MG132 appeared to be mediated by AMPK, and AMPK was found to induce the expression of Hpa2, thus establishing a loop that feeds itself where Hpa2 enhances AMPK phosphorylation that, in turn, induces Hpa2 expression, leading to attenuation of gastric tumorigenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	heparanase 2	Mus musculus	226-230
34435451-9	2021	Intriguingly, treatment with a proteasome inhibitor MG132 also decreased myosin replacement rate, although MG132 enhanced the accumulation of ubiquitinated myosin in the cytosol where replaceable myosin is pooled, suggesting that ubiquitinated myosin is not replaced by myosin in the myofibril.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	52-57	myosin heavy chain 14	Homo sapiens	73-79
34435451-9	2021	Intriguingly, treatment with a proteasome inhibitor MG132 also decreased myosin replacement rate, although MG132 enhanced the accumulation of ubiquitinated myosin in the cytosol where replaceable myosin is pooled, suggesting that ubiquitinated myosin is not replaced by myosin in the myofibril.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	myosin heavy chain 14	Homo sapiens	156-162
34445748-8	2021	Pretreatment with MG132, a proteasome inhibitor and lysosomal stabilizer, upregulated LAMP2 and autophagy and prevented HQ-induced oxidative damage in wildtype RPE cells but not cells transfected with shRNA against ATG5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	18-23	lysosomal associated membrane protein 2	Homo sapiens	86-91
34336846-9	2021	Cell functional experiments, co-immunoprecipitation, MG132 and ginkgolic acid treatment, western blot, and ChIP-Seq were used to identify the mechanism of S100A10 nuclear location.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	S100 calcium binding protein A10	Homo sapiens	155-162
34421601-8	2021	Furthermore, treatment with ubiquitin-proteasome inhibitor MG132 suppressing the ubiquitination of Cx43 ameliorated lipopolysaccharide-induced neuroinflammation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	59-64	gap junction protein, alpha 1	Rattus norvegicus	99-103
34376133-8	2022	To assess the ubiquitination pathway of degradation of EGFR in MDA-MB-231 cell line, MG-132 was used.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	85-91	epidermal growth factor receptor	Homo sapiens	55-59
34376133-10	2022	Upon Treatment with MG-132 and E2, EGFR expression did not reduce, suggesting that Estrogen degrades EGFR by ubiquitination pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	20-26	epidermal growth factor receptor	Homo sapiens	101-105
34483932-6	2021	Overexpression of USP5 could significantly extend the half-life of CyclinD1, while knockdown of USP5 decreased the protein level of CyclinD1, which could be restored by proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	ubiquitin specific peptidase 5	Homo sapiens	18-22
34483932-6	2021	Overexpression of USP5 could significantly extend the half-life of CyclinD1, while knockdown of USP5 decreased the protein level of CyclinD1, which could be restored by proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	cyclin D1	Homo sapiens	67-75
34483932-6	2021	Overexpression of USP5 could significantly extend the half-life of CyclinD1, while knockdown of USP5 decreased the protein level of CyclinD1, which could be restored by proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	ubiquitin specific peptidase 5	Homo sapiens	96-100
34483932-6	2021	Overexpression of USP5 could significantly extend the half-life of CyclinD1, while knockdown of USP5 decreased the protein level of CyclinD1, which could be restored by proteasome inhibitor MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	190-196	cyclin D1	Homo sapiens	132-140
34133238-7	2021	The pre-cytokinesis degradation of calponin 2 was attenuated by MG132 inhibition of the ubiquitin proteasome and inhibitor of protein kinase C (PKC), suggesting that PKC phosphorylation-triggered degradation of calponin 2 could determine the rate of cytokinesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	calponin 2	Homo sapiens	35-45
34275172-10	2021	Silencing PINK1 or PKA, or proteasome blockade using MG132, increased Mfn2 expression, enhanced mitochondrial fusion and induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	mitofusin 2	Homo sapiens	70-74
34273985-5	2021	The proteasome inhibitors (MG132) was used for detecting the beta-catenin ubiquitination-proteasome degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	27-32	catenin beta 1	Homo sapiens	61-73
