PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
31118030-7	2019	Confocal microscopic data indicated a synergism of NaIO3 and bafilomycin A1 on LC3 punctate formation, indicating the induction of autophagy.	bafilomycin A1	61-75	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	79-82
31108937-5	2019	Comparing the fluorescence characteristics of these proteins in response to intracellular pH changes induced by chloroquine or bafilomycin A1, we found that pHluorin-BACE1-mCherry is a better pH sensor for BACE1 because its fluorescence intensity responds to pH changes more dramatically and more quickly.	bafilomycin A1	127-141	beta-secretase 1	Homo sapiens	166-171
31108937-5	2019	Comparing the fluorescence characteristics of these proteins in response to intracellular pH changes induced by chloroquine or bafilomycin A1, we found that pHluorin-BACE1-mCherry is a better pH sensor for BACE1 because its fluorescence intensity responds to pH changes more dramatically and more quickly.	bafilomycin A1	127-141	beta-secretase 1	Homo sapiens	206-211
30805671-8	2019	Moreover, inhibiting A2AR by antagonist (SCH 58261) performed the same downstream biological effects as caffeine treatment, and autophagy inhibitor (BafilomycinA1) clearly abolished the caffeine-induced Bcl10 degradation and A20 suppression.	bafilomycin A1	149-162	B cell leukemia/lymphoma 10	Mus musculus	203-208
30805671-8	2019	Moreover, inhibiting A2AR by antagonist (SCH 58261) performed the same downstream biological effects as caffeine treatment, and autophagy inhibitor (BafilomycinA1) clearly abolished the caffeine-induced Bcl10 degradation and A20 suppression.	bafilomycin A1	149-162	tumor necrosis factor, alpha-induced protein 3	Mus musculus	225-228
30686534-5	2019	In contrast, genetic ablation (using ATG5-/- or ATG7-/- cells) or pharmacologic inhibition (the administration of bafilomycin A1 or chloroquine) of autophagy was found to block ferroptosis activator-induced HMGB1 release.	bafilomycin A1	114-128	high mobility group box 1	Homo sapiens	207-212
31327962-8	2019	Next, the drug bafilomycin A1 (BAF, 50 nM) was used to block the autophagic flux.	bafilomycin A1	15-29	BAF nuclear assembly factor 1	Homo sapiens	31-34
30893306-8	2019	Bafilomycin A1, a specific inhibitor of vacuolar-type proton ATPase (V-ATPase) which alkalizes acidic vesicles, abolished ZnT2-dependent zinc transport into intracellular vesicles.	bafilomycin A1	0-14	solute carrier family 30 member 2	Homo sapiens	122-126
30553838-9	2019	Autophagy was inhibited in ALR-knockdown mice and HepG2 cells, and autophagy inhibitor bafilomycin A1 attenuated the protective effects of ALR.	bafilomycin A1	87-101	growth factor, augmenter of liver regeneration	Homo sapiens	139-142
29486589-10	2019	Moreover, blocking autophagy with bafilomycin A1 or LC3B siRNA resulted in oxidant accumulation, NLRP3 inflammasome hyperactivation, and collagen deposition.	bafilomycin A1	34-48	NLR family pyrin domain containing 3	Homo sapiens	97-102
30789754-6	2019	Also, the inhibition of the lysosomal pathway with bafilomycin A1 (80 nM, 24 h) resulted in a significant increase in NPC1L1 protein levels.	bafilomycin A1	51-65	NPC1 like intracellular cholesterol transporter 1	Homo sapiens	118-124
30557043-6	2019	Inhibitors of bone resorption, such as alendronate, bafilomycin A1, and the PI3K inhibitor LY294002, suppressed the expression of Pmepa1 in osteoclasts.	bafilomycin A1	52-66	prostate transmembrane protein, androgen induced 1	Rattus norvegicus	130-136
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.	bafilomycin A1	65-79	G protein pathway suppressor 2	Mus musculus	160-164
30584497-6	2018	Anti-HRV1B activity of DEX via the glucocorticoid receptor (GCR)-dependent autophagy activation was assessed by blocking with chloroquine diphosphate salt or bafilomycin A1 treatment.	bafilomycin A1	158-172	nuclear receptor subfamily 3 group C member 1	Homo sapiens	60-63
29807114-3	2018	Further, SFN-NAC increased LC3 II/LC3 I and the number of LC3 punctas, but Western blot showed that SFN-NAC inhibited cell autophagy in response to a co-treatment of Bafilomycin A1 and SFN-NAC.	bafilomycin A1	166-180	RNA exonuclease 2	Homo sapiens	100-103
29807114-3	2018	Further, SFN-NAC increased LC3 II/LC3 I and the number of LC3 punctas, but Western blot showed that SFN-NAC inhibited cell autophagy in response to a co-treatment of Bafilomycin A1 and SFN-NAC.	bafilomycin A1	166-180	synuclein alpha	Homo sapiens	104-107
29807114-3	2018	Further, SFN-NAC increased LC3 II/LC3 I and the number of LC3 punctas, but Western blot showed that SFN-NAC inhibited cell autophagy in response to a co-treatment of Bafilomycin A1 and SFN-NAC.	bafilomycin A1	166-180	RNA exonuclease 2	Homo sapiens	100-103
29807114-3	2018	Further, SFN-NAC increased LC3 II/LC3 I and the number of LC3 punctas, but Western blot showed that SFN-NAC inhibited cell autophagy in response to a co-treatment of Bafilomycin A1 and SFN-NAC.	bafilomycin A1	166-180	synuclein alpha	Homo sapiens	104-107
30587795-6	2018	Morphologically, LT-IIc induced the formation of enlarged LAMP2+ autolysosomes, which was blocked by co-treatment with bafilomycin A1.	bafilomycin A1	119-133	lysosomal associated membrane protein 2	Homo sapiens	58-63
30282964-8	2018	The protective effects of TRPC6 ablation were prevented by autophagy inhibitors Chloroquine and Bafilomycin A1.	bafilomycin A1	96-110	transient receptor potential cation channel subfamily C member 6	Homo sapiens	26-31
29434757-8	2018	Autophagy flux analyzed by microtubule-associated protein 1 light chain 3 (LC3) turnover indicated that miR-221 reduced autophagy in CRC cells using different protease inhibitors (E64d and pepstatin A; Bafilomycin A1) in nutrient-rich medium or under starvation conditions.	bafilomycin A1	202-216	microRNA 221	Homo sapiens	104-111
29492987-7	2018	Preventing lysosome damage with bafilomycin A1 or CA-074-Me also counteracted SPION-induced IL-1beta release.	bafilomycin A1	32-46	interleukin 1 alpha	Mus musculus	92-100
28840510-6	2018	3-Methyl adenine did not change LC3 conversion; vinblastine and bafilomycin A1 decreased LAMP 2 expression in controls.	bafilomycin A1	64-78	lysosomal-associated membrane protein 2	Rattus norvegicus	89-95
29146131-10	2018	Furthermore, depigmentation in TSC2-KD melanocytes was accelerated by inhibiting autophagy (ATG7-KD or bafilomycin A1-pretreatment) and was completely reversed by induction of autophagy via mTOR-dependent (rapamycin) or mTOR-independent (SMER28) exposure.	bafilomycin A1	103-117	TSC complex subunit 2	Homo sapiens	31-35
28840510-7	2018	While cypermethrin increased LC3 conversion in the presence of 3-methyl adenine, LAMP 2 reduction was more pronounced in vinblastine and bafilomycin A1-treated cells.	bafilomycin A1	137-151	lysosomal-associated membrane protein 2	Rattus norvegicus	81-87
29080748-8	2018	By using NH4Cl and Bafilomycin A1 to inhibit the lysosomal degradative pathway, we found that the reduction of APP induced by SNX7 overexpression was prevented by such inhibition.	bafilomycin A1	19-33	sorting nexin 7	Homo sapiens	126-130
28128446-6	2017	AGE impairs autophagosomes" clearance in p53 negative cells as observed with an autophagosome maturation blocker-bafilomycinA1 treated cells.	bafilomycin A1	113-126	tumor protein p53	Homo sapiens	41-44
29203244-6	2018	In addition, ox-LDL increased LC3-II, Beclin 1, and p62 expressions in HUVECs, while these changes were nullified in the presence of treatment with bafilomycin A1 (BafA1, an inhibit autophagic flux inhibitor).	bafilomycin A1	148-162	beclin 1	Homo sapiens	38-46
29203244-6	2018	In addition, ox-LDL increased LC3-II, Beclin 1, and p62 expressions in HUVECs, while these changes were nullified in the presence of treatment with bafilomycin A1 (BafA1, an inhibit autophagic flux inhibitor).	bafilomycin A1	148-162	nucleoporin 62	Homo sapiens	52-55
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.	bafilomycin A1	134-138	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.	bafilomycin A1	80-84	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.	bafilomycin A1	77-81	cathepsin B	Homo sapiens	38-49
28106298-9	2017	Its role in autophagy was confirmed through decrease in the levels of LC3 II after pretreatment with IP3 R inhibitor and N acetyl cysteine.Moreover, inhibiting as well as silencing IP3 R-induced cell death in MCF-7 cells was attenuated by autophagic inhibitors (Bafilomycin A1 or 3-Methyladeneine).	bafilomycin A1	262-276	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	101-106
28106298-9	2017	Its role in autophagy was confirmed through decrease in the levels of LC3 II after pretreatment with IP3 R inhibitor and N acetyl cysteine.Moreover, inhibiting as well as silencing IP3 R-induced cell death in MCF-7 cells was attenuated by autophagic inhibitors (Bafilomycin A1 or 3-Methyladeneine).	bafilomycin A1	262-276	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	181-186
28214847-8	2017	Although free ubiquitin content was increased, the colocalization of it to CDK1 was markedly decreased in CD38-/- or baf treated CAMs.	bafilomycin A1	117-120	cyclin-dependent kinase 1	Mus musculus	75-79
27681126-4	2016	This depletion was independent of proteasomes, as it was not affected by the proteasome inhibitor MG132, but it was suppressed by bafilomycin A1, which led to the association of TRAF6 with autophagosomes.	bafilomycin A1	130-144	TNF receptor associated factor 6	Homo sapiens	178-183
28359055-8	2017	Treatment with bafilomycin A1 (an inhibitor of vacuolar H+-ATPase, a late autophagy inhibitor) further increase LC3-II and p62 levels, suggesting that degradation of autophagolysosome could be impaired.	bafilomycin A1	15-29	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	112-115
28359055-8	2017	Treatment with bafilomycin A1 (an inhibitor of vacuolar H+-ATPase, a late autophagy inhibitor) further increase LC3-II and p62 levels, suggesting that degradation of autophagolysosome could be impaired.	bafilomycin A1	15-29	nucleoporin 62	Homo sapiens	123-126
28101201-10	2016	Notably, following treatment of HepG2 cells with the autophagy inhibitor, BA1, the expression of apoptosis-related proteins, including Bax, Bak and p53, were significantly decreased (P<0.05), and cell viability was recovered to a certain extent.	bafilomycin A1	74-77	BCL2 associated X, apoptosis regulator	Homo sapiens	135-138
28101201-10	2016	Notably, following treatment of HepG2 cells with the autophagy inhibitor, BA1, the expression of apoptosis-related proteins, including Bax, Bak and p53, were significantly decreased (P<0.05), and cell viability was recovered to a certain extent.	bafilomycin A1	74-77	BCL2 antagonist/killer 1	Homo sapiens	140-143
28101201-10	2016	Notably, following treatment of HepG2 cells with the autophagy inhibitor, BA1, the expression of apoptosis-related proteins, including Bax, Bak and p53, were significantly decreased (P<0.05), and cell viability was recovered to a certain extent.	bafilomycin A1	74-77	tumor protein p53	Homo sapiens	148-151
27246695-8	2016	Paraquat-elicited changes in cardiac autophagy markers (LC3BII, LC3BII-to-LC3BI ratio and p62) were augmented by lysosomal inhibition using bafilomycin A1 in WT mice.	bafilomycin A1	140-154	nucleoporin 62	Mus musculus	90-93
26873723-9	2016	The decline in Cx43-protein levels, both as gap junctions and as hemichannels, could be prevented by the addition of bafilomycin A1, a lysosomal inhibitor, during the complete nutrient starvation period.	bafilomycin A1	117-131	gap junction protein alpha 1	Bos taurus	15-19
27513923-4	2016	Studies with Atg5 small interfering RNA (siRNA) and the autophagy inhibitors bafilomycin A1 (Baf) and chloroquine demonstrate that autophagy is required for AGGF1-mediated EC proliferation, migration, capillary tube formation, and aortic ring-based angiogenesis.	bafilomycin A1	77-91	angiogenic factor with G patch and FHA domains 1	Mus musculus	157-162
27513923-4	2016	Studies with Atg5 small interfering RNA (siRNA) and the autophagy inhibitors bafilomycin A1 (Baf) and chloroquine demonstrate that autophagy is required for AGGF1-mediated EC proliferation, migration, capillary tube formation, and aortic ring-based angiogenesis.	bafilomycin A1	93-96	angiogenic factor with G patch and FHA domains 1	Mus musculus	157-162
27226588-6	2016	Although the proteasome-specific inhibitors lactacystin and epoxomicin only moderately increase FoxO1 protein levels, the inhibitors of lysosomal proteolysis bafilomycin A1 and chloroquine restore the decreased FoxO1 levels in Zfat-deficient T cells to levels comparable with those in control cells.	bafilomycin A1	158-172	forkhead box O1	Mus musculus	211-216
27113027-5	2016	In addition, Akt reduction in adipose tissues of mice treated with curcumin could be recovered by administration of autophagy inhibitor bafilomycin A1 (BFA).	bafilomycin A1	136-150	thymoma viral proto-oncogene 1	Mus musculus	13-16
27113027-5	2016	In addition, Akt reduction in adipose tissues of mice treated with curcumin could be recovered by administration of autophagy inhibitor bafilomycin A1 (BFA).	bafilomycin A1	152-155	thymoma viral proto-oncogene 1	Mus musculus	13-16
27397870-9	2016	The formation of CaOx appears to be dependent on the cooperation between Prestin and the vATPase complex as treatment with bafilomycin A1 or concanamycin A abolishes the production of detectable CaOx.	bafilomycin A1	123-137	prestin	Drosophila melanogaster	73-80
27430213-9	2016	Further validation analyses were focused on V-ATPase and showed that two independent V-ATPase inhibitors (bafilomycin A1 and concanamycin A) are sensitive to SOX11 levels, causing reduced anti-proliferative response in SOX11 low cells.	bafilomycin A1	106-120	SRY-box transcription factor 11	Homo sapiens	158-163
27430213-9	2016	Further validation analyses were focused on V-ATPase and showed that two independent V-ATPase inhibitors (bafilomycin A1 and concanamycin A) are sensitive to SOX11 levels, causing reduced anti-proliferative response in SOX11 low cells.	bafilomycin A1	106-120	SRY-box transcription factor 11	Homo sapiens	219-224
26757341-11	2016	Small interfering RNA depletion of TPC2 alone or together with TPC1 increased both LC3II and p62 levels under basal conditions and in response to serum starvation, suggesting that, under conditions of severe energy depletion (serum plus glucose starvation), changes in the autophagic flux (as assessed by use of bafilomycin A1) occurred either when TPC1 or TPC2 were downregulated.	bafilomycin A1	312-326	two pore segment channel 2	Homo sapiens	35-39
