PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
20103630-3	2010	Surface plasmon resonance revealed up to several thousand-fold increased affinities of TRAIL(mim/DR5)-receptor complexes on generation of divalent and trivalent molecules, the latter of which was achieved with a conformationally restricted adamantane core.	Adamantane	240-250	TNF receptor superfamily member 10b	Homo sapiens	97-100
20103630-5	2010	In tumor models derived from human embryonic kidney cells or primary foreskin fibroblasts, TRAIL(mim/DR5) peptides exerted a cancer cell-selective action that could synergize with resveratrol in a manner independent of p53.	Resveratrol	180-191	TNF receptor superfamily member 10b	Homo sapiens	101-104
19877156-8	2010	Concerning the molecular mechanism mediating the dexamethasone-suppression of the TRAIL activity in pre-osteoclasts, but not in leukemic cells, we found that dexamethasone induced a significant down-regulation of the surface levels of TRAIL-R2 in cells of the osteoclastic lineage but not in leukemic cells.	Dexamethasone	49-62	TNF receptor superfamily member 10b	Homo sapiens	235-243
19877156-8	2010	Concerning the molecular mechanism mediating the dexamethasone-suppression of the TRAIL activity in pre-osteoclasts, but not in leukemic cells, we found that dexamethasone induced a significant down-regulation of the surface levels of TRAIL-R2 in cells of the osteoclastic lineage but not in leukemic cells.	Dexamethasone	158-171	TNF receptor superfamily member 10b	Homo sapiens	235-243
19949310-5	2010	Western blot analyses revealed that CDODO-Me-12 and CDODO-Me-11 downregulated the levels of anti-apoptosis proteins, c-FLIP, XIAP and Mcl-1, without altering the protein levels of Bcl-2 and the death receptors DR4 and DR5.	methyl 2-cyano-3,12-dioxooleana-1, 12-dien-30-oate	36-47	TNF receptor superfamily member 10b	Homo sapiens	218-221
20113484-10	2010	Interestingly, knockdown of DR5, but not DR4, prevented GGTI298/TRAIL-induced IkappaBalpha and p-Akt reduction, suggesting that DR5 mediates reduction of IkappaBalpha and p-Akt induced by GGTI298/TRAIL.	GGTI 298	56-63	TNF receptor superfamily member 10b	Homo sapiens	28-31
20113484-10	2010	Interestingly, knockdown of DR5, but not DR4, prevented GGTI298/TRAIL-induced IkappaBalpha and p-Akt reduction, suggesting that DR5 mediates reduction of IkappaBalpha and p-Akt induced by GGTI298/TRAIL.	GGTI 298	56-63	TNF receptor superfamily member 10b	Homo sapiens	128-131
20113484-10	2010	Interestingly, knockdown of DR5, but not DR4, prevented GGTI298/TRAIL-induced IkappaBalpha and p-Akt reduction, suggesting that DR5 mediates reduction of IkappaBalpha and p-Akt induced by GGTI298/TRAIL.	GGTI 298	188-195	TNF receptor superfamily member 10b	Homo sapiens	28-31
20113484-10	2010	Interestingly, knockdown of DR5, but not DR4, prevented GGTI298/TRAIL-induced IkappaBalpha and p-Akt reduction, suggesting that DR5 mediates reduction of IkappaBalpha and p-Akt induced by GGTI298/TRAIL.	GGTI 298	188-195	TNF receptor superfamily member 10b	Homo sapiens	128-131
20037825-12	2009	The expression of DR4 instead of DR5 was significantly increased in the EGCG group.	epigallocatechin gallate	72-76	TNF receptor superfamily member 10b	Homo sapiens	33-36
19943170-6	2010	Salt supplementation substantially reduces the Cd-induced elevation of IAA oxidase activity, thereby maintaining auxin levels in Cd-stressed plants, as indicated by DR5::GUS expression.	Salts	0-4	TNF receptor superfamily member 10b	Homo sapiens	165-168
19943170-6	2010	Salt supplementation substantially reduces the Cd-induced elevation of IAA oxidase activity, thereby maintaining auxin levels in Cd-stressed plants, as indicated by DR5::GUS expression.	Cadmium	47-49	TNF receptor superfamily member 10b	Homo sapiens	165-168
20003459-0	2009	2-Deoxy-D-glucose enhances TRAIL-induced apoptosis in human melanoma cells through XBP-1-mediated up-regulation of TRAIL-R2.	Deoxyglucose	0-17	TNF receptor superfamily member 10b	Homo sapiens	115-123
20003459-9	2009	Treatment with 2-DG up-regulated TRAIL death receptors, in particular, TRAIL-R2, on the melanoma cell surface.	Deoxyglucose	15-19	TNF receptor superfamily member 10b	Homo sapiens	71-79
20003459-12	2009	Moreover, XBP-1, which is known to be transcriptionally regulated by ATF6 and functionally activated by IRE1 alpha, was found to play an important role in 2-DG-mediated transcriptional up-regulation of TRAIL-R2 in melanoma cells.	Deoxyglucose	155-159	TNF receptor superfamily member 10b	Homo sapiens	202-210
19039521-5	2009	Bortezomib enhanced the sensitivity of ovarian cancer cells and tissue explants to an apoptosis-inducing TRAIL receptor antibody by upregulating the TRAIL receptor DR5.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	164-167
19903871-3	2009	We found that although AgNO(3) dramatically decreased root indole-3-acetic acid (IAA) responsiveness in inhibition of root elongation, promotion of DR5-beta-glucuronidase activity, and reduction of Aux/IAA protein levels, AVG had more mild effects.	agno	23-27	TNF receptor superfamily member 10b	Homo sapiens	148-151
19720557-0	2009	Esculetin enhances TRAIL-induced apoptosis through DR5 upregulation in human oral cancer SAS cells.	esculetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	51-54
19720557-5	2009	Furthermore, treatment with esculetin significantly increased TRAIL-induced apoptosis in SAS cells and the TRAIL-sensitizing effect was blocked by DR5/Fc chimera protein.	esculetin	28-37	TNF receptor superfamily member 10b	Homo sapiens	147-150
19720557-6	2009	Our results indicate that esculetin enhances TRAIL-induced apoptosis primarily through upregulation of DR5.	esculetin	26-35	TNF receptor superfamily member 10b	Homo sapiens	103-106
19731037-3	2009	In this study, we demonstrate that both Dox and Dox-CPPs can increase the density of the TRAIL receptors DR4 and DR5 at the plasma membrane and moderately sensitize MDA-MB 231 cells to exogeneously added recombinant TRAIL, as has already been shown for other chemotherapeutic drugs.	Doxorubicin	40-43	TNF receptor superfamily member 10b	Homo sapiens	113-116
19903871-3	2009	We found that although AgNO(3) dramatically decreased root indole-3-acetic acid (IAA) responsiveness in inhibition of root elongation, promotion of DR5-beta-glucuronidase activity, and reduction of Aux/IAA protein levels, AVG had more mild effects.	indoleacetic acid	59-79	TNF receptor superfamily member 10b	Homo sapiens	148-151
19903871-3	2009	We found that although AgNO(3) dramatically decreased root indole-3-acetic acid (IAA) responsiveness in inhibition of root elongation, promotion of DR5-beta-glucuronidase activity, and reduction of Aux/IAA protein levels, AVG had more mild effects.	indoleacetic acid	81-84	TNF receptor superfamily member 10b	Homo sapiens	148-151
19734228-10	2009	We next demonstrated by surface plasmon resonance that phosphorothioate-modified CpG ODNs directly bound to either TRAIL or lexatumumab and then decreased their binding to DR5.	Parathion	55-71	TNF receptor superfamily member 10b	Homo sapiens	172-175
19666002-3	2009	Here, we investigated whether the apoptotic process triggered by apple procyanidins involving the up-regulation of TRAIL-death receptors DR4/DR5 at the cell surface was dependent on cell membrane lipid-raft formation.	Proanthocyanidins	71-83	TNF receptor superfamily member 10b	Homo sapiens	141-144
19734228-11	2009	Finally, NK cell lysis of a DR5-sensitive MM cell line (NCI-H929) through TRAIL was partially inhibited by phosphorothioate-modified CpG ODNs.	Parathion	107-123	TNF receptor superfamily member 10b	Homo sapiens	28-31
19638488-8	2009	None of the death receptors that commonly initiate the extrinsic pathway: FAS, TNF-R1, and TRAIL-R2 are found to be responsible for triggering the apoptosis cascade induced by DHA and EPA.	Dihydroalprenolol	176-179	TNF receptor superfamily member 10b	Homo sapiens	91-99
19682913-2	2009	We previously found that isoflavonoid enhanced TRAIL-induced apoptosis in TRAIL-resistant cells, which is achieved through up-regulation of death receptor 5 (DR5).	isoflavonoid	25-37	TNF receptor superfamily member 10b	Homo sapiens	140-156
19682913-2	2009	We previously found that isoflavonoid enhanced TRAIL-induced apoptosis in TRAIL-resistant cells, which is achieved through up-regulation of death receptor 5 (DR5).	isoflavonoid	25-37	TNF receptor superfamily member 10b	Homo sapiens	158-161
19682913-4	2009	Of the isolates, cardamomin (6), the most potent compound, enhanced the expressions of DR5 and DR4 and decreased the Bcl-xL level in TRAIL-resistant DLD1 cells.	cardamonin	17-27	TNF receptor superfamily member 10b	Homo sapiens	87-90
19654295-3	2009	We found that zerumbone potentiated TRAIL-induced apoptosis in human HCT116 colon cancer cells and that this correlated with the up-regulation of TRAIL death receptor (DR) 4 and DR5.	zerumbone	14-23	TNF receptor superfamily member 10b	Homo sapiens	178-181
19464267-5	2009	In addition, we revealed that treatment with DMNB, a specific inhibitor of DNA-PK, resulted in an increase of DR4/DR5 mRNA levels and their surface expression and a decrease of c-FLIP mRNA levels in K562 cells.	4,5-dimethoxy-2-nitrobenzaldehyde	45-49	TNF receptor superfamily member 10b	Homo sapiens	114-117
19737941-0	2009	Suberoylanilide hydroxamic acid sensitizes human oral cancer cells to TRAIL-induced apoptosis through increase DR5 expression.	Vorinostat	0-31	TNF receptor superfamily member 10b	Homo sapiens	111-114
19737941-4	2009	Western blotting showed suberoylanilide hydroxamic acid increased Fas, Fas ligand, DR4, and DR5 protein expression and activated caspase-8 and caspase-9.	Vorinostat	24-55	TNF receptor superfamily member 10b	Homo sapiens	92-95
19737941-6	2009	Human recombinant DR5/Fc chimera protein but not Fas/Fc or DR4/Fc significantly inhibited apoptosis induced by suberoylanilide hydroxamic acid.	Vorinostat	111-142	TNF receptor superfamily member 10b	Homo sapiens	18-21
19737941-7	2009	These results suggest that suberoylanilide hydroxamic acid induces apoptosis mainly through activation of DR5/TRAIL death pathway.	Vorinostat	27-58	TNF receptor superfamily member 10b	Homo sapiens	106-109
19654295-11	2009	Overall, our results show that zerumbone can potentiate TRAIL-induced apoptosis through the reactive oxygen species-mediated activation of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase leading to DR4 and DR5 induction and resulting in enhancement of the anticancer effects of TRAIL.	zerumbone	31-40	TNF receptor superfamily member 10b	Homo sapiens	241-244
19654295-11	2009	Overall, our results show that zerumbone can potentiate TRAIL-induced apoptosis through the reactive oxygen species-mediated activation of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase leading to DR4 and DR5 induction and resulting in enhancement of the anticancer effects of TRAIL.	Reactive Oxygen Species	92-115	TNF receptor superfamily member 10b	Homo sapiens	241-244
19638488-8	2009	None of the death receptors that commonly initiate the extrinsic pathway: FAS, TNF-R1, and TRAIL-R2 are found to be responsible for triggering the apoptosis cascade induced by DHA and EPA.	Eicosapentaenoic Acid	184-187	TNF receptor superfamily member 10b	Homo sapiens	91-99
19343733-7	2009	In addition, increased expression of death receptor 5 protein was observed further supporting the proposed mechanism of apoptosis induction via the extrinsic pathway in 2-ME-exposed oesophageal carcinoma cells.	2-Methoxyestradiol	169-173	TNF receptor superfamily member 10b	Homo sapiens	37-53
19468286-0	2009	An agonistic monoclonal antibody against DR5 induces ROS production, sustained JNK activation and Endo G release in Jurkat leukemia cells.	Reactive Oxygen Species	53-56	TNF receptor superfamily member 10b	Homo sapiens	41-44
19468286-1	2009	We have previously reported that AD5-10, a novel agonistic monoclonal antibody against DR5, possessed a strong cytotoxic activity in various tumor cells, via induction of caspase-dependent and -independent signaling pathways.	ad5-10	33-39	TNF receptor superfamily member 10b	Homo sapiens	87-90
19493960-6	2009	An analysis of the DR5 reporter in vam3-4 indicated that VAM3 is involved in the proper pattern formation of auxin maxima in the leaf primordium.	vam3-4	35-41	TNF receptor superfamily member 10b	Homo sapiens	19-22
19493960-6	2009	An analysis of the DR5 reporter in vam3-4 indicated that VAM3 is involved in the proper pattern formation of auxin maxima in the leaf primordium.	vam3	57-61	TNF receptor superfamily member 10b	Homo sapiens	19-22
19594141-2	2009	In particular, cardenolide glycosides (1 and 2) from T. peruviana were shown to have a significant reversal effect on TRAIL resistance in human gastric adenocarcinoma cells, and real-time PCR showed that thevefolin (2) enhanced mRNA expression of death receptor 4 (DR4) and DR5.	cardenolide glycosides	15-37	TNF receptor superfamily member 10b	Homo sapiens	274-277
19345731-0	2009	Withaferin A sensitizes TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of death receptor 5 and down-regulation of c-FLIP.	withaferin A	0-12	TNF receptor superfamily member 10b	Homo sapiens	106-122
19345731-0	2009	Withaferin A sensitizes TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of death receptor 5 and down-regulation of c-FLIP.	Reactive Oxygen Species	56-79	TNF receptor superfamily member 10b	Homo sapiens	106-122
19345731-5	2009	Interestingly, a Wit A-induced increase in ROS levels preceded the up-regulation of CHOP and DR5.	Reactive Oxygen Species	43-46	TNF receptor superfamily member 10b	Homo sapiens	93-96
19345731-6	2009	The involvement of ROS in CHOP-mediated DR5 up-regulation was confirmed by the result that pretreatment with an antioxidant, NAC or catalase, inhibited Wit A-induced up-regulation of both CHOP and DR5.	Reactive Oxygen Species	19-22	TNF receptor superfamily member 10b	Homo sapiens	40-43
19345731-6	2009	The involvement of ROS in CHOP-mediated DR5 up-regulation was confirmed by the result that pretreatment with an antioxidant, NAC or catalase, inhibited Wit A-induced up-regulation of both CHOP and DR5.	Reactive Oxygen Species	19-22	TNF receptor superfamily member 10b	Homo sapiens	197-200
20641892-11	2004	Using HGS-ETR2 labeled with radioactive indium ((111)In) ((111)In -EC-HGS-ETR2), the investigators determined that the activity of HGS-ETR2 was increased because the pretreatment with paclitaxel upregulated the expression of TRAIL-R2 in Colo205 cell xenograft tumors in nude mice.	Paclitaxel	184-194	TNF receptor superfamily member 10b	Homo sapiens	225-233
19272388-7	2009	DR5-enhanced green fluorescent protein internalization was dependent on a dileucine-based internalization motif.	dileucine	74-83	TNF receptor superfamily member 10b	Homo sapiens	0-3
20641185-11	2004	Using HGS-ETR2 labeled with radioactive technetium ((99m)Tc) ((99m)Tc-EC-HGS-ETR2), the investigators determined that the activity of HGS-ETR2 was increased because the pretreatment with paclitaxel upregulated the expression of TRAIL-R2 in Colo205 cell xenograft tumors in nude mice.	Paclitaxel	187-197	TNF receptor superfamily member 10b	Homo sapiens	228-236
19037087-0	2009	Rottlerin induces apoptosis via death receptor 5 (DR5) upregulation through CHOP-dependent and PKC delta-independent mechanism in human malignant tumor cells.	rottlerin	0-9	TNF receptor superfamily member 10b	Homo sapiens	32-48
19037087-7	2009	These results suggest that rottlerin induces upregulation of DR5 via PKC delta-independent pathway.	rottlerin	27-36	TNF receptor superfamily member 10b	Homo sapiens	61-64
19264955-9	2009	Additionally, fisetin caused an increase in the protein levels of cleaved caspase-8, Fas ligand, death receptor 5, and TNF-related apoptosis-inducing ligand, and the caspase-8 inhibitor Z-IETD-FMK suppressed fisetin-induced apoptosis and the activation of caspase-3.	fisetin	14-21	TNF receptor superfamily member 10b	Homo sapiens	97-113
19037087-0	2009	Rottlerin induces apoptosis via death receptor 5 (DR5) upregulation through CHOP-dependent and PKC delta-independent mechanism in human malignant tumor cells.	rottlerin	0-9	TNF receptor superfamily member 10b	Homo sapiens	50-53
19037087-9	2009	Thus, DR5-mediated apoptosis, which is induced by rottlerin alone or by the combined treatment with rottlerin and TRAIL, may offer a new therapeutic strategy against cancer.	rottlerin	50-59	TNF receptor superfamily member 10b	Homo sapiens	6-9
19037087-9	2009	Thus, DR5-mediated apoptosis, which is induced by rottlerin alone or by the combined treatment with rottlerin and TRAIL, may offer a new therapeutic strategy against cancer.	rottlerin	100-109	TNF receptor superfamily member 10b	Homo sapiens	6-9
19037087-3	2009	We found that treatment with rottlerin significantly induces DR5 expression both at its messenger RNA and protein levels.	rottlerin	29-38	TNF receptor superfamily member 10b	Homo sapiens	61-64
19037087-4	2009	Downregulation of DR5 expression with small-interfering RNA (siRNA) efficiently attenuated rottlerin-induced apoptosis, showing that the critical role of DR5 in this cell death.	rottlerin	91-100	TNF receptor superfamily member 10b	Homo sapiens	18-21
19037087-4	2009	Downregulation of DR5 expression with small-interfering RNA (siRNA) efficiently attenuated rottlerin-induced apoptosis, showing that the critical role of DR5 in this cell death.	rottlerin	91-100	TNF receptor superfamily member 10b	Homo sapiens	154-157
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	0-9	TNF receptor superfamily member 10b	Homo sapiens	18-21
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	0-9	TNF receptor superfamily member 10b	Homo sapiens	164-167
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	0-9	TNF receptor superfamily member 10b	Homo sapiens	164-167
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	134-143	TNF receptor superfamily member 10b	Homo sapiens	164-167
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	134-143	TNF receptor superfamily member 10b	Homo sapiens	164-167
19037087-6	2009	Although rottlerin is known to be as an inhibitor of novel isoforms of protein kinase C (PKC), specifically PKC delta, not only suppression of PKC delta expression by siRNA but also overexpression of wild-type-PKC delta or dominant-negative-PKC delta did not affect the rottlerin-mediated induction of DR5 in our study.	rottlerin	9-18	TNF receptor superfamily member 10b	Homo sapiens	302-305
19379558-3	2009	The results showed that both TRAIL and DR5 protein and mRNA expressions in NB4, U937 and Jurkat cells increased after treated with sodium butyrate (SB) and in time-dependent manner.	Butyric Acid	131-146	TNF receptor superfamily member 10b	Homo sapiens	39-42
19351839-4	2009	Pretreatment of several melanoma lines just before gamma-irradiation with the inhibitor of ATM kinase KU-55933 suppressed p53 and nuclear factor-kappaB (NF-kappaB) activation but notably increased radiation-induced DR5 surface expression, down-regulated cFLIP (caspase-8 inhibitor) levels, and substantially enhanced exogenous TRAIL-induced apoptosis.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	102-110	TNF receptor superfamily member 10b	Homo sapiens	215-218
19379558-3	2009	The results showed that both TRAIL and DR5 protein and mRNA expressions in NB4, U937 and Jurkat cells increased after treated with sodium butyrate (SB) and in time-dependent manner.	Butyric Acid	148-150	TNF receptor superfamily member 10b	Homo sapiens	39-42
19276256-9	2009	Cisplatin significantly increased TRAIL-R2 expression at both the mRNA and the protein levels.	Cisplatin	0-9	TNF receptor superfamily member 10b	Homo sapiens	34-42
19223550-3	2009	We provide evidence that LY30-induced increase in intracellular H(2)O(2) up-regulates the expression of TRAIL receptors (DR4 and DR5) in SHEP-1 cells by activating mitogen-activated protein kinases, resulting in a significant amplification of TRAIL-mediated caspase-8 processing and activity, cytosolic translocation of cytochrome c, and cell death.	LY 303511	25-29	TNF receptor superfamily member 10b	Homo sapiens	129-132
19223002-4	2009	Oxaliplatin promoted death receptor 4 (DR4) and death receptor 5 (DR5) clustering into aggregated lipid rafts, while the cholesterol-sequestering agent nystatin partially prevented lipid raft aggregation, DR4 and DR5 clustering, and reduced apoptosis.	Oxaliplatin	0-11	TNF receptor superfamily member 10b	Homo sapiens	48-64
19223002-4	2009	Oxaliplatin promoted death receptor 4 (DR4) and death receptor 5 (DR5) clustering into aggregated lipid rafts, while the cholesterol-sequestering agent nystatin partially prevented lipid raft aggregation, DR4 and DR5 clustering, and reduced apoptosis.	Oxaliplatin	0-11	TNF receptor superfamily member 10b	Homo sapiens	66-69
19276284-4	2009	DESIGN: Effect of cisplatin alone or in combination with rhTRAIL or rhTRAIL-DR5 on DR5 surface expression, apoptosis, and cell survival of A2780 was measured.	Cisplatin	18-27	TNF receptor superfamily member 10b	Homo sapiens	83-86
19276284-7	2009	RESULTS: Cisplatin strongly enhanced DR5 surface expression.	Cisplatin	9-18	TNF receptor superfamily member 10b	Homo sapiens	37-40
19276284-8	2009	Both rhTRAIL and rhTRAIL-DR5 in combination with cisplatin induced high levels of caspase-3 activation, apoptosis, and cell kill, with rhTRAIL-DR5 being most potent.	Cisplatin	49-58	TNF receptor superfamily member 10b	Homo sapiens	143-146
19276284-10	2009	Intraperitoneal administration of rhTRAIL-DR5 delayed A2780 tumor progression, reflected in a mean light reduction of 68.3% (P = 0.015), whereas rhTRAIL or rhTRAIL-DR5 plus cisplatin resulted in 85% (P = 0.003) and 97% (P = 0.002) reduction compared with A2780 tumor progression in vehicle-treated animals.	Cisplatin	173-182	TNF receptor superfamily member 10b	Homo sapiens	42-45
19276284-12	2009	CONCLUSION: rhTRAIL-DR5 was superior over rhTRAIL in vitro and in vivo against DR5-expressing ovarian cancer also in combination with cisplatin.	Cisplatin	134-143	TNF receptor superfamily member 10b	Homo sapiens	20-23
19223002-4	2009	Oxaliplatin promoted death receptor 4 (DR4) and death receptor 5 (DR5) clustering into aggregated lipid rafts, while the cholesterol-sequestering agent nystatin partially prevented lipid raft aggregation, DR4 and DR5 clustering, and reduced apoptosis.	Nystatin	152-160	TNF receptor superfamily member 10b	Homo sapiens	213-216
19223550-3	2009	We provide evidence that LY30-induced increase in intracellular H(2)O(2) up-regulates the expression of TRAIL receptors (DR4 and DR5) in SHEP-1 cells by activating mitogen-activated protein kinases, resulting in a significant amplification of TRAIL-mediated caspase-8 processing and activity, cytosolic translocation of cytochrome c, and cell death.	Hydrogen Peroxide	64-72	TNF receptor superfamily member 10b	Homo sapiens	129-132
19223550-4	2009	Involvement of the death receptors was further confirmed by the ability of blocking antibodies against DR4 and/or DR5 to inhibit LY30-induced TRAIL sensitization.	LY 303511	129-133	TNF receptor superfamily member 10b	Homo sapiens	114-117
19223550-6	2009	Finally, small interfering RNA-mediated gene silencing of JNK and ERK inhibited LY30-induced increase in surface expression of DR4 and DR5, respectively.	LY 303511	80-84	TNF receptor superfamily member 10b	Homo sapiens	135-138
19230044-9	2009	Cytometry analysis revealed higher levels of DR5 expression on the surfaces of brefeldin-A-untreated cells than on the surfaces of brefeldin-A-treated cells, but brefeldin A treatment did not affect the total DR5 expression levels.	Brefeldin A	79-90	TNF receptor superfamily member 10b	Homo sapiens	45-48
19212626-10	2009	DDP facilitated the induction of expression of DR4 and DR5 significantly in cell line (P<0.05), but 5-FU influenced only the expression of DR5 significantly.	Fluorouracil	103-107	TNF receptor superfamily member 10b	Homo sapiens	142-145
18852135-4	2008	In addition, curcumin treatment of Burkitt"s lymphoma cell lines also causes up-regulation of DR5; however, this up-regulation does not result in apoptosis.	Curcumin	13-21	TNF receptor superfamily member 10b	Homo sapiens	94-97
19124248-2	2009	On screening for compounds that enhance DR5 expression using a luciferase assay with DLD-1/SacI, we previously identified 4"-demethyltoxicarol isoflavone (1) isolated from the leaves of Millettia brandisiana.	4'-demethyltoxicarol isoflavone	122-153	TNF receptor superfamily member 10b	Homo sapiens	40-43
19124248-7	2009	Furthermore, a MeOH extract of the bark of Ardisia colorata markedly enhanced DR5 activity in this screening system.	Methanol	15-19	TNF receptor superfamily member 10b	Homo sapiens	78-81
18978361-8	2009	RESULTS: Tunicamycin increases both DR5 mRNA (P < 0.005) and TRAIL-induced apoptosis (P < 0.0001) in ESC.	Tunicamycin	9-20	TNF receptor superfamily member 10b	Homo sapiens	36-39
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	43-54	TNF receptor superfamily member 10b	Homo sapiens	18-21
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	43-54	TNF receptor superfamily member 10b	Homo sapiens	75-78
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	146-157	TNF receptor superfamily member 10b	Homo sapiens	18-21
18778787-0	2009	Nitric oxide sensitizes tumor cells to TRAIL-induced apoptosis via inhibition of the DR5 transcription repressor Yin Yang 1.	Nitric Oxide	0-12	TNF receptor superfamily member 10b	Homo sapiens	85-88
18778787-1	2009	Treatment of TRAIL-resistant tumor cells with the nitric oxide donor DETANONOate sensitizes the tumor cells to TRAIL-induced apoptosis concomitantly with DR5 upregulation.	Nitric Oxide	50-62	TNF receptor superfamily member 10b	Homo sapiens	154-157
18778787-1	2009	Treatment of TRAIL-resistant tumor cells with the nitric oxide donor DETANONOate sensitizes the tumor cells to TRAIL-induced apoptosis concomitantly with DR5 upregulation.	2,2'-(hydroxynitrosohydrazono)bis-ethanamine	69-80	TNF receptor superfamily member 10b	Homo sapiens	154-157
18778787-2	2009	The mechanism of sensitization was examined based on the hypothesis that DETANONOate inhibits a transcription repressor Yin Yang 1 (YY1) that negatively regulates DR5 transcription.	2,2'-(hydroxynitrosohydrazono)bis-ethanamine	73-84	TNF receptor superfamily member 10b	Homo sapiens	163-166
18778787-3	2009	Treatment of the prostate carcinoma cell lines with DETANONOate inhibited both NF-kappaB and YY1 DNA-binding activities concomitantly with upregulation of DR5 expression.	2,2'-(hydroxynitrosohydrazono)bis-ethanamine	52-63	TNF receptor superfamily member 10b	Homo sapiens	155-158