34193603-6	2021	Functional domains analysis revealed that the C-terminal ubiquitin-fold domain was necessary for IRF3 degradation by Uba1 and the N-terminal DNA-binding domain of IRF3 was indispensable for the degradation by Uba1.The degradation of IRF3 was subsequently impaired by treatment with MG132, a ubiquitin proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-287	interferon regulatory factor 3	Homo sapiens	97-101
34193603-6	2021	Functional domains analysis revealed that the C-terminal ubiquitin-fold domain was necessary for IRF3 degradation by Uba1 and the N-terminal DNA-binding domain of IRF3 was indispensable for the degradation by Uba1.The degradation of IRF3 was subsequently impaired by treatment with MG132, a ubiquitin proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-287	interferon regulatory factor 3	Homo sapiens	163-167
34193603-6	2021	Functional domains analysis revealed that the C-terminal ubiquitin-fold domain was necessary for IRF3 degradation by Uba1 and the N-terminal DNA-binding domain of IRF3 was indispensable for the degradation by Uba1.The degradation of IRF3 was subsequently impaired by treatment with MG132, a ubiquitin proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-287	ubiquitin like modifier activating enzyme 1	Homo sapiens	209-213
34193603-6	2021	Functional domains analysis revealed that the C-terminal ubiquitin-fold domain was necessary for IRF3 degradation by Uba1 and the N-terminal DNA-binding domain of IRF3 was indispensable for the degradation by Uba1.The degradation of IRF3 was subsequently impaired by treatment with MG132, a ubiquitin proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	282-287	interferon regulatory factor 3	Homo sapiens	233-237
34230121-9	2021	Inhibition of proteasome activity by MG counteracts the Enz-mediated AR degradation transiently, whereas Bor showed no inhibition of the Enz-mediated AR degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-39	androgen receptor	Homo sapiens	69-71
34211022-4	2021	We show that the small molecule inhibitors MG132 (a 26S proteasome inhibitor used to block NF-kappaB signaling) and U0126 (a MAPK Kinase inhibitor used to block CCAAT-enhancer-binding proteins C/EBP) successfully block IL-1beta and TNF-alpha mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	nuclear factor kappa B subunit 1	Homo sapiens	91-100
34267496-5	2021	MG132 and chloroquine were used to inhibit the degradation of the WT and mutated EPHA2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	EPH receptor A2	Homo sapiens	81-86
34275032-2	2021	Overexpressed full-length (FL) CREBRF protein was stabilized by MG132; however, the intrinsic CREBRF expression in Neuro2a cells was negligible under all conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-69	CREB3 regulatory factor	Mus musculus	31-37
34211022-4	2021	We show that the small molecule inhibitors MG132 (a 26S proteasome inhibitor used to block NF-kappaB signaling) and U0126 (a MAPK Kinase inhibitor used to block CCAAT-enhancer-binding proteins C/EBP) successfully block IL-1beta and TNF-alpha mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	interleukin 1 alpha	Homo sapiens	219-227
34211022-4	2021	We show that the small molecule inhibitors MG132 (a 26S proteasome inhibitor used to block NF-kappaB signaling) and U0126 (a MAPK Kinase inhibitor used to block CCAAT-enhancer-binding proteins C/EBP) successfully block IL-1beta and TNF-alpha mRNA expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	tumor necrosis factor	Homo sapiens	232-241
34335925-11	2021	Inhibiting FOXM1 degradation with MG132 treatment affected neither palbociclib-induced G2/M cell cycle arrest nor expression of its target genes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	forkhead box M1	Homo sapiens	11-16
34222769-4	2021	Studies on the proteolytic regulation of ABI5, ABF1, and ABF3 in Arabidopsis thaliana have shown that the proteins have moderate degradation rates and accumulate in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	41-45
34222769-4	2021	Studies on the proteolytic regulation of ABI5, ABF1, and ABF3 in Arabidopsis thaliana have shown that the proteins have moderate degradation rates and accumulate in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	abscisic acid responsive element-binding factor 1	Arabidopsis thaliana	47-51
34222769-4	2021	Studies on the proteolytic regulation of ABI5, ABF1, and ABF3 in Arabidopsis thaliana have shown that the proteins have moderate degradation rates and accumulate in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	206-211	abscisic acid responsive elements-binding factor 3	Arabidopsis thaliana	57-61
34222769-9	2021	As previously seen for ABI5, ABF1, and ABF3, epitope-tagged constitutively expressed ABF2 degrades in seedlings treated with cycloheximide and is stabilized following treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	207-212	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	23-27