26757341-11	2016	Small interfering RNA depletion of TPC2 alone or together with TPC1 increased both LC3II and p62 levels under basal conditions and in response to serum starvation, suggesting that, under conditions of severe energy depletion (serum plus glucose starvation), changes in the autophagic flux (as assessed by use of bafilomycin A1) occurred either when TPC1 or TPC2 were downregulated.	bafilomycin A1	312-326	two pore channel 1	Mus musculus	63-67
26043797-8	2015	Pretreatment with the autophagy inhibitors LY294002, 3-methyladenine, chloroquine, and bafilomycin A1 enhanced the induction of apoptosis by MHY218, and this was accompanied by an increase in PARP cleavage.	bafilomycin A1	87-101	poly(ADP-ribose) polymerase 1	Homo sapiens	192-196
25981168-4	2015	We found that combined treatment with EGFR TKIs (erlotinib, gefitinib, or lapatinib) and vATPase inhibitors (bafilomycin A1 or concanamycin A) enhanced synergistic cell death compared to treatments with each drug alone.	bafilomycin A1	109-123	epidermal growth factor receptor	Homo sapiens	38-42
25981168-5	2015	Treatment with bafilomycin A1 or concanamycin A led to the induction of Bnip3 expression in an Hif-1alpha dependent manner.	bafilomycin A1	15-29	BCL2 interacting protein 3	Homo sapiens	72-77
25981168-5	2015	Treatment with bafilomycin A1 or concanamycin A led to the induction of Bnip3 expression in an Hif-1alpha dependent manner.	bafilomycin A1	15-29	hypoxia inducible factor 1 subunit alpha	Homo sapiens	95-105
26039928-7	2015	GH3 treatment with bafilomycin A1, a V-ATPase inhibitor, also blocked GH release, indicating mediation via impaired cellular acidification of V-ATPase.	bafilomycin A1	19-33	gonadotropin releasing hormone receptor	Rattus norvegicus	0-2
25853243-6	2015	We also found that TGFBIp was internalized by caveolae-mediated endocytosis, and the internalized TGFBIp accumulated after treatment with bafilomycin A1, an inhibitor of lysosomal degradation.	bafilomycin A1	138-152	transforming growth factor beta induced	Homo sapiens	19-25
25959678-2	2015	Based on studies with the V-ATPase inhibitor BafilomycinA1, lysosomal acidification is also thought to be required for fusion with incoming vesicles from the autophagic and endocytic pathways.	bafilomycin A1	45-58	Vacuolar H[+]-ATPase 26kD subunit	Drosophila melanogaster	26-34
25853243-6	2015	We also found that TGFBIp was internalized by caveolae-mediated endocytosis, and the internalized TGFBIp accumulated after treatment with bafilomycin A1, an inhibitor of lysosomal degradation.	bafilomycin A1	138-152	transforming growth factor beta induced	Homo sapiens	98-104
25376834-4	2015	Inhibition of autophagy by bafilomycin A1 or chloroquine treatment during amino acid scarcity abolished mTORC1 signaling, an effect that could be rescued by inhibiting protein synthesis or amino acid supplementation, respectively.	bafilomycin A1	27-41	CREB regulated transcription coactivator 1	Mus musculus	104-110
23192368-4	2013	K(IR)2.1 trafficking in HEK293 cells was studied by live cell imaging, immunofluorescence microscopy, and Western blot following pharmacological intervention with dynasore (Dyn), chlorpromazine (CPZ), bafilomycin A1 (Baf), or chloroquine (CQ).	bafilomycin A1	201-215	potassium inwardly rectifying channel subfamily J member 2	Homo sapiens	0-8
25617421-6	2015	Inhibition of autophagy with a PI3K inhibitor (3-MA), a ROS scavenger (NAC) or autophagosomal-lysosomal fusion inhibitors (bafilomycin A1 and chloroquine) rescued rMIF-induced vascular leakage, suggesting that autophagy mediates MIF-induced vascular leakage.	bafilomycin A1	123-137	macrophage migration inhibitory factor	Homo sapiens	164-167
26418500-8	2015	High phosphate further significantly up-regulated the mRNA levels of TGFB1, NFAT5 and SOX9, effects significantly blunted by additional treatment with bafilomycin A1 or methylamine.	bafilomycin A1	151-165	transforming growth factor beta 1	Homo sapiens	69-74
26418500-8	2015	High phosphate further significantly up-regulated the mRNA levels of TGFB1, NFAT5 and SOX9, effects significantly blunted by additional treatment with bafilomycin A1 or methylamine.	bafilomycin A1	151-165	nuclear factor of activated T cells 5	Homo sapiens	76-81
26418500-8	2015	High phosphate further significantly up-regulated the mRNA levels of TGFB1, NFAT5 and SOX9, effects significantly blunted by additional treatment with bafilomycin A1 or methylamine.	bafilomycin A1	151-165	SRY-box transcription factor 9	Homo sapiens	86-90
24977403-0	2014	Phagocytosis of bafilomycin A1-treated apoptotic neuroblastoma cells by bone marrow-derived dendritic cells initiates a CD8alpha+ lymphocyte response to neuroblastoma.	bafilomycin A1	16-30	CD8 antigen, alpha chain	Mus musculus	120-128
24687431-3	2014	In particular, Concanamycin A (CMA) and Bafilomycin A1 (Baf), inhibitors of vacuolar ATPase (V-ATPase), increased the secretion of CRELD2 without relying on its C-terminal structure.	bafilomycin A1	40-54	cysteine rich with EGF like domains 2	Homo sapiens	131-137
24321340-4	2014	Interestingly, CA-4-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitors (3-methyladenine and bafilomycin A1) or small interfering RNAs against the autophagic genes (Atg5 and Beclin 1).	bafilomycin A1	137-151	carbonic anhydrase 4	Homo sapiens	15-19
25484190-6	2014	Here, we attributed SNCA-induced toxicity mainly to secreted species in a cell culture model of SNCA aggregation and in SNCA transgenic mice: We showed that ALP inhibition by bafilomycinA1 reduced intracellular SNCA aggregation but increased secretion of smaller oligomers that exacerbated microenvironmental response including uptake, inflammation, and cellular damage.	bafilomycin A1	175-188	synuclein, alpha	Mus musculus	20-24
25484190-6	2014	Here, we attributed SNCA-induced toxicity mainly to secreted species in a cell culture model of SNCA aggregation and in SNCA transgenic mice: We showed that ALP inhibition by bafilomycinA1 reduced intracellular SNCA aggregation but increased secretion of smaller oligomers that exacerbated microenvironmental response including uptake, inflammation, and cellular damage.	bafilomycin A1	175-188	synuclein, alpha	Mus musculus	96-100
25484190-6	2014	Here, we attributed SNCA-induced toxicity mainly to secreted species in a cell culture model of SNCA aggregation and in SNCA transgenic mice: We showed that ALP inhibition by bafilomycinA1 reduced intracellular SNCA aggregation but increased secretion of smaller oligomers that exacerbated microenvironmental response including uptake, inflammation, and cellular damage.	bafilomycin A1	175-188	synuclein, alpha	Mus musculus	96-100
25484190-6	2014	Here, we attributed SNCA-induced toxicity mainly to secreted species in a cell culture model of SNCA aggregation and in SNCA transgenic mice: We showed that ALP inhibition by bafilomycinA1 reduced intracellular SNCA aggregation but increased secretion of smaller oligomers that exacerbated microenvironmental response including uptake, inflammation, and cellular damage.	bafilomycin A1	175-188	synuclein, alpha	Mus musculus	96-100
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	bafilomycin A1	316-330	kininogen 1	Homo sapiens	42-52
23674090-4	2013	We used bafilomycin A1 (BMA) as a specific inhibitor of Bcl-xL to examine the biological effects in UC cells in vitro and in vivo.	bafilomycin A1	8-22	BCL2 like 1	Homo sapiens	56-62
23674090-4	2013	We used bafilomycin A1 (BMA) as a specific inhibitor of Bcl-xL to examine the biological effects in UC cells in vitro and in vivo.	bafilomycin A1	24-27	BCL2 like 1	Homo sapiens	56-62
25451935-6	2015	In contrast, Ca(2+) transients induced via lysosome-targeted hTPC2 and endolysosome-targeted rTPC3 were abolished by bafilomycin A1 and markedly attenuated by thapsigargin.	bafilomycin A1	117-131	two pore segment channel 2	Homo sapiens	61-66
25218469-6	2014	In addition, the proteasomal inhibitor lactacystin (5muM) inhibited Ang II-mediated the reduction of mature hERG channel protein, but the lysosomal inhibitor bafilomycin A1 (1muM) had no effect on the protein.	bafilomycin A1	158-172	angiotensinogen	Homo sapiens	68-74
25181483-7	2014	The inhibition of lysosomal function by monensin or bafilomycin A1 after the occurrence of PrP(Sc) redistribution by CPZ or U18666A partly antagonized PrP(Sc) degradation, suggesting that the transfer of PrP(Sc) to late endosomes/lysosomes, possibly via alteration of the membrane trafficking machinery of cells, leads to PrP(Sc) degradation.	bafilomycin A1	52-66	prion protein	Mus musculus	91-94
25181483-7	2014	The inhibition of lysosomal function by monensin or bafilomycin A1 after the occurrence of PrP(Sc) redistribution by CPZ or U18666A partly antagonized PrP(Sc) degradation, suggesting that the transfer of PrP(Sc) to late endosomes/lysosomes, possibly via alteration of the membrane trafficking machinery of cells, leads to PrP(Sc) degradation.	bafilomycin A1	52-66	prion protein	Mus musculus	151-154
25181483-7	2014	The inhibition of lysosomal function by monensin or bafilomycin A1 after the occurrence of PrP(Sc) redistribution by CPZ or U18666A partly antagonized PrP(Sc) degradation, suggesting that the transfer of PrP(Sc) to late endosomes/lysosomes, possibly via alteration of the membrane trafficking machinery of cells, leads to PrP(Sc) degradation.	bafilomycin A1	52-66	prion protein	Mus musculus	151-154
25181483-7	2014	The inhibition of lysosomal function by monensin or bafilomycin A1 after the occurrence of PrP(Sc) redistribution by CPZ or U18666A partly antagonized PrP(Sc) degradation, suggesting that the transfer of PrP(Sc) to late endosomes/lysosomes, possibly via alteration of the membrane trafficking machinery of cells, leads to PrP(Sc) degradation.	bafilomycin A1	52-66	prion protein	Mus musculus	151-154
24695574-1	2014	ATP6V0C is the bafilomycin A1-binding subunit of vacuolar ATPase, an enzyme complex that critically regulates vesicular acidification.	bafilomycin A1	15-29	ATPase H+ transporting V0 subunit c	Homo sapiens	0-7
24695574-6	2014	Knockdown of ATP6V0C also sensitized cells to the accumulation of autophagy substrates and a reduction in neurite length following treatment with 1 nM bafilomycin A1, a concentration that did not produce such alterations in non-target control cells.	bafilomycin A1	151-165	ATPase H+ transporting V0 subunit c	Homo sapiens	13-20
24448802-8	2014	The macrolide antibiotic bafilomycin A1 inhibited CS-induced Ca(2+) release and prevented CFTR clearance from the plasma membrane, further linking cytoplasmic Ca(2+) and CFTR internalization.	bafilomycin A1	25-39	CF transmembrane conductance regulator	Homo sapiens	90-94
24448802-8	2014	The macrolide antibiotic bafilomycin A1 inhibited CS-induced Ca(2+) release and prevented CFTR clearance from the plasma membrane, further linking cytoplasmic Ca(2+) and CFTR internalization.	bafilomycin A1	25-39	CF transmembrane conductance regulator	Homo sapiens	170-174
24547878-9	2014	The autophagy inhibitor bafilomycin A1 (BaF) decreased 1-induced cell viability and increased pp38, pJNK, FasL, caspase-8 activation, and caspase-3 activation.	bafilomycin A1	24-38	BAF nuclear assembly factor 1	Homo sapiens	40-43
24547878-9	2014	The autophagy inhibitor bafilomycin A1 (BaF) decreased 1-induced cell viability and increased pp38, pJNK, FasL, caspase-8 activation, and caspase-3 activation.	bafilomycin A1	24-38	Fas ligand	Homo sapiens	106-110
24547878-9	2014	The autophagy inhibitor bafilomycin A1 (BaF) decreased 1-induced cell viability and increased pp38, pJNK, FasL, caspase-8 activation, and caspase-3 activation.	bafilomycin A1	24-38	caspase 8	Homo sapiens	112-121
24547878-9	2014	The autophagy inhibitor bafilomycin A1 (BaF) decreased 1-induced cell viability and increased pp38, pJNK, FasL, caspase-8 activation, and caspase-3 activation.	bafilomycin A1	24-38	caspase 3	Homo sapiens	138-147
23530046-11	2013	Acidic extracellular pH caused rapid intracellular acidification, and the IL-1beta-inducing effect of acidic medium could be mimicked by acidifying the cytosol with bafilomycin A1, a proton pump inhibitor.	bafilomycin A1	165-179	interleukin 1 beta	Homo sapiens	74-82
22962303-8	2012	Bafilomycin A1, a specific V-ATPase inhibitor, markedly slowed the intracellular pH (pHi) recovery after acid load in human HCC cells and retarded the growth of human HCC in orthotopic xenograft model.	bafilomycin A1	0-14	glucose-6-phosphate isomerase	Homo sapiens	85-88
23109342-8	2012	Inhibition of RNase L-induced autophagy using Bafilomycin A1 or 3-methyladenine suppressed viral growth in initial stages; in later stages autophagy promoted viral replication dampening the antiviral effect.	bafilomycin A1	46-60	ribonuclease L	Homo sapiens	14-21
22929013-3	2012	The packaging of glutamate was perturbed by blocking the vesicular glutamate transporter (VGlut) with bafilomycin A1.	bafilomycin A1	102-116	Vesicular glutamate transporter	Drosophila melanogaster	57-88
22929013-3	2012	The packaging of glutamate was perturbed by blocking the vesicular glutamate transporter (VGlut) with bafilomycin A1.	bafilomycin A1	102-116	Vesicular glutamate transporter	Drosophila melanogaster	90-95
21558123-8	2011	Bafilomycin A1 treatment also decreased exocytotic secretion from the regulated pathway, monitored by a CHGA chimera tagged with embryonic alkaline phosphatase.	bafilomycin A1	0-14	chromogranin A	Homo sapiens	104-108
22276961-4	2012	The high-K(+) -evoked overflow of beta-NAD(+)  is attenuated by cleavage of SNAP-25 with botulinum neurotoxin A, by inhibition of N-type voltage-dependent Ca(2+)  channels with omega-conotoxin GVIA, and by inhibition of the proton gradient of synaptic vesicles with bafilomycin A1, suggesting that beta-NAD(+)  is likely released via vesicle exocytosis.	bafilomycin A1	266-280	synaptosome associated protein 25	Rattus norvegicus	76-83
21613417-9	2011	Treatment with bafilomycin A1 (a proton pump inhibitor) and leupeptin (a lysosomal inhibitor) reversed WNK4 WT-mediated inhibition of Maxi K total protein expression.	bafilomycin A1	15-29	WNK lysine deficient protein kinase 4	Homo sapiens	103-107
22943412-3	2012	A decrease in iO2 (intracellular O2) to 0-10 muM, induced by Baf, is sufficient for stabilization of HIFs (hypoxia inducible factors) HIF-1alpha and HIF-2alpha, coupled with an increased expression of target genes including GLUT1 (glucose transporter 1), HIF PHD2 (prolyl hydroxylase domain 2) and CAIX (carbonic anhydrase IX).	bafilomycin A1	61-64	hypoxia inducible factor 1 subunit alpha	Homo sapiens	134-144