20209078-7	2009	In Smac-deficient cells, although TG-induced DR5 upregulation is not affected, activation of caspases 3, 9 and 8 is affected.	Thapsigargin	34-36	TNF receptor superfamily member 10b	Homo sapiens	45-48
20419043-6	2009	Sulindac sulfide-induced apoptosis is coupled with upregulation of death receptor 5 (DR5), and activation of caspases 3, 9 and 8 in Smac-proficient cells.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	67-83
20419043-6	2009	Sulindac sulfide-induced apoptosis is coupled with upregulation of death receptor 5 (DR5), and activation of caspases 3, 9 and 8 in Smac-proficient cells.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	85-88
20419043-7	2009	In Smac-deficient cells, although sulindac sulfide-induced DR5 upregulation is not altered, activation of caspases 3, 9 and 8 is affected.	sulindac sulfide	34-50	TNF receptor superfamily member 10b	Homo sapiens	59-62
19000651-4	2008	Nelfinavir sensitized ovarian cancer cells to treatment with an apoptosis-inducing TRAIL receptor antibody due to upregulation of the TRAIL receptor DR5 as shown by RT-PCR and FACScan analysis.	Nelfinavir	0-10	TNF receptor superfamily member 10b	Homo sapiens	149-152
19074830-6	2008	Allopurinol up-regulated the expression of a proapoptotic TRAIL receptor, death receptor 5 (DR5).	Allopurinol	0-11	TNF receptor superfamily member 10b	Homo sapiens	74-90
19074830-6	2008	Allopurinol up-regulated the expression of a proapoptotic TRAIL receptor, death receptor 5 (DR5).	Allopurinol	0-11	TNF receptor superfamily member 10b	Homo sapiens	92-95
19074830-7	2008	Allopurinol increased DR5 protein, mRNA, and promoter activity.	Allopurinol	0-11	TNF receptor superfamily member 10b	Homo sapiens	22-25
19074830-8	2008	Using DR5 small interfering RNA (siRNA), we showed that allopurinol-mediated DR5 up-regulation contributed to the enhancement of TRAIL effect by allopurinol.	Allopurinol	56-67	TNF receptor superfamily member 10b	Homo sapiens	6-9
19074830-8	2008	Using DR5 small interfering RNA (siRNA), we showed that allopurinol-mediated DR5 up-regulation contributed to the enhancement of TRAIL effect by allopurinol.	Allopurinol	56-67	TNF receptor superfamily member 10b	Homo sapiens	77-80
19074830-8	2008	Using DR5 small interfering RNA (siRNA), we showed that allopurinol-mediated DR5 up-regulation contributed to the enhancement of TRAIL effect by allopurinol.	Allopurinol	145-156	TNF receptor superfamily member 10b	Homo sapiens	6-9
19074830-8	2008	Using DR5 small interfering RNA (siRNA), we showed that allopurinol-mediated DR5 up-regulation contributed to the enhancement of TRAIL effect by allopurinol.	Allopurinol	145-156	TNF receptor superfamily member 10b	Homo sapiens	77-80
19074830-9	2008	Furthermore, we examined the mechanism of allopurinol-mediated DR5 up-regulation.	Allopurinol	42-53	TNF receptor superfamily member 10b	Homo sapiens	63-66
19074830-10	2008	DR5 promoter activity induced by allopurinol was diminished by a mutation of a CAAT/enhancer binding protein homologous protein (CHOP)-binding site.	Allopurinol	33-44	TNF receptor superfamily member 10b	Homo sapiens	0-3
19074830-11	2008	In addition, allopurinol also increased CHOP expression, suggesting that allopurinol induced DR5 expression via CHOP.	Allopurinol	13-24	TNF receptor superfamily member 10b	Homo sapiens	93-96
19074830-11	2008	In addition, allopurinol also increased CHOP expression, suggesting that allopurinol induced DR5 expression via CHOP.	Allopurinol	73-84	TNF receptor superfamily member 10b	Homo sapiens	93-96
19010914-2	2008	The rationale for using such a combination is that perifosine was recently described to increase TRAIL-R2 receptor expression and decrease the cellular FLICE-inhibitory protein (cFLIP) in human lung cancer cell lines.	perifosine	51-61	TNF receptor superfamily member 10b	Homo sapiens	97-105
19010914-4	2008	Perifosine, at concentrations below IC(50), dephosphorylated Akt and increased TRAIL-R2 levels, as shown by Western blot, reverse transcription-PCR, and flow cytometric analysis.	perifosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	79-87
19010914-7	2008	Up-regulation of TRAIL-R2 expression was dependent on a protein kinase Calpha/c-Jun-NH(2)-kinase 2/c-Jun signaling pathway activated by perifosine through reactive oxygen species production.	perifosine	136-146	TNF receptor superfamily member 10b	Homo sapiens	17-25
19010914-7	2008	Up-regulation of TRAIL-R2 expression was dependent on a protein kinase Calpha/c-Jun-NH(2)-kinase 2/c-Jun signaling pathway activated by perifosine through reactive oxygen species production.	Reactive Oxygen Species	155-178	TNF receptor superfamily member 10b	Homo sapiens	17-25
19010914-8	2008	Perifosine also synergized with TRAIL in primary AML cells displaying constitutive activation of the Akt pathway by inducing apoptosis, Akt dephosphorylation, TRAIL-R2 up-regulation, cFLIP-L and XIAP down-regulation, and c-Jun phosphorylation.	perifosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	159-167
18974136-12	2008	Interestingly, baicalein induced reactive oxygen species (ROS) and a ROS scavenger prevented DR5 expression and TRAIL sensitization in PC3 but not SW480 cells.	baicalein	15-24	TNF receptor superfamily member 10b	Homo sapiens	93-96
18974136-12	2008	Interestingly, baicalein induced reactive oxygen species (ROS) and a ROS scavenger prevented DR5 expression and TRAIL sensitization in PC3 but not SW480 cells.	Reactive Oxygen Species	69-72	TNF receptor superfamily member 10b	Homo sapiens	93-96
18980980-6	2008	Sulforaphane-induced apoptosis in PC-3 cells correlated with the generation of intracellular reactive oxygen species (ROS), collapse of mitochondrial membrane potential, activation of caspase-3 and caspase-9, and up-regulation of DR4 and DR5.	sulforaphane	0-12	TNF receptor superfamily member 10b	Homo sapiens	238-241
18980980-10	2008	Sulforaphane up-regulated the expressions of TRAIL-R1/DR4, TRAIL-R2/DR5, Bax and Bak and inhibited the activation of nuclear factor-kappaB P13K/AKT and MEK/ERK pathways in tumor tissues.	sulforaphane	0-12	TNF receptor superfamily member 10b	Homo sapiens	59-67
18980980-10	2008	Sulforaphane up-regulated the expressions of TRAIL-R1/DR4, TRAIL-R2/DR5, Bax and Bak and inhibited the activation of nuclear factor-kappaB P13K/AKT and MEK/ERK pathways in tumor tissues.	sulforaphane	0-12	TNF receptor superfamily member 10b	Homo sapiens	68-71
18680719-4	2008	DR5 but not DR4 siRNA efficiently blocked apoptosis induced by the co-treatment with kaempferol and TRAIL, indicating that DR5 up-regulation by kaempferol helps to enhance TRAIL actions.	kaempferol	85-95	TNF receptor superfamily member 10b	Homo sapiens	0-3
18680719-4	2008	DR5 but not DR4 siRNA efficiently blocked apoptosis induced by the co-treatment with kaempferol and TRAIL, indicating that DR5 up-regulation by kaempferol helps to enhance TRAIL actions.	kaempferol	85-95	TNF receptor superfamily member 10b	Homo sapiens	123-126
18680719-4	2008	DR5 but not DR4 siRNA efficiently blocked apoptosis induced by the co-treatment with kaempferol and TRAIL, indicating that DR5 up-regulation by kaempferol helps to enhance TRAIL actions.	kaempferol	144-154	TNF receptor superfamily member 10b	Homo sapiens	0-3
18680719-4	2008	DR5 but not DR4 siRNA efficiently blocked apoptosis induced by the co-treatment with kaempferol and TRAIL, indicating that DR5 up-regulation by kaempferol helps to enhance TRAIL actions.	kaempferol	144-154	TNF receptor superfamily member 10b	Homo sapiens	123-126
18636537-6	2008	Additionally, the induction of death receptor 5 (DR5), which contributes to Adriamycin-induced cytotoxicity, was not affected by NF-kappaB blockage.	Doxorubicin	76-86	TNF receptor superfamily member 10b	Homo sapiens	31-47
18636537-6	2008	Additionally, the induction of death receptor 5 (DR5), which contributes to Adriamycin-induced cytotoxicity, was not affected by NF-kappaB blockage.	Doxorubicin	76-86	TNF receptor superfamily member 10b	Homo sapiens	49-52
18852139-4	2008	Both DIM-C-pPhBr and DIM-C-pPhF resembled the classic ER stress inducer thapsigargin in pancreatic cancer cells and activated ER stress markers, such as glucose-related protein 78 and the c-Jun NH(2) kinase pathway, resulting in the induction of CCAAT/enhancer-binding protein homologous protein, death receptor 5, and the extrinsic apoptotic pathway.	dim-c-pphbr	5-16	TNF receptor superfamily member 10b	Homo sapiens	297-313
18852139-4	2008	Both DIM-C-pPhBr and DIM-C-pPhF resembled the classic ER stress inducer thapsigargin in pancreatic cancer cells and activated ER stress markers, such as glucose-related protein 78 and the c-Jun NH(2) kinase pathway, resulting in the induction of CCAAT/enhancer-binding protein homologous protein, death receptor 5, and the extrinsic apoptotic pathway.	dim-c-pphf	21-31	TNF receptor superfamily member 10b	Homo sapiens	297-313
18852146-0	2008	15-deoxy-Delta12,14-prostaglandin J2 up-regulates death receptor 5 gene expression in HCT116 cells: involvement of reactive oxygen species and C/EBP homologous transcription factor gene transcription.	14-prostaglandin j2	17-36	TNF receptor superfamily member 10b	Homo sapiens	50-66
18852146-1	2008	Although 15-deoxy-Delta(12,14)-prostaglandin J(2) (15dPGJ(2)) was reported to up-regulate death receptor 5 (DR5) protein expression and sensitize TRAIL-induced cytotoxicity, its action mechanism remains unclear.	15-deoxy-delta(12,14)-prostaglandin j	9-46	TNF receptor superfamily member 10b	Homo sapiens	90-106
18852146-1	2008	Although 15-deoxy-Delta(12,14)-prostaglandin J(2) (15dPGJ(2)) was reported to up-regulate death receptor 5 (DR5) protein expression and sensitize TRAIL-induced cytotoxicity, its action mechanism remains unclear.	15-deoxy-delta(12,14)-prostaglandin j	9-46	TNF receptor superfamily member 10b	Homo sapiens	108-111
18852146-6	2008	A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation.	Reactive Oxygen Species	48-71	TNF receptor superfamily member 10b	Homo sapiens	116-119
18852146-6	2008	A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation.	Reactive Oxygen Species	73-76	TNF receptor superfamily member 10b	Homo sapiens	116-119
18852146-6	2008	A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation.	Calcium	96-103	TNF receptor superfamily member 10b	Homo sapiens	116-119
18852146-11	2008	In summary, the effect of up-regulation of DR5 by 15dPGJ(2) in colon cancer cells is independent of PPAR-gamma and p53 but relies on CHOP induction through gene transcription involving ROS and calcium.	Reactive Oxygen Species	185-188	TNF receptor superfamily member 10b	Homo sapiens	43-46
19174554-0	2009	Mapatumumab and lexatumumab induce apoptosis in TRAIL-R1 and TRAIL-R2 antibody-resistant NSCLC cell lines when treated in combination with bortezomib.	Bortezomib	139-149	TNF receptor superfamily member 10b	Homo sapiens	61-69
20209078-2	2009	We have previously reported that TG induces apoptosis by engaging the death receptor 5 (DR5) and the intrinsic pathways.	Thapsigargin	33-35	TNF receptor superfamily member 10b	Homo sapiens	70-86
20209078-2	2009	We have previously reported that TG induces apoptosis by engaging the death receptor 5 (DR5) and the intrinsic pathways.	Thapsigargin	33-35	TNF receptor superfamily member 10b	Homo sapiens	88-91
20209078-6	2009	For example, ER stress inducing agent TG upregulates DR5, and activates caspases 3, 9 and 8 in Smac-proficient cells.	Thapsigargin	38-40	TNF receptor superfamily member 10b	Homo sapiens	53-56
18980244-0	2008	Quercetin sensitizes human hepatoma cells to TRAIL-induced apoptosis via Sp1-mediated DR5 up-regulation and proteasome-mediated c-FLIPS down-regulation.	Quercetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	86-89
18980244-5	2008	We found that quercetin treatment of HCC cells significantly up-regulated the mRNA and protein levels of DR5, a death receptor of TRAIL, in a transcription factor Sp1-dependent manner.	Quercetin	14-23	TNF receptor superfamily member 10b	Homo sapiens	105-108
18980244-7	2008	Finally, administration of small interfering RNA against DR5 or overexpression of c-FLIPS, but not c-FLIPL, significantly attenuated quercetin-stimulated TRAIL-induced apoptosis.	Quercetin	133-142	TNF receptor superfamily member 10b	Homo sapiens	57-60
18980244-8	2008	Collectively, these findings show that quercetin recovers TRAIL sensitivity in various HCC cells via up-regulation of DR5 and down-regulation of c-FLIPS.	Quercetin	39-48	TNF receptor superfamily member 10b	Homo sapiens	118-121
18852146-11	2008	In summary, the effect of up-regulation of DR5 by 15dPGJ(2) in colon cancer cells is independent of PPAR-gamma and p53 but relies on CHOP induction through gene transcription involving ROS and calcium.	Calcium	193-200	TNF receptor superfamily member 10b	Homo sapiens	43-46
18583568-3	2008	In HMCLs carrying a nonfunctional p53, cotreatment with PD strikingly elevates the (DR4 + DR5)/(DcR1 + DcR2) tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptors ratio and caspase-8 activation of ATO-treated cells.	Arsenic Trioxide	223-226	TNF receptor superfamily member 10b	Homo sapiens	90-93
18599488-0	2008	ABT-737 induces expression of the death receptor 5 and sensitizes human cancer cells to TRAIL-induced apoptosis.	ABT-737	0-7	TNF receptor superfamily member 10b	Homo sapiens	34-50
18794136-11	2008	Furthermore, salubrinal, an inhibitor of ER stress-induced apoptosis, inhibited JNK activation and up-regulation of CHOP and DR5 by CDDO-Me and protected cells from CDDO-Me-induced apoptosis.	salubrinal	13-23	TNF receptor superfamily member 10b	Homo sapiens	125-128
18794136-11	2008	Furthermore, salubrinal, an inhibitor of ER stress-induced apoptosis, inhibited JNK activation and up-regulation of CHOP and DR5 by CDDO-Me and protected cells from CDDO-Me-induced apoptosis.	bardoxolone methyl	132-139	TNF receptor superfamily member 10b	Homo sapiens	125-128
18794136-12	2008	Thus, ER stress seems to be important for CDDO-Me-induced JNK activation, CHOP and DR5 up-regulation, and apoptosis.	bardoxolone methyl	42-49	TNF receptor superfamily member 10b	Homo sapiens	83-86
18794136-13	2008	Collectively, we conclude that CDDO-Me triggers ER stress, leading to JNK-dependent, CHOP-mediated DR5 up-regulation and apoptosis.	bardoxolone methyl	31-38	TNF receptor superfamily member 10b	Homo sapiens	99-102
18794136-0	2008	Coupling of endoplasmic reticulum stress to CDDO-Me-induced up-regulation of death receptor 5 via a CHOP-dependent mechanism involving JNK activation.	bardoxolone methyl	44-51	TNF receptor superfamily member 10b	Homo sapiens	77-93
18794136-2	2008	We previously showed that CDDO-Me induces c-Jun NH(2)-terminal kinase (JNK)-dependent death receptor 5 (DR5) expression and augments death receptor-induced apoptosis.	bardoxolone methyl	26-33	TNF receptor superfamily member 10b	Homo sapiens	86-102
18794136-2	2008	We previously showed that CDDO-Me induces c-Jun NH(2)-terminal kinase (JNK)-dependent death receptor 5 (DR5) expression and augments death receptor-induced apoptosis.	bardoxolone methyl	26-33	TNF receptor superfamily member 10b	Homo sapiens	104-107
18794136-3	2008	The current study focused on addressing how CDDO-Me induces JNK-dependent DR5 expression.	bardoxolone methyl	44-51	TNF receptor superfamily member 10b	Homo sapiens	74-77
18794136-4	2008	Analysis of DR5 promoter regions defines that the CCAAT/enhancer binding protein homologous protein (CHOP) binding site is responsible for CDDO-Me-induced transactivation of the DR5 gene.	bardoxolone methyl	139-146	TNF receptor superfamily member 10b	Homo sapiens	12-15
18794136-4	2008	Analysis of DR5 promoter regions defines that the CCAAT/enhancer binding protein homologous protein (CHOP) binding site is responsible for CDDO-Me-induced transactivation of the DR5 gene.	bardoxolone methyl	139-146	TNF receptor superfamily member 10b	Homo sapiens	178-181
18794136-5	2008	Consistently, CDDO-Me induced DR5 expression and parallel CHOP up-regulation.	bardoxolone methyl	14-21	TNF receptor superfamily member 10b	Homo sapiens	30-33
18794136-6	2008	Blockade of CHOP up-regulation also abrogated CDDO-Me-induced DR5 expression.	bardoxolone methyl	46-53	TNF receptor superfamily member 10b	Homo sapiens	62-65
18794136-7	2008	These results indicate that CDDO-Me induces CHOP-dependent DR5 up-regulation.	bardoxolone methyl	28-35	TNF receptor superfamily member 10b	Homo sapiens	59-62
18599488-6	2008	Treatment with ABT-737 did not change the levels of c-FLIP, FADD, and caspase-8 but up-regulated the levels of the TRAIL receptor DR5.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	15-18	TNF receptor superfamily member 10b	Homo sapiens	130-133
18599488-7	2008	DR5 up-regulation induced by ABT-737 treatment occurred through a transcriptional mechanism, and mutagenesis studies demonstrated that the NF-kappaB site found in the DR5 promoter was essential for the ability of ABT-737 to increase the levels of this mRNA.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	29-32	TNF receptor superfamily member 10b	Homo sapiens	0-3
18599488-7	2008	DR5 up-regulation induced by ABT-737 treatment occurred through a transcriptional mechanism, and mutagenesis studies demonstrated that the NF-kappaB site found in the DR5 promoter was essential for the ability of ABT-737 to increase the levels of this mRNA.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	29-32	TNF receptor superfamily member 10b	Homo sapiens	167-170
18599488-7	2008	DR5 up-regulation induced by ABT-737 treatment occurred through a transcriptional mechanism, and mutagenesis studies demonstrated that the NF-kappaB site found in the DR5 promoter was essential for the ability of ABT-737 to increase the levels of this mRNA.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	213-216	TNF receptor superfamily member 10b	Homo sapiens	0-3
18599488-7	2008	DR5 up-regulation induced by ABT-737 treatment occurred through a transcriptional mechanism, and mutagenesis studies demonstrated that the NF-kappaB site found in the DR5 promoter was essential for the ability of ABT-737 to increase the levels of this mRNA.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	213-216	TNF receptor superfamily member 10b	Homo sapiens	167-170
18534188-0	2008	Hydrogen peroxide enhances TRAIL-induced cell death through up-regulation of DR5 in human astrocytic cells.	Hydrogen Peroxide	0-17	TNF receptor superfamily member 10b	Homo sapiens	77-80
18544564-7	2008	PS-341 (VELCADE, bortezomib), a proteasome inhibitor used to treat human cancer, increases the levels of both HIF-2alpha and c-Myc and elevates the level of DR5 in renal cancer, sensitizing renal cancer cells to TRAIL therapy.	Bortezomib	0-6	TNF receptor superfamily member 10b	Homo sapiens	157-160
18544564-7	2008	PS-341 (VELCADE, bortezomib), a proteasome inhibitor used to treat human cancer, increases the levels of both HIF-2alpha and c-Myc and elevates the level of DR5 in renal cancer, sensitizing renal cancer cells to TRAIL therapy.	Bortezomib	8-15	TNF receptor superfamily member 10b	Homo sapiens	157-160
18544564-7	2008	PS-341 (VELCADE, bortezomib), a proteasome inhibitor used to treat human cancer, increases the levels of both HIF-2alpha and c-Myc and elevates the level of DR5 in renal cancer, sensitizing renal cancer cells to TRAIL therapy.	Bortezomib	17-27	TNF receptor superfamily member 10b	Homo sapiens	157-160
18698026-2	2008	EXPERIMENTAL DESIGN: The activity of perifosine in combination with TRAIL was evaluated with experiments testing the effect of perifosine on DR4/DR5 expression by the use of chimeric blocking antibodies, as well as siRNA.	perifosine	37-47	TNF receptor superfamily member 10b	Homo sapiens	145-148
18698026-2	2008	EXPERIMENTAL DESIGN: The activity of perifosine in combination with TRAIL was evaluated with experiments testing the effect of perifosine on DR4/DR5 expression by the use of chimeric blocking antibodies, as well as siRNA.	perifosine	127-137	TNF receptor superfamily member 10b	Homo sapiens	145-148
18698026-3	2008	RESULTS: DR4 and DR5 expression was induced by exposure to single-agent perifosine.	perifosine	72-82	TNF receptor superfamily member 10b	Homo sapiens	17-20
19568915-12	2008	Isoliquiritigenin increased the amount of DR5 protein among TRAIL receptors.	isoliquiritigenin	0-17	TNF receptor superfamily member 10b	Homo sapiens	42-45
18534188-7	2008	H(2)O(2)-mediated cell death was blocked upon treatment with DR5:Fc protein, a TRAIL-specific antagonistic protein.	Hydrogen Peroxide	0-8	TNF receptor superfamily member 10b	Homo sapiens	61-64
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphbr	0-11	TNF receptor superfamily member 10b	Homo sapiens	68-84
18523266-0	2008	Proteasome inhibitors enhance TRAIL-induced apoptosis through the intronic regulation of DR5: involvement of NF-kappa B and reactive oxygen species-mediated p53 activation.	Reactive Oxygen Species	124-147	TNF receptor superfamily member 10b	Homo sapiens	89-92
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphf	16-26	TNF receptor superfamily member 10b	Homo sapiens	68-84
18636153-6	2008	In addition, SAHA up-regulated the death receptor DR5, inducing the activation of caspase-8 with the consequent cleavage of Bid.	Vorinostat	13-17	TNF receptor superfamily member 10b	Homo sapiens	50-53
18304628-2	2008	The addition of TRAIL significantly potentiated the cytotoxic effect of CDDO-Im, through mechanisms involving the induction of TRAIL-R1/TRAIL-R2 and downmodulation of TRAIL-R3/TRAIL-R4.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	72-79	TNF receptor superfamily member 10b	Homo sapiens	136-144
18523266-13	2008	These findings reveal that proteasome inhibitor-mediated NF-kappaB and ROS-dependent p53 activation are contributed to intronic regulation of DR5 transcription, and resulted in the subsequent enhancement of TRAIL-induced apoptosis in human lung cancer cells.	Reactive Oxygen Species	71-74	TNF receptor superfamily member 10b	Homo sapiens	142-145
18374381-4	2008	KTA induced cancer cell death treatment by triggering mitochondrial and death receptor 5 (DR5) apoptotic pathways, but did not act on the Fas receptor.	kotomolide A	0-3	TNF receptor superfamily member 10b	Homo sapiens	72-88
18374381-4	2008	KTA induced cancer cell death treatment by triggering mitochondrial and death receptor 5 (DR5) apoptotic pathways, but did not act on the Fas receptor.	kotomolide A	0-3	TNF receptor superfamily member 10b	Homo sapiens	90-93
18193086-4	2008	Although dipyridamole upregulated both DR4 and DR5 and increased their cell surface expression, RNA interference revealed a preferential dependence on DR5.	Dipyridamole	9-21	TNF receptor superfamily member 10b	Homo sapiens	47-50
18549619-3	2008	The cytotoxic effect was measured by MTT assay; cell apoptosis rate was determined by flow cytometry after Annexin V/PI staining; the expression level of DR5 on surface of HL-60 cells treated with Ara-C at different concentrations for 24 hours was determined by flow cytometry.	Cytarabine	197-202	TNF receptor superfamily member 10b	Homo sapiens	154-157
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	Cytarabine	37-42	TNF receptor superfamily member 10b	Homo sapiens	164-167
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	rstrail	45-52	TNF receptor superfamily member 10b	Homo sapiens	164-167
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	rstrail	104-111	TNF receptor superfamily member 10b	Homo sapiens	164-167
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	rstrail	104-111	TNF receptor superfamily member 10b	Homo sapiens	164-167
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	rstrail	104-111	TNF receptor superfamily member 10b	Homo sapiens	164-167
18549619-7	2008	When HL-60 cells treated with 5 and 10 mg/L of Ara-C for 24 hours, the expression level of DR5 on surface of HL-60 cells was higher than that in control group.	Cytarabine	47-52	TNF receptor superfamily member 10b	Homo sapiens	91-94
18549619-9	2008	Ara-C can upregulate DR5 expression on the surface of HL-60 cells and enhance the effect of rsTRAIL-inducing apoptosis.	Cytarabine	0-5	TNF receptor superfamily member 10b	Homo sapiens	21-24
18549619-12	2008	The mechanism may correlate with up-regulation of the expression level of DR5 and/or caspase-8 in HL-60 cells by Ara-C.	Cytarabine	113-118	TNF receptor superfamily member 10b	Homo sapiens	74-77
18193086-7	2008	In addition, a transcriptional mechanism powered by CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) induction was responsible for DR5 upregulation by dipyridamole.	Dipyridamole	167-179	TNF receptor superfamily member 10b	Homo sapiens	147-150
17957723-6	2008	DIM-C-pPhOCH(3) also activated the extrinsic apoptosis pathway through increased phosphorylation of c-jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5).	dim-c-pphoch(3)	0-15	TNF receptor superfamily member 10b	Homo sapiens	199-215
18187663-0	2008	Triptolide sensitizes AML cells to TRAIL-induced apoptosis via decrease of XIAP and p53-mediated increase of DR5.	triptolide	0-10	TNF receptor superfamily member 10b	Homo sapiens	109-112
18381960-1	2008	PURPOSE: This study was designed to evaluate the in vitro cytotoxicity and in vivo efficacy of TRA-8, a mouse monoclonal antibody that binds to the DR5 death receptor for tumor necrosis factor-related apoptosis-inducing ligand (also called Apo2L), alone and in combination with CPT-11, against human colon cancer cells and xenografts.	Irinotecan	278-284	TNF receptor superfamily member 10b	Homo sapiens	148-151
18483298-0	2008	Proteasome inhibitor PS-341 (VELCADE) induces stabilization of the TRAIL receptor DR5 mRNA through the 3"-untranslated region.	Bortezomib	21-27	TNF receptor superfamily member 10b	Homo sapiens	82-85
18483298-0	2008	Proteasome inhibitor PS-341 (VELCADE) induces stabilization of the TRAIL receptor DR5 mRNA through the 3"-untranslated region.	Bortezomib	29-36	TNF receptor superfamily member 10b	Homo sapiens	82-85
18483298-2	2008	PS-341 sensitizes prostate cancer cells to TRAIL-induced apoptosis by increasing TRAIL receptors (DR5), inhibiting protein degradation, and elevating DR5 mRNA.	Bortezomib	0-6	TNF receptor superfamily member 10b	Homo sapiens	98-101
18483298-2	2008	PS-341 sensitizes prostate cancer cells to TRAIL-induced apoptosis by increasing TRAIL receptors (DR5), inhibiting protein degradation, and elevating DR5 mRNA.	Bortezomib	0-6	TNF receptor superfamily member 10b	Homo sapiens	150-153