34222769-9	2021	As previously seen for ABI5, ABF1, and ABF3, epitope-tagged constitutively expressed ABF2 degrades in seedlings treated with cycloheximide and is stabilized following treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	207-212	abscisic acid responsive element-binding factor 1	Arabidopsis thaliana	29-33
34222769-9	2021	As previously seen for ABI5, ABF1, and ABF3, epitope-tagged constitutively expressed ABF2 degrades in seedlings treated with cycloheximide and is stabilized following treatment with the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	207-212	abscisic acid responsive elements-binding factor 3	Arabidopsis thaliana	39-43
34220184-5	2021	MG132 and chloroquine were used to inhibit the degradation of the WT and mutated EPHA2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	EPH receptor A2	Homo sapiens	81-86
34221996-13	2021	FUT11 knockdown significantly increased the degradation of PDK1 under hypoxia, while treatment with MG132 can relieve the degradation of PDK1 induced by FUT11 knockdown.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	pyruvate dehydrogenase kinase 1	Homo sapiens	59-63
34221996-13	2021	FUT11 knockdown significantly increased the degradation of PDK1 under hypoxia, while treatment with MG132 can relieve the degradation of PDK1 induced by FUT11 knockdown.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	pyruvate dehydrogenase kinase 1	Homo sapiens	137-141
34221996-13	2021	FUT11 knockdown significantly increased the degradation of PDK1 under hypoxia, while treatment with MG132 can relieve the degradation of PDK1 induced by FUT11 knockdown.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	fucosyltransferase 11	Homo sapiens	153-158
34106567-7	2021	Moreover, proteasome inhibitor, MG132, could rescue USP28 silence-induced degradation of FOXC1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	ubiquitin specific peptidase 28	Homo sapiens	52-57
34106567-7	2021	Moreover, proteasome inhibitor, MG132, could rescue USP28 silence-induced degradation of FOXC1.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	forkhead box C1	Homo sapiens	89-94
35427736-9	2022	As application of the proteasome inhibitor MG132 or overexpression of p38MAPK could reverse impaired differentiation of myoblasts induced by BaP, this may suggest potential related strategies for preventing tobacco-related skeletal muscle diseases or for respiratory rehabilitation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	43-48	prohibitin 2	Homo sapiens	141-144
34169395-4	2021	Co-immunoprecipitation, Western blot analysis, immunofluorescence microscopy, flow cytometry, quantitative-Polymerase Chain Reaction (qPCR), and the inhibition of p130 by MG132 inhibitor were employed to investigate the loss of p130 and its disruption in HPV 16/18 E7-transfected HaCaT cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	171-176	RB transcriptional corepressor like 2	Homo sapiens	163-167
34062977-6	2021	Using our existing protocol, inflammasome activation was induced in IL-1alpha-primed ARPE-19 cells with the proteasome and autophagy inhibitors MG-132 and bafilomycin A1, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	144-150	interleukin 1 alpha	Homo sapiens	68-77
34069945-8	2021	Furthermore, Wnt/beta-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	catenin beta 1	Homo sapiens	17-29
34069945-8	2021	Furthermore, Wnt/beta-catenin proved to be a potential pathway and related to P62 by using proteasome inhibitor (MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	nucleoporin 62	Homo sapiens	78-81
34631502-7	2021	In addition, treatment with MG132, a proteasome inhibitor, increased TCF3 protein levels, and there was not significant increase in TCF3 protein levels by methylmercury under these conditions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	transcription factor 3	Mus musculus	69-73
35427736-6	2022	Interestingly, treatment of proteasome inhibitor MG132 was able to reverse BaP-induced degradation of Hsp70/ MK2 and p38MAPK in myoblasts, implying BaP-mediated p38MAPK degradation is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	prohibitin 2	Homo sapiens	75-78
35427736-6	2022	Interestingly, treatment of proteasome inhibitor MG132 was able to reverse BaP-induced degradation of Hsp70/ MK2 and p38MAPK in myoblasts, implying BaP-mediated p38MAPK degradation is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	heat shock protein family A (Hsp70) member 4	Homo sapiens	102-107
35385822-5	2022	The expression of chTERT and telomerase activity were also significantly decreased when the NF-kappaB signaling pathway was blocked by p65 siRNA, MG132 or BAY 11-7082.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	146-151	nuclear factor kappa B subunit 1	Homo sapiens	92-101