22943412-3	2012	A decrease in iO2 (intracellular O2) to 0-10 muM, induced by Baf, is sufficient for stabilization of HIFs (hypoxia inducible factors) HIF-1alpha and HIF-2alpha, coupled with an increased expression of target genes including GLUT1 (glucose transporter 1), HIF PHD2 (prolyl hydroxylase domain 2) and CAIX (carbonic anhydrase IX).	bafilomycin A1	61-64	endothelial PAS domain protein 1	Homo sapiens	149-159
22943412-3	2012	A decrease in iO2 (intracellular O2) to 0-10 muM, induced by Baf, is sufficient for stabilization of HIFs (hypoxia inducible factors) HIF-1alpha and HIF-2alpha, coupled with an increased expression of target genes including GLUT1 (glucose transporter 1), HIF PHD2 (prolyl hydroxylase domain 2) and CAIX (carbonic anhydrase IX).	bafilomycin A1	61-64	solute carrier family 2 member 1	Homo sapiens	224-229
22943412-3	2012	A decrease in iO2 (intracellular O2) to 0-10 muM, induced by Baf, is sufficient for stabilization of HIFs (hypoxia inducible factors) HIF-1alpha and HIF-2alpha, coupled with an increased expression of target genes including GLUT1 (glucose transporter 1), HIF PHD2 (prolyl hydroxylase domain 2) and CAIX (carbonic anhydrase IX).	bafilomycin A1	61-64	solute carrier family 2 member 1	Homo sapiens	231-252
22943412-3	2012	A decrease in iO2 (intracellular O2) to 0-10 muM, induced by Baf, is sufficient for stabilization of HIFs (hypoxia inducible factors) HIF-1alpha and HIF-2alpha, coupled with an increased expression of target genes including GLUT1 (glucose transporter 1), HIF PHD2 (prolyl hydroxylase domain 2) and CAIX (carbonic anhydrase IX).	bafilomycin A1	61-64	carbonic anhydrase 9	Homo sapiens	298-302
22943412-3	2012	A decrease in iO2 (intracellular O2) to 0-10 muM, induced by Baf, is sufficient for stabilization of HIFs (hypoxia inducible factors) HIF-1alpha and HIF-2alpha, coupled with an increased expression of target genes including GLUT1 (glucose transporter 1), HIF PHD2 (prolyl hydroxylase domain 2) and CAIX (carbonic anhydrase IX).	bafilomycin A1	61-64	carbonic anhydrase 9	Homo sapiens	304-325
22647715-0	2012	Alpha-synuclein aggregation involves a bafilomycin A 1-sensitive autophagy pathway.	bafilomycin A1	39-54	synuclein, alpha	Mus musculus	0-15
23029002-5	2012	Moreover, phosphatidylinositol 3-kinase inhibition with 3-MA or inhibition of endosomal acidification with bafilomycin A1 hindered the release of TF-bearing NETs.	bafilomycin A1	107-121	coagulation factor III, tissue factor	Homo sapiens	146-148
21716324-5	2011	Bafilomycin A1, which inhibits endosomal acidification to block the TLR3 pathway, blocked the dsRNA-induced expression of TSLP, IL-8, IFN-beta, and other molecules including the dsRNA sensors, whereas it did not inhibit diacyllipopeptide-induced expression of TSLP and IL-8.	bafilomycin A1	0-14	toll like receptor 3	Homo sapiens	68-72
21716324-5	2011	Bafilomycin A1, which inhibits endosomal acidification to block the TLR3 pathway, blocked the dsRNA-induced expression of TSLP, IL-8, IFN-beta, and other molecules including the dsRNA sensors, whereas it did not inhibit diacyllipopeptide-induced expression of TSLP and IL-8.	bafilomycin A1	0-14	thymic stromal lymphopoietin	Homo sapiens	122-126
21716324-5	2011	Bafilomycin A1, which inhibits endosomal acidification to block the TLR3 pathway, blocked the dsRNA-induced expression of TSLP, IL-8, IFN-beta, and other molecules including the dsRNA sensors, whereas it did not inhibit diacyllipopeptide-induced expression of TSLP and IL-8.	bafilomycin A1	0-14	C-X-C motif chemokine ligand 8	Homo sapiens	128-132
21716324-5	2011	Bafilomycin A1, which inhibits endosomal acidification to block the TLR3 pathway, blocked the dsRNA-induced expression of TSLP, IL-8, IFN-beta, and other molecules including the dsRNA sensors, whereas it did not inhibit diacyllipopeptide-induced expression of TSLP and IL-8.	bafilomycin A1	0-14	interferon beta 1	Homo sapiens	134-142
21716324-5	2011	Bafilomycin A1, which inhibits endosomal acidification to block the TLR3 pathway, blocked the dsRNA-induced expression of TSLP, IL-8, IFN-beta, and other molecules including the dsRNA sensors, whereas it did not inhibit diacyllipopeptide-induced expression of TSLP and IL-8.	bafilomycin A1	0-14	thymic stromal lymphopoietin	Homo sapiens	260-264
21716324-5	2011	Bafilomycin A1, which inhibits endosomal acidification to block the TLR3 pathway, blocked the dsRNA-induced expression of TSLP, IL-8, IFN-beta, and other molecules including the dsRNA sensors, whereas it did not inhibit diacyllipopeptide-induced expression of TSLP and IL-8.	bafilomycin A1	0-14	C-X-C motif chemokine ligand 8	Homo sapiens	269-273
21807906-6	2011	Bafilomycin A1 (BafA), a specific inhibitor of vacuolar ATPase (vATPase) required for lysosomal function, increased the growth of the human pathogen Chlamydia trachomatis (L2) in wild-type murine fibroblasts and macrophages but inhibited growth in the autophagy-deficient ATG5(-/-) fibroblasts.	bafilomycin A1	0-14	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	47-62
21807906-6	2011	Bafilomycin A1 (BafA), a specific inhibitor of vacuolar ATPase (vATPase) required for lysosomal function, increased the growth of the human pathogen Chlamydia trachomatis (L2) in wild-type murine fibroblasts and macrophages but inhibited growth in the autophagy-deficient ATG5(-/-) fibroblasts.	bafilomycin A1	0-14	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	64-71
21807906-6	2011	Bafilomycin A1 (BafA), a specific inhibitor of vacuolar ATPase (vATPase) required for lysosomal function, increased the growth of the human pathogen Chlamydia trachomatis (L2) in wild-type murine fibroblasts and macrophages but inhibited growth in the autophagy-deficient ATG5(-/-) fibroblasts.	bafilomycin A1	16-20	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	47-62
21807906-6	2011	Bafilomycin A1 (BafA), a specific inhibitor of vacuolar ATPase (vATPase) required for lysosomal function, increased the growth of the human pathogen Chlamydia trachomatis (L2) in wild-type murine fibroblasts and macrophages but inhibited growth in the autophagy-deficient ATG5(-/-) fibroblasts.	bafilomycin A1	16-20	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	64-71
21289198-4	2011	Here, we demonstrate that four independent and highly selective inhibitors of vacuolar ATPase (bafilomycin A1, concanamycin A, archazolid B, and apicularen A) significantly elevate intracellular and secreted GRN.	bafilomycin A1	95-109	granulin precursor	Homo sapiens	208-211
21303699-4	2011	Moreover, the incubation of cells with ammonium chloride or bafilomycin A1 to produce the lysosomal dysfunction recently reported in Parkinson"s disease led to an increase in the release of alpha-synuclein in exosomes and a concomitant increase in alpha-synuclein transmission to recipient cells.	bafilomycin A1	60-74	synuclein alpha	Homo sapiens	190-205
21303699-4	2011	Moreover, the incubation of cells with ammonium chloride or bafilomycin A1 to produce the lysosomal dysfunction recently reported in Parkinson"s disease led to an increase in the release of alpha-synuclein in exosomes and a concomitant increase in alpha-synuclein transmission to recipient cells.	bafilomycin A1	60-74	synuclein alpha	Homo sapiens	248-263
21789015-9	2011	Moreover, treatment with bafilomycin A1 or folimycin restored total NKG2D levels in TGF-BETA1-treated NK cells.	bafilomycin A1	25-39	killer cell lectin like receptor K1	Homo sapiens	68-73
21789015-9	2011	Moreover, treatment with bafilomycin A1 or folimycin restored total NKG2D levels in TGF-BETA1-treated NK cells.	bafilomycin A1	25-39	transforming growth factor beta 1	Homo sapiens	84-93
21428909-4	2011	MMP-9 gene induction was sensitive toward treatment with the macrolide antibiotic bafilomycin A1, a vacuolar H(+)-ATPase inhibitor, and with the lysosomotropic agent chloroquine.	bafilomycin A1	82-96	matrix metallopeptidase 9	Homo sapiens	0-5
20104024-7	2010	Celecoxib-induced conversion of LC3 was due to autophagy induction, as supported using the lysosome inhibitor, bafilomycin A1, which produced an accumulation of LC3II.	bafilomycin A1	111-125	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	32-35
20570919-8	2010	Furthermore, the inhibition of intracellular acidification by treatment with bafilomycin A1 or chloroquine reproduced the phenotype observed for the (P)RR/ATP6AP2-deficient cardiomyocytes.	bafilomycin A1	77-91	ATPase, H+ transporting, lysosomal accessory protein 2	Mus musculus	155-162
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	bafilomycin A1	192-206	CD38 antigen	Mus musculus	39-43
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	bafilomycin A1	192-206	CD38 antigen	Mus musculus	61-65
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	bafilomycin A1	208-211	CD38 antigen	Mus musculus	39-43
20200208-8	2010	In isolated perfused septal coronary arteries from CD38(+/+) mice, FasL was found to significantly increase U-46619-induced vasoconstriction from 29.2 +/- 7.3 to 63.2 +/- 10.3%, which was abolished by Baf (100 nM).	bafilomycin A1	201-204	Fas ligand (TNF superfamily, member 6)	Mus musculus	67-71
19459857-4	2009	We investigated the apoptosis mechanism induced by cotreatment of Bcl-xL-overexpressing Ms-1 cells with BMA as a V-ATPase inhibitor and taxol (TXL) as an anticancer drug.	bafilomycin A1	104-107	BCL2 like 1	Homo sapiens	66-72
19594752-7	2009	The specific vacuolar ATPase (V-ATPase) inhibitors, bafilomycin A1 or FR167356, prevented vacuolization and drug uptake.	bafilomycin A1	52-66	dynein axonemal heavy chain 8	Homo sapiens	22-28
19594752-7	2009	The specific vacuolar ATPase (V-ATPase) inhibitors, bafilomycin A1 or FR167356, prevented vacuolization and drug uptake.	bafilomycin A1	52-66	dynein axonemal heavy chain 8	Homo sapiens	30-38
19864570-6	2009	The effects of beclin 1 overexpression on LC3 and alpha-syn accumulation were partially blocked by 3-MA and completely blocked by bafilomycin A1.	bafilomycin A1	130-144	beclin 1	Homo sapiens	15-23
19864570-6	2009	The effects of beclin 1 overexpression on LC3 and alpha-syn accumulation were partially blocked by 3-MA and completely blocked by bafilomycin A1.	bafilomycin A1	130-144	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	42-45
19864570-6	2009	The effects of beclin 1 overexpression on LC3 and alpha-syn accumulation were partially blocked by 3-MA and completely blocked by bafilomycin A1.	bafilomycin A1	130-144	synuclein alpha	Homo sapiens	50-59
17913823-4	2007	The ability of WNV(Vero) to induce IFN-alpha in pDCs did not require viral replication and was prevented by the treatment of cells with bafilomycin A1 and chloroquine, suggesting that it was dependent on endosomal Toll-like receptor recognition.	bafilomycin A1	136-150	interferon alpha 1	Homo sapiens	35-44
19448082-8	2009	The primary transport system driving base secretion into the lumen appears to be a bafilomycin-A(1)-sensitive, electrogenic H(+) V-ATPase located on the basal membrane, which extrudes acid into the haemolymph, as inferred from the extracellular pH gradients detected adjacent to the basal membrane.	bafilomycin A1	83-99	Vacuolar H[+]-ATPase 55kD subunit	Drosophila melanogaster	129-137
18632865-3	2008	The entry of ENTV Env pseudovirions was substantially inhibited by bafilomycin A1 (BafA1) but was surprisingly enhanced by lysosomotropic agents and lysosomal protease inhibitors following a 4- to 6-h treatment period; of note, prolonged treatment with BafA1 or ammonium chloride completely blocked ENTV entry.	bafilomycin A1	83-88	envelope protein	Jaagsiekte sheep retrovirus	18-21
18408955-5	2008	Acidotropic probes (LysoSensor and DAMP) accumulate in non-pigmented Pmel17-positive melanosomes, and DAMP accumulation is sensitive to bafilomycin A1, a specific inhibitor of V-ATPase.	bafilomycin A1	136-150	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	176-184
17638544-4	2007	When the cells were pretreated with two structurally different lysosomal vesicle function inhibitors, bafilomycin A1 (Baf) and glycyl-L-phenylalanine-beta-naphthylamide (GPN), the FasL-induced LRs clustering was substantially blocked, and corresponding ROS production significantly decreased.	bafilomycin A1	102-116	Fas ligand	Homo sapiens	180-184
16895977-9	2006	Our findings suggest that the V-ATPase inhibitors bafilomycin A1 and concanamycin A similarly induce NO production and the newly produced NO participates partially in the V-ATPase inhibitor-induced apoptosis in RAW 264.7 cells.	bafilomycin A1	50-64	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	30-38
17604018-4	2007	Treatment with bafilomycin A1, an MMP-2 activator, or GM6001, an MMP inhibitor, at the pre-condensation stage resulted in the inhibition or promotion of chondrogenesis, respectively.	bafilomycin A1	15-29	matrix metallopeptidase 2	Homo sapiens	34-39
17431216-7	2007	In contrast, caspase-8 but not caspase-9 activation was blocked by the destruction of lysosomes (preincubation with Gly-Phe beta-naphthylamide, a cathepsin C substrate), loss of lysosomal acidity (bafilomycin A1), or inhibition of cathepsin L or D. Using pepstatin A-BODIPY FL conjugate, we confirmed translocation of cathepsin D out of lysosomes in response to menadione.	bafilomycin A1	197-211	caspase 8	Homo sapiens	13-22
16895977-2	2006	Bafilomycin A1 and concanamycin A activated nuclear factor (NF)-kappaB and activator protein-1 and decreased the level of IkappaB-alpha and increased that of phosphorylated c-Jun N-terminal kinase (JNK).	bafilomycin A1	0-14	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	122-135
16895977-9	2006	Our findings suggest that the V-ATPase inhibitors bafilomycin A1 and concanamycin A similarly induce NO production and the newly produced NO participates partially in the V-ATPase inhibitor-induced apoptosis in RAW 264.7 cells.	bafilomycin A1	50-64	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	171-179
16895977-2	2006	Bafilomycin A1 and concanamycin A activated nuclear factor (NF)-kappaB and activator protein-1 and decreased the level of IkappaB-alpha and increased that of phosphorylated c-Jun N-terminal kinase (JNK).	bafilomycin A1	0-14	mitogen-activated protein kinase 8	Mus musculus	173-196
16473958-8	2006	In the presence of Baf (100 nM), this ET-1-induced two-phase [Ca2+]i response was completely abolished, whereas Rya (50 microM) only markedly blocked the ET-1-induced large global Ca2+ increase.	bafilomycin A1	19-22	endothelin 1	Homo sapiens	38-42