18483298-7	2008	In LNCaP cells treated with PS-341, small interfering RNA-mediated knockdown of HuR markedly decreases the half-life of DR5 mRNA, indicating that HuR is essential for mRNA stabilization.	Bortezomib	28-34	TNF receptor superfamily member 10b	Homo sapiens	120-123
17968315-0	2008	Celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 expression via GADD153/CHOP.	Celecoxib	0-9	TNF receptor superfamily member 10b	Homo sapiens	57-73
17968315-3	2008	Here we report that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the ligand for DR5, to induce apoptosis in COX-2-positive and -negative cancer cells.	Celecoxib	36-45	TNF receptor superfamily member 10b	Homo sapiens	93-109
17968315-3	2008	Here we report that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the ligand for DR5, to induce apoptosis in COX-2-positive and -negative cancer cells.	Celecoxib	36-45	TNF receptor superfamily member 10b	Homo sapiens	111-114
17968315-3	2008	Here we report that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the ligand for DR5, to induce apoptosis in COX-2-positive and -negative cancer cells.	Celecoxib	36-45	TNF receptor superfamily member 10b	Homo sapiens	215-218
17968315-3	2008	Here we report that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the ligand for DR5, to induce apoptosis in COX-2-positive and -negative cancer cells.	ON09310	74-81	TNF receptor superfamily member 10b	Homo sapiens	93-109
17968315-3	2008	Here we report that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the ligand for DR5, to induce apoptosis in COX-2-positive and -negative cancer cells.	ON09310	74-81	TNF receptor superfamily member 10b	Homo sapiens	111-114
17968315-3	2008	Here we report that COX-2-selective celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), the ligand for DR5, to induce apoptosis in COX-2-positive and -negative cancer cells.	ON09310	74-81	TNF receptor superfamily member 10b	Homo sapiens	215-218
18413750-6	2008	Furthermore, the OSU-03012/EGFR inhibitor combination induced GADD153-mediated up-regulation of death receptor 5 expression and subsequent activation of the extrinsic apoptosis pathway.	OSU 03012	17-26	TNF receptor superfamily member 10b	Homo sapiens	96-112
18423123-8	2008	RESULTS: The positive rate of DR5 on SMMC-7721 cells was 95.0%.	smmc	37-41	TNF receptor superfamily member 10b	Homo sapiens	30-33
18187663-5	2008	Furthermore, triptolide increased DR5 levels in OCI-AML3, while the DR5 increase was blunted in p53-knockdown OCI-AML3 and p53-mutated U937 cells, confirming a role for p53 in the regulation of DR5.	triptolide	13-23	TNF receptor superfamily member 10b	Homo sapiens	34-37
18341587-7	2008	Transient knockdown of the transcription factor GADD153/C/EBP homologous protein and application of the synthetic c-Jun N-terminal kinase inhibitor SP600125 indicated that enhanced DR5 expression occurred independently of GADD153/C/EBP homologous protein, but required activation of the c-Jun N-terminal kinase/c-Jun signaling pathway.	pyrazolanthrone	148-156	TNF receptor superfamily member 10b	Homo sapiens	181-184
17957723-6	2008	DIM-C-pPhOCH(3) also activated the extrinsic apoptosis pathway through increased phosphorylation of c-jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5).	dim-c-pphoch(3)	0-15	TNF receptor superfamily member 10b	Homo sapiens	217-220
18164688-0	2008	Rosiglitazone promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by reactive oxygen species-mediated up-regulation of death receptor 5 and down-regulation of c-FLIP.	Rosiglitazone	0-13	TNF receptor superfamily member 10b	Homo sapiens	150-166
18164688-9	2008	Taken together, the results of this study demonstrate that rosiglitazone enhances TRAIL-induced apoptosis in various cancer cells by ROS-mediated DR5 up-regulation and down-regulation of c-FLIPs.	Rosiglitazone	59-72	TNF receptor superfamily member 10b	Homo sapiens	146-149
18164688-9	2008	Taken together, the results of this study demonstrate that rosiglitazone enhances TRAIL-induced apoptosis in various cancer cells by ROS-mediated DR5 up-regulation and down-regulation of c-FLIPs.	Reactive Oxygen Species	133-136	TNF receptor superfamily member 10b	Homo sapiens	146-149
18222423-4	2008	Our observations indicated that resveratrol, a polyphenolic phytoalexin, decreased STAT3 and NF-kappaB activation, while activating JNK-cJun that finally suppressed expression of cFLIP and Bcl-xL proteins and increased sensitivity to exogenous TRAIL in DR5-positive melanomas.	Resveratrol	32-43	TNF receptor superfamily member 10b	Homo sapiens	253-256
18222423-5	2008	Interestingly, resveratrol did not increase surface expression of DR5 in human melanomas, while gamma-irradiation or sodium arsenite treatment substantially upregulated DR5 expression.	sodium arsenite	117-132	TNF receptor superfamily member 10b	Homo sapiens	169-172
18222423-6	2008	Hence, an initial increase in DR5 surface expression (either by gamma-irradiation or arsenite), and subsequent downregulation of antiapoptotic cFLIP and Bcl-xL (by resveratrol), appear to constitute an efficient approach to reactivate apoptotic death pathways in TRAIL-resistant human melanomas.	arsenite	85-93	TNF receptor superfamily member 10b	Homo sapiens	30-33
18164688-0	2008	Rosiglitazone promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by reactive oxygen species-mediated up-regulation of death receptor 5 and down-regulation of c-FLIP.	Reactive Oxygen Species	100-123	TNF receptor superfamily member 10b	Homo sapiens	150-166
18164688-4	2008	We found that treatment with rosiglitazone significantly induces DR5 expression at both its mRNA and its protein levels, accompanying the generation of reactive oxygen species (ROS).	Rosiglitazone	29-42	TNF receptor superfamily member 10b	Homo sapiens	65-68
18164688-4	2008	We found that treatment with rosiglitazone significantly induces DR5 expression at both its mRNA and its protein levels, accompanying the generation of reactive oxygen species (ROS).	Reactive Oxygen Species	152-175	TNF receptor superfamily member 10b	Homo sapiens	65-68
18164688-4	2008	We found that treatment with rosiglitazone significantly induces DR5 expression at both its mRNA and its protein levels, accompanying the generation of reactive oxygen species (ROS).	Reactive Oxygen Species	177-180	TNF receptor superfamily member 10b	Homo sapiens	65-68
18164688-5	2008	Both treatment with DR5/Fc chimeric protein and silencing of DR5 expression using small interfering RNAs attenuated rosiglitazone plus TRAIL-induced apoptosis, showing the critical role of DR5 in this cell death.	Rosiglitazone	116-129	TNF receptor superfamily member 10b	Homo sapiens	61-64
18164688-5	2008	Both treatment with DR5/Fc chimeric protein and silencing of DR5 expression using small interfering RNAs attenuated rosiglitazone plus TRAIL-induced apoptosis, showing the critical role of DR5 in this cell death.	Rosiglitazone	116-129	TNF receptor superfamily member 10b	Homo sapiens	61-64
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Glutathione	18-21	TNF receptor superfamily member 10b	Homo sapiens	68-71
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Glutathione	18-21	TNF receptor superfamily member 10b	Homo sapiens	219-222
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Rosiglitazone	46-59	TNF receptor superfamily member 10b	Homo sapiens	68-71
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Rosiglitazone	46-59	TNF receptor superfamily member 10b	Homo sapiens	219-222
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Rosiglitazone	144-157	TNF receptor superfamily member 10b	Homo sapiens	219-222
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Reactive Oxygen Species	185-188	TNF receptor superfamily member 10b	Homo sapiens	68-71
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Reactive Oxygen Species	185-188	TNF receptor superfamily member 10b	Homo sapiens	219-222
18164688-6	2008	Pretreatment with GSH significantly inhibited rosiglitazone-induced DR5 up-regulation and the cell death induced by the combined treatment with rosiglitazone and TRAIL, suggesting that ROS mediate rosiglitazone-induced DR5 up-regulation, contributing to TRAIL-mediated apoptosis.	Rosiglitazone	144-157	TNF receptor superfamily member 10b	Homo sapiens	219-222
18006694-4	2008	The association of FADD with DR5 results in the formation of death-inducing signaling complex (DISC) to trigger the downstream apoptotic signaling cascade.	fadd	19-23	TNF receptor superfamily member 10b	Homo sapiens	29-32
18036820-0	2008	A novel sesquiterpenoid dimer parviflorene F induces apoptosis by up-regulating the expression of TRAIL-R2 and a caspase-dependent mechanism.	sesquiterpenoid	8-23	TNF receptor superfamily member 10b	Homo sapiens	98-106
18036820-0	2008	A novel sesquiterpenoid dimer parviflorene F induces apoptosis by up-regulating the expression of TRAIL-R2 and a caspase-dependent mechanism.	parviflorene F	30-44	TNF receptor superfamily member 10b	Homo sapiens	98-106
18022315-0	2008	RRR-gamma-tocopherol induces human breast cancer cells to undergo apoptosis via death receptor 5 (DR5)-mediated apoptotic signaling.	Tocopherols	9-20	TNF receptor superfamily member 10b	Homo sapiens	80-96
18022315-0	2008	RRR-gamma-tocopherol induces human breast cancer cells to undergo apoptosis via death receptor 5 (DR5)-mediated apoptotic signaling.	Tocopherols	9-20	TNF receptor superfamily member 10b	Homo sapiens	98-101
18022315-2	2008	gammaT was shown to induce cancer cells but not normal cells to undergo apoptosis, sensitize cancer cells to Tumor necrosis factor-Related Apoptosis-Inducing Ligand (TRAIL)-induced apoptosis, and increase death receptor 5 (DR5) mRNA, protein and cell surface expression.	gamma-Tocopherol	0-6	TNF receptor superfamily member 10b	Homo sapiens	205-221
18022315-2	2008	gammaT was shown to induce cancer cells but not normal cells to undergo apoptosis, sensitize cancer cells to Tumor necrosis factor-Related Apoptosis-Inducing Ligand (TRAIL)-induced apoptosis, and increase death receptor 5 (DR5) mRNA, protein and cell surface expression.	gamma-Tocopherol	0-6	TNF receptor superfamily member 10b	Homo sapiens	223-226
18022315-3	2008	Knockdown of DR5 attenuated gammaT-induced apoptosis.	gamma-Tocopherol	28-34	TNF receptor superfamily member 10b	Homo sapiens	13-16
18022315-5	2008	Thus, gammaT is a potent pro-apoptotic agent for human breast cancer cells inducing apoptosis via activation of DR5-mediated apoptotic pathway.	gamma-Tocopherol	6-12	TNF receptor superfamily member 10b	Homo sapiens	112-115
18177927-11	2008	IHC revealed an increase in DR5 expression in tumor slices treated with cisplatin for 24 h. IHC and Western blotting demonstrated TRA-8-induced cell death via apoptosis and activation of caspase 3 and 8.	Cisplatin	72-81	TNF receptor superfamily member 10b	Homo sapiens	28-31
18202802-0	2008	Induction of apoptosis by pectenotoxin-2 is mediated with the induction of DR4/DR5, Egr-1 and NAG-1, activation of caspases and modulation of the Bcl-2 family in p53-deficient Hep3B hepatocellular carcinoma cells.	pectenotoxin 2	26-40	TNF receptor superfamily member 10b	Homo sapiens	79-82
17703232-5	2007	Notably, disulfide-bonded fusion proteins of the THD of mTRAIL and mCD95L with a subdomain of the tenascin-C (TNC) oligomerization domain, which still assembled into trimers, efficiently interacted with their cognate cellular receptors and robustly stimulated CD95 and TRAILR2 signaling after secondary cross-linking.	Disulfides	9-18	TNF receptor superfamily member 10b	Homo sapiens	269-276
18097593-0	2008	Sp1 is involved in 8-chloro-adenosine-upregulated death receptor 5 expression in human hepatoma cells.	8-chloro	19-27	TNF receptor superfamily member 10b	Homo sapiens	50-66
18097593-0	2008	Sp1 is involved in 8-chloro-adenosine-upregulated death receptor 5 expression in human hepatoma cells.	Adenosine	28-37	TNF receptor superfamily member 10b	Homo sapiens	50-66
18097593-4	2008	In the present study, we demonstrated by Western blot and real-time PCR that 8-Cl-Ado selectively up-regulated death receptor 5 (DR5), but not death receptor 4 (DR4), at both protein and RNA levels in human hepatoma cell line BEL-7402.	8-chloroadenosine	77-85	TNF receptor superfamily member 10b	Homo sapiens	111-127
18097593-4	2008	In the present study, we demonstrated by Western blot and real-time PCR that 8-Cl-Ado selectively up-regulated death receptor 5 (DR5), but not death receptor 4 (DR4), at both protein and RNA levels in human hepatoma cell line BEL-7402.	8-chloroadenosine	77-85	TNF receptor superfamily member 10b	Homo sapiens	129-132
18097593-6	2008	Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) confirmed that 8-Cl-Ado treatment facilitated transcription factor Sp1 binding to its cis-element -198/-189 in the DR5 promoter, suggesting that Sp1 is at least one of the 8-Cl-Ado-responsive transcription factors.	8-chloroadenosine	100-108	TNF receptor superfamily member 10b	Homo sapiens	200-203
18097593-6	2008	Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) confirmed that 8-Cl-Ado treatment facilitated transcription factor Sp1 binding to its cis-element -198/-189 in the DR5 promoter, suggesting that Sp1 is at least one of the 8-Cl-Ado-responsive transcription factors.	8-cl	100-104	TNF receptor superfamily member 10b	Homo sapiens	200-203
18097593-6	2008	Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) confirmed that 8-Cl-Ado treatment facilitated transcription factor Sp1 binding to its cis-element -198/-189 in the DR5 promoter, suggesting that Sp1 is at least one of the 8-Cl-Ado-responsive transcription factors.	beta-apocarotenoid-14',13'-dioxygenase	105-108	TNF receptor superfamily member 10b	Homo sapiens	200-203
18097593-8	2008	These data allowed us to draw a conclusion that 8-Cl-Ado-enhanced DR5 expression is regulated by Sp1 binding to the -198/-189 cis-element in DR5 promoter without affecting NF-kappaB activity in the hepatoma cells.	8-chloroadenosine	48-56	TNF receptor superfamily member 10b	Homo sapiens	66-69
18097593-8	2008	These data allowed us to draw a conclusion that 8-Cl-Ado-enhanced DR5 expression is regulated by Sp1 binding to the -198/-189 cis-element in DR5 promoter without affecting NF-kappaB activity in the hepatoma cells.	8-chloroadenosine	48-56	TNF receptor superfamily member 10b	Homo sapiens	141-144
17922852-0	2007	Low concentrations of doxorubicin sensitizes human solid cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-receptor (R) 2-mediated apoptosis by inducing TRAIL-R2 expression.	Doxorubicin	22-33	TNF receptor superfamily member 10b	Homo sapiens	183-191
17922852-7	2007	Low concentrations of doxorubicin (0.1 and 1 microg/mL) significantly increased TRAIL-R2 expression at both the mRNA and protein levels.	Doxorubicin	22-33	TNF receptor superfamily member 10b	Homo sapiens	80-88
17922852-11	2007	These findings suggest that doxorubicin sensitizes solid cancer cells to TRAIL-R2-mediated apoptosis by inducing TRAIL-R2 expression, and that the combination treatment with lexatumumab and doxorubicin might be a promising targeted therapy for cancers, including RCC, prostate, bladder, and lung cancers.	Doxorubicin	28-39	TNF receptor superfamily member 10b	Homo sapiens	73-81
17922852-11	2007	These findings suggest that doxorubicin sensitizes solid cancer cells to TRAIL-R2-mediated apoptosis by inducing TRAIL-R2 expression, and that the combination treatment with lexatumumab and doxorubicin might be a promising targeted therapy for cancers, including RCC, prostate, bladder, and lung cancers.	Doxorubicin	28-39	TNF receptor superfamily member 10b	Homo sapiens	113-121
17922852-11	2007	These findings suggest that doxorubicin sensitizes solid cancer cells to TRAIL-R2-mediated apoptosis by inducing TRAIL-R2 expression, and that the combination treatment with lexatumumab and doxorubicin might be a promising targeted therapy for cancers, including RCC, prostate, bladder, and lung cancers.	Doxorubicin	190-201	TNF receptor superfamily member 10b	Homo sapiens	73-81
17922852-11	2007	These findings suggest that doxorubicin sensitizes solid cancer cells to TRAIL-R2-mediated apoptosis by inducing TRAIL-R2 expression, and that the combination treatment with lexatumumab and doxorubicin might be a promising targeted therapy for cancers, including RCC, prostate, bladder, and lung cancers.	Doxorubicin	190-201	TNF receptor superfamily member 10b	Homo sapiens	113-121
18172319-0	2008	Arsenic trioxide sensitizes human glioma cells, but not normal astrocytes, to TRAIL-induced apoptosis via CCAAT/enhancer-binding protein homologous protein-dependent DR5 up-regulation.	Arsenic Trioxide	0-16	TNF receptor superfamily member 10b	Homo sapiens	166-169
18172319-6	2008	The involvement of CHOP in this process was confirmed by siRNA-mediated CHOP suppression, which not only attenuated As(2)O(3)-induced DR5 up-regulation but also inhibited the As(2)O(3)-stimulated TRAIL-induced apoptosis.	(2)o(3)	118-125	TNF receptor superfamily member 10b	Homo sapiens	134-137
18172319-6	2008	The involvement of CHOP in this process was confirmed by siRNA-mediated CHOP suppression, which not only attenuated As(2)O(3)-induced DR5 up-regulation but also inhibited the As(2)O(3)-stimulated TRAIL-induced apoptosis.	(2)o(3)	177-184	TNF receptor superfamily member 10b	Homo sapiens	134-137
18172319-10	2008	In addition, As(2)O(3)-mediated up-regulation of CHOP and DR5, as well as partial proteolytic processing of procaspase-3 by TRAIL, was not induced in astrocytes.	(2)o(3)	15-22	TNF receptor superfamily member 10b	Homo sapiens	58-61
17703232-5	2007	Notably, disulfide-bonded fusion proteins of the THD of mTRAIL and mCD95L with a subdomain of the tenascin-C (TNC) oligomerization domain, which still assembled into trimers, efficiently interacted with their cognate cellular receptors and robustly stimulated CD95 and TRAILR2 signaling after secondary cross-linking.	Thiamine	49-52	TNF receptor superfamily member 10b	Homo sapiens	269-276
17982676-6	2007	Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests.	Fluorouracil	58-62	TNF receptor superfamily member 10b	Homo sapiens	180-189
18065493-7	2007	We show that TRAIL activates the canonical caspase-dependent pathway, whereas treatment with cycloheximide increases the sensitivity of MG-63 cells to TRAIL and anti-DR5 and can also sensitize hPOB-tert cells to both agents.	Cycloheximide	93-106	TNF receptor superfamily member 10b	Homo sapiens	166-169
17893044-7	2007	In addition, cells treated with hydrogen peroxide expressed less X-linked inhibitor of apoptosis protein (XIAP) and survivin which, like cFLIP(S), are short-half-life proteins with an antiapoptotic function while expression levels of DR5, caspases-8, -9, -3, and Bax are maintained.	Hydrogen Peroxide	32-49	TNF receptor superfamily member 10b	Homo sapiens	234-257
18006776-5	2007	DIM-C-pPhtBu also induced several common proapoptotic responses in ACHN and 786-0 cells, including increased expression of nonsteroidal anti-inflammatory drug-activated gene-1 and endoplasmic reticulum stress, which activates death receptor 5 and the extrinsic pathway of apoptosis.	1,1-bis(3'-indolyl)-1-(4-t-butylphenyl)methane	0-12	TNF receptor superfamily member 10b	Homo sapiens	226-242
17689858-6	2007	These results indicate that caspase-3 is a key regulator of apoptosis in response to combined genistein and TRAIL in human gastric adenocarcinoma AGS cells through the activation of DR5 and mitochondrial dysfunction.	Genistein	94-103	TNF receptor superfamily member 10b	Homo sapiens	182-185
17652336-0	2007	Thapsigargin sensitizes human melanoma cells to TRAIL-induced apoptosis by up-regulation of TRAIL-R2 through the unfolded protein response.	Thapsigargin	0-12	TNF receptor superfamily member 10b	Homo sapiens	92-100
17652336-3	2007	We show in this study that the endoplasmic reticulum stress inducer, thapsigargin (TG), selectively up-regulated TRAIL-R2 and enhanced TRAIL-induced apoptosis in melanoma cells.	Thapsigargin	69-81	TNF receptor superfamily member 10b	Homo sapiens	113-121
17652336-3	2007	We show in this study that the endoplasmic reticulum stress inducer, thapsigargin (TG), selectively up-regulated TRAIL-R2 and enhanced TRAIL-induced apoptosis in melanoma cells.	Thapsigargin	83-85	TNF receptor superfamily member 10b	Homo sapiens	113-121
17684158-6	2007	To determine the underlying mechanism of the synergy between DMC and TRAIL, we have demonstrated that DMC induces a CCAAT/enhancer binding protein homologous protein-dependent expression of DR5, a major TRAIL receptor, and reduces the levels of cellular FLICE-inhibitory protein (c-FLIP) (both the long and short forms), key inhibitors of death receptor-mediated apoptosis, by facilitating c-FLIP degradation through a ubiquitin/proteasome-dependent mechanism.	2,5-dimethylcelecoxib	61-64	TNF receptor superfamily member 10b	Homo sapiens	190-193
17684158-6	2007	To determine the underlying mechanism of the synergy between DMC and TRAIL, we have demonstrated that DMC induces a CCAAT/enhancer binding protein homologous protein-dependent expression of DR5, a major TRAIL receptor, and reduces the levels of cellular FLICE-inhibitory protein (c-FLIP) (both the long and short forms), key inhibitors of death receptor-mediated apoptosis, by facilitating c-FLIP degradation through a ubiquitin/proteasome-dependent mechanism.	2,5-dimethylcelecoxib	102-105	TNF receptor superfamily member 10b	Homo sapiens	190-193
17684158-7	2007	It is noteworthy that enforced expression of c-FLIP or silencing of DR5 expression using DR5 small interfering RNA abrogated the enhanced effects on induction of apoptosis by the combination of DMC and TRAIL, indicating that both DR5 up-regulation and c-FLIP reduction contribute to cooperative induction of apoptosis by the combination of DMC and TRAIL.	2,5-dimethylcelecoxib	194-197	TNF receptor superfamily member 10b	Homo sapiens	68-71
17684158-7	2007	It is noteworthy that enforced expression of c-FLIP or silencing of DR5 expression using DR5 small interfering RNA abrogated the enhanced effects on induction of apoptosis by the combination of DMC and TRAIL, indicating that both DR5 up-regulation and c-FLIP reduction contribute to cooperative induction of apoptosis by the combination of DMC and TRAIL.	2,5-dimethylcelecoxib	194-197	TNF receptor superfamily member 10b	Homo sapiens	89-92
17684158-7	2007	It is noteworthy that enforced expression of c-FLIP or silencing of DR5 expression using DR5 small interfering RNA abrogated the enhanced effects on induction of apoptosis by the combination of DMC and TRAIL, indicating that both DR5 up-regulation and c-FLIP reduction contribute to cooperative induction of apoptosis by the combination of DMC and TRAIL.	2,5-dimethylcelecoxib	194-197	TNF receptor superfamily member 10b	Homo sapiens	89-92
17684158-7	2007	It is noteworthy that enforced expression of c-FLIP or silencing of DR5 expression using DR5 small interfering RNA abrogated the enhanced effects on induction of apoptosis by the combination of DMC and TRAIL, indicating that both DR5 up-regulation and c-FLIP reduction contribute to cooperative induction of apoptosis by the combination of DMC and TRAIL.	2,5-dimethylcelecoxib	340-343	TNF receptor superfamily member 10b	Homo sapiens	68-71
17684158-7	2007	It is noteworthy that enforced expression of c-FLIP or silencing of DR5 expression using DR5 small interfering RNA abrogated the enhanced effects on induction of apoptosis by the combination of DMC and TRAIL, indicating that both DR5 up-regulation and c-FLIP reduction contribute to cooperative induction of apoptosis by the combination of DMC and TRAIL.	2,5-dimethylcelecoxib	340-343	TNF receptor superfamily member 10b	Homo sapiens	89-92
17684158-7	2007	It is noteworthy that enforced expression of c-FLIP or silencing of DR5 expression using DR5 small interfering RNA abrogated the enhanced effects on induction of apoptosis by the combination of DMC and TRAIL, indicating that both DR5 up-regulation and c-FLIP reduction contribute to cooperative induction of apoptosis by the combination of DMC and TRAIL.	2,5-dimethylcelecoxib	340-343	TNF receptor superfamily member 10b	Homo sapiens	89-92
17684158-8	2007	Together, we conclude that DMC sensitizes human NSCLC cells to TRAIL-induced apoptosis via induction of DR5 and down-regulation of c-FLIP.	2,5-dimethylcelecoxib	27-30	TNF receptor superfamily member 10b	Homo sapiens	104-107
17671697-0	2007	Regulation of DR-5 protein and mitochondrial transmembrane potential by gemcitabine, a possible mechanism of gemcitabine-enhanced TRAIL-induced apoptosis.	gemcitabine	72-83	TNF receptor superfamily member 10b	Homo sapiens	14-18
17548900-0	2007	Induction of death receptor 5 and suppression of survivin contribute to sensitization of TRAIL-induced cytotoxicity by quercetin in non-small cell lung cancer cells.	Quercetin	119-128	TNF receptor superfamily member 10b	Homo sapiens	13-29
17548900-3	2007	Quercetin increased expression of death receptor (DR) 5, whereas it had no effect on that of other components of the death-inducing signaling complex.	Quercetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	34-55
17548900-7	2007	These results suggest the pathways for regulation of DR5 and survivin expression by quercetin are distinct.	Quercetin	84-93	TNF receptor superfamily member 10b	Homo sapiens	53-56
17548900-8	2007	Importantly, suppression of survivin-sensitized TRAIL-induced cell death and blockage of DR5 expression suppressed the synergistic cytotoxicity induced by quercetin and TRAIL co-treatment.	Quercetin	155-164	TNF receptor superfamily member 10b	Homo sapiens	89-92
17548900-9	2007	On the whole, our data show that quercetin sensitizes TRAIL-induced cytotoxicity in lung cancer cells through two independent pathways: induction of DR5 and suppression of survivin expression, which may underlie the mechanism of the lung cancer preventive activity of quercetin.	Quercetin	33-42	TNF receptor superfamily member 10b	Homo sapiens	149-152
17585340-0	2007	LY303511 amplifies TRAIL-induced apoptosis in tumor cells by enhancing DR5 oligomerization, DISC assembly, and mitochondrial permeabilization.	LY 303511	0-8	TNF receptor superfamily member 10b	Homo sapiens	71-74
17585340-7	2007	We link this execution signal to the ability of LY30 to downregulate cFLIP(S) and oligomerize DR5, thus facilitating the signaling of the death initiating signaling complex.	ly30	48-52	TNF receptor superfamily member 10b	Homo sapiens	94-97
17804742-0	2007	Silibinin sensitizes human glioma cells to TRAIL-mediated apoptosis via DR5 up-regulation and down-regulation of c-FLIP and survivin.	Silybin	0-9	TNF receptor superfamily member 10b	Homo sapiens	72-75