35427736-6	2022	Interestingly, treatment of proteasome inhibitor MG132 was able to reverse BaP-induced degradation of Hsp70/ MK2 and p38MAPK in myoblasts, implying BaP-mediated p38MAPK degradation is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	MAPK activated protein kinase 2	Homo sapiens	109-112
35427736-6	2022	Interestingly, treatment of proteasome inhibitor MG132 was able to reverse BaP-induced degradation of Hsp70/ MK2 and p38MAPK in myoblasts, implying BaP-mediated p38MAPK degradation is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	mitogen-activated protein kinase 14	Homo sapiens	117-124
35427736-6	2022	Interestingly, treatment of proteasome inhibitor MG132 was able to reverse BaP-induced degradation of Hsp70/ MK2 and p38MAPK in myoblasts, implying BaP-mediated p38MAPK degradation is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	prohibitin 2	Homo sapiens	148-151
35427736-6	2022	Interestingly, treatment of proteasome inhibitor MG132 was able to reverse BaP-induced degradation of Hsp70/ MK2 and p38MAPK in myoblasts, implying BaP-mediated p38MAPK degradation is proteasome-dependent.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	mitogen-activated protein kinase 14	Homo sapiens	161-168
35331835-9	2022	Moreover, we observed that TRIM25-mediated XRCC5 degradation was reversed by proteasome inhibitor MG-132 or lysosome inhibitor 3-MA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	tripartite motif containing 25	Homo sapiens	27-33
35331835-9	2022	Moreover, we observed that TRIM25-mediated XRCC5 degradation was reversed by proteasome inhibitor MG-132 or lysosome inhibitor 3-MA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-104	X-ray repair cross complementing 5	Homo sapiens	43-48
35631459-6	2022	The depletion of c-Met was mediated by ubiquitin-proteasomal degradation following co-treatment with artonin F, with the proteasome inhibitor MG132 reversing its c-Met-targeting effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-22
35405432-3	2022	Separate groups of model rats were pretreated with the TRAF6 inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-78	TNF receptor associated factor 6	Rattus norvegicus	55-60
35405432-7	2022	Pre-treatment with MG-132 significantly alleviated pancreatic and intestinal pathological scores, reduced serum levels of amylase, IL-1beta, and IL-6, and ameliorated apoptosis of mucosal cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	interleukin 1 alpha	Rattus norvegicus	131-139
35405432-7	2022	Pre-treatment with MG-132 significantly alleviated pancreatic and intestinal pathological scores, reduced serum levels of amylase, IL-1beta, and IL-6, and ameliorated apoptosis of mucosal cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-25	interleukin 6	Rattus norvegicus	145-149
35405432-8	2022	MG-132 reduced intestinal barrier injury, including serum levels of diamine oxidase and lipopolysaccharide, and intestinal expressions of ZO-1 and occludin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	amine oxidase, copper containing 1	Rattus norvegicus	68-83
35405432-8	2022	MG-132 reduced intestinal barrier injury, including serum levels of diamine oxidase and lipopolysaccharide, and intestinal expressions of ZO-1 and occludin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	tight junction protein 1	Rattus norvegicus	138-142
35405432-8	2022	MG-132 reduced intestinal barrier injury, including serum levels of diamine oxidase and lipopolysaccharide, and intestinal expressions of ZO-1 and occludin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	occludin	Rattus norvegicus	147-155
35613681-7	2022	MG132, a proteasome inhibitor, attenuated 1-NP-induced AKAP1 degradation and downstream pDRP1 (Ser637) reduction, thereby ameliorating 1-NP-downregulated steroidogenesis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	A kinase (PRKA) anchor protein 1	Mus musculus	55-60
35631459-6	2022	The depletion of c-Met was mediated by ubiquitin-proteasomal degradation following co-treatment with artonin F, with the proteasome inhibitor MG132 reversing its c-Met-targeting effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	142-147	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	162-167
35588657-7	2022	The proteasome inhibitor, MG132 restored the level of RIPK1 reduced by C-316-1, suggesting that C-316-1 limits necroptosis by promoting the degradation of RIPK1 rather than by reducing its production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	receptor interacting serine/threonine kinase 1	Homo sapiens	54-59