16895977-2	2006	Bafilomycin A1 and concanamycin A activated nuclear factor (NF)-kappaB and activator protein-1 and decreased the level of IkappaB-alpha and increased that of phosphorylated c-Jun N-terminal kinase (JNK).	bafilomycin A1	0-14	mitogen-activated protein kinase 8	Mus musculus	198-201
16473958-8	2006	In the presence of Baf (100 nM), this ET-1-induced two-phase [Ca2+]i response was completely abolished, whereas Rya (50 microM) only markedly blocked the ET-1-induced large global Ca2+ increase.	bafilomycin A1	19-22	endothelin 1	Homo sapiens	154-158
16473958-9	2006	Functional studies showed that 100 nM Baf significantly attenuated ET-1-induced maximal constriction from 82.26 +/- 4.42% to 51.80 +/- 4.36%.	bafilomycin A1	38-41	endothelin 1	Homo sapiens	67-71
16443004-8	2006	K-independent proton transport activity was significantly inhibited by the H(+)-ATPase inhibitor bafilomycin A(1) (BAF, 10 nM) with luminal applied in both WT and KO mice.	bafilomycin A1	97-113	b-associated fitness	Mus musculus	115-118
16622236-7	2006	The IL-8 secretion in response to P. aeruginosa DNA was decreased by treatments that inhibit acidification of intracellular organelles, using chloroquine, a pH-neutralizing compound, or bafilomycin A1, an inhibitor of vacuolar H+-ATPase.	bafilomycin A1	186-200	C-X-C motif chemokine ligand 8	Homo sapiens	4-8
15847604-10	2005	Thrombin, but not ADP or AVP, reduces the rise in [Ca2+]c evoked by nigericin and bafilomycin A1.	bafilomycin A1	82-96	coagulation factor II, thrombin	Homo sapiens	0-8
16227281-10	2005	By using small interfering RNA against the mu2 subunit of adaptor protein 2, dominant negative dynamin construct K44A, and the lysosomotropic agents bafilomycin A1 and ammonium chloride, we also demonstrated that surface TNFR1 was internalized by RID by a clathrin-dependent process involving mu2 and dynamin, followed by degradation of TNFR1 via an endosomal/lysosomal pathway.	bafilomycin A1	149-163	TNF receptor superfamily member 1A	Homo sapiens	221-226
15847604-10	2005	Thrombin, but not ADP or AVP, reduces the rise in [Ca2+]c evoked by nigericin and bafilomycin A1.	bafilomycin A1	82-96	carbonic anhydrase 2	Homo sapiens	51-54
15885844-9	2005	The PLL-SU5%/DNA complex seems to be internalized via SUR-mediated endocytosis pathway as suggested by vacuolar ATPases inhibition by Bafilomycin A1.	bafilomycin A1	134-148	ATP binding cassette subfamily C member 8	Rattus norvegicus	54-57
16133868-5	2005	Although we found no evidence for a direct involvement of lysosomal cathepsins, bafilomycin A1 and ammonium chloride significantly attenuated TNF toxicity.	bafilomycin A1	80-94	tumor necrosis factor	Rattus norvegicus	142-145
12900525-8	2003	The recognition of HSV-2 by TLR9 was mediated through an endocytic pathway that was inhibited by chloroquine or bafilomycin A1.	bafilomycin A1	112-126	toll like receptor 9	Homo sapiens	28-32
15638326-0	2004	Biosynthetic investigations of the V-type ATPase inhibitors bafilomycin A1, B1 and concanamycin A.	bafilomycin A1	60-74	dynein axonemal heavy chain 8	Homo sapiens	42-48
15102616-6	2004	Furthermore, whereas the internalized receptors exhibit rapid recycling, treatment with proton pump inhibitors (bafilomycin-A1 and concanamycin A) or brefeldin A, Golgi disrupting agents, reduces PTH/PTHrP receptor recycling.	bafilomycin A1	112-126	parathyroid hormone 1 receptor	Homo sapiens	196-214
14985124-3	2004	The UGA4 protein was located on the vacuolar membrane as determined by the effects of bafilomycin A1 and by indirect immunofluorescence microscopy.	bafilomycin A1	86-100	Uga4p	Saccharomyces cerevisiae S288C	4-8
15542860-7	2005	The effect of bafilomycin A1 on CgA secretion depends on a sorting determinant located within the amino terminus (CgA-(1-115)) but not the C-terminal region of the granin.	bafilomycin A1	14-28	chromogranin A	Rattus norvegicus	32-35
15542860-7	2005	The effect of bafilomycin A1 on CgA secretion depends on a sorting determinant located within the amino terminus (CgA-(1-115)) but not the C-terminal region of the granin.	bafilomycin A1	14-28	chromogranin A	Rattus norvegicus	114-117
15166000-4	2004	Correspondingly, the amount of small responsive GLUT4 vesicles in concanamycin A- and bafilomycin A1-treated cells is decreased.	bafilomycin A1	86-100	solute carrier family 2 member 4	Homo sapiens	48-53
14561721-10	2003	These findings suggest that bafilomycin A(1)-induced apoptosis in MKN-1 cells is mediated by other proteases released after lysosomal dysfunction followed by activation of caspase-3 in a cytochrome c-independent manner.	bafilomycin A1	28-44	caspase 3	Homo sapiens	172-181
14561721-10	2003	These findings suggest that bafilomycin A(1)-induced apoptosis in MKN-1 cells is mediated by other proteases released after lysosomal dysfunction followed by activation of caspase-3 in a cytochrome c-independent manner.	bafilomycin A1	28-44	cytochrome c, somatic	Homo sapiens	187-199
11812790-5	2002	The translocation of tyrosinase out of the endoplasmic reticulum and the induction of cell pigmentation in the presence of the ionophore monensin or the specific V-ATPase inhibitors concanamycin A and bafilomycin A1 supported a role for V-ATPases in this process.	bafilomycin A1	201-215	tyrosinase	Homo sapiens	21-31
12675272-4	2003	Bafilomycin A1 and 5-(N-ethyl-N-isopropyl)amiloride (EIPA) were used to delineate the activities of the H+-pump and NHE, respectively.	bafilomycin A1	0-14	solute carrier family 9 member C1	Homo sapiens	116-119
12547648-6	2003	Likewise, another V-type ATPase inhibitor, bafilomycinA1 facilitated GDNF release from C6, U87MG and T98G glioma cells, in a concentration-dependent manner.	bafilomycin A1	43-56	glial cell derived neurotrophic factor	Homo sapiens	69-73
12675272-10	2003	Similarly, pHi recovery from NH4Cl prepulse acid-loads (pHo 7.4) was sensitive to both EIPA and bafilomycin A1.	bafilomycin A1	96-110	glucose-6-phosphate isomerase	Homo sapiens	11-14
11812790-5	2002	The translocation of tyrosinase out of the endoplasmic reticulum and the induction of cell pigmentation in the presence of the ionophore monensin or the specific V-ATPase inhibitors concanamycin A and bafilomycin A1 supported a role for V-ATPases in this process.	bafilomycin A1	201-215	dynein axonemal heavy chain 8	Homo sapiens	162-170
11773703-3	2002	Exposure of neonatal rat cardiomyocytes to the established apoptotic agents, bafilomycin A1 (BAF) or staurosporine (STAU) induced apoptosis and caused a decrease in PP-1 activity of 35%.	bafilomycin A1	77-91	BAF nuclear assembly factor 1	Rattus norvegicus	93-96
11773703-3	2002	Exposure of neonatal rat cardiomyocytes to the established apoptotic agents, bafilomycin A1 (BAF) or staurosporine (STAU) induced apoptosis and caused a decrease in PP-1 activity of 35%.	bafilomycin A1	77-91	neuropeptide Y receptor Y4	Rattus norvegicus	165-169
12498152-4	2002	Based on these results and comparing them to existing models of the adenovirus entry, we propose a refined model in which there are two pathways of adenoviral entry: the first one involves the epsilon-COP as the downstream effector of the acidification and can be blocked by bafilomycin A1 and the second one is a pH-independent pathway.	bafilomycin A1	275-289	coatomer subunit epsilon	Cricetulus griseus	193-204
11799150-7	2002	Inhibition of adenovirus penetration with bafilomycin A1 or ammonium chloride attenuated the activation of ERK-p38 and IP-10 mRNA expression following infection, suggesting that endosomal escape was required to trigger these pathways.	bafilomycin A1	42-56	mitogen-activated protein kinase 1	Homo sapiens	107-110
11799150-7	2002	Inhibition of adenovirus penetration with bafilomycin A1 or ammonium chloride attenuated the activation of ERK-p38 and IP-10 mRNA expression following infection, suggesting that endosomal escape was required to trigger these pathways.	bafilomycin A1	42-56	mitogen-activated protein kinase 1	Homo sapiens	111-114
11799150-7	2002	Inhibition of adenovirus penetration with bafilomycin A1 or ammonium chloride attenuated the activation of ERK-p38 and IP-10 mRNA expression following infection, suggesting that endosomal escape was required to trigger these pathways.	bafilomycin A1	42-56	C-X-C motif chemokine ligand 10	Homo sapiens	119-124
10231559-0	1999	Induction of hydroxyapatite resorptive activity in bone marrow cell populations resistant to bafilomycin A1 by a factor with restricted expression to bone and brain, neurochondrin.	bafilomycin A1	93-107	neurochondrin	Mus musculus	166-179
11390405-5	2001	Bafilomycin A1, but not a specific proteasome inhibitor, prevented early degradation of palmitoylation-deficient CCR5 and promoted its accumulation in lysosomal compartments.	bafilomycin A1	0-14	C-C motif chemokine receptor 5	Homo sapiens	113-117
10784591-6	2000	Bafilomycin A1 was used to analyze the association between GFP-ATP7B and the late endosomes.	bafilomycin A1	0-14	ATPase copper transporting beta	Homo sapiens	59-68
11432741-7	2001	Inhibitor studies revealed that the heterologously produced A1 ATPase is insensitive to azide, dicyclohexylcarbodiimide and bafilomycin A1, but sensitive to diethylstilbestrol and its analogues dienestrol and hexestrol.	bafilomycin A1	124-138	ATPase	Escherichia coli	63-69
10922469-1	2000	In this study, we describe the activation of melanogenesis by selective vacuolar type H(+)-ATPase inhibitors (bafilomycin A1 and concanamycin A) in amelanotic human and mouse melanoma cells which express tyrosinase but show no melanogenesis.	bafilomycin A1	110-124	tyrosinase	Mus musculus	204-214
10446931-10	1999	These calcitonin effects on endocytotic and re-exocytotic pathways were inhibited by 100 nM cytochalasin D, 100 nM nocodazole, 0.1 to 1 microM bafilomycin A1, or 0.1 mM monodansyl cadaverine.	bafilomycin A1	143-157	Calcitonin gene-related peptide	Sus scrofa	6-16
10231559-4	1999	By means of this method, we isolated a factor with 16% leucine residues, termed neurochondrin, that induces hydroxyapatite resorptive activity in bone marrow cells resistant to bafilomycin A1, an inhibitor of macrophage- and osteoclast-mediated resorption.	bafilomycin A1	177-191	neurochondrin	Mus musculus	80-93
10201953-5	1999	Using whole blood from healthy donors and flow cytometry, we found that colchicine (0.1-10 mM), cytochalasin D (1000 microM), NH4Cl (10-50 mM), and bafilomycin A1 (0.1-3 microM) significantly reduced the affinity of FITC-HBP for CD14-positive monocytes.	bafilomycin A1	148-162	azurocidin 1	Homo sapiens	221-224
10217271-4	1999	The macrolides bafilomycin A1 (BAF) and concanamycin A (CON) block lysosomal acidification through selective inhibition of the V-type ATPase.	bafilomycin A1	15-29	BAF nuclear assembly factor 1	Rattus norvegicus	31-34
10201953-5	1999	Using whole blood from healthy donors and flow cytometry, we found that colchicine (0.1-10 mM), cytochalasin D (1000 microM), NH4Cl (10-50 mM), and bafilomycin A1 (0.1-3 microM) significantly reduced the affinity of FITC-HBP for CD14-positive monocytes.	bafilomycin A1	148-162	CD14 molecule	Homo sapiens	229-233
10201953-6	1999	Using isolated human monocytes and ELISA, we found that colchicine (0.1 mM), cytochalasin D (30 and 300 microM), NH4Cl (30 mM), and bafilomycin A1 (1 microM) significantly reduced the effect of HBP (10 microg/ml) to enhance LPS (10 ng/ml)-induced TNF-alpha release after 24 h. These findings demonstrate that internalization of HBP in monocytes is essential for the enhancement of LPS-induced TNF-alpha release.	bafilomycin A1	132-146	azurocidin 1	Homo sapiens	194-197
10201953-6	1999	Using isolated human monocytes and ELISA, we found that colchicine (0.1 mM), cytochalasin D (30 and 300 microM), NH4Cl (30 mM), and bafilomycin A1 (1 microM) significantly reduced the effect of HBP (10 microg/ml) to enhance LPS (10 ng/ml)-induced TNF-alpha release after 24 h. These findings demonstrate that internalization of HBP in monocytes is essential for the enhancement of LPS-induced TNF-alpha release.	bafilomycin A1	132-146	tumor necrosis factor	Homo sapiens	247-256
10201953-6	1999	Using isolated human monocytes and ELISA, we found that colchicine (0.1 mM), cytochalasin D (30 and 300 microM), NH4Cl (30 mM), and bafilomycin A1 (1 microM) significantly reduced the effect of HBP (10 microg/ml) to enhance LPS (10 ng/ml)-induced TNF-alpha release after 24 h. These findings demonstrate that internalization of HBP in monocytes is essential for the enhancement of LPS-induced TNF-alpha release.	bafilomycin A1	132-146	azurocidin 1	Homo sapiens	328-331
10201953-6	1999	Using isolated human monocytes and ELISA, we found that colchicine (0.1 mM), cytochalasin D (30 and 300 microM), NH4Cl (30 mM), and bafilomycin A1 (1 microM) significantly reduced the effect of HBP (10 microg/ml) to enhance LPS (10 ng/ml)-induced TNF-alpha release after 24 h. These findings demonstrate that internalization of HBP in monocytes is essential for the enhancement of LPS-induced TNF-alpha release.	bafilomycin A1	132-146	tumor necrosis factor	Homo sapiens	393-402
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	tumor protein p53	Homo sapiens	83-86
10195692-5	1999	When cells were treated with the fungal metabolite brefeldin A or with the specific vacuolar H+-ATPase inhibitor bafilomycin A1, the processing of SgII and the release of its cleavage products were strongly inhibited, indicating that its processing commenced in the later compartments of the secretory pathway.	bafilomycin A1	113-127	secretogranin II S homeolog	Xenopus laevis	147-151
9657902-6	1998	Following acid loading in NaCl Ringers with a 20 mm NH4Cl prepulse, pHi recovery was partially inhibited by exposure to either Na-free (NMGCl) Ringers, 100 microM DMA or 20 microM bafilomycin A1.	bafilomycin A1	180-194	glucose-6-phosphate isomerase	Bos taurus	68-71
9808725-5	1998	45Ca2+ pumping into vesicles from ECA1 transformants was detected after the H+/Ca2+-antiport activity was eliminated with bafilomycin A1 and gramicidin D. The pump had a high affinity for Ca2+ (Km = 30 nM) and displayed two affinities for ATP (Km of 20 and 235 microM).	bafilomycin A1	122-136	ER-type Ca2+-ATPase 1	Arabidopsis thaliana	34-38
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	tumor protein p53	Homo sapiens	99-102
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	cyclin dependent kinase inhibitor 1A	Homo sapiens	188-191