17804742-4	2007	Silibinin treatment up-regulated DR5, a death receptor of TRAIL, in a transcription factor CHOP-dependent manner.	Silybin	0-9	TNF receptor superfamily member 10b	Homo sapiens	33-36
17876056-5	2007	We report that quercetin enhanced TRAIL-induced apoptosis by causing the redistribution of DR4 and DR5 into lipid rafts.	Quercetin	15-24	TNF receptor superfamily member 10b	Homo sapiens	99-102
18253090-3	2007	In an effort to understand the mechanism by which CDDO-Me induces apoptosis, particularly in human lung cancer cells, we previously demonstrated that CDDO-Me induces apoptosis involving c-Jun N-terminal kinase (JNK)-dependent upregulation of death receptor 5 (DR5) expression.	bardoxolone methyl	50-57	TNF receptor superfamily member 10b	Homo sapiens	242-258
18253090-3	2007	In an effort to understand the mechanism by which CDDO-Me induces apoptosis, particularly in human lung cancer cells, we previously demonstrated that CDDO-Me induces apoptosis involving c-Jun N-terminal kinase (JNK)-dependent upregulation of death receptor 5 (DR5) expression.	bardoxolone methyl	50-57	TNF receptor superfamily member 10b	Homo sapiens	260-263
18253090-3	2007	In an effort to understand the mechanism by which CDDO-Me induces apoptosis, particularly in human lung cancer cells, we previously demonstrated that CDDO-Me induces apoptosis involving c-Jun N-terminal kinase (JNK)-dependent upregulation of death receptor 5 (DR5) expression.	bardoxolone methyl	150-157	TNF receptor superfamily member 10b	Homo sapiens	242-258
18253090-3	2007	In an effort to understand the mechanism by which CDDO-Me induces apoptosis, particularly in human lung cancer cells, we previously demonstrated that CDDO-Me induces apoptosis involving c-Jun N-terminal kinase (JNK)-dependent upregulation of death receptor 5 (DR5) expression.	bardoxolone methyl	150-157	TNF receptor superfamily member 10b	Homo sapiens	260-263
17786298-8	2007	We present, herein, one potential novel sensitizing agent, namely, nitric oxide (NO) that has been shown to sensitize TRAIL-resistant tumor cells to TRAIL apoptosis via its inhibitory effect on the transcription factors NF-kappaB and Yin Yang 1 (YY1), concomitantly with upregulation of DR5.	Nitric Oxide	67-79	TNF receptor superfamily member 10b	Homo sapiens	287-290
17875785-0	2007	Bortezomib sensitizes non-Hodgkin"s lymphoma cells to apoptosis induced by antibodies to tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors TRAIL-R1 and TRAIL-R2.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	176-184
17936227-9	2007	The DR5 cluster is characterized by a Glu in beta 9 and its polymorphism is connected with preferred anchors at beta 9 of the binding peptide, while the DQ3 cluster is characterized by Glu B86 and Leu B87, which allows the binding of large hydrophobic amino acids at p1 of the binding peptide.	Glutamic Acid	38-41	TNF receptor superfamily member 10b	Homo sapiens	4-7
17936227-9	2007	The DR5 cluster is characterized by a Glu in beta 9 and its polymorphism is connected with preferred anchors at beta 9 of the binding peptide, while the DQ3 cluster is characterized by Glu B86 and Leu B87, which allows the binding of large hydrophobic amino acids at p1 of the binding peptide.	Glutamic Acid	185-188	TNF receptor superfamily member 10b	Homo sapiens	4-7
17936227-9	2007	The DR5 cluster is characterized by a Glu in beta 9 and its polymorphism is connected with preferred anchors at beta 9 of the binding peptide, while the DQ3 cluster is characterized by Glu B86 and Leu B87, which allows the binding of large hydrophobic amino acids at p1 of the binding peptide.	Leucine	197-200	TNF receptor superfamily member 10b	Homo sapiens	4-7
17767167-4	2007	Biochemical analysis of DR5 identified several ectodomain O-(N-acetyl galactosamine-galactose-sialic acid) structures.	o-(n-acetyl galactosamine-galactose	58-93	TNF receptor superfamily member 10b	Homo sapiens	24-27
17767167-4	2007	Biochemical analysis of DR5 identified several ectodomain O-(N-acetyl galactosamine-galactose-sialic acid) structures.	N-Acetylneuraminic Acid	94-105	TNF receptor superfamily member 10b	Homo sapiens	24-27
17671697-0	2007	Regulation of DR-5 protein and mitochondrial transmembrane potential by gemcitabine, a possible mechanism of gemcitabine-enhanced TRAIL-induced apoptosis.	gemcitabine	109-120	TNF receptor superfamily member 10b	Homo sapiens	14-18
17671697-7	2007	In addition, the gemcitabine pretreatment up-regulated DR-5 and p53 protein expression in a time-dependent manner, which suggests the possible involvement of the p53 protein as a transcriptional factor for DR-5 up-regulation.	gemcitabine	17-28	TNF receptor superfamily member 10b	Homo sapiens	55-59
17671697-7	2007	In addition, the gemcitabine pretreatment up-regulated DR-5 and p53 protein expression in a time-dependent manner, which suggests the possible involvement of the p53 protein as a transcriptional factor for DR-5 up-regulation.	gemcitabine	17-28	TNF receptor superfamily member 10b	Homo sapiens	206-210
17671697-8	2007	Thus, we report our findings that gemcitabine enhanced the TRAIL-induced apoptosis and the apoptotic signals are mediated by DR-5-dependent pathway and mitochondrial pathway.	gemcitabine	34-45	TNF receptor superfamily member 10b	Homo sapiens	125-129
17671697-9	2007	Taken together, gemcitabine enhanced TRAIL-induced apoptosis via DR-5 up-regulation and lowering MTP, and suggest that gemcitabine may be used as a successful chemotherapeutic agent for ligand type tumor therapy combined with TRAIL.	gemcitabine	16-27	TNF receptor superfamily member 10b	Homo sapiens	65-69
17671697-9	2007	Taken together, gemcitabine enhanced TRAIL-induced apoptosis via DR-5 up-regulation and lowering MTP, and suggest that gemcitabine may be used as a successful chemotherapeutic agent for ligand type tumor therapy combined with TRAIL.	gemcitabine	119-130	TNF receptor superfamily member 10b	Homo sapiens	65-69
17699792-6	2007	EABE-induced apoptosis in HL-60 cells correlated with increased levels of reactive oxygen species, the death receptor 5 (DR5), and caspase activation and decreased levels of the mitochondrial membrane potential.	ethacrynic acid butyl ester	0-4	TNF receptor superfamily member 10b	Homo sapiens	103-119
17825219-7	2007	RESULTS: Human DR5 extracellular fragment gene was successfully amplified and high level expression was obtained in E.coli BL21 (DE3) induced by 0.1 mmol/L IPTG.	Isopropyl Thiogalactoside	156-160	TNF receptor superfamily member 10b	Homo sapiens	15-18
17825219-8	2007	The DR5 extracellular fragment protein was identified by SDS-PAGE and Western blot analysis.	Sodium Dodecyl Sulfate	57-60	TNF receptor superfamily member 10b	Homo sapiens	4-7
17699792-6	2007	EABE-induced apoptosis in HL-60 cells correlated with increased levels of reactive oxygen species, the death receptor 5 (DR5), and caspase activation and decreased levels of the mitochondrial membrane potential.	ethacrynic acid butyl ester	0-4	TNF receptor superfamily member 10b	Homo sapiens	121-124
17699792-7	2007	Pretreatment with antioxidants, either N-acetylcysteine or catalase, completely blocked EABE-induced apoptosis, H2O2 accumulation, and up-regulation of DR5 levels.	Acetylcysteine	39-55	TNF receptor superfamily member 10b	Homo sapiens	152-155
17699792-7	2007	Pretreatment with antioxidants, either N-acetylcysteine or catalase, completely blocked EABE-induced apoptosis, H2O2 accumulation, and up-regulation of DR5 levels.	ethacrynic acid butyl ester	88-92	TNF receptor superfamily member 10b	Homo sapiens	152-155
17520194-1	2007	Previous studies indicated that signalling via CD95 and DR5 is greatly enhanced by the formation of ceramide-enriched membrane platforms.	Ceramides	100-108	TNF receptor superfamily member 10b	Homo sapiens	56-59
17520194-4	2007	The latter served DR5 to cluster after application of very low doses of TRAIL in combination with doxorubicin.	Doxorubicin	98-109	TNF receptor superfamily member 10b	Homo sapiens	18-21
17520194-5	2007	Genetic deficiency of the ASM abrogated doxorubicin-induced ceramide release, as well as clustering of DR5 and apoptosis induced by the combined treatment of doxorubicin and TRAIL.	Doxorubicin	158-169	TNF receptor superfamily member 10b	Homo sapiens	103-106
17620439-6	2007	Enhanced surface expression of TRAIL-R2, but also TRAIL-R1, was associated with bortezomib treatment, which is likely to contribute to the increased processing of caspase-8 in the combination treatment.	Bortezomib	80-90	TNF receptor superfamily member 10b	Homo sapiens	31-39
17690453-0	2007	Tryptophol induces death receptor (DR) 5-mediated apoptosis in U937 cells.	tryptophol	0-10	TNF receptor superfamily member 10b	Homo sapiens	19-40
17690453-4	2007	In this study, we found that tryptophol enhances formation of a death-inducing signaling complex including death receptor (DR) 5.	tryptophol	29-39	TNF receptor superfamily member 10b	Homo sapiens	107-128
17690453-6	2007	These results indicate that tryptophol induces apoptosis through DR5 and that the resistance of PBL to tryptophol-induced apoptosis might be due to competition from DcR1.	tryptophol	28-38	TNF receptor superfamily member 10b	Homo sapiens	65-68
17470478-10	2007	Oleic acid treatment led to upregulation of the cognate TRAIL receptor death receptor 5 (DR5) but not death receptor 4 (DR4).	Oleic Acid	0-10	TNF receptor superfamily member 10b	Homo sapiens	71-87
17470478-10	2007	Oleic acid treatment led to upregulation of the cognate TRAIL receptor death receptor 5 (DR5) but not death receptor 4 (DR4).	Oleic Acid	0-10	TNF receptor superfamily member 10b	Homo sapiens	89-92
17470478-14	2007	CONCLUSION: Our results suggest that FFA induced hepatocyte steatosis sensitises to TRAIL by a DR5 mediated JNK dependent mechanism.	Fatty Acids, Nonesterified	37-40	TNF receptor superfamily member 10b	Homo sapiens	95-98
17604333-8	2007	Despite the activation of both caspase-8 and caspase-9, perifosine strikingly induced the expression of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor, death receptor 5, and down-regulated cellular FLICE-inhibitory protein (c-FLIP), an endogenous inhibitor of the extrinsic apoptotic pathway, with limited modulatory effects on the expression of other genes including Bcl-2, Bcl-X(L), PUMA, and survivin.	perifosine	56-66	TNF receptor superfamily member 10b	Homo sapiens	182-198
17604333-9	2007	Silencing of either caspase-8 or death receptor 5 attenuated perifosine-induced apoptosis.	perifosine	61-71	TNF receptor superfamily member 10b	Homo sapiens	33-49
17493934-0	2007	The farnesyltransferase inhibitor lonafarnib induces CCAAT/enhancer-binding protein homologous protein-dependent expression of death receptor 5, leading to induction of apoptosis in human cancer cells.	lonafarnib	34-44	TNF receptor superfamily member 10b	Homo sapiens	127-143
17493934-5	2007	In this study, we investigated the modulation of DR5 by the FTI lonafarnib and the involvement of DR5 up-regulation in FTI-induced apoptosis.	lonafarnib	64-74	TNF receptor superfamily member 10b	Homo sapiens	49-52
17493934-7	2007	Lonafarnib up-regulated DR5 expression, increased cell-surface DR5 distribution, and enhanced tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.	lonafarnib	0-10	TNF receptor superfamily member 10b	Homo sapiens	24-27
17493934-7	2007	Lonafarnib up-regulated DR5 expression, increased cell-surface DR5 distribution, and enhanced tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.	lonafarnib	0-10	TNF receptor superfamily member 10b	Homo sapiens	63-66
17493934-8	2007	Overexpression of a dominant-negative Fas-associated death domain mutant or silencing of DR5 expression using small interfering RNA attenuated lonafarnib-induced apoptosis.	lonafarnib	143-153	TNF receptor superfamily member 10b	Homo sapiens	89-92
17493934-9	2007	These results indicate a critical role of the DR5-mediated extrinsic apoptotic pathway in lonafarnib-induced apoptosis.	lonafarnib	90-100	TNF receptor superfamily member 10b	Homo sapiens	46-49
17493934-10	2007	By analyzing the DR5 promoter, we found that lonafarnib induced a CCAAT/enhancer-binding protein homologous protein (CHOP)-dependent transactivation of the DR5 promoter.	lonafarnib	45-55	TNF receptor superfamily member 10b	Homo sapiens	17-20
17493934-10	2007	By analyzing the DR5 promoter, we found that lonafarnib induced a CCAAT/enhancer-binding protein homologous protein (CHOP)-dependent transactivation of the DR5 promoter.	lonafarnib	45-55	TNF receptor superfamily member 10b	Homo sapiens	156-159
17493934-11	2007	Lonafarnib increased CHOP expression, whereas silencing of CHOP expression abrogated lonafarnib-induced DR5 expression.	lonafarnib	85-95	TNF receptor superfamily member 10b	Homo sapiens	104-107
17493934-12	2007	These results thus indicate that lonafarnib induces CHOP-dependent DR5 up-regulation.	lonafarnib	33-43	TNF receptor superfamily member 10b	Homo sapiens	67-70
17493934-13	2007	We conclude that CHOP-dependent DR5 up-regulation contributes to lonafarnib-induced apoptosis.	lonafarnib	65-75	TNF receptor superfamily member 10b	Homo sapiens	32-35
17510428-0	2007	The farnesyltransferase inhibitor R115777 up-regulates the expression of death receptor 5 and enhances TRAIL-induced apoptosis in human lung cancer cells.	tipifarnib	34-41	TNF receptor superfamily member 10b	Homo sapiens	73-89
17579120-11	2007	Halocynthiaxanthin markedly up-regulated a TRAIL receptor, death receptor 5 (DR5), among the death receptor-related genes, suggesting a possible mechanism for the combined effects.	halocynthiaxanthin	0-18	TNF receptor superfamily member 10b	Homo sapiens	59-75
17579120-11	2007	Halocynthiaxanthin markedly up-regulated a TRAIL receptor, death receptor 5 (DR5), among the death receptor-related genes, suggesting a possible mechanism for the combined effects.	halocynthiaxanthin	0-18	TNF receptor superfamily member 10b	Homo sapiens	77-80
17510429-0	2007	The proteasome inhibitor PS-341 (bortezomib) up-regulates DR5 expression leading to induction of apoptosis and enhancement of TRAIL-induced apoptosis despite up-regulation of c-FLIP and survivin expression in human NSCLC cells.	Bortezomib	25-31	TNF receptor superfamily member 10b	Homo sapiens	58-61
17510429-5	2007	Blockage of PS-341-induced DR5 up-regulation using DR5 small interfering RNA (siRNA) rendered cells less sensitive to apoptosis induced by either PS-341 or its combination with TRAIL, indicating that DR5 up-regulation mediates PS-341-induced apoptosis and enhancement of TRAIL-induced apoptosis in human NSCLC cells.	Bortezomib	12-18	TNF receptor superfamily member 10b	Homo sapiens	51-54
17510429-5	2007	Blockage of PS-341-induced DR5 up-regulation using DR5 small interfering RNA (siRNA) rendered cells less sensitive to apoptosis induced by either PS-341 or its combination with TRAIL, indicating that DR5 up-regulation mediates PS-341-induced apoptosis and enhancement of TRAIL-induced apoptosis in human NSCLC cells.	Bortezomib	146-152	TNF receptor superfamily member 10b	Homo sapiens	27-30
17510429-0	2007	The proteasome inhibitor PS-341 (bortezomib) up-regulates DR5 expression leading to induction of apoptosis and enhancement of TRAIL-induced apoptosis despite up-regulation of c-FLIP and survivin expression in human NSCLC cells.	Bortezomib	33-43	TNF receptor superfamily member 10b	Homo sapiens	58-61
17510429-5	2007	Blockage of PS-341-induced DR5 up-regulation using DR5 small interfering RNA (siRNA) rendered cells less sensitive to apoptosis induced by either PS-341 or its combination with TRAIL, indicating that DR5 up-regulation mediates PS-341-induced apoptosis and enhancement of TRAIL-induced apoptosis in human NSCLC cells.	Bortezomib	146-152	TNF receptor superfamily member 10b	Homo sapiens	27-30
17510429-3	2007	In the present study, we show that PS-341 induced caspase-8-dependent apoptosis, cooperated with TRAIL to induce apoptosis, and up-regulated death receptor 5 (DR5) expression in human non-small cell lung cancer (NSCLC) cells.	Bortezomib	35-41	TNF receptor superfamily member 10b	Homo sapiens	141-157
17510429-3	2007	In the present study, we show that PS-341 induced caspase-8-dependent apoptosis, cooperated with TRAIL to induce apoptosis, and up-regulated death receptor 5 (DR5) expression in human non-small cell lung cancer (NSCLC) cells.	Bortezomib	35-41	TNF receptor superfamily member 10b	Homo sapiens	159-162
17510429-4	2007	DR5 induction correlated with the ability of PS-341 to induce apoptosis.	Bortezomib	45-51	TNF receptor superfamily member 10b	Homo sapiens	0-3
17510429-5	2007	Blockage of PS-341-induced DR5 up-regulation using DR5 small interfering RNA (siRNA) rendered cells less sensitive to apoptosis induced by either PS-341 or its combination with TRAIL, indicating that DR5 up-regulation mediates PS-341-induced apoptosis and enhancement of TRAIL-induced apoptosis in human NSCLC cells.	Bortezomib	12-18	TNF receptor superfamily member 10b	Homo sapiens	27-30
17510429-5	2007	Blockage of PS-341-induced DR5 up-regulation using DR5 small interfering RNA (siRNA) rendered cells less sensitive to apoptosis induced by either PS-341 or its combination with TRAIL, indicating that DR5 up-regulation mediates PS-341-induced apoptosis and enhancement of TRAIL-induced apoptosis in human NSCLC cells.	Bortezomib	12-18	TNF receptor superfamily member 10b	Homo sapiens	51-54
17440103-8	2007	Finally, N-acetylcysteine, an inhibitor of ROS, inhibits sanguinarine-induced generation of ROS, up-regulation of DR5, Bax conformational changes, activation of caspase-3, and down-regulation of IAPs.	Acetylcysteine	9-25	TNF receptor superfamily member 10b	Homo sapiens	114-117
17440103-3	2007	Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid).	sanguinarine	19-31	TNF receptor superfamily member 10b	Homo sapiens	83-99
17440103-8	2007	Finally, N-acetylcysteine, an inhibitor of ROS, inhibits sanguinarine-induced generation of ROS, up-regulation of DR5, Bax conformational changes, activation of caspase-3, and down-regulation of IAPs.	sanguinarine	57-69	TNF receptor superfamily member 10b	Homo sapiens	114-117
17440103-3	2007	Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid).	sanguinarine	19-31	TNF receptor superfamily member 10b	Homo sapiens	101-104
17440103-3	2007	Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid).	Reactive Oxygen Species	135-158	TNF receptor superfamily member 10b	Homo sapiens	83-99
17440103-9	2007	Taken together, our findings suggest that sanguinarine is a potent inducer of apoptosis of PEL cells via up-regulation of DR5 and raise the possibility that this agent may be of value in the development of novel therapeutic approaches for the treatment of PEL.	sanguinarine	42-54	TNF receptor superfamily member 10b	Homo sapiens	122-125
17440103-3	2007	Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid).	Reactive Oxygen Species	135-158	TNF receptor superfamily member 10b	Homo sapiens	101-104
17440103-3	2007	Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid).	Reactive Oxygen Species	160-163	TNF receptor superfamily member 10b	Homo sapiens	83-99
17432717-9	2007	Expression of the death receptors DR5 and DR4 in two cell lines (A172 and U251) upregulated significantly when they were used in combination hTRAIL/TMZ treatment (p < 0.05 compared with baseline control), leading to activation of caspase-8 and caspase-3 (p < 0.05 compared with baseline control) and confirming an extrinsic apoptotic pathway.	Temozolomide	148-151	TNF receptor superfamily member 10b	Homo sapiens	34-37
17440103-3	2007	Our data show that sanguinarine treatment of PEL cells results in up-regulation of death receptor 5 (DR5) expression via generation of reactive oxygen species (ROS) and causes activation of caspase-8 and truncation of Bid (tBid).	Reactive Oxygen Species	160-163	TNF receptor superfamily member 10b	Homo sapiens	101-104
17409433-8	2007	Whereas treatment with R-flurbiprofen or ibuprofen resulted in a massive induction of p75(NTR) protein levels, the expression of Fas, p55(TNFR), DR3, DR4, DR5, and DR6 remained largely unchanged.	Ibuprofen	41-50	TNF receptor superfamily member 10b	Homo sapiens	155-158
17575157-0	2007	Tunicamycin sensitizes human melanoma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by up-regulation of TRAIL-R2 via the unfolded protein response.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	141-149
17575157-3	2007	We show in this study that the endoplasmic reticulum (ER) stress inducer, tunicamycin, selectively up-regulated the cell surface expression of TRAIL-R2, but not other members of the TNF receptor family, and enhanced TRAIL-induced apoptosis in cultured melanoma cells and fresh melanoma isolates.	Tunicamycin	74-85	TNF receptor superfamily member 10b	Homo sapiens	143-151
17575157-4	2007	Tunicamycin-mediated sensitization of melanoma cells to TRAIL-induced apoptosis was associated with increased activation of the caspase cascade and reduction in mitochondrial membrane potential and was inhibited by a recombinant TRAIL-R2/Fc chimeric protein.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	229-237
17575157-9	2007	Moreover, the transcription factor CCAAT/enhancer-binding protein homologous protein seemed to be involved in the up-regulation of TRAIL-R2 by tunicamycin, but its role varied between different melanoma lines.	Tunicamycin	143-154	TNF receptor superfamily member 10b	Homo sapiens	131-139
16936710-6	2007	In addition, the increased expression of DR5 receptor after beta amyloid treatment was sustained by p53 transcriptional activity, as demonstrated by the data showing that the p53 inhibitor Pifithrin alpha prevented both beta amyloid-induced DR5 induction and cell death.	pifithrin	189-204	TNF receptor superfamily member 10b	Homo sapiens	41-44
17326159-6	2007	RNA interference and TRAIL receptor blockage experiments revealed that in bortezomib-treated hepatoma cells TRAIL-R1/TRAIL-R2 up-regulation, enhanced TRAIL DISC formation and cFLIPL down-regulation in addition to accumulation of Bak cooperatively sensitized for TRAIL.	Bortezomib	74-84	TNF receptor superfamily member 10b	Homo sapiens	117-125
17363481-0	2007	High-resolution single-photon emission computed tomography and X-ray computed tomography imaging of Tc-99m-labeled anti-DR5 antibody in breast tumor xenografts.	Technetium	100-106	TNF receptor superfamily member 10b	Homo sapiens	120-123
17273769-4	2007	In this study, we report that fenretinide induces death receptor 5 (DR5)/TRAIL-R2 up-regulation via the induction of the transcription factor CHOP in colon cancer cell lines.	Fenretinide	30-41	TNF receptor superfamily member 10b	Homo sapiens	73-81
17273769-5	2007	Fenretinide induced DR5 expression at protein and mRNA levels.	Fenretinide	0-11	TNF receptor superfamily member 10b	Homo sapiens	20-23
17273769-6	2007	Furthermore, fenretinide increased DR5 promoter activity and the enhanced activity decreased by mutation of the CHOP binding site.	Fenretinide	13-24	TNF receptor superfamily member 10b	Homo sapiens	35-38
17273769-10	2007	Fenretinide and TRAIL cooperatively activated caspase-3, -8, -10 and -9 and cleavage of Bid and PARP, and this activation was also blocked in the presence of DR5/Fc chimeric protein.	Fenretinide	0-11	TNF receptor superfamily member 10b	Homo sapiens	158-161
17273769-0	2007	Fenretinide up-regulates DR5/TRAIL-R2 expression via the induction of the transcription factor CHOP and combined treatment with fenretinide and TRAIL induces synergistic apoptosis in colon cancer cell lines.	Fenretinide	0-11	TNF receptor superfamily member 10b	Homo sapiens	25-28
17273769-0	2007	Fenretinide up-regulates DR5/TRAIL-R2 expression via the induction of the transcription factor CHOP and combined treatment with fenretinide and TRAIL induces synergistic apoptosis in colon cancer cell lines.	Fenretinide	0-11	TNF receptor superfamily member 10b	Homo sapiens	29-37
17273769-4	2007	In this study, we report that fenretinide induces death receptor 5 (DR5)/TRAIL-R2 up-regulation via the induction of the transcription factor CHOP in colon cancer cell lines.	Fenretinide	30-41	TNF receptor superfamily member 10b	Homo sapiens	50-66
17273769-4	2007	In this study, we report that fenretinide induces death receptor 5 (DR5)/TRAIL-R2 up-regulation via the induction of the transcription factor CHOP in colon cancer cell lines.	Fenretinide	30-41	TNF receptor superfamily member 10b	Homo sapiens	68-71
17363481-1	2007	A murine, apoptosis-inducing monoclonal antibody (mTRA-8) targeting human DR5 was radiolabeled with Tc-99m.	mtra	50-54	TNF receptor superfamily member 10b	Homo sapiens	74-77
17363481-1	2007	A murine, apoptosis-inducing monoclonal antibody (mTRA-8) targeting human DR5 was radiolabeled with Tc-99m.	tc-99	100-105	TNF receptor superfamily member 10b	Homo sapiens	74-77
17363481-4	2007	Scatchard assays showed specific and high binding affinity of Tc-99m-mTRA-8 to DR5; the killing efficacy of mTRA-8 was unchanged by Tc-99m labeling.	tc-99m-mtra-8	62-75	TNF receptor superfamily member 10b	Homo sapiens	79-82
17363481-4	2007	Scatchard assays showed specific and high binding affinity of Tc-99m-mTRA-8 to DR5; the killing efficacy of mTRA-8 was unchanged by Tc-99m labeling.	mtra-8	69-75	TNF receptor superfamily member 10b	Homo sapiens	79-82
17363481-4	2007	Scatchard assays showed specific and high binding affinity of Tc-99m-mTRA-8 to DR5; the killing efficacy of mTRA-8 was unchanged by Tc-99m labeling.	tc-99	62-67	TNF receptor superfamily member 10b	Homo sapiens	79-82
17286903-0	2007	[Enhancement of glioma cell apoptosis induced by anti-human DR5/DR4 monoclonal antibodies by sub-toxic dose of doxorubicin in human].	Doxorubicin	111-122	TNF receptor superfamily member 10b	Homo sapiens	60-63
17105846-7	2007	Asoprisnil treatment significantly (P < 0.05) increased TRAIL, DR4, and DR5 contents in cultured leiomyoma cells in a dose-dependent manner with a cleavage of caspase-8, -7, and -3, and decreased X-linked chromosome-linked inhibitor of apoptosis protein contents.	asoprisnil	0-10	TNF receptor superfamily member 10b	Homo sapiens	75-78
17286903-7	2007	CONCLUSION: Subtoxic doxorubicin applied with antibodies caused higher cell death rate of glioma cells, which may be relevant to DR4/DR5, the release of cytochrome C and FLIP and Ca2+ concentration.	Doxorubicin	21-32	TNF receptor superfamily member 10b	Homo sapiens	133-136