35588657-7	2022	The proteasome inhibitor, MG132 restored the level of RIPK1 reduced by C-316-1, suggesting that C-316-1 limits necroptosis by promoting the degradation of RIPK1 rather than by reducing its production.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	receptor interacting serine/threonine kinase 1	Homo sapiens	155-160
35232219-10	2022	Retaining Hif1alpha stability using CoCl2 or MG132 abolished the protective effect of capsaicin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	hypoxia inducible factor 1, alpha subunit	Mus musculus	10-19
35568791-3	2022	For instance, it was reported that the decrease in protein synthesis upon the 26S proteasomal inhibition by MG132 or bortezomib is mediated by increased eIF2alpha phosphorylation in an HRI-dependent manner in mouse embryonic fibroblast cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	eukaryotic translation initiation factor 2A	Mus musculus	153-162
35568791-3	2022	For instance, it was reported that the decrease in protein synthesis upon the 26S proteasomal inhibition by MG132 or bortezomib is mediated by increased eIF2alpha phosphorylation in an HRI-dependent manner in mouse embryonic fibroblast cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	eukaryotic translation initiation factor 2 alpha kinase 1	Mus musculus	185-188
35524269-0	2022	The anti-tumor effect of proteasome inhibitor MG132 for human adenoid cystic carcinoma: correlate with the emerging role of Nrf2/Keap1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	NFE2 like bZIP transcription factor 2	Homo sapiens	124-128
35524269-0	2022	The anti-tumor effect of proteasome inhibitor MG132 for human adenoid cystic carcinoma: correlate with the emerging role of Nrf2/Keap1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	kelch like ECH associated protein 1	Homo sapiens	129-134
35524269-7	2022	The application of MG132 induced the up-regulation of Nrf2/Keap1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	NFE2 like bZIP transcription factor 2	Homo sapiens	54-58
35524269-7	2022	The application of MG132 induced the up-regulation of Nrf2/Keap1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	19-24	kelch like ECH associated protein 1	Homo sapiens	59-64
35524269-8	2022	Furthermore, inhibition of Nrf2 attenuated the therapeutic effects of MG132 for ACC (both ML385 + MG132 10microM P = 0.0013; 40microM P = 0.0057; 70microM P = 0.0003 versus MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
35524269-8	2022	Furthermore, inhibition of Nrf2 attenuated the therapeutic effects of MG132 for ACC (both ML385 + MG132 10microM P = 0.0013; 40microM P = 0.0057; 70microM P = 0.0003 versus MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
35524269-8	2022	Furthermore, inhibition of Nrf2 attenuated the therapeutic effects of MG132 for ACC (both ML385 + MG132 10microM P = 0.0013; 40microM P = 0.0057; 70microM P = 0.0003 versus MG132).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	173-178	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
35524269-10	2022	CONCLUSIONS: Our results revealed that proteasome inhibitors MG132 could inhibit the cell viability and induce the apoptosis of ACC through Nrf2/Keap1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	NFE2 like bZIP transcription factor 2	Homo sapiens	140-144
35524269-10	2022	CONCLUSIONS: Our results revealed that proteasome inhibitors MG132 could inhibit the cell viability and induce the apoptosis of ACC through Nrf2/Keap1 signaling pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	kelch like ECH associated protein 1	Homo sapiens	145-150
35628386-9	2022	Differently, the proteasome inhibitor MG132 reverted TNFalpha effect, indicating the involvement of proteasomal degradation in Cx43 reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	tumor necrosis factor	Homo sapiens	53-61
35628386-9	2022	Differently, the proteasome inhibitor MG132 reverted TNFalpha effect, indicating the involvement of proteasomal degradation in Cx43 reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	gap junction protein alpha 1	Homo sapiens	127-131
35569519-4	2022	Though the RP2 protein could be readily recovered by proteasome inhibitors, e.g., MG132, their applications for RP2-related RP therapy were limited by their nonspecific characterization.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	82-87	RP2 activator of ARL3 GTPase	Homo sapiens	11-14
35563650-8	2022	After treatment with the proteosome inhibitor MG132, the migration, adhesion and angiogenesis caused by FXR overexpression were all reversed in bladder cancer cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	46-51	nuclear receptor subfamily 1 group H member 4	Homo sapiens	104-107