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	tumor protein p53	Homo sapiens	99-102
9157016-7	1997	Using antibodies against the myc epitope and the early endosomal autoantigen EEA1 as markers, we found that endosomes in wild-type and mutant MDCK cells rapidly tubulate in the presence of bafilomycin A1, an inhibitor of vacuolar H(+)-ATPase.	bafilomycin A1	189-203	early endosome antigen 1	Canis lupus familiaris	77-81
9200012-2	1997	Specific inhibitors of vacuolar H(+)-ATPase (V-ATPase), concanamycin A and bafilomycin A1, abolish bone resorption by osteoclasts.	bafilomycin A1	75-89	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	23-43
9374657-8	1997	Bafilomycin A1 (0.1 microM; an inhibitor of vacuolar H(+)-ATPase) inhibited the pHi increase caused by high K+.	bafilomycin A1	0-14	glucose-6-phosphate isomerase	Oryctolagus cuniculus	80-83
9321906-6	1997	In the absence of peritubular sodium, pHi recovery was inhibited by luminal bafilomycin A1 but not by luminal Sch-28080 addition or by luminal potassium removal.	bafilomycin A1	76-90	glucose-6-phosphate isomerase	Oryctolagus cuniculus	38-41
9207248-3	1997	Addition of 10(-8) M bafilomycin A1 to osteoclasts cultured on bone induced a rapid decrease of the pHi, while addition of amiloride had only a minor effect.	bafilomycin A1	21-35	glucose-6-phosphate isomerase	Rattus norvegicus	100-103
9153255-5	1997	We show that removal of transferrin from sorting endosomes and accumulation in the peri-centriolar endocytic recycling compartment takes place normally in bafilomycin A1-treated cells.	bafilomycin A1	155-169	transferrin	Homo sapiens	24-35
8910293-4	1996	The transport of [3H]ACh by human VAChT was dependent upon the addition of exogenous ATP at 37 degrees C. Uptake was abolished by low temperature (4 degrees C), the proton ionophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (2.5 microM) and bafilomycin A1 (1 microM), a specific inhibitor of the vesicular H+-ATPase.	bafilomycin A1	250-264	solute carrier family 18 member A3	Homo sapiens	34-39
8943309-6	1996	Treatment of fibroblasts with either bafilomycin A1 or 3-methyladenine indicates that proteolytic cleavage of SAP precursor begins as early as in the late endosomes.	bafilomycin A1	37-51	SH2 domain containing 1A	Homo sapiens	110-113
8941214-6	1996	BafilomycinA1 and NH4Cl, both of which raise the intragranular pH to neutral, inhibited the eosinophil peroxidase exocytosis induced by platelet-activating factor.	bafilomycin A1	0-13	eosinophil peroxidase	Homo sapiens	92-113
9151711-5	1997	Inhibitors of lysosomal function (bafilomycin A1, folimycin) markedly reduced zeta chain degradation, leading to the accumulation of zeta chain in large Lamp1(+) vesicles.	bafilomycin A1	34-48	lysosomal associated membrane protein 1	Homo sapiens	153-158
7890753-0	1995	The vacuolar H(+)-ATPase inhibitor bafilomycin A1 differentially affects proteolytic processing of mutant and wild-type beta-amyloid precursor protein.	bafilomycin A1	35-49	amyloid beta precursor protein	Homo sapiens	120-150
8741216-5	1996	Thus, quantitative lmmunogold labeling showed that the Baf-induced alkalinization reduced the transfer of internalized Cat.Au to lysosomes, as defined by their content of human lysosome-associated membrane protein 1 (h-lamp-1) and cathepsin D.	bafilomycin A1	55-58	lysosomal associated membrane protein 1	Homo sapiens	177-215
8741216-5	1996	Thus, quantitative lmmunogold labeling showed that the Baf-induced alkalinization reduced the transfer of internalized Cat.Au to lysosomes, as defined by their content of human lysosome-associated membrane protein 1 (h-lamp-1) and cathepsin D.	bafilomycin A1	55-58	cathepsin D	Homo sapiens	231-242
8626546-7	1996	Treatment of the cells with bafilomycin A1, an inhibitor for the proton pump of the lysosomes, inhibited intracellular degradation of the LDL and prevented down-regulations of the mRNA and the cell surface TM antigen levels caused by oxidized LDL.	bafilomycin A1	28-42	thrombomodulin	Homo sapiens	206-208
8546711-5	1996	Here we have shown that bafilomycin A1, a specific inhibitor of V-ATPase, inhibits endosome acidification and mitogen-induced DNA synthesis in Swiss 3T3 fibroblasts.	bafilomycin A1	24-38	ATPase, H+ transporting, lysosomal V0 subunit D2	Mus musculus	64-72
7642700-3	1995	Toward this purpose, bafilomycin A1 (Baf), a specific inhibitor of the vacuolar proton pump, was used to inhibit acidification of the vacuolar system.	bafilomycin A1	21-35	BAF nuclear assembly factor 1	Homo sapiens	37-40
7890753-1	1995	We analyzed the effect of the vacuolar H(+)-ATPase inhibitor bafilomycin A1 (bafA1) on the processing of beta-amyloid precursor protein (beta APP).	bafilomycin A1	61-75	amyloid beta precursor protein	Homo sapiens	105-135
7890753-1	1995	We analyzed the effect of the vacuolar H(+)-ATPase inhibitor bafilomycin A1 (bafA1) on the processing of beta-amyloid precursor protein (beta APP).	bafilomycin A1	77-82	amyloid beta precursor protein	Homo sapiens	105-135
7852298-4	1995	In contrast, the robust production of A beta from a human neuroglioma-derived cell line (HS683) transfected with WT APP, or from primary human mixed brain cultures (HMBC) expressing genomic WT APP, were also effectively inhibited by baf A.	bafilomycin A1	233-238	amyloid beta precursor protein	Homo sapiens	38-44
7518670-1	1994	We examined the effect of bafilomycin A1 (BAF), an inhibitor of vacuolar-type H(+)-ATPases, on macrophages activation (measured as increased nitrite production and leishmanicidal activity) induced by interferon gamma alone or together with lipopolysaccharide or tumour necrosis factor alpha.	bafilomycin A1	26-40	BAF nuclear assembly factor 1	Homo sapiens	42-45
7864640-3	1995	Under these conditions IL-1-stimulated proteoglycan degradation was inhibited by bafilomycin A1 with an IC50 of < 10 nM in both chondrocyte monolayers and articular cartilage explants.	bafilomycin A1	81-95	interleukin 1 alpha	Homo sapiens	23-27
7864640-6	1995	Tumor necrosis factor-alpha and retinoic acid also stimulated proteoglycan degradation in chondrocyte monolayers, and in both cases the response was inhibited by bafilomycin A1.	bafilomycin A1	162-176	tumor necrosis factor	Homo sapiens	0-27
7864640-8	1995	IL-1 also stimulated the synthesis and secretion of prostromelysin by chondrocyte monolayers, however, under conditions in which IL-1 stimulated proteoglycan release was totally blocked by bafilomycin A1, there was no effect on IL-1-stimulated stromelysin secretion or stromelysin enzyme activity.	bafilomycin A1	189-203	interleukin 1 alpha	Homo sapiens	0-4
7864640-8	1995	IL-1 also stimulated the synthesis and secretion of prostromelysin by chondrocyte monolayers, however, under conditions in which IL-1 stimulated proteoglycan release was totally blocked by bafilomycin A1, there was no effect on IL-1-stimulated stromelysin secretion or stromelysin enzyme activity.	bafilomycin A1	189-203	interleukin 1 alpha	Homo sapiens	129-133
7864640-8	1995	IL-1 also stimulated the synthesis and secretion of prostromelysin by chondrocyte monolayers, however, under conditions in which IL-1 stimulated proteoglycan release was totally blocked by bafilomycin A1, there was no effect on IL-1-stimulated stromelysin secretion or stromelysin enzyme activity.	bafilomycin A1	189-203	interleukin 1 alpha	Homo sapiens	129-133
7864795-12	1995	We conclude that the TRHR-TRH system is unique among recycling receptors because, after RL sequestration, the TRHR-TRH complex becomes dissociated intracellularly via a bafilomycin A1-sensitive, acidic pH-dependent mechanism, and both the unoccupied TRHR and TRH recycle disassociated from each other.	bafilomycin A1	169-183	thyrotropin releasing hormone receptor	Rattus norvegicus	21-25
7864795-12	1995	We conclude that the TRHR-TRH system is unique among recycling receptors because, after RL sequestration, the TRHR-TRH complex becomes dissociated intracellularly via a bafilomycin A1-sensitive, acidic pH-dependent mechanism, and both the unoccupied TRHR and TRH recycle disassociated from each other.	bafilomycin A1	169-183	thyrotropin releasing hormone receptor	Rattus norvegicus	110-114
7864795-12	1995	We conclude that the TRHR-TRH system is unique among recycling receptors because, after RL sequestration, the TRHR-TRH complex becomes dissociated intracellularly via a bafilomycin A1-sensitive, acidic pH-dependent mechanism, and both the unoccupied TRHR and TRH recycle disassociated from each other.	bafilomycin A1	169-183	thyrotropin releasing hormone receptor	Rattus norvegicus	110-114
7840150-13	1995	Bafilomycin A1 and pCMBS did not inhibit the initial amiloride-sensitive portion of recovery, but they did inhibit a late component of recovery when pHi was above 7.0.	bafilomycin A1	0-14	glucose-6-phosphate isomerase 1	Mus musculus	149-152
8006950-5	1994	(iii) The internal application of the vacuolar H(+)-ATPase inhibitors N-ethylmaleimide (NEM), NO3- and bafilomycin A1 (BFA) depolarized the membrane by 15 +/- 2, 18 +/- 2 and 16 +/- 2 mV, respectively.	bafilomycin A1	119-122	NBL1, DAN family BMP antagonist	Mus musculus	94-97
8169833-1	1994	Bafilomycin A1, an inhibitor of vacuolar adenosine triphosphatase, was tested for its ability to antagonize botulinum neurotoxins (serotypes A-G), tetanus toxin and phospholipase A2 neurotoxins (notexin, beta-bungarotoxin, taipoxin and textilotoxin) on the mouse phrenic nerve-hemidiaphragm preparation.	bafilomycin A1	0-14	phospholipase A2, group IB, pancreas	Mus musculus	165-181
1832676-11	1991	In the presence of 1 microM bafilomycin A1, 125I-labeled epidermal growth factor (EGF) bound to the cell surface at 4 degrees C was internalized normally into the cells at 37 degrees C but was not degraded at all, in marked contrast to the rapid degradation of 125I-EGF in the control cells without the drug.	bafilomycin A1	28-42	epidermal growth factor	Mus musculus	57-80
1314493-3	1992	Second, at 37 degrees C, pHi recovery after acute intracellular acidification caused by 40 mM acetate addition to cell suspension was inhibited 36% by 200-400 nM bafilomycin A1, a macrolide antibiotic that specifically inhibits vacuolar-type H(+)-ATPase at submicromolar concentrations.	bafilomycin A1	162-176	glucose-6-phosphate isomerase	Rattus norvegicus	25-28
8253856-7	1993	The functional importance of V-type H+ ATPase-activity in preserving pHi homeostasis at acidic extracellular pH levels was reflected by the impairment of O2- production at pHo 6.70 when H+ ATPase activity was inhibited: bafilomycin A1 reduced O2- production from 13.9 +/- 1.0 to 9.3 +/- 0.6 nmoles/10(6) cells/40 min, in control and bafilomycin A1-treated cells, respectively (P < 0.05), while EPA had no effect.	bafilomycin A1	220-234	glucose-6-phosphate isomerase 1	Mus musculus	69-72
1317456-3	1992	In the absence of Na+ in the superfusion solutions, pHi recovered from the acid load by a mechanism inhibited by 0.1 microM bafilomycin A1, a specific inhibitor of a vacuolar-type H(+)-ATPase.	bafilomycin A1	124-138	glucose-6-phosphate isomerase	Rattus norvegicus	52-55
1660409-1	1991	Bafilomycin A1, a selective inhibitor of vacuolar H(+)-ATPase, induced neurite outgrowth of PC12 cells dose- and time-dependently: more than 50% of the cells extended neurite-like spikes after 24 h treatment with 100 nM bafilomycin A1.	bafilomycin A1	220-234	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	12-61
1832676-11	1991	In the presence of 1 microM bafilomycin A1, 125I-labeled epidermal growth factor (EGF) bound to the cell surface at 4 degrees C was internalized normally into the cells at 37 degrees C but was not degraded at all, in marked contrast to the rapid degradation of 125I-EGF in the control cells without the drug.	bafilomycin A1	28-42	epidermal growth factor	Mus musculus	82-85
1832676-11	1991	In the presence of 1 microM bafilomycin A1, 125I-labeled epidermal growth factor (EGF) bound to the cell surface at 4 degrees C was internalized normally into the cells at 37 degrees C but was not degraded at all, in marked contrast to the rapid degradation of 125I-EGF in the control cells without the drug.	bafilomycin A1	28-42	epidermal growth factor	Mus musculus	266-269
34105096-13	2022	The intervention of bafilomycin A1 and rapamycin in HSCs strongly supported the notion that inhibition of autophagy enhanced alpha -SMA protein expression levels (P<0.01).	bafilomycin A1	20-34	immunoglobulin mu binding protein 2	Mus musculus	132-135
1651328-5	1991	Furthermore, although no specific protease inhibitor assayed could affect this processing, NGFR degradation and truncation were retarded by treatment with: 1) the weak base amines, ammonium chloride or methylamine; 2) the carboxylic ionophore, monensin; or 3) the vacuolar ATPase inhibitor, bafilomycin A1, all agents that dissipate endosomal/lysosomal proton gradients via alternate mechanisms.	bafilomycin A1	291-305	nerve growth factor receptor	Homo sapiens	91-95
33236955-3	2021	NH4Cl and bafilomycin A1, but not the proteasomal inhibitor MG132, prevented the FAC-mediated decrease in TfR1 protein levels, thus indicating lysosomal involvement.	bafilomycin A1	10-24	transferrin receptor	Homo sapiens	106-110
34933095-7	2022	In Abeta(1-42)-, A53T-alpha-synuclein-, or Q74-induced BV-2 cells, PSS significantly inhibited NLRP3 inflammasome activation, which was attenuated by bafilomycin A1 (an autophagy inhibitor) and SHP099 (an SHP-2 inhibitor).	bafilomycin A1	150-164	NLR family, pyrin domain containing 3	Mus musculus	95-100
34905649-6	2022	Moreover, rapamycin successfully restores the impaired autophagic flux and alleviates liver senescence in GDF11 overexpression mice, while the GDF11 knockdown-mediated benefits are abolished by the autophagy inhibitor bafilomycin A1.	bafilomycin A1	218-232	growth differentiation factor 11	Mus musculus	143-148
34954677-4	2021	BPA treatment significantly increased the levels of autophagy-regulated proteins including Beclin-1 and LC3-II along with the decrease of p62, accompanied by the elevation of autophagy flux and the accumulation of acidic vacuoles, which was blocked by the autophagy inhibitor bafilomycin A1 (BafA1).	bafilomycin A1	276-290	beclin 1	Homo sapiens	91-99
34954677-4	2021	BPA treatment significantly increased the levels of autophagy-regulated proteins including Beclin-1 and LC3-II along with the decrease of p62, accompanied by the elevation of autophagy flux and the accumulation of acidic vacuoles, which was blocked by the autophagy inhibitor bafilomycin A1 (BafA1).	bafilomycin A1	276-290	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	104-107