17499001-8	2007	However, SAHA induces, in addition to p21(WAF1/CIP1) also re-expression of DR5.	Vorinostat	9-13	TNF receptor superfamily member 10b	Homo sapiens	75-78
17003375-7	2007	A Fas/CD95-deficient MM subline expressing DR4 and DR5 was resistant to edelfosine.	ammonium ferrous sulfate	2-5	TNF receptor superfamily member 10b	Homo sapiens	51-54
17849272-0	2007	The Effect of N-nitrosodimethylamine on TRAIL and DR5 expression in human neutrophils--preliminary study.	Dimethylnitrosamine	14-36	TNF receptor superfamily member 10b	Homo sapiens	50-53
17145888-6	2006	Treatment with As(2)O(3) plus BSO, but not with As(2)O(3) alone, increased the levels of death receptor (DR) 5 protein and caspase-8 cleavage.	Arsenic Trioxide	15-24	TNF receptor superfamily member 10b	Homo sapiens	89-110
17649723-6	2007	DR5 expression increased while P65 decreased as the doses of doxorubicin increased when KM3 cells treated with doxorubicin (0.5, 1.0, 2.0 and 4.0 microg/ml) plus 20 ng/ml TRAIL.	Doxorubicin	61-72	TNF receptor superfamily member 10b	Homo sapiens	0-3
17649723-6	2007	DR5 expression increased while P65 decreased as the doses of doxorubicin increased when KM3 cells treated with doxorubicin (0.5, 1.0, 2.0 and 4.0 microg/ml) plus 20 ng/ml TRAIL.	Doxorubicin	111-122	TNF receptor superfamily member 10b	Homo sapiens	0-3
17649723-7	2007	CONCLUSION: Increasing the expression of DR5 and nuclear transferring of P65 are the important molecular mechanism by which doxorubicin enhances TRAIL-inducing apoptosis of KM3 cells.	Doxorubicin	124-135	TNF receptor superfamily member 10b	Homo sapiens	41-44
17145853-3	2006	Our previous work has shown that celecoxib induces death receptor 5 expression, resulting in induction of apoptosis and enhancement of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human lung cancer cells.	Celecoxib	33-42	TNF receptor superfamily member 10b	Homo sapiens	51-67
17143496-0	2007	Phytosphingosine in combination with TRAIL sensitizes cancer cells to TRAIL through synergistic up-regulation of DR4 and DR5.	phytosphingosine	0-16	TNF receptor superfamily member 10b	Homo sapiens	121-124
17143496-9	2007	These results indicate that phytosphingosine sensitizes cancer cells to TRAIL through the synergistic up-regulation of DR4 and DR5 in an NF-kappaB-dependent fashion resulting in caspase-8 activation and subsequent mitochondrial dysfunction.	phytosphingosine	28-44	TNF receptor superfamily member 10b	Homo sapiens	127-130
17070520-6	2006	Arsenite treatment upregulated surface levels of death receptors, TRAIL-R1 and TRAIL-R2, through increased translocation of these proteins from cytoplasm to the cell surface.	arsenite	0-8	TNF receptor superfamily member 10b	Homo sapiens	79-87
17145853-7	2006	Collectively, we conclude that celecoxib induces apoptosis in human lung cancer cells through activation of the extrinsic apoptotic pathway, primarily by induction of death receptor 5 and down-regulation of c-FLIP.	Celecoxib	31-40	TNF receptor superfamily member 10b	Homo sapiens	167-183
17145888-7	2006	The JNK inhibitor SP600125 inhibited the increase in DR5 protein and attenuated apoptosis induced by treatment with As(2)O(3) plus BSO.	pyrazolanthrone	18-26	TNF receptor superfamily member 10b	Homo sapiens	53-56
17257501-3	2006	Cytotoxicity exerted by FasL/anti-DR5 mAb on tumor cell lines was measured by MTT assay and the induced apoptosis was determined by agarose gel electrophoresis.	monooxyethylene trimethylolpropane tristearate	78-81	TNF receptor superfamily member 10b	Homo sapiens	34-37
16859704-4	2006	Despite great differences in overall size and structure, the DR5-binding peptides and antibodies shared a tripeptide motif, which was conserved within a disulfide-constrained loop of the peptides and the third complementarity determining region of the antibody heavy chains.	tripeptide K-26	106-116	TNF receptor superfamily member 10b	Homo sapiens	61-64
16435155-4	2006	TSA induced the transcription of TRAIL death receptor DR5 without affecting the transcription of DR4 and the decoy receptors; DcR1 and DcR2.	trichostatin A	0-3	TNF receptor superfamily member 10b	Homo sapiens	54-57
16571651-0	2006	Sulforaphane enhances TRAIL-induced apoptosis through the induction of DR5 expression in human osteosarcoma cells.	sulforaphane	0-12	TNF receptor superfamily member 10b	Homo sapiens	71-74
17148761-4	2006	Paclitaxel significantly increased in vivo expression of TRAIL-R1 and TRAIL-R2 in a time-dependent manner.	Paclitaxel	0-10	TNF receptor superfamily member 10b	Homo sapiens	70-78
17148761-5	2006	The imaging results were confirmed by immunoblots for steady-state protein levels (>20-fold increase in TRAIL-R1 and TRAIL-R2 levels in tumor xenografts by 48 h after paclitaxel administration).	Paclitaxel	170-180	TNF receptor superfamily member 10b	Homo sapiens	120-128
16613838-0	2006	Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis through CHOP-independent DR5 upregulation.	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	128-131
16613838-2	2006	In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, is a potent enhancer of TRAIL-induced apoptosis through upregulation of DR5 expression.	Curcumin	30-38	TNF receptor superfamily member 10b	Homo sapiens	167-170
16613838-3	2006	Both treatment with DR5/Fc chimeric protein and silencing of DR5 expression using small interfering RNA (siRNA) attenuated curcumin plus TRAIL-induced apoptosis, showing that the critical role of DR5 in this cell death.	Curcumin	123-131	TNF receptor superfamily member 10b	Homo sapiens	20-23
16613838-3	2006	Both treatment with DR5/Fc chimeric protein and silencing of DR5 expression using small interfering RNA (siRNA) attenuated curcumin plus TRAIL-induced apoptosis, showing that the critical role of DR5 in this cell death.	Curcumin	123-131	TNF receptor superfamily member 10b	Homo sapiens	61-64
16613838-3	2006	Both treatment with DR5/Fc chimeric protein and silencing of DR5 expression using small interfering RNA (siRNA) attenuated curcumin plus TRAIL-induced apoptosis, showing that the critical role of DR5 in this cell death.	Curcumin	123-131	TNF receptor superfamily member 10b	Homo sapiens	61-64
16613838-6	2006	Taken together, the present study demonstrates that curcumin enhances TRAIL-induced apoptosis by CHOP-independent upregulation of DR5.	Curcumin	52-60	TNF receptor superfamily member 10b	Homo sapiens	130-133
16636669-3	2006	Ceramide-enriched membrane platforms serve to cluster DR5 upon stimulation.	Ceramides	0-8	TNF receptor superfamily member 10b	Homo sapiens	54-57
16636669-7	2006	Our data indicate that ceramide-enriched membrane platforms are required for the signaling of TRAIL-DR5 complexes under physiological conditions.	Ceramides	23-31	TNF receptor superfamily member 10b	Homo sapiens	100-103
16859704-4	2006	Despite great differences in overall size and structure, the DR5-binding peptides and antibodies shared a tripeptide motif, which was conserved within a disulfide-constrained loop of the peptides and the third complementarity determining region of the antibody heavy chains.	Disulfides	153-162	TNF receptor superfamily member 10b	Homo sapiens	61-64
16859704-5	2006	The X-ray crystal structure of an antibody in complex with DR5 revealed that the tripeptide motif is buried at the core of the interface, confirming its central role in antigen recognition.	tripeptide K-26	81-91	TNF receptor superfamily member 10b	Homo sapiens	59-62
16820931-8	2006	Flavopiridol up-regulated TRAIL, TRAIL-R1 and TRAIL-R2 in both cell lines.	alvocidib	0-12	TNF receptor superfamily member 10b	Homo sapiens	46-54
16550602-8	2006	Treatment with SAHA increased cell surface expression of DR5 but not DR4.	Vorinostat	15-19	TNF receptor superfamily member 10b	Homo sapiens	57-60
16891469-3	2006	Here, we report that 15d-PGJ(2) induces DR5 expression at both mRNA and protein levels, resulting in the synergistic sensitization of TRAIL-induced apoptosis in human neoplastic cells, such as Jurkat human leukemia cells or PC3 human prostate cancer cells.	15d-pgj	21-28	TNF receptor superfamily member 10b	Homo sapiens	40-43
16923369-8	2006	Expression of DR5 protein was not detected in SKNDZ cells but an increased DR5 protein expression was found after treatment with adriamycin or etoposide.	Doxorubicin	129-139	TNF receptor superfamily member 10b	Homo sapiens	14-17
16923369-8	2006	Expression of DR5 protein was not detected in SKNDZ cells but an increased DR5 protein expression was found after treatment with adriamycin or etoposide.	Doxorubicin	129-139	TNF receptor superfamily member 10b	Homo sapiens	75-78
16923369-8	2006	Expression of DR5 protein was not detected in SKNDZ cells but an increased DR5 protein expression was found after treatment with adriamycin or etoposide.	Etoposide	143-152	TNF receptor superfamily member 10b	Homo sapiens	14-17
16923369-8	2006	Expression of DR5 protein was not detected in SKNDZ cells but an increased DR5 protein expression was found after treatment with adriamycin or etoposide.	Etoposide	143-152	TNF receptor superfamily member 10b	Homo sapiens	75-78
16753135-5	2006	DR5 but not DR4 engagement by TRAIL attenuated cellular ATP levels by robustly stimulating P-gp ATPase activity, and thus triggered P-gp-dependent apoptosis by depletion of the cellular ATP pool.	Adenosine Triphosphate	56-59	TNF receptor superfamily member 10b	Homo sapiens	0-3
16753135-5	2006	DR5 but not DR4 engagement by TRAIL attenuated cellular ATP levels by robustly stimulating P-gp ATPase activity, and thus triggered P-gp-dependent apoptosis by depletion of the cellular ATP pool.	Adenosine Triphosphate	96-99	TNF receptor superfamily member 10b	Homo sapiens	0-3
16699947-9	2006	Sulindac sulfide caused apoptosis, and induced expression of DR-5 and NAG-1 in Hep3B cells.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	61-65
16699949-3	2006	Herein, we have demonstrated that the induction of apoptosis by the proteasome inhibitors, MG-132 and PS-341 (bortezomib, Velcade), in primary CLL cells and the Burkitt lymphoma cell line, BJAB, is associated with up-regulation of TRAIL and its death receptors, DR4 and DR5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-97	TNF receptor superfamily member 10b	Homo sapiens	270-273
16699949-3	2006	Herein, we have demonstrated that the induction of apoptosis by the proteasome inhibitors, MG-132 and PS-341 (bortezomib, Velcade), in primary CLL cells and the Burkitt lymphoma cell line, BJAB, is associated with up-regulation of TRAIL and its death receptors, DR4 and DR5.	Bortezomib	102-108	TNF receptor superfamily member 10b	Homo sapiens	270-273
16699949-3	2006	Herein, we have demonstrated that the induction of apoptosis by the proteasome inhibitors, MG-132 and PS-341 (bortezomib, Velcade), in primary CLL cells and the Burkitt lymphoma cell line, BJAB, is associated with up-regulation of TRAIL and its death receptors, DR4 and DR5.	Bortezomib	122-129	TNF receptor superfamily member 10b	Homo sapiens	270-273
16699949-5	2006	MG-132 treatment increases binding of DR5 to the adaptor protein FADD, and causes caspase-8 activation and cleavage of pro-apoptotic BID.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	TNF receptor superfamily member 10b	Homo sapiens	38-41
16699949-7	2006	MG-132 also increases apoptosis and DR5 expression in normal B-cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-6	TNF receptor superfamily member 10b	Homo sapiens	36-39
16891471-6	2006	However, these cells did undergo apoptosis in response to another form of recombinant TRAIL, histidine-tagged TRAIL, suggesting differing contributions of DR4 and DR5 in the response to these two forms of TRAIL.	Histidine	93-102	TNF receptor superfamily member 10b	Homo sapiens	163-166
16891469-7	2006	DR5/Fc chimera protein, zVAD-fmk pancaspase inhibitor, and caspase-8 inhibitor efficiently blocked the activation of these apoptotic signal mediators and the induction of apoptotic cell death enhanced by cotreatment with 15d-PGJ(2) and TRAIL.	15d-pgj	221-228	TNF receptor superfamily member 10b	Homo sapiens	0-3
16891469-8	2006	Moreover, a double-stranded small interfering RNA targeting DR5 gene, which suppressed DR5 up-regulation by 15d-PGJ(2), significantly attenuated apoptosis induced by cotreatment with 15d-PGJ(2) and TRAIL.	15d-pgj	108-115	TNF receptor superfamily member 10b	Homo sapiens	60-63
16891469-8	2006	Moreover, a double-stranded small interfering RNA targeting DR5 gene, which suppressed DR5 up-regulation by 15d-PGJ(2), significantly attenuated apoptosis induced by cotreatment with 15d-PGJ(2) and TRAIL.	15d-pgj	108-115	TNF receptor superfamily member 10b	Homo sapiens	87-90
16891469-8	2006	Moreover, a double-stranded small interfering RNA targeting DR5 gene, which suppressed DR5 up-regulation by 15d-PGJ(2), significantly attenuated apoptosis induced by cotreatment with 15d-PGJ(2) and TRAIL.	15d-pgj	183-190	TNF receptor superfamily member 10b	Homo sapiens	60-63
16891469-8	2006	Moreover, a double-stranded small interfering RNA targeting DR5 gene, which suppressed DR5 up-regulation by 15d-PGJ(2), significantly attenuated apoptosis induced by cotreatment with 15d-PGJ(2) and TRAIL.	15d-pgj	183-190	TNF receptor superfamily member 10b	Homo sapiens	87-90
16740726-5	2006	Sensitization to Apo2L/TRAIL mediated by cardiac glycosides was accompanied by up-regulation of death receptors 4 (DR4) and 5 (DR5) on both RNA and protein levels.	Glycosides	49-59	TNF receptor superfamily member 10b	Homo sapiens	127-130
17147249-0	2006	[Adriamycin enhances anti-human DR5 monoclonal antibody (mDRA-6) induced HL-60 cells apoptosis].	Doxorubicin	1-11	TNF receptor superfamily member 10b	Homo sapiens	32-35
16740726-7	2006	Blocking of up-regulation of DR4 and DR5 alone significantly reduced cell death after combined treatment with cardiac glycosides and Apo2L/TRAIL.	Glycosides	118-128	TNF receptor superfamily member 10b	Homo sapiens	37-40
16740726-8	2006	Combined silencing of DR4 and DR5 abrogated the ability of cardiac glycosides and Apo2L/TRAIL to induce apoptosis in an additive manner.	Glycosides	67-77	TNF receptor superfamily member 10b	Homo sapiens	30-33
16740726-9	2006	To our knowledge, this is the first demonstration that glycosides up-regulate DR4 and DR5, thereby reverting the resistance of lung cancer cells to Apo2/TRAIL-induced apoptosis.	Glycosides	55-65	TNF receptor superfamily member 10b	Homo sapiens	86-89
16452234-0	2006	Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5.	sulforaphane	0-12	TNF receptor superfamily member 10b	Homo sapiens	198-201
16582599-0	2006	Depletion of intracellular glutathione contributes to JNK-mediated death receptor 5 upregulation and apoptosis induction by the novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me).	Glutathione	27-38	TNF receptor superfamily member 10b	Homo sapiens	67-83
16582599-0	2006	Depletion of intracellular glutathione contributes to JNK-mediated death receptor 5 upregulation and apoptosis induction by the novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me).	triterpenoid TP-222	144-156	TNF receptor superfamily member 10b	Homo sapiens	67-83
16582599-0	2006	Depletion of intracellular glutathione contributes to JNK-mediated death receptor 5 upregulation and apoptosis induction by the novel synthetic triterpenoid methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate (CDDO-Me).	methyl-2-cyano-3, 12-dioxooleana-1, 9-dien-28-oate	157-207	TNF receptor superfamily member 10b	Homo sapiens	67-83
16582599-2	2006	We previously demonstrated that CDDO-Me induces a c-Jun N-terminal kinase (JNK)-mediated DR5 expression and apoptosis.	bardoxolone methyl	32-39	TNF receptor superfamily member 10b	Homo sapiens	89-92
16582599-3	2006	This study revealed the mechanism by which CDDO-Me induces JNK activation and subsequent DR5 upregulation and apoptosis.	bardoxolone methyl	43-50	TNF receptor superfamily member 10b	Homo sapiens	89-92
16582599-4	2006	To determine whether CDDO-Me activates JNK and induces DR5 expression and apoptosis via oxidative stress by inducing the generation of reactive oxygen species (ROS), we examined the effects of various antioxidants on JNK activation, DR5 upregulation, and apoptosis induction by CDDO-Me.	bardoxolone methyl	21-28	TNF receptor superfamily member 10b	Homo sapiens	55-58
16582599-11	2006	Furthermore, these thiol antioxidants abrogated CDDO-Me-induced DR5 expression, whereas the GSH-depleting agent diethylmaleate also upregulated DR5 expression at concentrations that deplete intracellular GSH, demonstrating that GSH depletion can cause DR5 upregulation.	Sulfhydryl Compounds	19-24	TNF receptor superfamily member 10b	Homo sapiens	64-67
16582599-11	2006	Furthermore, these thiol antioxidants abrogated CDDO-Me-induced DR5 expression, whereas the GSH-depleting agent diethylmaleate also upregulated DR5 expression at concentrations that deplete intracellular GSH, demonstrating that GSH depletion can cause DR5 upregulation.	bardoxolone methyl	48-55	TNF receptor superfamily member 10b	Homo sapiens	64-67
16582599-11	2006	Furthermore, these thiol antioxidants abrogated CDDO-Me-induced DR5 expression, whereas the GSH-depleting agent diethylmaleate also upregulated DR5 expression at concentrations that deplete intracellular GSH, demonstrating that GSH depletion can cause DR5 upregulation.	Glutathione	92-95	TNF receptor superfamily member 10b	Homo sapiens	144-147
16582599-11	2006	Furthermore, these thiol antioxidants abrogated CDDO-Me-induced DR5 expression, whereas the GSH-depleting agent diethylmaleate also upregulated DR5 expression at concentrations that deplete intracellular GSH, demonstrating that GSH depletion can cause DR5 upregulation.	Glutathione	92-95	TNF receptor superfamily member 10b	Homo sapiens	144-147
16582599-12	2006	Collectively, we conclude that CDDO-Me activates the JNK pathway via depletion of intracellular GSH, leading to DR5 upregulation and induction of apoptosis.	bardoxolone methyl	31-38	TNF receptor superfamily member 10b	Homo sapiens	112-115
16582599-12	2006	Collectively, we conclude that CDDO-Me activates the JNK pathway via depletion of intracellular GSH, leading to DR5 upregulation and induction of apoptosis.	Glutathione	96-99	TNF receptor superfamily member 10b	Homo sapiens	112-115
16529749-0	2006	Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis.	alpha-Tocopherol	0-26	TNF receptor superfamily member 10b	Homo sapiens	43-46
16529749-2	2006	We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.	alpha-Tocopherol	13-22	TNF receptor superfamily member 10b	Homo sapiens	51-54
16529749-4	2006	Treatment with sub-lethal doses of alpha-TOS restored expression of DR4 and DR5.	alpha-Tocopherol	35-44	TNF receptor superfamily member 10b	Homo sapiens	76-79
16332727-0	2006	3,3"-diindolylmethane (DIM) and its derivatives induce apoptosis in pancreatic cancer cells through endoplasmic reticulum stress-dependent upregulation of DR5.	3,3'-diindolylmethane	0-21	TNF receptor superfamily member 10b	Homo sapiens	155-158
16332727-5	2006	The subsequent downstream effects of DIM/DIM-C-pPhtBu- and Tg-induced ER stress included CHOP-dependent induction of death receptor DR5 and subsequent cleavage of caspase 8, caspase 3, Bid and PARP.	Thapsigargin	59-61	TNF receptor superfamily member 10b	Homo sapiens	132-135
16531263-4	2006	Additional in vitro studies revealed that the apoptosis of erythroblasts and the expression of FasL, TRAIL, TRAIL-R1 and TRAIL-R2 was lower in cultures with thalidomide than in control cultures.	Thalidomide	157-168	TNF receptor superfamily member 10b	Homo sapiens	121-129
16434995-4	2006	Arsenic trioxide led to increased cell surface expression of DR5 (death receptor 5), inhibition of the serine/threonine kinase Akt and downregulation of the short isoform of FLIP (FLICE-inhibitory protein, FLIPS).	Arsenic Trioxide	0-16	TNF receptor superfamily member 10b	Homo sapiens	61-64
16434995-4	2006	Arsenic trioxide led to increased cell surface expression of DR5 (death receptor 5), inhibition of the serine/threonine kinase Akt and downregulation of the short isoform of FLIP (FLICE-inhibitory protein, FLIPS).	Arsenic Trioxide	0-16	TNF receptor superfamily member 10b	Homo sapiens	66-82
16452234-4	2006	We found that sulforaphane treatment significantly up-regulated mRNA and protein levels of DR5, a death receptor of TRAIL.	sulforaphane	14-26	TNF receptor superfamily member 10b	Homo sapiens	91-94
16452234-6	2006	Pretreatment with N-acetyl-l-cysteine and overexpression of catalase inhibited sulforaphane-induced up-regulation of DR5 and almost completely blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-37	TNF receptor superfamily member 10b	Homo sapiens	117-120
16452234-6	2006	Pretreatment with N-acetyl-l-cysteine and overexpression of catalase inhibited sulforaphane-induced up-regulation of DR5 and almost completely blocked the cotreatment-induced apoptosis.	sulforaphane	79-91	TNF receptor superfamily member 10b	Homo sapiens	117-120
16452234-7	2006	Furthermore, the sulforaphane-mediated sensitization to TRAIL was efficiently reduced by administration of a blocking antibody or small interfering RNAs for DR5.	sulforaphane	17-29	TNF receptor superfamily member 10b	Homo sapiens	157-160
16452234-8	2006	These results collectively indicate that sulforaphane-induced generation of ROS and the subsequent up-regulation of DR5 are critical for triggering and amplifying TRAIL-induced apoptotic signaling.	sulforaphane	41-53	TNF receptor superfamily member 10b	Homo sapiens	116-119
16452234-0	2006	Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5.	Reactive Oxygen Species	148-171	TNF receptor superfamily member 10b	Homo sapiens	198-201
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Cholesterol	338-349	TNF receptor superfamily member 10b	Homo sapiens	205-208
16397266-6	2006	HDAC inhibition, especially with sodium butyrate and trichostatin A, led to increased TRAIL-R2 gene transcription that correlated with increased TRAIL-R2 surface expression.	Butyric Acid	33-48	TNF receptor superfamily member 10b	Homo sapiens	86-94
16397266-6	2006	HDAC inhibition, especially with sodium butyrate and trichostatin A, led to increased TRAIL-R2 gene transcription that correlated with increased TRAIL-R2 surface expression.	Butyric Acid	33-48	TNF receptor superfamily member 10b	Homo sapiens	145-153
16397266-6	2006	HDAC inhibition, especially with sodium butyrate and trichostatin A, led to increased TRAIL-R2 gene transcription that correlated with increased TRAIL-R2 surface expression.	trichostatin A	53-67	TNF receptor superfamily member 10b	Homo sapiens	86-94
16397266-6	2006	HDAC inhibition, especially with sodium butyrate and trichostatin A, led to increased TRAIL-R2 gene transcription that correlated with increased TRAIL-R2 surface expression.	trichostatin A	53-67	TNF receptor superfamily member 10b	Homo sapiens	145-153
16357153-0	2005	Cyclooxygenase-2 inhibition sensitizes human colon carcinoma cells to TRAIL-induced apoptosis through clustering of DR5 and concentrating death-inducing signaling complex components into ceramide-enriched caveolae.	Ceramides	187-195	TNF receptor superfamily member 10b	Homo sapiens	116-119
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Ceramides	359-367	TNF receptor superfamily member 10b	Homo sapiens	205-208
15987718-0	2005	Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5 (DR5).	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	159-175
15987718-0	2005	Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5 (DR5).	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	177-180
16227396-7	2005	Given that sulindac sulfide activated caspase-8 and increased membrane death receptor (DR4 and DR5) protein levels, we evaluated its combination with the endogenous death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	sulindac sulfide	11-27	TNF receptor superfamily member 10b	Homo sapiens	95-98
15987718-0	2005	Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5 (DR5).	Reactive Oxygen Species	110-133	TNF receptor superfamily member 10b	Homo sapiens	159-175
15987718-0	2005	Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5 (DR5).	Reactive Oxygen Species	110-133	TNF receptor superfamily member 10b	Homo sapiens	177-180
15987718-5	2005	We found that treatment with curcumin significantly induces death receptor 5 (DR5) expression both at its mRNA and protein levels, accompanying the generation of the reactive oxygen species (ROS).	Curcumin	29-37	TNF receptor superfamily member 10b	Homo sapiens	60-76
15987718-5	2005	We found that treatment with curcumin significantly induces death receptor 5 (DR5) expression both at its mRNA and protein levels, accompanying the generation of the reactive oxygen species (ROS).	Curcumin	29-37	TNF receptor superfamily member 10b	Homo sapiens	78-81
15987718-5	2005	We found that treatment with curcumin significantly induces death receptor 5 (DR5) expression both at its mRNA and protein levels, accompanying the generation of the reactive oxygen species (ROS).	Reactive Oxygen Species	166-189	TNF receptor superfamily member 10b	Homo sapiens	60-76
15987718-5	2005	We found that treatment with curcumin significantly induces death receptor 5 (DR5) expression both at its mRNA and protein levels, accompanying the generation of the reactive oxygen species (ROS).	Reactive Oxygen Species	166-189	TNF receptor superfamily member 10b	Homo sapiens	78-81
15987718-5	2005	We found that treatment with curcumin significantly induces death receptor 5 (DR5) expression both at its mRNA and protein levels, accompanying the generation of the reactive oxygen species (ROS).	Reactive Oxygen Species	191-194	TNF receptor superfamily member 10b	Homo sapiens	60-76
15987718-5	2005	We found that treatment with curcumin significantly induces death receptor 5 (DR5) expression both at its mRNA and protein levels, accompanying the generation of the reactive oxygen species (ROS).	Reactive Oxygen Species	191-194	TNF receptor superfamily member 10b	Homo sapiens	78-81
15987718-6	2005	Not only the pretreatment with N-acetylcystine but also the ectopic expression of peroxiredoxin II, an antioxidative protein, dramatically inhibited the apoptosis induced by curcumin and TRAIL in combination, blocking the curcumin-mediated DR5 upregulation.	N-monoacetylcystine	31-46	TNF receptor superfamily member 10b	Homo sapiens	240-243
15987718-6	2005	Not only the pretreatment with N-acetylcystine but also the ectopic expression of peroxiredoxin II, an antioxidative protein, dramatically inhibited the apoptosis induced by curcumin and TRAIL in combination, blocking the curcumin-mediated DR5 upregulation.	Curcumin	174-182	TNF receptor superfamily member 10b	Homo sapiens	240-243