35563720-8	2022	Elevated cAMP or NLS-ActinR62D reduced the half-life of RelA/p65, which was reversed by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	RELA proto-oncogene, NF-kB subunit	Homo sapiens	56-60
35417031-8	2022	Moreover, the dinaciclib-induced decrease of Oct4 and Nanog protein expression was able to be restored by co-treatment with MG-132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	124-130	POU class 5 homeobox 1	Homo sapiens	45-49
35563720-8	2022	Elevated cAMP or NLS-ActinR62D reduced the half-life of RelA/p65, which was reversed by the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	113-118	RELA proto-oncogene, NF-kB subunit	Homo sapiens	61-64
35529443-7	2022	Furthermore, through the use of the protein synthesis inhibitor CHX and the proteasome synthesis inhibitor MG-132, rutaecarpine was found to promote the expreesions of PGK1 and NRF2 by accelerating PGK1 ubiquitination to reduce PGK1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-113	phosphoglycerate kinase 1	Rattus norvegicus	168-172
35410635-8	2022	Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	mitogen-activated protein kinase 14	Mus musculus	55-58
35410635-8	2022	Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	jun proto-oncogene	Mus musculus	80-85
35410635-8	2022	Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	189-194	jun proto-oncogene	Mus musculus	152-157
35529443-7	2022	Furthermore, through the use of the protein synthesis inhibitor CHX and the proteasome synthesis inhibitor MG-132, rutaecarpine was found to promote the expreesions of PGK1 and NRF2 by accelerating PGK1 ubiquitination to reduce PGK1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-113	NFE2 like bZIP transcription factor 2	Rattus norvegicus	177-181
35529443-7	2022	Furthermore, through the use of the protein synthesis inhibitor CHX and the proteasome synthesis inhibitor MG-132, rutaecarpine was found to promote the expreesions of PGK1 and NRF2 by accelerating PGK1 ubiquitination to reduce PGK1 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-113	phosphoglycerate kinase 1	Rattus norvegicus	198-202
35409357-10	2022	We found that MG132 prevented the OC-mediated decrease in STAR protein levels following 8Br-cAMP stimulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	steroidogenic acute regulatory protein	Mus musculus	58-62
35388084-4	2022	Stress signaling via p38, JNK and c-Jun was active even after 24 h of MG-132 treatment, while the survival-mediating Akt phosphorylation declined and the executor of apoptosis (caspase-3) was activated by that time and apoptosis was also observable.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	mitogen activated protein kinase 14	Rattus norvegicus	21-24
35388084-4	2022	Stress signaling via p38, JNK and c-Jun was active even after 24 h of MG-132 treatment, while the survival-mediating Akt phosphorylation declined and the executor of apoptosis (caspase-3) was activated by that time and apoptosis was also observable.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-76	mitogen-activated protein kinase 8	Rattus norvegicus	26-29
35379791-9	2022	Furthermore, ERalpha overexpression reduced the protein levels of FMNL2 in breast cancer cells, which were reversed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	estrogen receptor 1	Homo sapiens	13-20
35379791-9	2022	Furthermore, ERalpha overexpression reduced the protein levels of FMNL2 in breast cancer cells, which were reversed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	119-124	formin like 2	Homo sapiens	66-71
35043173-10	2022	MTZ-mediated beta-catenin downregulation was recovered by MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	catenin (cadherin associated protein), beta 1	Mus musculus	13-25
35202579-8	2022	Mechanistically, gelsevirine promoted STING K48-linked poly-ubiquitination and MG-132 (a proteasome inhibitor) reversed the inhibitive effects of gelsevirine on IL-1beta-induced activation of STING/TBK1 pathway in chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	interleukin 1 alpha	Mus musculus	161-169
35202579-8	2022	Mechanistically, gelsevirine promoted STING K48-linked poly-ubiquitination and MG-132 (a proteasome inhibitor) reversed the inhibitive effects of gelsevirine on IL-1beta-induced activation of STING/TBK1 pathway in chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-85	TANK-binding kinase 1	Mus musculus	198-202
35247157-7	2022	Compared to ACK1-knockdown cells, ACK1-rescued cells exhibited a restored p27 expression after MG132 treatment and showed an elevated level of ubiquitinated p27.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	dynactin subunit 6	Homo sapiens	74-77
35408930-8	2022	Finally, MG-132-mediated proteasome inhibition sensitized VHL wild-type cells to zafirlukast-induced cell death and inhibition of HIF-2alpha rescued zafirlukast- and MG-132-triggered cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	von Hippel-Lindau tumor suppressor	Homo sapiens	58-61