34954677-4	2021	BPA treatment significantly increased the levels of autophagy-regulated proteins including Beclin-1 and LC3-II along with the decrease of p62, accompanied by the elevation of autophagy flux and the accumulation of acidic vacuoles, which was blocked by the autophagy inhibitor bafilomycin A1 (BafA1).	bafilomycin A1	276-290	nucleoporin 62	Homo sapiens	138-141
34954677-4	2021	BPA treatment significantly increased the levels of autophagy-regulated proteins including Beclin-1 and LC3-II along with the decrease of p62, accompanied by the elevation of autophagy flux and the accumulation of acidic vacuoles, which was blocked by the autophagy inhibitor bafilomycin A1 (BafA1).	bafilomycin A1	292-297	beclin 1	Homo sapiens	91-99
34954677-4	2021	BPA treatment significantly increased the levels of autophagy-regulated proteins including Beclin-1 and LC3-II along with the decrease of p62, accompanied by the elevation of autophagy flux and the accumulation of acidic vacuoles, which was blocked by the autophagy inhibitor bafilomycin A1 (BafA1).	bafilomycin A1	292-297	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	104-107
34954677-4	2021	BPA treatment significantly increased the levels of autophagy-regulated proteins including Beclin-1 and LC3-II along with the decrease of p62, accompanied by the elevation of autophagy flux and the accumulation of acidic vacuoles, which was blocked by the autophagy inhibitor bafilomycin A1 (BafA1).	bafilomycin A1	292-297	nucleoporin 62	Homo sapiens	138-141
34434265-8	2021	The decrease in apoptosis caused by IKKepsilon knockdown was reversed when the autophagic flow was blocked using bafilomycin A1.	bafilomycin A1	113-127	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	36-46
34536391-11	2021	Bafilomycin A1 (BafA1) is a late autophagy inhibitor, aggravated cell damage and apoptosis and counteracted the enhancement of autophagy activation and protective effects of neuritin.	bafilomycin A1	0-14	neuritin 1	Homo sapiens	174-182
34536391-11	2021	Bafilomycin A1 (BafA1) is a late autophagy inhibitor, aggravated cell damage and apoptosis and counteracted the enhancement of autophagy activation and protective effects of neuritin.	bafilomycin A1	16-21	neuritin 1	Homo sapiens	174-182
34520793-5	2021	Our results showed that DM enhanced autophagy in association with an accumulation of autophagosomes and increase in the levels of autophagy markers LC3-II/LC3-I ratio and p62 which were much elevated in the presence of lysosomal inhibitors bafilomycin A1 and chloroquine.	bafilomycin A1	240-254	nucleoporin 62	Homo sapiens	171-174
34425162-4	2021	Pretreatment of HNE cells with the specific vacuolar H+-ATPase inhibitor bafilomycin A1 reduced the RV-C03 RNA levels in the ASL; inflammatory cytokines, including interleukin (IL)-1beta, IL-6 and IL-8, in the supernatant; the mRNA expression of the RV-C receptor cadherin-related family member 3 (CDHR3) in the cells; and the number of acidic endosomes where RV-B RNA enters the cytoplasm.	bafilomycin A1	73-87	interleukin 1 alpha	Homo sapiens	164-186
34425162-4	2021	Pretreatment of HNE cells with the specific vacuolar H+-ATPase inhibitor bafilomycin A1 reduced the RV-C03 RNA levels in the ASL; inflammatory cytokines, including interleukin (IL)-1beta, IL-6 and IL-8, in the supernatant; the mRNA expression of the RV-C receptor cadherin-related family member 3 (CDHR3) in the cells; and the number of acidic endosomes where RV-B RNA enters the cytoplasm.	bafilomycin A1	73-87	interleukin 6	Homo sapiens	188-192
34425162-4	2021	Pretreatment of HNE cells with the specific vacuolar H+-ATPase inhibitor bafilomycin A1 reduced the RV-C03 RNA levels in the ASL; inflammatory cytokines, including interleukin (IL)-1beta, IL-6 and IL-8, in the supernatant; the mRNA expression of the RV-C receptor cadherin-related family member 3 (CDHR3) in the cells; and the number of acidic endosomes where RV-B RNA enters the cytoplasm.	bafilomycin A1	73-87	C-X-C motif chemokine ligand 8	Homo sapiens	197-201
34425162-4	2021	Pretreatment of HNE cells with the specific vacuolar H+-ATPase inhibitor bafilomycin A1 reduced the RV-C03 RNA levels in the ASL; inflammatory cytokines, including interleukin (IL)-1beta, IL-6 and IL-8, in the supernatant; the mRNA expression of the RV-C receptor cadherin-related family member 3 (CDHR3) in the cells; and the number of acidic endosomes where RV-B RNA enters the cytoplasm.	bafilomycin A1	73-87	cadherin related family member 3	Homo sapiens	298-303
34571747-10	2021	Immunofluorescence evidenced the accumulation of LC3B puncta in U87Mg cells pretreated with autophagy inhibitor Bafilomycin A1.	bafilomycin A1	112-126	microtubule associated protein 1 light chain 3 beta	Homo sapiens	49-53
34127226-4	2021	Further studies show that fucoidan promotes autophagy showed by the expression of p62/SQSTM1 and microtubule-associated protein light chain 3 (LC3) II, which can be blocked by autophagy inhibitors 3-MA and bafilomycin A1.	bafilomycin A1	206-220	sequestosome 1	Homo sapiens	82-85
34127226-4	2021	Further studies show that fucoidan promotes autophagy showed by the expression of p62/SQSTM1 and microtubule-associated protein light chain 3 (LC3) II, which can be blocked by autophagy inhibitors 3-MA and bafilomycin A1.	bafilomycin A1	206-220	sequestosome 1	Homo sapiens	86-92
34127226-4	2021	Further studies show that fucoidan promotes autophagy showed by the expression of p62/SQSTM1 and microtubule-associated protein light chain 3 (LC3) II, which can be blocked by autophagy inhibitors 3-MA and bafilomycin A1.	bafilomycin A1	206-220	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	143-146
34410949-11	2021	Autophagy inhibitors including 3-methyladenine (3-MA), chloroquine (CQ) and bafilomycin A1 (Baf) significantly alleviated the autophagic cell death effect of gadodiamide on normal brain glial SVG P12 cells.	bafilomycin A1	76-90	BAF nuclear assembly factor 1	Homo sapiens	92-95
34360859-6	2021	This process was suppressed by knockdown of the Cx43 gene and by bafilomycin A1, an inhibitor of vacuolar ATPase.	bafilomycin A1	65-79	gap junction protein alpha 1	Homo sapiens	48-52
34378314-8	2021	The results suggested that silencing of SLC26A4-AS1 led to declined ITPR1 level, up-regulation of ETS1 promoted ITPR1 expression, and either ETS1 knockdown or autophagy inhibitor Bafilomycin A1 could mitigate the promoting effects of SLC26A4-AS1 overexpression on PTC cell autophagy.	bafilomycin A1	179-193	SLC26A4 antisense RNA 1	Homo sapiens	234-245
34062228-6	2021	In conclusion, claudin-1 might be a barrier for CSFV infection in PK-15 cells, while CSFV bypasses the barrier through lysosome mediated degradation of claudin-1, which could be repressed by bafilomycin A1.	bafilomycin A1	191-205	claudin 1	Sus scrofa	15-24
34062228-6	2021	In conclusion, claudin-1 might be a barrier for CSFV infection in PK-15 cells, while CSFV bypasses the barrier through lysosome mediated degradation of claudin-1, which could be repressed by bafilomycin A1.	bafilomycin A1	191-205	claudin 1	Sus scrofa	152-161
34185060-9	2021	The decreased levels of ATP7A and Atox1 proteins were restored by the antioxidant N-acetylcysteine and the lysosomal inhibitor bafilomycin A1.	bafilomycin A1	127-141	ATPase copper transporting alpha	Homo sapiens	24-29
34252168-5	2021	Endosomal acidification inhibitors like BafilomycinA1 and NH4Cl, which inhibit the CG pathway, reduce the uptake of RBD and impede Spike-pseudoviral infection in both AGS and AGS-ACE2 cells.	bafilomycin A1	40-53	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	131-136
34252168-5	2021	Endosomal acidification inhibitors like BafilomycinA1 and NH4Cl, which inhibit the CG pathway, reduce the uptake of RBD and impede Spike-pseudoviral infection in both AGS and AGS-ACE2 cells.	bafilomycin A1	40-53	angiotensin converting enzyme 2	Homo sapiens	179-183
34252168-6	2021	The inhibition by BafilomycinA1 was found to be distinct from Chloroquine which neither affects RBD uptake nor alters endosomal pH, yet attenuates Spike-pseudovirus entry.	bafilomycin A1	18-31	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	147-152
34185060-9	2021	The decreased levels of ATP7A and Atox1 proteins were restored by the antioxidant N-acetylcysteine and the lysosomal inhibitor bafilomycin A1.	bafilomycin A1	127-141	antioxidant 1 copper chaperone	Homo sapiens	34-39
34177609-6	2021	Interestingly, nicotine significantly promoted dynamin-related protein 1 (Drp1)-mediated mitochondrial fission and suppressed mitofusin (MFN)-mediated fusion, which was also observed in the bafilomycin A1-treated group.	bafilomycin A1	190-204	dynamin 1-like	Rattus norvegicus	47-72
34080667-7	2021	In addition, pretreatment with the autophagy inhibitor bafilomycin A1 attenuated CXCR4 abrogation-induced cell death.	bafilomycin A1	55-69	chemokine (C-X-C motif) receptor 4	Mus musculus	81-86
34335562-8	2021	Additionally, analysis of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) and NLR with CARD domain-containing 4 (NLRC4) in J774A.1 cells indicated that spvC decreased the protein levels of NLRP3 and NLRC4, which were significantly changed by autophagy inhibitor Bafilomycin A1.	bafilomycin A1	315-329	NLR family, pyrin domain containing 3	Mus musculus	120-125
34335562-8	2021	Additionally, analysis of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) and NLR with CARD domain-containing 4 (NLRC4) in J774A.1 cells indicated that spvC decreased the protein levels of NLRP3 and NLRC4, which were significantly changed by autophagy inhibitor Bafilomycin A1.	bafilomycin A1	315-329	NLR family, CARD domain containing 4	Mus musculus	166-171
34335562-8	2021	Additionally, analysis of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) and NLR with CARD domain-containing 4 (NLRC4) in J774A.1 cells indicated that spvC decreased the protein levels of NLRP3 and NLRC4, which were significantly changed by autophagy inhibitor Bafilomycin A1.	bafilomycin A1	315-329	Salmonella plasmid virulence protein C	Salmonella enterica subsp. enterica serovar Typhimurium	205-209
34335562-8	2021	Additionally, analysis of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) and NLR with CARD domain-containing 4 (NLRC4) in J774A.1 cells indicated that spvC decreased the protein levels of NLRP3 and NLRC4, which were significantly changed by autophagy inhibitor Bafilomycin A1.	bafilomycin A1	315-329	NLR family, pyrin domain containing 3	Mus musculus	242-247
34335562-8	2021	Additionally, analysis of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) and NLR with CARD domain-containing 4 (NLRC4) in J774A.1 cells indicated that spvC decreased the protein levels of NLRP3 and NLRC4, which were significantly changed by autophagy inhibitor Bafilomycin A1.	bafilomycin A1	315-329	NLR family, CARD domain containing 4	Mus musculus	252-257
34079802-6	2021	Inhibition of autophagy by inhibitors like leupeptin, chloroquine (CQ), and Bafilomycin A1 (Baf-A1) blocks the degradation of B7H3 in glioma cells.	bafilomycin A1	76-90	CD276 antigen	Mus musculus	126-130
34093174-9	2021	In addition, when the fusion of autophagosomes with lysosomes was blocked by Bafilomycin A1, the degradation of p62 induced by Dex during the autophagy process was suspended.	bafilomycin A1	77-91	nucleoporin 62	Homo sapiens	112-115
34079802-6	2021	Inhibition of autophagy by inhibitors like leupeptin, chloroquine (CQ), and Bafilomycin A1 (Baf-A1) blocks the degradation of B7H3 in glioma cells.	bafilomycin A1	92-98	CD276 antigen	Mus musculus	126-130
34184748-8	2021	Mechanistically, TMEM100 was demonstrated to induce autophagy in A549 cells via inhibiting the PI3K/AKT signaling pathway, whereas inhibiting autophagy using bafilomycin A1 significantly enhanced TMEM100-induced apoptosis to compensate for the cell death.	bafilomycin A1	158-172	transmembrane protein 100	Homo sapiens	196-203
35366539-10	2022	Moreover, treatment with bafilomycin A1, an inhibitor of lysosomal protein degradation, restored Glut1 protein levels by siRNA of LDHA.	bafilomycin A1	25-39	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	97-102
35435531-7	2022	Deletion of mTOR relieved autophagosome-lysosome fusion dysfunction and ameliorated apoptosis of CD4 + T cells in CLP mice, but this rescued phenotype was abolished by treatment with bafilomycin A1, a specific A-L fusion inhibitor.	bafilomycin A1	183-197	mechanistic target of rapamycin kinase	Mus musculus	12-16
35435531-7	2022	Deletion of mTOR relieved autophagosome-lysosome fusion dysfunction and ameliorated apoptosis of CD4 + T cells in CLP mice, but this rescued phenotype was abolished by treatment with bafilomycin A1, a specific A-L fusion inhibitor.	bafilomycin A1	183-197	CD4 antigen	Mus musculus	97-100
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.	bafilomycin A1	155-169	interleukin 1 alpha	Homo sapiens	68-77
34257560-12	2021	After treatment with bafilomycin A1, proliferation was inhibited in both cell types, but the effects were more prominent in the cells overexpressing CUL4A.	bafilomycin A1	21-35	cullin 4A	Homo sapiens	149-154
35366539-10	2022	Moreover, treatment with bafilomycin A1, an inhibitor of lysosomal protein degradation, restored Glut1 protein levels by siRNA of LDHA.	bafilomycin A1	25-39	lactate dehydrogenase A	Mus musculus	130-134
35179568-4	2022	Inhibition of autophagic flux by chloroquine or bafilomycin A1 were sufficient to induce eNOS monomerization and lowers nitric oxide bioavailability through raising mitochondrial reactive oxygen species (mtROS).	bafilomycin A1	48-62	nitric oxide synthase 3	Homo sapiens	89-93
35122618-6	2022	LC3 II was increased at 8 h (p = 0.043) and 24 h (p = 0.015) of recovery, whereas p62 was elevated at 2 h (p = 0.002) and 8 h (p < 0.001) of recovery, but returned to baseline by 24 h. In Bafilomycin A1 treated cells, p62 was further increased immediately following HT (p = 0.041).	bafilomycin A1	188-202	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	0-3
35122618-6	2022	LC3 II was increased at 8 h (p = 0.043) and 24 h (p = 0.015) of recovery, whereas p62 was elevated at 2 h (p = 0.002) and 8 h (p < 0.001) of recovery, but returned to baseline by 24 h. In Bafilomycin A1 treated cells, p62 was further increased immediately following HT (p = 0.041).	bafilomycin A1	188-202	nucleoporin 62	Homo sapiens	82-85
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	NLR family pyrin domain containing 3	Homo sapiens	97-102