15987718-7	2005	Taken together, the present study demonstrates that curcumin enhances TRAIL-induced apoptosis by ROS-mediated DR5 upregulation.	Curcumin	52-60	TNF receptor superfamily member 10b	Homo sapiens	110-113
15987718-7	2005	Taken together, the present study demonstrates that curcumin enhances TRAIL-induced apoptosis by ROS-mediated DR5 upregulation.	Reactive Oxygen Species	97-100	TNF receptor superfamily member 10b	Homo sapiens	110-113
16123594-4	2005	NFkappaB activation induces death receptor 5 (DR5) expression following DNA damaging agent etoposide treatment but not following growth factor EGF treatment.	Etoposide	91-100	TNF receptor superfamily member 10b	Homo sapiens	28-44
16123594-4	2005	NFkappaB activation induces death receptor 5 (DR5) expression following DNA damaging agent etoposide treatment but not following growth factor EGF treatment.	Etoposide	91-100	TNF receptor superfamily member 10b	Homo sapiens	46-49
16024638-4	2005	This effect was associated with the ability of CD437 to induce the expression of DR4 and DR5.	CD 437	47-52	TNF receptor superfamily member 10b	Homo sapiens	89-92
16098063-0	2005	Activity of selective fully human agonistic antibodies to the TRAIL death receptors TRAIL-R1 and TRAIL-R2 in primary and cultured lymphoma cells: induction of apoptosis and enhancement of doxorubicin- and bortezomib-induced cell death.	Doxorubicin	188-199	TNF receptor superfamily member 10b	Homo sapiens	97-105
16098063-0	2005	Activity of selective fully human agonistic antibodies to the TRAIL death receptors TRAIL-R1 and TRAIL-R2 in primary and cultured lymphoma cells: induction of apoptosis and enhancement of doxorubicin- and bortezomib-induced cell death.	Bortezomib	205-215	TNF receptor superfamily member 10b	Homo sapiens	97-105
16127151-5	2005	A specific role for p53 in TRAIL-R2-mediated apoptosis was indicated by the ability of p53 siRNA to significantly reduce RASF apoptosis and by the reduced apoptosis of RASFs bearing p53 mutations on treatment with anti-DR5 antibody or anti-DR5 antibody plus lactacystin.	lactacystin	258-269	TNF receptor superfamily member 10b	Homo sapiens	27-35
15963948-3	2005	Our previous studies have shown that luteolin, a naturally occurring flavonoid, induces the up-regulation of death receptor 5 (DR5), which is a receptor for TRAIL.	Flavonoids	69-78	TNF receptor superfamily member 10b	Homo sapiens	109-125
15963948-3	2005	Our previous studies have shown that luteolin, a naturally occurring flavonoid, induces the up-regulation of death receptor 5 (DR5), which is a receptor for TRAIL.	Flavonoids	69-78	TNF receptor superfamily member 10b	Homo sapiens	127-130
16024639-2	2005	In this study, we showed that tunicamycin, a naturally occurring antibiotic, is a potent enhancer of TRAIL-induced apoptosis through up-regulation of DR5 expression.	Tunicamycin	30-41	TNF receptor superfamily member 10b	Homo sapiens	150-153
16024639-4	2005	The tunicamycin-mediated enhancement of TRAIL-induced apoptosis was markedly blocked by a recombinant human DR5/Fc chimeric protein.	Tunicamycin	4-15	TNF receptor superfamily member 10b	Homo sapiens	108-111
16024639-5	2005	Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	150-153
16024639-6	2005	Tunicamycin up-regulated DR5 expression at the mRNA and protein levels in a dose-dependent manner.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	25-28
16024639-7	2005	Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression.	Tunicamycin	17-28	TNF receptor superfamily member 10b	Homo sapiens	88-91
16024639-7	2005	Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression.	Tunicamycin	17-28	TNF receptor superfamily member 10b	Homo sapiens	183-186
16024639-8	2005	Tunicamycin increased DR5 promoter activity and this enhanced activity was diminished by mutation of a CHOP-binding site.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	22-25
16024639-9	2005	In addition, suppression of CHOP expression by small interfering RNA reduced the tunicamycin-mediated induction of DR5.	Tunicamycin	81-92	TNF receptor superfamily member 10b	Homo sapiens	115-118
16024639-10	2005	Of note, tunicamycin-mediated induction of CHOP and DR5 protein expression was not observed in normal human peripheral blood mononuclear cells.	Tunicamycin	9-20	TNF receptor superfamily member 10b	Homo sapiens	52-55
15994939-0	2005	Proteasome inhibitor MG132 induces death receptor 5 through CCAAT/enhancer-binding protein homologous protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF receptor superfamily member 10b	Homo sapiens	35-51
15994939-11	2005	Furthermore, CHOP small interfering RNA attenuated the DR5 up-regulation due to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	TNF receptor superfamily member 10b	Homo sapiens	55-58
15994939-3	2005	In this study, we report that CCAAT/enhancer-binding protein homologous protein (CHOP) is a regulator of DR5 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	TNF receptor superfamily member 10b	Homo sapiens	105-108
15994939-12	2005	These results indicate that the proteasome inhibitor MG132 induces DR5 expression through CHOP up-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	TNF receptor superfamily member 10b	Homo sapiens	67-70
15994939-4	2005	MG132 induced DR5 expression at a protein and mRNA level in prostate cancer DU145 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10b	Homo sapiens	14-17
15994939-5	2005	Furthermore, MG132 increased DR5 promoter activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	13-18	TNF receptor superfamily member 10b	Homo sapiens	29-32
16082182-5	2005	Subsequent studies showed that combined treatment with bortezomib or MG132 resulted in an increase of death receptor (DR) 5 and Bik at protein levels but had no effects on protein levels of DR4, Bax, Bak, Bcl-2, Bcl-XL or Flice-inhibitory protein (FLIP).	Bortezomib	55-65	TNF receptor superfamily member 10b	Homo sapiens	102-123
15994939-6	2005	Using a series of deletion mutant plasmids containing DR5 promoters of various sizes, we found that MG132 stimulated the promoter activity via the region of -289 to -253.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	100-105	TNF receptor superfamily member 10b	Homo sapiens	54-57
16082182-5	2005	Subsequent studies showed that combined treatment with bortezomib or MG132 resulted in an increase of death receptor (DR) 5 and Bik at protein levels but had no effects on protein levels of DR4, Bax, Bak, Bcl-2, Bcl-XL or Flice-inhibitory protein (FLIP).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	TNF receptor superfamily member 10b	Homo sapiens	102-123
15994939-9	2005	An electrophoretic mobility shift assay showed that CHOP directly bound to the MG132-responsive site on the DR5 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	TNF receptor superfamily member 10b	Homo sapiens	108-111
16082182-7	2005	Blocking JNK activation with the JNK inhibitor SP600125 attenuated DR5 increase, but enhancement of apoptosis induction and increase of Bik protein were not affected.	pyrazolanthrone	47-55	TNF receptor superfamily member 10b	Homo sapiens	67-70
15930300-7	2005	From a mechanistic standpoint, we show that CDDO and CDDO-Im down-regulate the antiapoptotic protein c-FLIP(L), and up-regulate cell surface TRAIL receptors DR4 and DR5.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	44-48	TNF receptor superfamily member 10b	Homo sapiens	165-168
15942663-4	2005	LY294002 increased Hep3B cell susceptibility to chemotherapy-induced apoptosis by enhancing the expression of DR4 and DR5 and the activation of caspase-8 and -3.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	TNF receptor superfamily member 10b	Homo sapiens	118-121
15964798-4	2005	Herein, we determined that etoposide-induced DR5 expression requires the first intronic region of the DR5 gene.	Etoposide	27-36	TNF receptor superfamily member 10b	Homo sapiens	45-48
15964798-4	2005	Herein, we determined that etoposide-induced DR5 expression requires the first intronic region of the DR5 gene.	Etoposide	27-36	TNF receptor superfamily member 10b	Homo sapiens	102-105
16026644-2	2005	Low doses of SAHA or TSA enhanced the cytotoxic and apoptotic effects of TRAIL and upregulated the surface expression of TRAIL death receptors (DR4 and/or DR5).	trichostatin A	21-24	TNF receptor superfamily member 10b	Homo sapiens	155-158
15850806-11	2005	Deletion and mutation of the DR5, but not the IR6 element, abolished the atRA-mediated activity.	Tretinoin	73-77	TNF receptor superfamily member 10b	Homo sapiens	29-32
15850806-13	2005	In addition to the functional DR5, the region contains many other potential sequence elements that are required to maximize the atRA-mediated induction.	Tretinoin	128-132	TNF receptor superfamily member 10b	Homo sapiens	30-33
15930300-7	2005	From a mechanistic standpoint, we show that CDDO and CDDO-Im down-regulate the antiapoptotic protein c-FLIP(L), and up-regulate cell surface TRAIL receptors DR4 and DR5.	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole	53-60	TNF receptor superfamily member 10b	Homo sapiens	165-168
15956246-7	2005	Many gene expression changes observed following in vitro SN-38 exposure were also seen following in vivo administration of 10 or 15 mg/m(2) CPT-11; notably, proapoptotic changes included reduced transcription of survivin pathway-associated genes and increased transcription of death receptor 5.	Irinotecan	57-62	TNF receptor superfamily member 10b	Homo sapiens	277-293
15956246-7	2005	Many gene expression changes observed following in vitro SN-38 exposure were also seen following in vivo administration of 10 or 15 mg/m(2) CPT-11; notably, proapoptotic changes included reduced transcription of survivin pathway-associated genes and increased transcription of death receptor 5.	Irinotecan	140-146	TNF receptor superfamily member 10b	Homo sapiens	277-293
15767547-8	2005	The mRNAs of death receptors 4 and 5 (DR4 and DR5) were induced in leukemia cells undergoing apoptosis after boswellic acid acetate treatment.	boswellic acid acetate	109-131	TNF receptor superfamily member 10b	Homo sapiens	46-49
15339846-4	2005	In addition, CD40 ligation in vitro and in vivo induces CLL cells to express the proapoptotic protein, BH3 interacting domain death agonist (Bid), which can facilitate crosstalk between mitochondrial-dependent, apoptosis-inducing pathways and death receptors, such as death receptor 5 (DR5).	BH 3	103-106	TNF receptor superfamily member 10b	Homo sapiens	268-284
15339846-4	2005	In addition, CD40 ligation in vitro and in vivo induces CLL cells to express the proapoptotic protein, BH3 interacting domain death agonist (Bid), which can facilitate crosstalk between mitochondrial-dependent, apoptosis-inducing pathways and death receptors, such as death receptor 5 (DR5).	BH 3	103-106	TNF receptor superfamily member 10b	Homo sapiens	286-289
15806306-0	2005	IFN-gamma/JAK/STAT pathway-induced inhibition of DR4 and DR5 expression on endothelial cells is cancelled by cycloheximide-sensitive mechanism: novel finding of cycloheximide-regulating death receptor expression.	Cycloheximide	109-122	TNF receptor superfamily member 10b	Homo sapiens	57-60
15806306-6	2005	IFN-gamma/JAK/STAT-induced suppression was regulated by cycloheximide (CHX)-sensitive mechanism since the use of CHX mimicked the action of chemical inhibition of JAK in regard to DR4/DR5 expression as well as TRAIL-mediated endothelial cell apoptosis.	Cycloheximide	56-69	TNF receptor superfamily member 10b	Homo sapiens	184-187
15806306-6	2005	IFN-gamma/JAK/STAT-induced suppression was regulated by cycloheximide (CHX)-sensitive mechanism since the use of CHX mimicked the action of chemical inhibition of JAK in regard to DR4/DR5 expression as well as TRAIL-mediated endothelial cell apoptosis.	Cycloheximide	71-74	TNF receptor superfamily member 10b	Homo sapiens	184-187
15949263-5	2005	The expression of DR5 on MM and KM3 cells was up-regulated after chemotherapy and exposure to doxorubicin (P < 0.	Doxorubicin	94-105	TNF receptor superfamily member 10b	Homo sapiens	18-21
15949263-8	2005	Up-regulated DR5 on KM3 cells after incubating with doxorubicin and after chemotherapy suggests the cytotoxic agents might enhance the apoptosis of MM cells.	Doxorubicin	52-63	TNF receptor superfamily member 10b	Homo sapiens	13-16
15767547-9	2005	These data taken together suggest that boswellic acid acetate induces myeloid leukemia cell apoptosis through activation of caspase-8 by induced expression of DR4 and DR5, and that the activated caspase-8 either directly activates caspase-3 by cleavage or indirectly by cleaving Bid, which in turn decreases mitochondria membrane potential.	boswellic acid acetate	39-61	TNF receptor superfamily member 10b	Homo sapiens	167-170
15735044-6	2005	Fenretinide treatment also increased levels of the death receptor DR5 and caused mitochondrial membrane depolarization.	Fenretinide	0-11	TNF receptor superfamily member 10b	Homo sapiens	66-69
15802865-5	2005	The post-irradiation treatment of the cells with N-acetyl-L-cysteine (NAC) abolished the up-regulation of the expression of Fas and DR5 on the plasma membrane.	Acetylcysteine	49-68	TNF receptor superfamily member 10b	Homo sapiens	132-135
15735044-9	2005	We conclude that fenretinide induces apoptosis in all three histologic subtypes of meningioma and exerts diverse cellular effects, including DR5 up-regulation, modulation of retinoid receptor levels, and inhibition of IGF-I-induced proliferation.	Fenretinide	17-28	TNF receptor superfamily member 10b	Homo sapiens	141-144
15572759-10	2004	Celecoxib treatment induced the expression of death receptors, particularly that of DR5.	Celecoxib	0-9	TNF receptor superfamily member 10b	Homo sapiens	84-87
15748438-3	2005	The results showed that (1) TRAIL, DR4 and DR5 were highly expressed in both patient group and CR group, while the DcR1 and DcR2 were poorly expressed.	Chromium	95-97	TNF receptor superfamily member 10b	Homo sapiens	43-46
15748438-4	2005	(2) The level of DR5 expression in CR group was higher than that in patient group.	Chromium	35-37	TNF receptor superfamily member 10b	Homo sapiens	17-20
15748438-5	2005	(3) The level of DR5 was higher than DR4 in both patient group and CR group.	Chromium	67-69	TNF receptor superfamily member 10b	Homo sapiens	17-20
15897917-4	2005	TRAIL receptor-1 (DR4) and TRAIL receptor-2 (DR5) were upregulated under the treatment of doxorubicin and verified to be responsible for TRAIL-mediated signal transduction.	Doxorubicin	90-101	TNF receptor superfamily member 10b	Homo sapiens	45-48
15719269-4	2005	Our data show that gliomas preferentially express TRAIL R2 and that treatment with topotecan, a topoisomerase I inhibitor, significantly up-regulates its expression as detected by flow cytometry and western blotting.	Topotecan	83-92	TNF receptor superfamily member 10b	Homo sapiens	50-58
15572759-11	2004	Overexpression of a dominant negative Fas-associated death domain mutant, but not of BCL2, reduced the level of celecoxib-induced apoptosis, and silencing of DR5 expression by DR5 siRNA suppressed celecoxib-induced caspase 8 activation and apoptosis.	Celecoxib	197-206	TNF receptor superfamily member 10b	Homo sapiens	158-161
15572759-11	2004	Overexpression of a dominant negative Fas-associated death domain mutant, but not of BCL2, reduced the level of celecoxib-induced apoptosis, and silencing of DR5 expression by DR5 siRNA suppressed celecoxib-induced caspase 8 activation and apoptosis.	Celecoxib	197-206	TNF receptor superfamily member 10b	Homo sapiens	176-179
15322075-2	2004	We and others have reported previously that DR5 expression is up-regulated in thapsigargin (THG)-treated human cancer cells.	Thapsigargin	78-90	TNF receptor superfamily member 10b	Homo sapiens	44-47
15480430-0	2004	Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells.	Resveratrol	86-97	TNF receptor superfamily member 10b	Homo sapiens	32-35
15322075-2	2004	We and others have reported previously that DR5 expression is up-regulated in thapsigargin (THG)-treated human cancer cells.	Thapsigargin	92-95	TNF receptor superfamily member 10b	Homo sapiens	44-47
15322075-6	2004	In addition to HCT116 cells, inhibition of CHOP or DR5 induction also attenuated THG-induced cell death in other cancer cell lines including LNCaP, A2780S, and DU145, indicating that CHOP and DR5 are critical for ER stress-mediated apoptosis in human carcinoma cells.	Thapsigargin	81-84	TNF receptor superfamily member 10b	Homo sapiens	192-195
15322075-3	2004	Here, we provide evidence that CHOP is involved in THG up-regulation of DR5, which is a critical step for ER stress-induced apoptosis in human cancer cells.	Thapsigargin	51-54	TNF receptor superfamily member 10b	Homo sapiens	72-75
15322075-4	2004	In human colon cancer HCT116 cells, knockdown of DR5 by siRNA blocked THG-induced Bax conformational change along with caspase-3 activation and cell death.	Thapsigargin	70-73	TNF receptor superfamily member 10b	Homo sapiens	49-52
15322075-5	2004	Moreover, inhibition of CHOP expression attenuated DR5 up-regulation and apoptosis induced by THG, whereas ectopic expression of DR5 restored the sensitivity of CHOP siRNA-transfected cells to THG-induced apoptosis.	Thapsigargin	193-196	TNF receptor superfamily member 10b	Homo sapiens	129-132
15322075-6	2004	In addition to HCT116 cells, inhibition of CHOP or DR5 induction also attenuated THG-induced cell death in other cancer cell lines including LNCaP, A2780S, and DU145, indicating that CHOP and DR5 are critical for ER stress-mediated apoptosis in human carcinoma cells.	Thapsigargin	81-84	TNF receptor superfamily member 10b	Homo sapiens	51-54
15334061-7	2004	Knockdown of FLIP expression in MM cell lines, by a FLIPsiRNA, re-established the normal response to apoptosis induced by Fas or DR4/DR5, which was blocked by pretreatment with the caspase-8 inhibitor z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	201-211	TNF receptor superfamily member 10b	Homo sapiens	133-136
15492278-6	2004	In addition, some of the changes observed in SWB77 were opposite to those seen in methionine-dependent tumors, including expression of p21, TRAIL-R2, and TIEG.	Methionine	82-92	TNF receptor superfamily member 10b	Homo sapiens	140-148
15180942-7	2004	Moreover, temporal expressions of DR-4 and DR-5 induced by sulindac sulfide were similar to that of NAG-1.	sulindac sulfide	59-75	TNF receptor superfamily member 10b	Homo sapiens	43-47
15142888-0	2004	Sodium butyrate sensitizes TRAIL-mediated apoptosis by induction of transcription from the DR5 gene promoter through Sp1 sites in colon cancer cells.	Butyric Acid	0-15	TNF receptor superfamily member 10b	Homo sapiens	91-94
15492284-0	2004	c-Jun NH2-terminal kinase-mediated up-regulation of death receptor 5 contributes to induction of apoptosis by the novel synthetic triterpenoid methyl-2-cyano-3,12-dioxooleana-1, 9-dien-28-oate in human lung cancer cells.	triterpenoid TP-222	130-142	TNF receptor superfamily member 10b	Homo sapiens	52-68
15492284-0	2004	c-Jun NH2-terminal kinase-mediated up-regulation of death receptor 5 contributes to induction of apoptosis by the novel synthetic triterpenoid methyl-2-cyano-3,12-dioxooleana-1, 9-dien-28-oate in human lung cancer cells.	methyl-2-cyano-3,12-dioxooleana-1, 9-dien-28-oate	143-192	TNF receptor superfamily member 10b	Homo sapiens	52-68
15492284-4	2004	We found that CDDO-Me not only activated caspase-8 but also induced expression of DRs, particularly DR5, in a p53-independent mechanism.	bardoxolone methyl	14-21	TNF receptor superfamily member 10b	Homo sapiens	100-103
15492284-6	2004	Moreover, silencing of DR5 expression using small interfering RNA suppressed apoptosis induced by CDDO-Me alone or by combination of CDDO-Me and TRAIL, indicating that DR5 up-regulation is required for induction of apoptosis by CDDO-Me and for enhancement of TRAIL-induced apoptosis by CDDO-Me.	bardoxolone methyl	98-105	TNF receptor superfamily member 10b	Homo sapiens	23-26
15492284-6	2004	Moreover, silencing of DR5 expression using small interfering RNA suppressed apoptosis induced by CDDO-Me alone or by combination of CDDO-Me and TRAIL, indicating that DR5 up-regulation is required for induction of apoptosis by CDDO-Me and for enhancement of TRAIL-induced apoptosis by CDDO-Me.	bardoxolone methyl	133-140	TNF receptor superfamily member 10b	Homo sapiens	23-26
15492284-6	2004	Moreover, silencing of DR5 expression using small interfering RNA suppressed apoptosis induced by CDDO-Me alone or by combination of CDDO-Me and TRAIL, indicating that DR5 up-regulation is required for induction of apoptosis by CDDO-Me and for enhancement of TRAIL-induced apoptosis by CDDO-Me.	bardoxolone methyl	133-140	TNF receptor superfamily member 10b	Homo sapiens	23-26
15492284-6	2004	Moreover, silencing of DR5 expression using small interfering RNA suppressed apoptosis induced by CDDO-Me alone or by combination of CDDO-Me and TRAIL, indicating that DR5 up-regulation is required for induction of apoptosis by CDDO-Me and for enhancement of TRAIL-induced apoptosis by CDDO-Me.	bardoxolone methyl	133-140	TNF receptor superfamily member 10b	Homo sapiens	23-26
15142888-3	2004	In this study, we demonstrate for the first time that sodium butyrate selectively up-regulated DR5 but had no effect on the expression of the other TNF-alpha-related apoptosis-inducing ligand (TRAIL) receptor, DR4.	Butyric Acid	54-69	TNF receptor superfamily member 10b	Homo sapiens	95-98
15142888-4	2004	Sodium butyrate-induced expression of DR5 involves the putative Sp1 site within the DR5 promoter region.	Butyric Acid	0-15	TNF receptor superfamily member 10b	Homo sapiens	38-41
15374982-0	2004	Inducible silencing of KILLER/DR5 in vivo promotes bioluminescent colon tumor xenograft growth and confers resistance to chemotherapeutic agent 5-fluorouracil.	Fluorouracil	144-158	TNF receptor superfamily member 10b	Homo sapiens	23-33
15142888-4	2004	Sodium butyrate-induced expression of DR5 involves the putative Sp1 site within the DR5 promoter region.	Butyric Acid	0-15	TNF receptor superfamily member 10b	Homo sapiens	84-87
15142888-5	2004	Using a combination of the electrophoretic mobility shift assay and the luciferase reporter assay, we found that a specific Sp1 site (located at -195 bp relative to the transcription start site) is required for sodium butyrate-mediated activation of the DR5 promoter.	Butyric Acid	211-226	TNF receptor superfamily member 10b	Homo sapiens	254-257
15208660-3	2004	Here, we report that histone deacetylase inhibitors (HDACIs) such as trichostatin A (TSA), sodium butyrate, and suberoylanilide hydroxamic acid (SAHA) upregulated DR5 expression in various human malignant tumor cells.	trichostatin A	69-83	TNF receptor superfamily member 10b	Homo sapiens	163-166
15155747-11	2004	Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5.	Tunicamycin	67-78	TNF receptor superfamily member 10b	Homo sapiens	144-154
15208660-3	2004	Here, we report that histone deacetylase inhibitors (HDACIs) such as trichostatin A (TSA), sodium butyrate, and suberoylanilide hydroxamic acid (SAHA) upregulated DR5 expression in various human malignant tumor cells.	trichostatin A	85-88	TNF receptor superfamily member 10b	Homo sapiens	163-166
15208660-3	2004	Here, we report that histone deacetylase inhibitors (HDACIs) such as trichostatin A (TSA), sodium butyrate, and suberoylanilide hydroxamic acid (SAHA) upregulated DR5 expression in various human malignant tumor cells.	Butyric Acid	91-106	TNF receptor superfamily member 10b	Homo sapiens	163-166
15208660-3	2004	Here, we report that histone deacetylase inhibitors (HDACIs) such as trichostatin A (TSA), sodium butyrate, and suberoylanilide hydroxamic acid (SAHA) upregulated DR5 expression in various human malignant tumor cells.	Vorinostat	112-143	TNF receptor superfamily member 10b	Homo sapiens	163-166
15208660-3	2004	Here, we report that histone deacetylase inhibitors (HDACIs) such as trichostatin A (TSA), sodium butyrate, and suberoylanilide hydroxamic acid (SAHA) upregulated DR5 expression in various human malignant tumor cells.	Vorinostat	145-149	TNF receptor superfamily member 10b	Homo sapiens	163-166
15201983-4	2004	We showed that the expression of death receptor DR5, but not DR4 was up-regulated and the decoy receptor DcR1 was down-regulated in the cells treated with 8-Cl-Ado and the recombinant soluble TRAIL (rsTRAIL, 95-281 a.a.).	8-chloroadenosine	155-163	TNF receptor superfamily member 10b	Homo sapiens	48-51
15201983-8	2004	Our results provided evidence for the first time that 8-Cl-Ado sensitizes the human hepatoma cells BEL-7402 to rsTRAIL-induced apoptosis by up-regulating DR5 expression, inactivating the NF-kappaB activity, and signaling by the caspase-dependent and -independent pathway.	8-chloroadenosine	54-62	TNF receptor superfamily member 10b	Homo sapiens	154-157
14739940-6	2004	Preincubation with E-17-beta completely prevented both TRAIL-induced DR4 and DR5 upregulation and apoptosis.	e-17-beta	19-28	TNF receptor superfamily member 10b	Homo sapiens	77-80
15077162-6	2004	This cytotoxicity was partially inhibited by addition of TRAILR2/Fc fusion protein, indicating that the secreted TRAIL mediates, at least in part, the apoptotic effect displayed by the supernatants of stimulated SK-N-MC cells.	sk-n-mc	212-219	TNF receptor superfamily member 10b	Homo sapiens	57-64
14691451-0	2004	Proteasome inhibitor MG132 upregulates death receptor 5 and cooperates with Apo2L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF receptor superfamily member 10b	Homo sapiens	39-55
14561739-0	2004	Bile acids up-regulate death receptor 5/TRAIL-receptor 2 expression via a c-Jun N-terminal kinase-dependent pathway involving Sp1.	Bile Acids and Salts	0-10	TNF receptor superfamily member 10b	Homo sapiens	23-39
14691451-5	2004	Here, we report that proteasome inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -deficient HCT116 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	TNF receptor superfamily member 10b	Homo sapiens	72-88
14691451-8	2004	These results suggest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 by upregulating DR5 effectively cooperates with Apo2L/TRAIL to overcome Bax deficiency-induced resistance to Apo2L/TRAIL.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	111-116	TNF receptor superfamily member 10b	Homo sapiens	133-136