35408930-8	2022	Finally, MG-132-mediated proteasome inhibition sensitized VHL wild-type cells to zafirlukast-induced cell death and inhibition of HIF-2alpha rescued zafirlukast- and MG-132-triggered cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-15	endothelial PAS domain protein 1	Homo sapiens	130-140
35408930-8	2022	Finally, MG-132-mediated proteasome inhibition sensitized VHL wild-type cells to zafirlukast-induced cell death and inhibition of HIF-2alpha rescued zafirlukast- and MG-132-triggered cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	166-172	endothelial PAS domain protein 1	Homo sapiens	130-140
35336982-9	2022	The I226R-induced NEMO degradation could be prevented by treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	pI226R	African swine fever virus	4-9
35336982-9	2022	The I226R-induced NEMO degradation could be prevented by treatment with MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	72-77	inhibitor of nuclear factor kappa B kinase regulatory subunit gamma	Homo sapiens	18-22
35305671-13	2022	Our data show that overexpression of ANAPC2 significantly reduces KRAS protein levels, which is reversed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	anaphase promoting complex subunit 2	Mus musculus	37-43
35305671-13	2022	Our data show that overexpression of ANAPC2 significantly reduces KRAS protein levels, which is reversed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	108-113	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	66-70
35247157-7	2022	Compared to ACK1-knockdown cells, ACK1-rescued cells exhibited a restored p27 expression after MG132 treatment and showed an elevated level of ubiquitinated p27.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	tyrosine kinase non receptor 2	Homo sapiens	34-38
35238869-6	2022	Proteasome (bortezomib, MG132) and caspase-1 (VX-765, Z-VAD-FMK) inhibitors block NLRP1 activation and downstream pyroptosis, respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	NLR family pyrin domain containing 1	Homo sapiens	82-87
34699308-6	2022	Proteasome inhibitor MG-132 decreased FUNDC1 ubiquitination level while protease activator MF-094 increased FUNDC1 ubiquitination level.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	FUN14 domain containing 1	Homo sapiens	38-44
35074488-10	2022	However, the proteasome inhibitor MG132 blocked DHT-induced Nrf2 inhibition, suggesting a post-translational regulation manner.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	NFE2 like bZIP transcription factor 2	Homo sapiens	60-64
35203681-8	2022	GATA2 protein expression was rescued by the proteasome inhibitor MG132 and partly by mutating the target site of the E3 ligase FBXW7.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	65-70	GATA binding protein 2	Homo sapiens	0-5
35203681-9	2022	Moreover, MG132-mediated proteasome inhibition induced AR mRNA and additional luminal marker gene transcription in the prostate transit amplifying cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	10-15	androgen receptor	Homo sapiens	55-57
35042442-9	2022	The hyperthermia-induced degradation of TAK1 and MEKK2 was rescued by either the proteasome inhibitor MG132 or the calpain inhibitor ALLN; however, RAF1 was not affected by the inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-107	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	40-44
35130601-0	2022	(Experimental study of proteasome inhibitor MG132 up-regulates Wnt/beta-catenin signaling pathway to improve osteoporosis).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	catenin beta 1	Rattus norvegicus	67-79
35130601-12	2022	CONCLUSION: MG-132, a ubiquitin proteasome inhibitor, can regulate Wnt/beta-catenin signaling pathway by inhibiting the degradation of beta-catenin protein, and delaying the occurrence and development of osteoporosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-18	catenin beta 1	Rattus norvegicus	71-83
35130601-12	2022	CONCLUSION: MG-132, a ubiquitin proteasome inhibitor, can regulate Wnt/beta-catenin signaling pathway by inhibiting the degradation of beta-catenin protein, and delaying the occurrence and development of osteoporosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	12-18	catenin beta 1	Rattus norvegicus	135-147
35042442-9	2022	The hyperthermia-induced degradation of TAK1 and MEKK2 was rescued by either the proteasome inhibitor MG132 or the calpain inhibitor ALLN; however, RAF1 was not affected by the inhibitors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	102-107	mitogen-activated protein kinase kinase kinase 2	Homo sapiens	49-54