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	NLR family pyrin domain containing 3	Homo sapiens	202-207
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	caspase 1	Homo sapiens	220-226
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	S100 calcium binding protein A10	Homo sapiens	227-230
35092164-7	2022	While blocking the fusion of autophagosomes with lysosomes by bafilomycin A1(BafA1), the reduced NLRP3 inflammasome activity induced by RAPA was significantly restored, with increased protein levels of NLRP3 and cleaved Casp-1(p10), as well as IL-1beta secretion.	bafilomycin A1	62-76	interleukin 1 alpha	Homo sapiens	244-252
34996966-3	2022	Here we scrutinize this approach and show that bafilomycin A1 (BafA) but not chloroquine is suitable for flux quantification due to the stimulating effect of chloroquine on non-canonical LC3B-lipidation.	bafilomycin A1	47-61	microtubule associated protein 1 light chain 3 beta	Homo sapiens	187-191
35387562-9	2022	Thus, we demonstrate that bafilomycin A1 treatment from 2.5 up to 24 h does not inhibit fusion between autophagosomes and lysosomes, but leads to the accumulation of LC3-positive material inside autolysosomes.	bafilomycin A1	26-40	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	166-169
35348729-8	2022	The increased efficacy of mTOR inhibition plus T-DM1 was abrogated by lysosome inhibitors (chloroquine and bafilomycin A1).	bafilomycin A1	107-121	mechanistic target of rapamycin kinase	Homo sapiens	26-30
35023829-5	2022	Phenotypical analysis of pikfyve zebrafish mutants revealed that loss of Pikfyve caused aberrant vacuolation (accumulation of Rab7+Lc3+ amphisomes) in lens cells, which was significantly alleviated by treatment with the V-ATPase inhibitor bafilomycin A1 (Baf-A1).	bafilomycin A1	239-253	phosphoinositide kinase, FYVE finger containing	Danio rerio	25-32
35023829-5	2022	Phenotypical analysis of pikfyve zebrafish mutants revealed that loss of Pikfyve caused aberrant vacuolation (accumulation of Rab7+Lc3+ amphisomes) in lens cells, which was significantly alleviated by treatment with the V-ATPase inhibitor bafilomycin A1 (Baf-A1).	bafilomycin A1	239-253	phosphoinositide kinase, FYVE finger containing	Danio rerio	73-80
35624155-9	2022	Pharmacological inhibition of autophagy by bafilomycin A1 increased polyUb-p62 and polyUb-p53 in the cytoplasm, indicating that p53 protein levels and subcellular localization were regulated by polyUb-p62 and autophagy.	bafilomycin A1	43-57	sequestosome 1	Mus musculus	75-78
35624155-9	2022	Pharmacological inhibition of autophagy by bafilomycin A1 increased polyUb-p62 and polyUb-p53 in the cytoplasm, indicating that p53 protein levels and subcellular localization were regulated by polyUb-p62 and autophagy.	bafilomycin A1	43-57	transformation related protein 53, pseudogene	Mus musculus	90-93
35624155-9	2022	Pharmacological inhibition of autophagy by bafilomycin A1 increased polyUb-p62 and polyUb-p53 in the cytoplasm, indicating that p53 protein levels and subcellular localization were regulated by polyUb-p62 and autophagy.	bafilomycin A1	43-57	transformation related protein 53, pseudogene	Mus musculus	128-131
35007347-5	2022	In contrast, the inhibitors of endosomal acidification bafilomycin A1 and chloroquine increased levels of LC3-II, due to reduced degradation in acidic lysosomes.	bafilomycin A1	55-69	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	106-112
34996966-5	2022	When rapamycin was combined with saturating concentrations of BafA, no significant further increase of LC3B lipidation could be detected over the levels induced by the late-stage inhibitor.	bafilomycin A1	62-66	microtubule associated protein 1 light chain 3 beta	Homo sapiens	103-107
34996966-3	2022	Here we scrutinize this approach and show that bafilomycin A1 (BafA) but not chloroquine is suitable for flux quantification due to the stimulating effect of chloroquine on non-canonical LC3B-lipidation.	bafilomycin A1	63-67	microtubule associated protein 1 light chain 3 beta	Homo sapiens	187-191
33676894-5	2021	Overexpression of Vps24, a protein that sorts transmembrane proteins into lysosomes via the multivesicular body (MVB) pathway, accelerated whereas the lysosome inhibitor bafilomycin A1 completely prevented PKC-mediated Kv1.5 degradation.	bafilomycin A1	170-184	potassium voltage-gated channel subfamily A member 5	Homo sapiens	219-224
34048091-5	2021	Pre-incubation of retina with bafilomycin A1 (an inhibitor of neurotransmitter uptake into synaptic vesicles) abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a vesicular source of glutamate activates AII NMDARs, whereas a non-vesicular source activates A17 NMDARs.	bafilomycin A1	30-44	NLR family pyrin domain containing 3	Homo sapiens	144-147
34048091-5	2021	Pre-incubation of retina with bafilomycin A1 (an inhibitor of neurotransmitter uptake into synaptic vesicles) abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a vesicular source of glutamate activates AII NMDARs, whereas a non-vesicular source activates A17 NMDARs.	bafilomycin A1	30-44	NLR family pyrin domain containing 3	Homo sapiens	225-228
34048091-5	2021	Pre-incubation of retina with bafilomycin A1 (an inhibitor of neurotransmitter uptake into synaptic vesicles) abolished NMDAR-mediated noise in AII, but not A17 amacrines, suggesting a vesicular source of glutamate activates AII NMDARs, whereas a non-vesicular source activates A17 NMDARs.	bafilomycin A1	30-44	immunoglobulin kappa variable 2-30	Homo sapiens	278-281
32724177-10	2021	Cotreatment with the autophagy inhibitor 3-MA or bafilomycin A1 abrogated the in vivo and in vitro neuroprotective effects of GM1 ganglioside.	bafilomycin A1	49-63	coenzyme Q10A	Mus musculus	126-129
33727633-8	2021	The mRNA levels of AE2 in each KO cell did not change, and the downregulation of AE2 in L-IRBIT KO cells was inhibited by bafilomycin A1.	bafilomycin A1	122-136	solute carrier family 4 member 2	Homo sapiens	81-84
33727633-8	2021	The mRNA levels of AE2 in each KO cell did not change, and the downregulation of AE2 in L-IRBIT KO cells was inhibited by bafilomycin A1.	bafilomycin A1	122-136	adenosylhomocysteinase like 1	Homo sapiens	90-95
34035861-9	2021	The number of GFP-LC3 puncta in HCs following exposure to HDN was increased compared with that observed in HCs without HDN exposure under the H/R conditions after bafilomycin A1 treatment.	bafilomycin A1	163-177	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	18-21
33145969-0	2021	Bafilomycin A1 enhances NLRP3 inflammasome activation in human monocytes independent of lysosomal acidification.	bafilomycin A1	0-14	NLR family pyrin domain containing 3	Homo sapiens	24-29
33145969-3	2021	Here we report that pharmacological inhibition of V-ATPase with bafilomycin A1 exacerbated LPS-induced NLRP3 inflammasome activation in primary human monocytes.	bafilomycin A1	64-78	NLR family pyrin domain containing 3	Homo sapiens	103-108
33749503-4	2021	Our data revealed that LC3-II formation and SQSTM1/p62 degradation were noted in H2O2-activated human platelets, which could be blocked by 3-methyladenine and bafilomycin A1, indicating that platelet activation may cause platelet autophagy.	bafilomycin A1	159-173	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	23-26
33749503-4	2021	Our data revealed that LC3-II formation and SQSTM1/p62 degradation were noted in H2O2-activated human platelets, which could be blocked by 3-methyladenine and bafilomycin A1, indicating that platelet activation may cause platelet autophagy.	bafilomycin A1	159-173	sequestosome 1	Homo sapiens	44-50
33749503-4	2021	Our data revealed that LC3-II formation and SQSTM1/p62 degradation were noted in H2O2-activated human platelets, which could be blocked by 3-methyladenine and bafilomycin A1, indicating that platelet activation may cause platelet autophagy.	bafilomycin A1	159-173	sequestosome 1	Homo sapiens	51-54
33869205-9	2021	Inhibiting miR-22 promoted autophagic flux confirmed by an increased LC3II/GAPDH ratio and reduced p62 protein level under bafilomycin A1 conditions.	bafilomycin A1	123-137	microRNA 22	Mus musculus	11-17
33486901-11	2021	So, the cumulative effect of oncogenic p62 should be considered when using autophagy inhibitors, especially drugs that act at the last stage of autophagy such as chloroquine and bafilomycin A1.	bafilomycin A1	178-192	nucleoporin 62	Homo sapiens	39-42
33746976-5	2021	The use of pharmacological agents, rapamycin and bafilomycin A1, reveals that RipA activates PI3K-AKT-mTORC1 signaling cascade that ultimately culminates in the inhibition of autophagy initiating kinase ULK1 (Unc-51 like autophagy activating kinase).	bafilomycin A1	49-63	CREB regulated transcription coactivator 1	Mus musculus	102-108
33639976-10	2021	Moreover, in the hACE2 transgenic mice model of SARS-CoV-2 infection, chloroquine and bafilomycin A1 reduced viral replication in lung tissues and alleviated viral pneumonia with reduced inflammatory exudation and infiltration in peribronchiolar and perivascular tissues, as well as improved structures of alveolar septum and pulmonary alveoli.	bafilomycin A1	86-100	angiotensin converting enzyme 2	Homo sapiens	17-22
33668422-4	2021	In vitro experiments using mouse and human cardiac fibroblasts confirmed that blockade of autophagy with Bafilomycin A1 inhibited fibroblast-to-myofibroblast transition induced by transforming growth factor (TGF)-beta.	bafilomycin A1	105-119	transforming growth factor alpha	Homo sapiens	180-217
33668885-11	2021	Furthermore, inhibition of lysosomal hyperpolarization with Bafilomycin A1 blocked LMP and NLRP3 activation, suggesting a causal relation between lysosomal hyperpolarization and LMP.	bafilomycin A1	60-74	NLR family, pyrin domain containing 3	Mus musculus	91-96
33421769-5	2021	The lysosome inhibitor bafilomycin A1 or deletion of nuclear receptor coactivator 4 (NCOA4) inhibited cystine deprivation-induced decrease in FTH1 protein levels and cell death.	bafilomycin A1	23-37	ferritin heavy chain 1	Homo sapiens	142-146
33526785-10	2021	Inhibition of autophagy using bafilomycin A1 or Beclin1 siRNA leads to reversal of Neu2-induced apoptosis suggesting their possible relationship.	bafilomycin A1	30-44	neuraminidase 2	Homo sapiens	83-87
33384144-6	2021	We find that when 14 was co-administrated with Bafilomycin A1 (BAF) in PC3 cells, rapid necrotic cell death occurred with no cleaved caspase-3 and cleaved PARP activation and increasing the expression of survivin.	bafilomycin A1	47-61	poly(ADP-ribose) polymerase 1	Homo sapiens	155-159
33285240-7	2021	The lysosome inhibitor bafilomycin A1 increased xCT protein levels in the absence of EGF or in the presence of EGF and Torin 1.	bafilomycin A1	23-37	solute carrier family 7 member 11	Homo sapiens	48-51
33526785-13	2021	Such changes were absent in the presence of bafilomycin A1 indicating the involvement of autophagy in Neu2-induced anoikis.	bafilomycin A1	44-58	neuraminidase 2	Homo sapiens	102-106
33459130-4	2021	Accumulation of LC3-II in elicited atg7-/- macrophages in response to bafilomycin A1 validated these data.	bafilomycin A1	70-84	Atg7p	Saccharomyces cerevisiae S288C	35-39
33552025-10	2020	Consistent with this mechanism, inhibition of autophagolysosome maturation with bafilomycin A1 abrogated the ability of THP-PKR macrophages to limit replication of Mtb, whereas pharmacological activation of autophagy enhanced the anti-mycobacterial effect of PKR overexpression.	bafilomycin A1	80-94	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	124-127
33453994-7	2020	Consistent with high-dose liproxstatin-1 protecting via a lysosomal mechanism, we further de-monstrated that loss of viability induced by alpha-synuclein PFFs was attenuated by chloroquine and bafilomycin A1 as well as the lysosomal cysteine protease inhibitors, leupeptin, E-64D, and Ca-074-Me, but not other autophagy or lysosomal enzyme inhibitors.	bafilomycin A1	193-207	synuclein, alpha	Mus musculus	138-153
32976350-0	2020	Phagocytosis of Bafilomycin A1-treated Apoptotic Neuroblastoma Cells by Bone Marrow-derived Dendritic Cells Initiates a CD8alpha+ Lymphocyte Response to Neuroblastoma: Erratum.	bafilomycin A1	16-30	CD8a molecule	Homo sapiens	120-128
33308286-11	2020	Additionally, bafilomycin A1, an autophagy inhibitor, reversed the ATP13A2-induced stemness of colon cancer cells.	bafilomycin A1	14-28	ATPase cation transporting 13A2	Homo sapiens	67-74
32950809-7	2020	Mechanistically, bafilomycin A1 and Atg5 small interfering RNA were used to evaluate the possible mechanism of autophagy activated by irisin, and it was identified that irisin may upregulate autophagy by increasing the Atg12-Atg5-Atg16L complex.	bafilomycin A1	17-31	fibronectin type III domain containing 5	Homo sapiens	169-175
33292101-7	2020	Bioinformatics analysis of GEO data, GSE60570 accession number, revealed that p38 signalling induction and DNA damage response are among the main disrupted signalling pathways in bafilomycin A1-treated RPE-1 cells.	bafilomycin A1	179-193	mitogen-activated protein kinase 14	Homo sapiens	78-81
32810509-10	2020	Using LB-100, a PP2A inhibitor, AICAR, an agonist of AMPK, and bafilomycin A1 (Baf-A1), an autophagy inhibitor, we discover that FTY720 induces ferroptosis and autophagy through the PP2A/AMPK pathway, and ferroptosis and autophagy can reinforce each other.	bafilomycin A1	63-77	protein phosphatase 2 phosphatase activator	Homo sapiens	182-186
32810509-10	2020	Using LB-100, a PP2A inhibitor, AICAR, an agonist of AMPK, and bafilomycin A1 (Baf-A1), an autophagy inhibitor, we discover that FTY720 induces ferroptosis and autophagy through the PP2A/AMPK pathway, and ferroptosis and autophagy can reinforce each other.	bafilomycin A1	63-77	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	187-191
32736005-9	2020	Bafilomycin A1 almost completely prevented the generation of cytoplasmic vacuoles and significantly attenuated cytotoxicity induced by maduramicin, along with downregulation of K-Ras and upregulation of Rac1.	bafilomycin A1	0-14	KRAS proto-oncogene, GTPase	Gallus gallus	177-182
32736005-9	2020	Bafilomycin A1 almost completely prevented the generation of cytoplasmic vacuoles and significantly attenuated cytotoxicity induced by maduramicin, along with downregulation of K-Ras and upregulation of Rac1.	bafilomycin A1	0-14	ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1)	Gallus gallus	203-207