14561739-1	2004	Bile acids up-regulate death receptor 5 (DR5)/TRAIL-receptor 2 (TRAIL-R2) expression thereby sensitizing hepatocytes to TRAIL-mediated apoptosis.	Bile Acids and Salts	0-10	TNF receptor superfamily member 10b	Homo sapiens	23-39
14561739-1	2004	Bile acids up-regulate death receptor 5 (DR5)/TRAIL-receptor 2 (TRAIL-R2) expression thereby sensitizing hepatocytes to TRAIL-mediated apoptosis.	Bile Acids and Salts	0-10	TNF receptor superfamily member 10b	Homo sapiens	41-44
14561739-1	2004	Bile acids up-regulate death receptor 5 (DR5)/TRAIL-receptor 2 (TRAIL-R2) expression thereby sensitizing hepatocytes to TRAIL-mediated apoptosis.	Bile Acids and Salts	0-10	TNF receptor superfamily member 10b	Homo sapiens	64-72
14561739-2	2004	However, the precise mechanism by which bile acids enhance DR5/TRAIL-R2 expression is unknown.	Bile Acids and Salts	40-50	TNF receptor superfamily member 10b	Homo sapiens	59-62
14561739-2	2004	However, the precise mechanism by which bile acids enhance DR5/TRAIL-R2 expression is unknown.	Bile Acids and Salts	40-50	TNF receptor superfamily member 10b	Homo sapiens	63-71
14561739-3	2004	Although several bile acids enhanced DR5/TRAIL-R2 expression, deoxycholic acid (DCA) was the most potent.	Bile Acids and Salts	17-27	TNF receptor superfamily member 10b	Homo sapiens	37-40
14561739-3	2004	Although several bile acids enhanced DR5/TRAIL-R2 expression, deoxycholic acid (DCA) was the most potent.	Bile Acids and Salts	17-27	TNF receptor superfamily member 10b	Homo sapiens	41-49
14561739-4	2004	DCA stimulated JNK activation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.	Deoxycholic Acid	0-3	TNF receptor superfamily member 10b	Homo sapiens	81-84
14561739-4	2004	DCA stimulated JNK activation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.	Deoxycholic Acid	0-3	TNF receptor superfamily member 10b	Homo sapiens	85-93
14561739-4	2004	DCA stimulated JNK activation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.	pyrazolanthrone	52-60	TNF receptor superfamily member 10b	Homo sapiens	81-84
14561739-4	2004	DCA stimulated JNK activation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.	pyrazolanthrone	52-60	TNF receptor superfamily member 10b	Homo sapiens	85-93
14561739-4	2004	DCA stimulated JNK activation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.	Deoxycholic Acid	69-72	TNF receptor superfamily member 10b	Homo sapiens	81-84
14561739-4	2004	DCA stimulated JNK activation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.	Deoxycholic Acid	69-72	TNF receptor superfamily member 10b	Homo sapiens	85-93
14561739-7	2004	JNK inhibition with SP600125 also blocked binding of Sp1 to the DR5/TRAIL-R2 promoter.	pyrazolanthrone	20-28	TNF receptor superfamily member 10b	Homo sapiens	64-67
14561739-7	2004	JNK inhibition with SP600125 also blocked binding of Sp1 to the DR5/TRAIL-R2 promoter.	pyrazolanthrone	20-28	TNF receptor superfamily member 10b	Homo sapiens	68-76
14561739-9	2004	In conclusion, Sp1 is a bile acid-responsive transcription factor that mediates DR5/TRAIL-R2 gene expression downstream of JNK.	Bile Acids and Salts	24-33	TNF receptor superfamily member 10b	Homo sapiens	80-83
14561739-9	2004	In conclusion, Sp1 is a bile acid-responsive transcription factor that mediates DR5/TRAIL-R2 gene expression downstream of JNK.	Bile Acids and Salts	24-33	TNF receptor superfamily member 10b	Homo sapiens	84-92
12904602-8	2003	Western blot and flow cytometric analyses revealed that doxorubicin significantly increased the expression of DR5, and somewhat up-regulated the expression of DR4 and DcR2.	Doxorubicin	56-67	TNF receptor superfamily member 10b	Homo sapiens	110-113
14500373-4	2003	The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells.	Paclitaxel	28-38	TNF receptor superfamily member 10b	Homo sapiens	179-182
14720446-8	2003	Vp16 or Ara-C upregulated DR5 gene expression and augmented Apo2L-induced apoptosis in HL-60 cells.	Cytarabine	8-13	TNF receptor superfamily member 10b	Homo sapiens	26-29
14720446-10	2003	Ara-C or Vp16 upregulated DR5 gene expression and increased the sensitivity of HL-60 to Apo2L-induced cytotoxicity.	Cytarabine	0-5	TNF receptor superfamily member 10b	Homo sapiens	26-29
14520473-4	2003	We also show that the caspase-9-specific inhibitor z-LEHD-fmk inhibits drug-mediated apoptosis, leading to decreased PARP and caspase-3 cleavage, and reduced DR5 expression.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	51-61	TNF receptor superfamily member 10b	Homo sapiens	158-161
12811515-12	2003	Furthermore, the increase in TRAIL/Apo-2L sensitivity following topotecan treatment correlated with increased expression of TRAIL-R1 and TRAIL-R2 and decreased intracellular levels of the antiapoptotic protein survivin.	Topotecan	64-73	TNF receptor superfamily member 10b	Homo sapiens	137-145
12811515-14	2003	The sensitivity of DU-145 cells to TRAIL/Apo-2L was dramatically increased when combined with topotecan, suggesting that low-dose topotecan treatment to upregulate TRAIL-R1 and TRAIL-R2 and downregulate survivin, followed by TRAIL/Apo-2L administration, may be a viable therapy for treating cancer of the prostate.	Topotecan	130-139	TNF receptor superfamily member 10b	Homo sapiens	177-185
14500373-4	2003	The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells.	Vincristine	40-51	TNF receptor superfamily member 10b	Homo sapiens	179-182
14500373-4	2003	The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells.	Vinblastine	53-64	TNF receptor superfamily member 10b	Homo sapiens	179-182
14500373-4	2003	The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells.	Etoposide	66-75	TNF receptor superfamily member 10b	Homo sapiens	179-182
14500373-4	2003	The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells.	Camptothecin	77-89	TNF receptor superfamily member 10b	Homo sapiens	179-182
14500373-4	2003	The chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, camptothecin, and Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAIL resulted in apoptosis of both TRAIL-sensitive and -resistant cells.	Doxorubicin	95-105	TNF receptor superfamily member 10b	Homo sapiens	179-182
14500373-6	2003	TRAIL induces apoptosis in Adriamycin-resistant MCF7 cells already expressing high levels of death receptors DR4 and DR5.	Doxorubicin	27-37	TNF receptor superfamily member 10b	Homo sapiens	117-120
12838325-7	2003	Importantly, treatment of resistant cells with the chemotherapeutic agents doxorubicin, cisplatin and etoposide reversed the resistance to Apo2L/TRAIL, which was associated with drug-induced upregulation of mRNA encoding the death receptors DR4 and DR5.	Doxorubicin	75-86	TNF receptor superfamily member 10b	Homo sapiens	249-252
12902978-2	2003	PS-341 treatment by itself does not affect the levels of Bax, Bak, caspases 3 and 8, c-Flip or FADD, but elevates levels of TRAIL receptors DR4 and DR5.	Bortezomib	0-6	TNF receptor superfamily member 10b	Homo sapiens	148-151
12838325-7	2003	Importantly, treatment of resistant cells with the chemotherapeutic agents doxorubicin, cisplatin and etoposide reversed the resistance to Apo2L/TRAIL, which was associated with drug-induced upregulation of mRNA encoding the death receptors DR4 and DR5.	Cisplatin	88-97	TNF receptor superfamily member 10b	Homo sapiens	249-252
12838325-7	2003	Importantly, treatment of resistant cells with the chemotherapeutic agents doxorubicin, cisplatin and etoposide reversed the resistance to Apo2L/TRAIL, which was associated with drug-induced upregulation of mRNA encoding the death receptors DR4 and DR5.	Etoposide	102-111	TNF receptor superfamily member 10b	Homo sapiens	249-252
12835727-4	2003	DR4 expression was increased when Jurkat cells were treated with TRAIL, and DR5 expression increased after exposing Molt-4 cells to TRAIL plus a low dose of doxorubicin for 24 h. The expression of DR4 and DR5 in UCB mononuclear cells was unchanged after treatment with TRAIL, a low-dose doxorubicin, or TRAIL plus a low dose of doxorubicin.	Doxorubicin	157-168	TNF receptor superfamily member 10b	Homo sapiens	76-79
12835727-4	2003	DR4 expression was increased when Jurkat cells were treated with TRAIL, and DR5 expression increased after exposing Molt-4 cells to TRAIL plus a low dose of doxorubicin for 24 h. The expression of DR4 and DR5 in UCB mononuclear cells was unchanged after treatment with TRAIL, a low-dose doxorubicin, or TRAIL plus a low dose of doxorubicin.	Doxorubicin	287-298	TNF receptor superfamily member 10b	Homo sapiens	205-208
12835727-4	2003	DR4 expression was increased when Jurkat cells were treated with TRAIL, and DR5 expression increased after exposing Molt-4 cells to TRAIL plus a low dose of doxorubicin for 24 h. The expression of DR4 and DR5 in UCB mononuclear cells was unchanged after treatment with TRAIL, a low-dose doxorubicin, or TRAIL plus a low dose of doxorubicin.	Doxorubicin	157-168	TNF receptor superfamily member 10b	Homo sapiens	205-208
12835727-4	2003	DR4 expression was increased when Jurkat cells were treated with TRAIL, and DR5 expression increased after exposing Molt-4 cells to TRAIL plus a low dose of doxorubicin for 24 h. The expression of DR4 and DR5 in UCB mononuclear cells was unchanged after treatment with TRAIL, a low-dose doxorubicin, or TRAIL plus a low dose of doxorubicin.	Doxorubicin	287-298	TNF receptor superfamily member 10b	Homo sapiens	205-208
12684208-3	2003	Bile acid modulation of death-receptor signaling is multifactorial and includes trafficking of Fas to the cell surface, enhancing TRAIL-R2/DR5 expression, and suppression of function of cFLIP, an antiapoptotic protein modulating death-receptor function.	Bile Acids and Salts	0-9	TNF receptor superfamily member 10b	Homo sapiens	130-138
12763223-6	2003	Coincubation of TRAIL and doxorubicin led to the overexpression of TRAIL-R2 resulting in a synergistic effect of doxorubicin and TRAIL in TRAIL-sensitive cell lines and in the overcoming of TRAIL-resistance in all of the TRAIL-resistant cell lines, except HTB-91, which lacked caspase 8 expression.	Doxorubicin	26-37	TNF receptor superfamily member 10b	Homo sapiens	67-75
12763223-6	2003	Coincubation of TRAIL and doxorubicin led to the overexpression of TRAIL-R2 resulting in a synergistic effect of doxorubicin and TRAIL in TRAIL-sensitive cell lines and in the overcoming of TRAIL-resistance in all of the TRAIL-resistant cell lines, except HTB-91, which lacked caspase 8 expression.	Doxorubicin	113-124	TNF receptor superfamily member 10b	Homo sapiens	67-75
12684208-3	2003	Bile acid modulation of death-receptor signaling is multifactorial and includes trafficking of Fas to the cell surface, enhancing TRAIL-R2/DR5 expression, and suppression of function of cFLIP, an antiapoptotic protein modulating death-receptor function.	Bile Acids and Salts	0-9	TNF receptor superfamily member 10b	Homo sapiens	139-142
12584736-0	2003	Enhancement of TRAIL/Apo2L-mediated apoptosis by adriamycin through inducing DR4 and DR5 in renal cell carcinoma cells.	Doxorubicin	49-59	TNF receptor superfamily member 10b	Homo sapiens	85-88
12730681-0	2003	Effect of Bax deficiency on death receptor 5 and mitochondrial pathways during endoplasmic reticulum calcium pool depletion-induced apoptosis.	Calcium	101-108	TNF receptor superfamily member 10b	Homo sapiens	28-44
14716031-0	2003	Death receptor 5 and Bcl-2 protein expression as predictors of tumor response to gemcitabine and cisplatin in patients with advanced non-small-cell lung cancer.	gemcitabine	81-92	TNF receptor superfamily member 10b	Homo sapiens	0-16
12610517-6	2003	We show that genotoxic agents such as cisplatin, doxorubicin and camptothecin, in addition to UV radiation, can induce TRAIL-R2 on the cell surface of TRAIL receptor-negative tumour cells.	Cisplatin	38-47	TNF receptor superfamily member 10b	Homo sapiens	119-127
12610517-6	2003	We show that genotoxic agents such as cisplatin, doxorubicin and camptothecin, in addition to UV radiation, can induce TRAIL-R2 on the cell surface of TRAIL receptor-negative tumour cells.	Doxorubicin	49-60	TNF receptor superfamily member 10b	Homo sapiens	119-127
12610517-6	2003	We show that genotoxic agents such as cisplatin, doxorubicin and camptothecin, in addition to UV radiation, can induce TRAIL-R2 on the cell surface of TRAIL receptor-negative tumour cells.	Camptothecin	65-77	TNF receptor superfamily member 10b	Homo sapiens	119-127
12670894-6	2003	Caspase-8 processing is dependent on de novo protein synthesis; DR5 expression is strongly up-regulated by THG treatment.	Thapsigargin	107-110	TNF receptor superfamily member 10b	Homo sapiens	64-67
12569362-7	2003	A DR5 retinoic acid responsive element was observed in the LTR.	Tretinoin	6-19	TNF receptor superfamily member 10b	Homo sapiens	2-5
12543804-0	2003	2-methoxyestradiol up-regulates death receptor 5 and induces apoptosis through activation of the extrinsic pathway.	2-Methoxyestradiol	0-18	TNF receptor superfamily member 10b	Homo sapiens	32-48
14716031-0	2003	Death receptor 5 and Bcl-2 protein expression as predictors of tumor response to gemcitabine and cisplatin in patients with advanced non-small-cell lung cancer.	Cisplatin	97-106	TNF receptor superfamily member 10b	Homo sapiens	0-16
12642685-3	2002	This resistance was determined by failure to form the TRAIL-DISC and by decreased TRAIL-R1 and TRAIL-R2 levels after androgen deprivation; the capacity of TRAIL to induce DISC formation was completely restored in the presence of DHT.	Dihydrotestosterone	229-232	TNF receptor superfamily member 10b	Homo sapiens	95-103
12390973-6	2002	A blocking experiment with monoclonal antibodies directed against TRAIL-R1 and TRAIL-R2 revealed that TRAIL-R1 is mainly involved in TRAIL-induced apoptosis of ahOL.	ahol	160-164	TNF receptor superfamily member 10b	Homo sapiens	79-87
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	20-26	TNF receptor superfamily member 10b	Homo sapiens	67-70
12388624-2	2002	We have recently demonstrated, however, that bile acids increase TRAIL-R2/DR5 expression in a human liver cell line and render these cells susceptible to TRAIL-mediated apoptosis.	Bile Acids and Salts	45-55	TNF receptor superfamily member 10b	Homo sapiens	65-73
12388624-2	2002	We have recently demonstrated, however, that bile acids increase TRAIL-R2/DR5 expression in a human liver cell line and render these cells susceptible to TRAIL-mediated apoptosis.	Bile Acids and Salts	45-55	TNF receptor superfamily member 10b	Homo sapiens	74-77
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	20-26	TNF receptor superfamily member 10b	Homo sapiens	149-152
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	88-94	TNF receptor superfamily member 10b	Homo sapiens	67-70
12384541-9	2002	Tumors treated with CPT-11 showed increased membrane expression of DR5, suggesting that CPT-11 may increase sensitivity to TRAIL by up-regulation of DR5.	Irinotecan	88-94	TNF receptor superfamily member 10b	Homo sapiens	149-152
12203115-2	2002	Here we report that two different NSAIDs, sulindac sulfide and SC-"236 engage the death receptor 5 (DR5) and mitochondrial pathways to mediate apoptosis in human colon cancer cells.	sulindac sulfide	42-58	TNF receptor superfamily member 10b	Homo sapiens	82-98
12207174-7	2002	Blockage of NFkappaB activation either by expression of dominant negative IkappaB or treatment with proteasome inhibitor lactacystin eliminates TRAIL induced DR5 expression.	lactacystin	121-132	TNF receptor superfamily member 10b	Homo sapiens	158-161
12203115-2	2002	Here we report that two different NSAIDs, sulindac sulfide and SC-"236 engage the death receptor 5 (DR5) and mitochondrial pathways to mediate apoptosis in human colon cancer cells.	sulindac sulfide	42-58	TNF receptor superfamily member 10b	Homo sapiens	100-103
12203115-2	2002	Here we report that two different NSAIDs, sulindac sulfide and SC-"236 engage the death receptor 5 (DR5) and mitochondrial pathways to mediate apoptosis in human colon cancer cells.	4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide	63-70	TNF receptor superfamily member 10b	Homo sapiens	82-98
12203115-2	2002	Here we report that two different NSAIDs, sulindac sulfide and SC-"236 engage the death receptor 5 (DR5) and mitochondrial pathways to mediate apoptosis in human colon cancer cells.	4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide	63-70	TNF receptor superfamily member 10b	Homo sapiens	100-103
12203115-3	2002	We show that sulindac sulfide and SC-"236-induced apoptosis is coupled with upregulation of DR5, caspase 8 activation and Bid cleavage.	sulindac sulfide	13-29	TNF receptor superfamily member 10b	Homo sapiens	92-95
12203115-3	2002	We show that sulindac sulfide and SC-"236-induced apoptosis is coupled with upregulation of DR5, caspase 8 activation and Bid cleavage.	4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide	34-41	TNF receptor superfamily member 10b	Homo sapiens	92-95
12203115-5	2002	We further show that sulindac sulfide and SC-"236-induced DR5 upregulation occurs independent of the COX inhibitory effects of these NSAIDs.	sulindac sulfide	21-37	TNF receptor superfamily member 10b	Homo sapiens	58-61
12203115-5	2002	We further show that sulindac sulfide and SC-"236-induced DR5 upregulation occurs independent of the COX inhibitory effects of these NSAIDs.	4-(5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide	42-49	TNF receptor superfamily member 10b	Homo sapiens	58-61
11916527-1	2002	The relationship between p53 gene status and the expression of DR5 and Fas was evaluated as a function of sensitivity of 11 acute lymphoblastic leukemia cell lines to adriamycin, etoposide, vincristine, methotrexate and dexamethasone.	Doxorubicin	167-177	TNF receptor superfamily member 10b	Homo sapiens	63-66
12203115-7	2002	For example, sulindac sulfide upregulates DR5 in both Bax-deficient and proficient cells, but Apo2L/TRAIL efficiently potentiates sulindac sulfide-induced apoptosis as well as activation of caspase-8, -9 and -3 only in Bax-proficient cells.	sulindac sulfide	13-29	TNF receptor superfamily member 10b	Homo sapiens	42-45
12208739-6	2002	Sulindac sulfide treatment restored DR-5 expression and, when combined with TRAIL, reduced cell viability to a greater extent than did either drug alone.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	36-40
12034736-0	2002	Bisindolylmaleimide VIII enhances DR5-mediated apoptosis through the MKK4/JNK/p38 kinase and the mitochondrial pathways.	bisindolylmaleimide	0-19	TNF receptor superfamily member 10b	Homo sapiens	34-37
12432279-6	2002	Selenium upregulation of DR5 was coupled with caspase 8 activation and Bid cleavage thereby suggesting the existence of a potential cross-talk between the DR5 and the mitochondrial pathways.	Selenium	0-8	TNF receptor superfamily member 10b	Homo sapiens	155-158
12432279-7	2002	Thus, our results suggest that DR5 is specifically regulated by selenium and its activation may play an important role in selenium-mediated chemoprevention.	Selenium	64-72	TNF receptor superfamily member 10b	Homo sapiens	31-34
12432279-7	2002	Thus, our results suggest that DR5 is specifically regulated by selenium and its activation may play an important role in selenium-mediated chemoprevention.	Selenium	122-130	TNF receptor superfamily member 10b	Homo sapiens	31-34
12496481-6	2002	TRAIL receptor mRNAs (DR4, DR5, and DcR2) were induced by doxorubicin but these changes were not reflected at the protein level.	Doxorubicin	58-69	TNF receptor superfamily member 10b	Homo sapiens	27-30
12432279-0	2002	Death receptor 5 regulation during selenium-mediated apoptosis in human prostate cancer cells.	Selenium	35-43	TNF receptor superfamily member 10b	Homo sapiens	0-16
12432279-4	2002	Here we report that selenium-mediated apoptosis appears to involve membrane death receptor, DR5-dependent pathway in human prostate cancer cells.	Selenium	20-28	TNF receptor superfamily member 10b	Homo sapiens	92-95
12432279-5	2002	Selenium specifically upregulated DR5 expression but not that of DR4.	Selenium	0-8	TNF receptor superfamily member 10b	Homo sapiens	34-37
12432279-6	2002	Selenium upregulation of DR5 was coupled with caspase 8 activation and Bid cleavage thereby suggesting the existence of a potential cross-talk between the DR5 and the mitochondrial pathways.	Selenium	0-8	TNF receptor superfamily member 10b	Homo sapiens	25-28
11916527-1	2002	The relationship between p53 gene status and the expression of DR5 and Fas was evaluated as a function of sensitivity of 11 acute lymphoblastic leukemia cell lines to adriamycin, etoposide, vincristine, methotrexate and dexamethasone.	Etoposide	179-188	TNF receptor superfamily member 10b	Homo sapiens	63-66
11916527-1	2002	The relationship between p53 gene status and the expression of DR5 and Fas was evaluated as a function of sensitivity of 11 acute lymphoblastic leukemia cell lines to adriamycin, etoposide, vincristine, methotrexate and dexamethasone.	Vincristine	190-201	TNF receptor superfamily member 10b	Homo sapiens	63-66
11916527-1	2002	The relationship between p53 gene status and the expression of DR5 and Fas was evaluated as a function of sensitivity of 11 acute lymphoblastic leukemia cell lines to adriamycin, etoposide, vincristine, methotrexate and dexamethasone.	Methotrexate	203-215	TNF receptor superfamily member 10b	Homo sapiens	63-66
11916527-1	2002	The relationship between p53 gene status and the expression of DR5 and Fas was evaluated as a function of sensitivity of 11 acute lymphoblastic leukemia cell lines to adriamycin, etoposide, vincristine, methotrexate and dexamethasone.	Dexamethasone	220-233	TNF receptor superfamily member 10b	Homo sapiens	63-66
11802207-0	2002	TRAIL, FasL and a blocking anti-DR5 antibody augment paclitaxel-induced apoptosis in human non-small-cell lung cancer.	Paclitaxel	53-63	TNF receptor superfamily member 10b	Homo sapiens	32-35
11965535-0	2002	Endoplasmic reticulum calcium pool depletion-induced apoptosis is coupled with activation of the death receptor 5 pathway.	Calcium	22-29	TNF receptor superfamily member 10b	Homo sapiens	97-113
11965535-3	2002	In this study, we demonstrate for the first time that TG-mediated perturbations in Ca(2+) homeostasis are coupled with activation of the death receptor 5 (DR5)-dependent apoptotic pathway in human cancer cells.	Thapsigargin	54-56	TNF receptor superfamily member 10b	Homo sapiens	137-153
11965535-3	2002	In this study, we demonstrate for the first time that TG-mediated perturbations in Ca(2+) homeostasis are coupled with activation of the death receptor 5 (DR5)-dependent apoptotic pathway in human cancer cells.	Thapsigargin	54-56	TNF receptor superfamily member 10b	Homo sapiens	155-158
11965535-9	2002	The TG-induced increase in DR5 expression appeared to occur as a consequence of TG-induced endoplasmic reticulum (ER) Ca(2+) pool depletion.	Thapsigargin	4-6	TNF receptor superfamily member 10b	Homo sapiens	27-30
11802207-10	2002	The combination treatments, FasL+PA, TRAIL+PA or PA+anti-DR5 antibody, greatly enhance PA-apoptotic effect in most cell lines.	Paclitaxel	49-52	TNF receptor superfamily member 10b	Homo sapiens	57-60
12794242-8	2002	PMA also increased the expression of TRAIL receptors DR4 and DR5; this expression was inhibited by the PKC inhibitors GF109203x, Go6983, and Ro-31-8220 and the MEK inhibitor UO126, suggesting a role for conventional PKC isoforms and MEK in the regulation of TRAIL receptor expression.	bisindolylmaleimide I	118-127	TNF receptor superfamily member 10b	Homo sapiens	61-64
11803469-2	2002	We demonstrate that in H157 human lung carcinoma cells, etoposide and doxorubicin induce the NF-kappaB-dependent expression of both pro- and anti-apoptotic proteins including TRAIL and its death receptor, DR5, and IAPs.	Etoposide	56-65	TNF receptor superfamily member 10b	Homo sapiens	205-208
11803469-2	2002	We demonstrate that in H157 human lung carcinoma cells, etoposide and doxorubicin induce the NF-kappaB-dependent expression of both pro- and anti-apoptotic proteins including TRAIL and its death receptor, DR5, and IAPs.	Doxorubicin	70-81	TNF receptor superfamily member 10b	Homo sapiens	205-208
12174820-7	2002	p53 target genes such as p21WAF1/Cip1, and KILLER/DR5 were upregulated by CP-31398, but their expression did not correlate with arrest or apoptosis induction.	CP 31398	74-82	TNF receptor superfamily member 10b	Homo sapiens	43-53
12174820-8	2002	Combination of CP-31398 and TRAIL or chemotherapeutic agents enhanced cancer cell killing effect possibly through upregulation of p53-regulated genes such as KILLER/DR5.	CP 31398	15-23	TNF receptor superfamily member 10b	Homo sapiens	158-168
12794242-8	2002	PMA also increased the expression of TRAIL receptors DR4 and DR5; this expression was inhibited by the PKC inhibitors GF109203x, Go6983, and Ro-31-8220 and the MEK inhibitor UO126, suggesting a role for conventional PKC isoforms and MEK in the regulation of TRAIL receptor expression.	2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimide	129-135	TNF receptor superfamily member 10b	Homo sapiens	61-64
12794242-8	2002	PMA also increased the expression of TRAIL receptors DR4 and DR5; this expression was inhibited by the PKC inhibitors GF109203x, Go6983, and Ro-31-8220 and the MEK inhibitor UO126, suggesting a role for conventional PKC isoforms and MEK in the regulation of TRAIL receptor expression.	U 0126	174-179	TNF receptor superfamily member 10b	Homo sapiens	61-64
11498783-7	2001	Although the basal mRNA levels of these genes did not depend on the presence of p53, we observed a p53-dependent induction of all these targets in response to gamma-irradiation and a p53-independent regulation for p21 and KILLER/DR5 in response to dexamethasone.	Dexamethasone	248-261	TNF receptor superfamily member 10b	Homo sapiens	222-232
11677215-1	2001	BACKGROUND & AIMS: The KILLER/death receptor (DR)5 has been identified as a potent inducer of apoptosis, and mapped to chromosome 8p21-22, showing frequent allelic loss in gastric cancer.	Adenosine Monophosphate	12-15	TNF receptor superfamily member 10b	Homo sapiens	27-54
11507096-0	2001	The bile acid glycochenodeoxycholate induces trail-receptor 2/DR5 expression and apoptosis.	Bile Acids and Salts	4-13	TNF receptor superfamily member 10b	Homo sapiens	62-65
11507096-0	2001	The bile acid glycochenodeoxycholate induces trail-receptor 2/DR5 expression and apoptosis.	Glycochenodeoxycholic Acid	14-36	TNF receptor superfamily member 10b	Homo sapiens	62-65
11507096-8	2001	GCDC treatment increased expression of TRAIL-R2/DR5 mRNA and protein 10-fold while expression of TRAIL-R1 was unchanged.	Glycochenodeoxycholic Acid	0-4	TNF receptor superfamily member 10b	Homo sapiens	39-47