33201170-4	2020	This process is blocked by bafilomycin A1 that binds and inhibits the vacuolar ATPase (V-ATPase) and by SopF, a bacterial effector that catalytically modifies the V-ATPase to inhibit LC3B lipidation via ATG16L1.	bafilomycin A1	27-41	microtubule associated protein 1 light chain 3 beta	Homo sapiens	183-187
33201170-4	2020	This process is blocked by bafilomycin A1 that binds and inhibits the vacuolar ATPase (V-ATPase) and by SopF, a bacterial effector that catalytically modifies the V-ATPase to inhibit LC3B lipidation via ATG16L1.	bafilomycin A1	27-41	autophagy related 16 like 1	Homo sapiens	203-210
32792197-6	2020	In addition, we found that treatment with ursolic acid promotes melanosomal degradation, and bafilomycin A1 inhibition of autophagosome-lysosome fusion blocked the removal of melanosomes in alpha-MSH-stimulated B16F1 cells.	bafilomycin A1	93-107	STAM binding protein	Mus musculus	190-199
32943718-6	2020	Rubicon overexpression or administration of bafilomycin A1 or chloroquine, an inhibitor of late-stage autophagy, suppressed autophagy and activated the type 1 IFN pathway.	bafilomycin A1	44-58	interferon alpha 1	Homo sapiens	159-162
33029288-4	2020	The role of autophagy and AMP-activated protein kinase (AMPK) was determined by treating NSCLC cells with bafilomycin A1, an autophagy inhibitor, and compound C, an AMPK inhibitor.	bafilomycin A1	106-120	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	56-60
33029288-7	2020	Treatment with bafilomycin A1 markedly reduced cell viability but increased proportions of sub-G1 phase cells and annexin V-positive cells in H460 cells.	bafilomycin A1	15-29	annexin A5	Homo sapiens	114-123
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.	bafilomycin A1	76-90	serine/threonine kinase 39	Homo sapiens	161-165
32693673-8	2020	Moreover, the LAPTM4B-overexpression-mediated benefits were abolished by knockdown of lysosome-associated membrane protein-2 (an autophagosome-lysosome fusion protein) in vitro and by the autophagy inhibitor bafilomycin A1 in vivo.	bafilomycin A1	208-222	lysosomal-associated protein transmembrane 4B	Mus musculus	14-21
33041800-8	2020	When in the presence of bafilomycin A1 (BAF), the Ubc9 adenovirus plus OGD group presented a higher level of LC3 II and GFP-LC3 puncta than the OGD group.	bafilomycin A1	24-38	ubiquitin-conjugating enzyme E2I	Mus musculus	50-54
33041800-8	2020	When in the presence of bafilomycin A1 (BAF), the Ubc9 adenovirus plus OGD group presented a higher level of LC3 II and GFP-LC3 puncta than the OGD group.	bafilomycin A1	40-43	ubiquitin-conjugating enzyme E2I	Mus musculus	50-54
32708051-10	2020	The autophagy inhibitor bafilomycin A1, but not the proteasome inhibitor MG132, inhibited the beta-cryptoxanthin-induced decrease in p62 and LC3-II expressions.	bafilomycin A1	24-38	nucleoporin 62	Mus musculus	133-136
32685103-11	2020	In addition, both bafilomycin A1 (a lysosome inhibitor) and an AMPK inhibitor (compound c) markedly prevented salidroside-induced autophagic degradation of p-Src and caveolin-1.	bafilomycin A1	18-32	Rous sarcoma oncogene	Mus musculus	158-161
32453975-4	2020	Consistently, melatonin treatment during in vitro maturation also attenuated the meiotic defects induced by H2O2 by regulating autophagy and SIRT1, which could be abolished by SIRT1 inhibitor, Ex527 and autophagy inhibitor Bafilomycin A1 (Baf A1).	bafilomycin A1	223-237	sirtuin 1	Mus musculus	176-181
32469087-7	2020	Concurrently, HMGB1 impaired insulin sensitivities by attenuating the abundance of insulin receptor substrate-1, Akt phosphorylation, GLUT4 translocation, and glucose uptake in granulosa cells, which were reversed by blocking autophagy pathways with siRNA-mediated knockdown of ATG7 or with chloroquine and bafilomycin A1, the lysosome inhibitors.	bafilomycin A1	307-321	high mobility group box 1	Homo sapiens	14-19
32463725-10	2020	Similarly, pretreatment of the lysosomal inhibitor, bafilomycin A1 reversed the inhibitory effects of 14-3-3gamma on BK protein expression.	bafilomycin A1	52-66	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein gamma	Homo sapiens	102-113
32685103-11	2020	In addition, both bafilomycin A1 (a lysosome inhibitor) and an AMPK inhibitor (compound c) markedly prevented salidroside-induced autophagic degradation of p-Src and caveolin-1.	bafilomycin A1	18-32	caveolin 1, caveolae protein	Mus musculus	166-176
32626542-12	2020	We found that after treatment with proteasomal inhibitor MG132 and lysosomal inhibitor bafilomycin A1, MDR3 expression of V399L was significantly increased.	bafilomycin A1	87-101	ATP binding cassette subfamily B member 4	Homo sapiens	103-107
32549199-3	2020	We have shown that silencing of PKCepsilon by siRNA inhibited basal and starvation-induced autophagy in T47D breast cancer cells as determined by the decrease in LC3-II, increase in p62, and decrease in autophagy puncta both in the presence and absence of bafilomycin A1.	bafilomycin A1	256-270	protein kinase C epsilon	Homo sapiens	32-42
32265299-8	2020	The lysosome inhibitor bafilomycin A1 suppressed xCT down-regulation in HD-cultured glioblastoma cells and in Torin 1-treated cells grown at low density.	bafilomycin A1	23-37	solute carrier family 7 member 11	Homo sapiens	49-52
32397873-3	2021	CASP9-deficient cells demonstrate the missorting of CTSD (cathepsin D) and other acid hydrolases, accumulation of late endosomes, and reduced degradation of bafilomycin A1-sensitive proteins.	bafilomycin A1	157-171	caspase 9	Homo sapiens	0-5
31902824-7	2020	The expression levels of CD81 in HEK293T cells treated with a proteasome inhibitor (lactacystin) and lysosome inhibitors (chloroquine and bafilomycin A1) were analyzed by flow cytometry.	bafilomycin A1	138-152	CD81 molecule	Homo sapiens	25-29
32414129-4	2020	Inhibition of autophagy by a chemical agent (such as chloroquine, bafilomycin A1, or 3-methyladenine) increases the AHR protein levels in HeLa cells whereas activation of autophagy by short-term nutrition deprivation reduces its levels.	bafilomycin A1	66-80	aryl hydrocarbon receptor	Homo sapiens	116-119
32248306-8	2020	The protective effect of CARD9 on cardiomyocytes against H/R-induced oxidative stress was abolished by treatment with autophagy inhibitors, 3-methyladenine (3-MA) or Bafilomycin A1(BafA1).	bafilomycin A1	166-180	caspase recruitment domain family, member 9	Mus musculus	25-30
32209654-4	2020	We found that administration of autophagic inhibitors such as chloroquine or bafilomycin A1, or depletion of autophagy-related 5 (ATG5), results in accumulation of intracellular VEGFA, indicating that VEGFA is a basal autophagic substrate.	bafilomycin A1	77-91	vascular endothelial growth factor A	Mus musculus	178-183
32209654-4	2020	We found that administration of autophagic inhibitors such as chloroquine or bafilomycin A1, or depletion of autophagy-related 5 (ATG5), results in accumulation of intracellular VEGFA, indicating that VEGFA is a basal autophagic substrate.	bafilomycin A1	77-91	vascular endothelial growth factor A	Mus musculus	201-206
32273718-12	2020	The autophagy inhibitor Bafilomycin A1 (BafA1) repressed both autophagy and apoptosis, indicating that miR-126 induced autophagy was responsible for the induction of apoptosis.	bafilomycin A1	24-38	microRNA 126	Homo sapiens	103-110
32273718-12	2020	The autophagy inhibitor Bafilomycin A1 (BafA1) repressed both autophagy and apoptosis, indicating that miR-126 induced autophagy was responsible for the induction of apoptosis.	bafilomycin A1	40-45	microRNA 126	Homo sapiens	103-110
30621446-5	2020	Importantly, the protective effects of isopsoralen against IL-1beta were blocked by pretreatment with autophagy inhibitor 3-MA and bafilomycin A1.	bafilomycin A1	131-145	interleukin 1 beta	Rattus norvegicus	59-67
31794745-7	2020	Whereas inhibition of degradation of autolysosomes by bafilomycin A1 (Baf-A1) reversed functional recovery caused by Tubastatin A, revealing the association between tubulin acetylation and autophagy, which supports HDAC6 inhibition as a potential target for SCI treatment.	bafilomycin A1	70-76	histone deacetylase 6	Mus musculus	215-220
31836471-8	2020	Further, alpha-Synuclein mRNA was decreased by the inhibition of autophagy by using inhibitor bafilomycin A1 or by silencing Atg5 with siRNA.	bafilomycin A1	94-108	synuclein, alpha	Mus musculus	9-24
31696568-6	2020	In contrast, inactivation of autophagy by 3-methyladenine or Bafilomycin A1 could attenuate OPG-mediated inhibition of OC differentiation via the AMPK/mTOR/p70S6K signalling pathway.	bafilomycin A1	61-75	TNF receptor superfamily member 11b	Homo sapiens	92-95
31544984-12	2020	The late autophagy inhibitor bafilomycin A1 (Baf-A1) and the Wnt/beta-catenin pathway inhibitor PKF115-584 reversed the effects of LRP6 on trophoblast autophagy, migration and invasion.	bafilomycin A1	29-43	LDL receptor related protein 6	Homo sapiens	131-135
31544984-12	2020	The late autophagy inhibitor bafilomycin A1 (Baf-A1) and the Wnt/beta-catenin pathway inhibitor PKF115-584 reversed the effects of LRP6 on trophoblast autophagy, migration and invasion.	bafilomycin A1	45-51	LDL receptor related protein 6	Homo sapiens	131-135
31952347-5	2020	The proteasome inhibitor MG132 and the autophagy inhibitor bafilomycin A1 were found to upregulate the PDCD4 levels.	bafilomycin A1	59-73	programmed cell death 4	Homo sapiens	103-108
31696568-6	2020	In contrast, inactivation of autophagy by 3-methyladenine or Bafilomycin A1 could attenuate OPG-mediated inhibition of OC differentiation via the AMPK/mTOR/p70S6K signalling pathway.	bafilomycin A1	61-75	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	146-150
30924217-11	2019	MR formation and ROS production were significantly inhibited in thoracic aorta from AngII-induced rats treated with bafilomycin A1 and amitriptyline.	bafilomycin A1	116-130	angiotensinogen	Rattus norvegicus	84-89
31960608-10	2020	The addition of autophagy inhibitors 3-methyladenine (10 mM) or bafilomycin A1 (10 muM) reduced caffeine-dependent lipid utilization by approximately 30%.	bafilomycin A1	64-78	latexin	Homo sapiens	83-86
31889041-8	2019	Therefore, whether melatonin regulates the amylin expression/oligomerization in thapsigargin- or tunicamycin-combined with Bafilomycin A1 (autophagy inhibitor) or MG132 (proteasome inhibitor) treatments were investigated.	bafilomycin A1	123-137	islet amyloid polypeptide	Rattus norvegicus	43-49
31889041-9	2019	Amylin expression/oligomerization with melatonin treatment was significantly decreased in the thapsigargin- or tunicamycin-combined Bafilomycin A1 or MG132 treatments.	bafilomycin A1	132-146	islet amyloid polypeptide	Rattus norvegicus	0-6
31657331-16	2019	In Baf+LPS group, PD-L1 mRNA expression was significantly up-regulated as compared with that in LPS stimulation group [12-hour PD-L1 mRNA (2-DeltaDeltaCT): 109.1+-7.4 vs. 72.2+-10.0, P &lt; 0.01].	bafilomycin A1	3-6	CD274 antigen	Mus musculus	18-23
31657331-16	2019	In Baf+LPS group, PD-L1 mRNA expression was significantly up-regulated as compared with that in LPS stimulation group [12-hour PD-L1 mRNA (2-DeltaDeltaCT): 109.1+-7.4 vs. 72.2+-10.0, P &lt; 0.01].	bafilomycin A1	3-6	CD274 antigen	Mus musculus	127-132
31657331-19	2019	On the contrary, the expressions of PD-L1, LC3 and p62 in the Baf+LPS group were significantly up-regulated, indicating that the binding of autophagy and lysosome was blocked, and autophagy was not smooth.	bafilomycin A1	62-65	CD274 antigen	Mus musculus	36-41
31657331-19	2019	On the contrary, the expressions of PD-L1, LC3 and p62 in the Baf+LPS group were significantly up-regulated, indicating that the binding of autophagy and lysosome was blocked, and autophagy was not smooth.	bafilomycin A1	62-65	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	43-46
31657331-19	2019	On the contrary, the expressions of PD-L1, LC3 and p62 in the Baf+LPS group were significantly up-regulated, indicating that the binding of autophagy and lysosome was blocked, and autophagy was not smooth.	bafilomycin A1	62-65	nucleoporin 62	Mus musculus	51-54
31116586-6	2019	Inhibiting mTORC1 with everolimus rapidly increased cyclin D1 degradation, whereas 3-methyladenine, chloroquine, and bafilomycin A1, the classic autophagy inhibitors, could attenuate everolimus-induced cyclin D1 degradation.	bafilomycin A1	117-131	cyclin D1	Homo sapiens	202-211
31541377-7	2019	Mn-induced degradation of ZIP14 was blocked by bafilomycin A1, which increased localization of the transporter in Lamp1-positive vesicles.	bafilomycin A1	47-61	solute carrier family 39 member 14	Homo sapiens	26-31
31541377-7	2019	Mn-induced degradation of ZIP14 was blocked by bafilomycin A1, which increased localization of the transporter in Lamp1-positive vesicles.	bafilomycin A1	47-61	lysosomal associated membrane protein 1	Homo sapiens	114-119
31707034-12	2019	The efficacy of CA on A53T alpha-synuclein degradation was reversed by the autophagy inhibitor bafilomycin A1 and the JNK inhibitor SP600125.	bafilomycin A1	95-109	synuclein, alpha	Mus musculus	27-42
31332960-9	2019	The protein levels of LC3-II and p62 were increased in cells overexpression of wild-type and mutant WDR45 while the protein levels were not increased in cells overexpression of mutant WDR45 upon treatment with autophagy inhibitor Bafilomycin A1.	bafilomycin A1	230-244	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	22-25
31332960-9	2019	The protein levels of LC3-II and p62 were increased in cells overexpression of wild-type and mutant WDR45 while the protein levels were not increased in cells overexpression of mutant WDR45 upon treatment with autophagy inhibitor Bafilomycin A1.	bafilomycin A1	230-244	WD repeat domain 45	Homo sapiens	184-189
31332960-10	2019	Results from confocal microscopy revealed that LC3-positive puncta were increased in cells expressing both wild-type and mutant WDR45 while the number of LC3-positive puncta was not increased in cells expressing mutant WDR45 upon treatment with Bafilomycin A1.	bafilomycin A1	245-259	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	47-50
31332960-10	2019	Results from confocal microscopy revealed that LC3-positive puncta were increased in cells expressing both wild-type and mutant WDR45 while the number of LC3-positive puncta was not increased in cells expressing mutant WDR45 upon treatment with Bafilomycin A1.	bafilomycin A1	245-259	WD repeat domain 45	Homo sapiens	219-224
30909132-6	2019	Primary HNECs were treated with HNE, bafilomycin A1, and SP600125.	bafilomycin A1	37-51	elastase, neutrophil expressed	Homo sapiens	8-11