11507096-8	2001	GCDC treatment increased expression of TRAIL-R2/DR5 mRNA and protein 10-fold while expression of TRAIL-R1 was unchanged.	Glycochenodeoxycholic Acid	0-4	TNF receptor superfamily member 10b	Homo sapiens	48-51
11507096-9	2001	Furthermore, aggregation of TRAIL-R2/DR5, but not TRAIL-R1/DR4 was observed following GCDC treatment of the cells.	Glycochenodeoxycholic Acid	86-90	TNF receptor superfamily member 10b	Homo sapiens	28-36
11507096-9	2001	Furthermore, aggregation of TRAIL-R2/DR5, but not TRAIL-R1/DR4 was observed following GCDC treatment of the cells.	Glycochenodeoxycholic Acid	86-90	TNF receptor superfamily member 10b	Homo sapiens	37-40
11507096-10	2001	Induction of TRAIL-R2/DR5 expression and apoptosis by bile acids provides new insights into the mechanisms of hepatocyte apoptosis and the regulation of TRAIL-R2/DR5 expression.	Bile Acids and Salts	54-64	TNF receptor superfamily member 10b	Homo sapiens	13-21
11507096-10	2001	Induction of TRAIL-R2/DR5 expression and apoptosis by bile acids provides new insights into the mechanisms of hepatocyte apoptosis and the regulation of TRAIL-R2/DR5 expression.	Bile Acids and Salts	54-64	TNF receptor superfamily member 10b	Homo sapiens	22-25
11507096-10	2001	Induction of TRAIL-R2/DR5 expression and apoptosis by bile acids provides new insights into the mechanisms of hepatocyte apoptosis and the regulation of TRAIL-R2/DR5 expression.	Bile Acids and Salts	54-64	TNF receptor superfamily member 10b	Homo sapiens	153-161
11507096-10	2001	Induction of TRAIL-R2/DR5 expression and apoptosis by bile acids provides new insights into the mechanisms of hepatocyte apoptosis and the regulation of TRAIL-R2/DR5 expression.	Bile Acids and Salts	54-64	TNF receptor superfamily member 10b	Homo sapiens	162-165
11559570-0	2001	Sulindac sulfide-induced apoptosis involves death receptor 5 and the caspase 8-dependent pathway in human colon and prostate cancer cells.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	44-60
11559570-5	2001	Sulindac sulfide up-regulated DR5 and activated the proximal caspase 8 in various different colon and prostate cancer cell lines.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	30-33
11559570-6	2001	Sulindac sulfide specifically up-regulated the DR5 levels but had no effect on the levels of other DRs including DR4, Fas, and tumor necrosis factor receptor 1.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	47-50
11559570-9	2001	Our results indicated that by blocking the DR5-dependent apoptotic pathway, dominant-negative Fas-associated death domain did indeed inhibit sulindac sulfide-induced apoptosis.	sulindac sulfide	141-157	TNF receptor superfamily member 10b	Homo sapiens	43-46
11559570-10	2001	Furthermore, exogenous tumor necrosis factor-related apoptosis-inducing ligand, the ligand for DR5, also potentiated sulindac sulfide-induced apoptosis in all of the cell lines tested, thereby further supporting the involvement of DR5 in sulindac sulfide-induced apoptosis.	sulindac sulfide	117-133	TNF receptor superfamily member 10b	Homo sapiens	95-98
11559570-10	2001	Furthermore, exogenous tumor necrosis factor-related apoptosis-inducing ligand, the ligand for DR5, also potentiated sulindac sulfide-induced apoptosis in all of the cell lines tested, thereby further supporting the involvement of DR5 in sulindac sulfide-induced apoptosis.	sulindac sulfide	117-133	TNF receptor superfamily member 10b	Homo sapiens	231-234
11559570-10	2001	Furthermore, exogenous tumor necrosis factor-related apoptosis-inducing ligand, the ligand for DR5, also potentiated sulindac sulfide-induced apoptosis in all of the cell lines tested, thereby further supporting the involvement of DR5 in sulindac sulfide-induced apoptosis.	sulindac sulfide	238-254	TNF receptor superfamily member 10b	Homo sapiens	95-98
11559570-11	2001	Thus, our results demonstrate that sulindac sulfide also engages the membrane DR pathway involving DR5 and proximal caspase 8 to induce apoptosis.	sulindac sulfide	35-51	TNF receptor superfamily member 10b	Homo sapiens	99-102
11751478-7	2001	Adriamycin treatment modestly up-regulated Apo2L/TRAIL-R2 (DR5) and had no effect on the expression of Fas-associated death domain, c-FLIP, Bcl-2, Bcl(xL), Bax, and IAP family members (cIAP-1, cIAP-2, XIAP, and survivin).	Doxorubicin	0-10	TNF receptor superfamily member 10b	Homo sapiens	49-57
11751478-7	2001	Adriamycin treatment modestly up-regulated Apo2L/TRAIL-R2 (DR5) and had no effect on the expression of Fas-associated death domain, c-FLIP, Bcl-2, Bcl(xL), Bax, and IAP family members (cIAP-1, cIAP-2, XIAP, and survivin).	Doxorubicin	0-10	TNF receptor superfamily member 10b	Homo sapiens	59-62
11468181-7	2001	Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the effect of TRAIL not only against MM cells sensitive to, but also against those resistant to, Dex- or Dox-induced apoptosis.	Doxorubicin	0-3	TNF receptor superfamily member 10b	Homo sapiens	54-70
11468181-7	2001	Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the effect of TRAIL not only against MM cells sensitive to, but also against those resistant to, Dex- or Dox-induced apoptosis.	Doxorubicin	0-3	TNF receptor superfamily member 10b	Homo sapiens	72-75
11468181-7	2001	Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the effect of TRAIL not only against MM cells sensitive to, but also against those resistant to, Dex- or Dox-induced apoptosis.	Dexamethasone	203-206	TNF receptor superfamily member 10b	Homo sapiens	54-70
11468181-7	2001	Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the effect of TRAIL not only against MM cells sensitive to, but also against those resistant to, Dex- or Dox-induced apoptosis.	Doxorubicin	211-214	TNF receptor superfamily member 10b	Homo sapiens	54-70
11468181-7	2001	Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the effect of TRAIL not only against MM cells sensitive to, but also against those resistant to, Dex- or Dox-induced apoptosis.	Doxorubicin	211-214	TNF receptor superfamily member 10b	Homo sapiens	72-75
11212279-5	2001	Treatment with paclitaxel or taxotere increased DR4 and/or DR5 protein levels (up to 8-fold) without affecting the protein levels of DcR1 and DcR2, Apo-2L/TRAIL, Fas, or Fas ligand.	Paclitaxel	15-25	TNF receptor superfamily member 10b	Homo sapiens	59-62
11234890-9	2001	Cotreatment with STI-571 significantly enhanced Apo-2L/TRAIL-induced apoptosis (P < 0.01) as well as increased the processing of caspase-9 and -3 and XIAP, without affecting the levels of DR4, DR5, decoy receptors, or c-FLIP(L).	Imatinib Mesylate	17-24	TNF receptor superfamily member 10b	Homo sapiens	196-199
11139340-4	2001	beta-Lapachone, a topoisomerase inhibitor, increased KILLER/DR5 mRNA in colon cancer cell lines with wild-type p53 but not with mutant p53.	beta-lapachone	0-14	TNF receptor superfamily member 10b	Homo sapiens	53-63
11139340-5	2001	In contrast, betulinic acid, a novel chemotherapeutic compound, induced apoptosis and KILLER/DR5 mRNA in melanoma and glioblastoma cells through a p53-independent mechanism.	betulinic acid	13-27	TNF receptor superfamily member 10b	Homo sapiens	86-96
11139340-6	2001	The synthetic glucocorticoid dexamethasone elevated KILLER/DR5 mRNA in glioblastoma, ovarian cancer, and colon cancer cell lines with mutant p53 undergoing apoptosis, and this induction was inhibited by the transcriptional inhibitor actinomycin D.	Dexamethasone	29-42	TNF receptor superfamily member 10b	Homo sapiens	52-62
11139340-6	2001	The synthetic glucocorticoid dexamethasone elevated KILLER/DR5 mRNA in glioblastoma, ovarian cancer, and colon cancer cell lines with mutant p53 undergoing apoptosis, and this induction was inhibited by the transcriptional inhibitor actinomycin D.	Dactinomycin	233-246	TNF receptor superfamily member 10b	Homo sapiens	52-62
11212279-5	2001	Treatment with paclitaxel or taxotere increased DR4 and/or DR5 protein levels (up to 8-fold) without affecting the protein levels of DcR1 and DcR2, Apo-2L/TRAIL, Fas, or Fas ligand.	Docetaxel	29-37	TNF receptor superfamily member 10b	Homo sapiens	59-62
11139287-6	2000	Topotecan, a novel topoisomerase I inhibitor, induced upregulation of TRAIL-R2 as well as downregulation of TRAIL.	Topotecan	0-9	TNF receptor superfamily member 10b	Homo sapiens	70-78
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Doxorubicin	60-71	TNF receptor superfamily member 10b	Homo sapiens	82-85
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Etoposide	44-53	TNF receptor superfamily member 10b	Homo sapiens	90-93
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Cytarabine	55-60	TNF receptor superfamily member 10b	Homo sapiens	90-93
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Doxorubicin	65-76	TNF receptor superfamily member 10b	Homo sapiens	90-93
11212279-6	2001	Up-regulation of DR4 and DR5 was not preceded by the induction of their mRNA levels but was inhibited by cotreatment with cycloheximide.	Cycloheximide	122-135	TNF receptor superfamily member 10b	Homo sapiens	25-28
11212279-9	2001	These findings indicate that up-regulation of DR4 and DR5 protein levels by treatment with paclitaxel enhances subsequent Apo-2L/TRAIL-induced apoptosis of human prostate cancer cells.	Paclitaxel	91-101	TNF receptor superfamily member 10b	Homo sapiens	54-57
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Etoposide	39-48	TNF receptor superfamily member 10b	Homo sapiens	82-85
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	TNF receptor superfamily member 10b	Homo sapiens	82-85
10893485-1	2000	The cholecystokinin A receptor (CCK-AR) modulates CCK-stimulated dopamine release in the posterior nucleus accumbens, and its gene is mapped to 4p15.2-15.1 with the dopamine receptor 5 (DR5) gene.	Dopamine	65-73	TNF receptor superfamily member 10b	Homo sapiens	165-184
10930093-0	2000	Coordinated regulation of two TRAIL-R2/KILLER/DR5 mRNA isoforms by DNA damaging agents, serum and 17beta-estradiol in human breast cancer cells.	Estradiol	98-114	TNF receptor superfamily member 10b	Homo sapiens	30-38
10930093-0	2000	Coordinated regulation of two TRAIL-R2/KILLER/DR5 mRNA isoforms by DNA damaging agents, serum and 17beta-estradiol in human breast cancer cells.	Estradiol	98-114	TNF receptor superfamily member 10b	Homo sapiens	39-49
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	63-73	TNF receptor superfamily member 10b	Homo sapiens	162-170
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	63-73	TNF receptor superfamily member 10b	Homo sapiens	171-181
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	138-148	TNF receptor superfamily member 10b	Homo sapiens	162-170
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	138-148	TNF receptor superfamily member 10b	Homo sapiens	171-181
11002424-9	2000	Because CD437 induced the expression of DR4, DR5 and Fas, we examined the effects of combining CD437 and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and Fas ligand, respectively, in HPC cells.	CD 437	8-13	TNF receptor superfamily member 10b	Homo sapiens	45-48
10893485-1	2000	The cholecystokinin A receptor (CCK-AR) modulates CCK-stimulated dopamine release in the posterior nucleus accumbens, and its gene is mapped to 4p15.2-15.1 with the dopamine receptor 5 (DR5) gene.	Dopamine	65-73	TNF receptor superfamily member 10b	Homo sapiens	186-189
10693703-12	2000	Expression of TRAIL (a ligand for DR4 and DR5) was significantly lower in CCSK and RTK than in normal kidney (9.5+/-1.5% v. 56.1+/-10.1%; P = .01).	ccsk	74-78	TNF receptor superfamily member 10b	Homo sapiens	42-45
10777207-9	2000	In p53-wild-type but not -mutant or -null cell lines, doxorubicin treatment stabilized p53 protein, and increased specific binding to BS2 as revealed by EMSA, and upregulated the KILLER/DR5 promoter-luciferase reporter gene.	Doxorubicin	54-65	TNF receptor superfamily member 10b	Homo sapiens	179-189
10706092-3	2000	Here we show that the DNA-damaging chemotherapeutic drugs, cis-diamminedichloroplatinum(II) (CDDP) and etoposide, elicited increased expression of DR5 in human glioma cells.	Cisplatin	59-91	TNF receptor superfamily member 10b	Homo sapiens	147-150
10706092-3	2000	Here we show that the DNA-damaging chemotherapeutic drugs, cis-diamminedichloroplatinum(II) (CDDP) and etoposide, elicited increased expression of DR5 in human glioma cells.	Cisplatin	93-97	TNF receptor superfamily member 10b	Homo sapiens	147-150
10706092-3	2000	Here we show that the DNA-damaging chemotherapeutic drugs, cis-diamminedichloroplatinum(II) (CDDP) and etoposide, elicited increased expression of DR5 in human glioma cells.	Etoposide	103-112	TNF receptor superfamily member 10b	Homo sapiens	147-150
10706092-4	2000	Exposure of such cells in vitro to soluble human TRAIL in combination with CDDP or etoposide resulted in synergistic cell death that could be blocked by soluble TRAIL-neutralizing DR5-Fc or the caspase inhibitors, Z-Asp-CH2-DCB and CrmA.	Cisplatin	75-79	TNF receptor superfamily member 10b	Homo sapiens	180-183
10706092-4	2000	Exposure of such cells in vitro to soluble human TRAIL in combination with CDDP or etoposide resulted in synergistic cell death that could be blocked by soluble TRAIL-neutralizing DR5-Fc or the caspase inhibitors, Z-Asp-CH2-DCB and CrmA.	Etoposide	83-92	TNF receptor superfamily member 10b	Homo sapiens	180-183
10706092-4	2000	Exposure of such cells in vitro to soluble human TRAIL in combination with CDDP or etoposide resulted in synergistic cell death that could be blocked by soluble TRAIL-neutralizing DR5-Fc or the caspase inhibitors, Z-Asp-CH2-DCB and CrmA.	benzyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene	214-227	TNF receptor superfamily member 10b	Homo sapiens	180-183
10706092-4	2000	Exposure of such cells in vitro to soluble human TRAIL in combination with CDDP or etoposide resulted in synergistic cell death that could be blocked by soluble TRAIL-neutralizing DR5-Fc or the caspase inhibitors, Z-Asp-CH2-DCB and CrmA.	crma	232-236	TNF receptor superfamily member 10b	Homo sapiens	180-183
10676636-6	2000	Biochemical analysis of the signaling events induced by TRAIL revealed that PK could be sensitized for TRAIL and, similarly, for TRAIL-R1- and TRAIL-R2-specific apoptosis by pretreatment of the cells with cycloheximide (CHX).	Cycloheximide	205-218	TNF receptor superfamily member 10b	Homo sapiens	143-151
10676636-6	2000	Biochemical analysis of the signaling events induced by TRAIL revealed that PK could be sensitized for TRAIL and, similarly, for TRAIL-R1- and TRAIL-R2-specific apoptosis by pretreatment of the cells with cycloheximide (CHX).	Cycloheximide	220-223	TNF receptor superfamily member 10b	Homo sapiens	143-151
9311998-5	1997	TRAIL-R2 contains two extracellular cysteine-rich repeats, typical for TNF receptor (TNFR) family members, and a cytoplasmic death domain.	Cysteine	36-44	TNF receptor superfamily member 10b	Homo sapiens	0-8
10933923-2	2000	We previously identified the death domain containing proapoptotic TRAIL death receptor KILLER/DR5 (TRAIL-R2) as an upregulated transcript following exposure of cancer cells, with wild-type but not with mutant or degraded p53 proteins, to a cytotoxic dose of adriamycin.	Doxorubicin	258-268	TNF receptor superfamily member 10b	Homo sapiens	87-97
10933923-2	2000	We previously identified the death domain containing proapoptotic TRAIL death receptor KILLER/DR5 (TRAIL-R2) as an upregulated transcript following exposure of cancer cells, with wild-type but not with mutant or degraded p53 proteins, to a cytotoxic dose of adriamycin.	Doxorubicin	258-268	TNF receptor superfamily member 10b	Homo sapiens	99-107
10594023-4	2000	The mechanism of the synergistic effect results from the etoposide-mediated increase in the expression of the death receptors 4 (DR4) and 5 (DR5).	Etoposide	57-66	TNF receptor superfamily member 10b	Homo sapiens	141-144
10594023-5	2000	Inhibition of NF-kappaB activation by expression of kinase-inactive MEK kinase 1(MEKK1) or dominant-negative IkappaB (DeltaIkappaB) blocked the increase in DR4 and DR5 expression following etoposide treatment.	Etoposide	189-198	TNF receptor superfamily member 10b	Homo sapiens	164-167
9563466-1	1998	The death receptor (DR) KILLER/DR5 gene has recently been identified as a doxorubicin-regulated transcript that was also induced by exogenous wild-type p53 in p53-negative cells.	Doxorubicin	74-85	TNF receptor superfamily member 10b	Homo sapiens	24-34
9563466-6	1998	Just like other p53-regulated genes, ionizing radiation induction of KILLER/DR5 occurs in p53 wild-type cells, whereas methyl methanesulfonate regulation of KILLER/DR5 occurs in a p53-dependent and -independent manner.	Methyl Methanesulfonate	119-142	TNF receptor superfamily member 10b	Homo sapiens	157-167
10597242-6	1999	Inhibition of transcription by Actinomycin D blocks both KILLER/DR5 and p21 induction in cells undergoing p53-dependent apoptosis.	Dactinomycin	31-44	TNF receptor superfamily member 10b	Homo sapiens	57-67
10336890-6	1999	Despite the altered polarity, the DR5-bound heterodimer was able to recruit the nuclear receptor coactivator ACTR in a vitamin D-dependent fashion.	Vitamin D	119-128	TNF receptor superfamily member 10b	Homo sapiens	34-37
10327056-8	1999	These results suggest that CD437-induced apoptosis is more extensive in NSCLC cells that express wild-type p53, possibly due to the involvement of the p53 regulated genes Killer/DR5, and Bax although CD437 can also induce apoptosis by means of a p53-independent mechanism.	CD 437	27-32	TNF receptor superfamily member 10b	Homo sapiens	178-181
9856825-9	1998	Deletion of the DR1d or DR5 sites reduced retinoid-induced promoter activity by 63% and 27%, respectively.	Retinoids	42-50	TNF receptor superfamily member 10b	Homo sapiens	24-27
9486405-6	1998	All patients with pSS, with or without autoantibodies to Ro and La, were found to have at least one of the HLA-DRB1 types DR2, DR3 or DR5.	pss	18-21	TNF receptor superfamily member 10b	Homo sapiens	134-137
7654186-1	1995	Functional retinoic acid response elements (RAREs) have been described wherein the direct repeats are separated by 1, 2 or 5 bp (termed DR1, DR2 and DR5 respectively).	Tretinoin	11-24	TNF receptor superfamily member 10b	Homo sapiens	149-152
7565738-3	1995	The greatest RA-dependent transactivation, seen with DR15, was similar to that observed with the canonical DR5.	Tretinoin	13-15	TNF receptor superfamily member 10b	Homo sapiens	107-110
8139911-1	1994	The polymorphic nature of sequences which act as retinoic acid response elements (RAREs and RXREs) in transactivation assays in mammalian cells, suggests that elements consisting of a direct repetition of a half site motif, separated by 1 to 5 base pairs (DR1 to DR5), are targets for retinoic acid (RA) signalling.	Tretinoin	82-84	TNF receptor superfamily member 10b	Homo sapiens	263-266
7558913-1	1995	Susceptibility to developing CD is widely accepted to be primarily associated with a particular HLA-DQ alpha beta heterodimer encoded by the DQA1*0501 and DQB1*0201 alleles in cis position on the DR3,DQ2 haplotype or in trans position by DR5,DQ7/DR7,DQ2 heterozygotes.	Cadmium	29-31	TNF receptor superfamily member 10b	Homo sapiens	238-241
7558913-5	1995	Furthermore, our data also show that those carrying the genotype DR5,DQ7/DR7,DQ2 have a significantly increased risk of developing CD as compared to those that are non-DR7 positive, also carrying the CD-associated HLA-DQ alpha beta heterodimer.	Cadmium	131-133	TNF receptor superfamily member 10b	Homo sapiens	65-68
7558913-5	1995	Furthermore, our data also show that those carrying the genotype DR5,DQ7/DR7,DQ2 have a significantly increased risk of developing CD as compared to those that are non-DR7 positive, also carrying the CD-associated HLA-DQ alpha beta heterodimer.	Cadmium	200-202	TNF receptor superfamily member 10b	Homo sapiens	65-68
7706255-0	1995	Retinoic acid induction of human tissue-type plasminogen activator gene expression via a direct repeat element (DR5) located at -7 kilobases.	Tretinoin	0-13	TNF receptor superfamily member 10b	Homo sapiens	112-115
7706255-5	1995	A functional retinoic acid response element (RARE), consisting of a direct repeat of the GGGTCA motif spaced by 5 nucleotides (t-PA/DR5), was localized at -7.3 kilobases.	Tretinoin	13-26	TNF receptor superfamily member 10b	Homo sapiens	132-135
7706255-5	1995	A functional retinoic acid response element (RARE), consisting of a direct repeat of the GGGTCA motif spaced by 5 nucleotides (t-PA/DR5), was localized at -7.3 kilobases.	gggtca	89-95	TNF receptor superfamily member 10b	Homo sapiens	132-135
7706255-6	1995	The t-PA/DR5 element interacted with the heterodimer composed of retinoic acid receptor alpha and retinoid X receptor alpha in vitro, whereas its mutation abolished induction by RA in transient expression.	Tretinoin	178-180	TNF receptor superfamily member 10b	Homo sapiens	9-12
16287099-6	2006	MG132 massively induced TRAIL receptor DR4 and DR5 membrane expression in HeLa, whereas in SiHa only DR5 membrane expression was upregulated from almost undetectable to high levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10b	Homo sapiens	47-50
8409432-7	1993	Finally, bulk sequencing profiles contained signals from further putative anchor residues clustering in the NH2-terminal region:tyrosine, phenylalanine, leucine, isoleucine, and valine are enriched at positions 2 to 4 in DR1, DR5, and DR6, however, at positions 4 to 6 in DR3.	Tyrosine	128-136	TNF receptor superfamily member 10b	Homo sapiens	226-229
8409432-7	1993	Finally, bulk sequencing profiles contained signals from further putative anchor residues clustering in the NH2-terminal region:tyrosine, phenylalanine, leucine, isoleucine, and valine are enriched at positions 2 to 4 in DR1, DR5, and DR6, however, at positions 4 to 6 in DR3.	Valine	178-184	TNF receptor superfamily member 10b	Homo sapiens	226-229
8151585-0	1994	Association of HLA-DR5 with mucocutaneous lesions in patients with rheumatoid arthritis receiving gold sodium thiomalate.	Gold Sodium Thiomalate	98-120	TNF receptor superfamily member 10b	Homo sapiens	19-22
1993839-6	1991	For DR2 and DR3 the shortest peptide was residues 6-15, an additional serine (residue 5) was required for DR1 and DR7 and an aspartic acid (residue 4) for DR4, DR5, and DR6.	Aspartic Acid	125-138	TNF receptor superfamily member 10b	Homo sapiens	160-163
1899160-0	1991	HLA-DR1, -DR5, and -DR8 antigen disparities are associated with acute steroid-resistant rejection and poor kidney graft survival.	Steroids	70-77	TNF receptor superfamily member 10b	Homo sapiens	10-13
1673331-2	1991	The 285-fold doxorubicin-resistant colon adenocarcinoma subline, LoVo/DR5, was found to overexpress the mRNA for P-glycoprotein without the concomitant requirement of MDR1 gene amplification, suggesting that relatively high levels of P-glycoprotein mediated multiple drug resistance may occur by transcriptional activation of the gene.	Doxorubicin	13-24	TNF receptor superfamily member 10b	Homo sapiens	70-73
33767436-7	2021	We showed that CRISPR/Cas9 mediated silencing of DR5 could block Bortezomib-mediated re-sensitization, demonstrating its critical role.	Bortezomib	65-75	TNF receptor superfamily member 10b	Homo sapiens	49-52
26074143-0	2015	RAD001 (everolimus) enhances TRAIL cytotoxicity in human leukemic Jurkat T cells by upregulating DR5.	Everolimus	8-18	TNF receptor superfamily member 10b	Homo sapiens	97-100
26074143-3	2015	In the present study, we showed that the Akt/mTOR inhibitor RAD001 (everolimus) induced cell death in a dose-dependent manner and enhanced TRAIL-induced apoptosis in human leukemic Jurkat T cells, which show PI3K/Akt/mTOR pathway activation and basal expression levels of death receptor (DR) 5 (TRAIL-R2).	Everolimus	68-78	TNF receptor superfamily member 10b	Homo sapiens	272-293
26074143-3	2015	In the present study, we showed that the Akt/mTOR inhibitor RAD001 (everolimus) induced cell death in a dose-dependent manner and enhanced TRAIL-induced apoptosis in human leukemic Jurkat T cells, which show PI3K/Akt/mTOR pathway activation and basal expression levels of death receptor (DR) 5 (TRAIL-R2).	Everolimus	68-78	TNF receptor superfamily member 10b	Homo sapiens	295-303
16287099-14	2006	Our results indicate that not only DR4 and DR5 upregulation but also XIAP inactivation contribute to rhTRAIL sensitization by MG132 in cervical cancer cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-131	TNF receptor superfamily member 10b	Homo sapiens	43-46
16287099-9	2006	Although p53 siRNA partially inhibited MG132-induced DR5 upregulation in HeLa and SiHa, no effect on rhTRAIL-induced apoptosis was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	TNF receptor superfamily member 10b	Homo sapiens	53-56
34926196-0	2021	Combination of oridonin and TRAIL induces apoptosis in uveal melanoma cells by upregulating DR5.	oridonin	15-23	TNF receptor superfamily member 10b	Homo sapiens	92-95
34288496-0	2022	Pyronaridine induces apoptosis in Non-small cell lung cancer cells by upregulating DR5 expression and inhibiting EGFR.	pyronaridine	0-12	TNF receptor superfamily member 10b	Homo sapiens	83-86
34288496-4	2022	The data showed that pyronaridine could upregulate the expression of TRAIL (TNF-related apoptosis-inducing ligand)-mediated DR5 (Death receptor 5) to promote cellular apoptosis.	pyronaridine	21-33	TNF receptor superfamily member 10b	Homo sapiens	124-127
34288496-4	2022	The data showed that pyronaridine could upregulate the expression of TRAIL (TNF-related apoptosis-inducing ligand)-mediated DR5 (Death receptor 5) to promote cellular apoptosis.	pyronaridine	21-33	TNF receptor superfamily member 10b	Homo sapiens	129-145
34926196-9	2021	The Western blot results showed that the protein expression levels of the DR5, a-caspase-3, and BAX increased, while the expression levels of the anti-apoptosis-related proteins XIAP and BCL-2 were suppressed when TRAIL and oridonin simultaneously administered to MUM-2B cells.	oridonin	224-232	TNF receptor superfamily member 10b	Homo sapiens	74-77
34926196-10	2021	Interfering the expression of DR5 gene in MUM-2B cells could reverse the inhibitory effect of oridonin and TRAIL on the proliferation and apoptosis induction of MUM-2B cells.	oridonin	94-102	TNF receptor superfamily member 10b	Homo sapiens	30-33
34926196-11	2021	CONCLUSION: The inhibitory effects of oridonin and TRAIL on MUM-2B cells are significantly enhanced when they were administered as a combined treatment, which may ascribe to up-regulation of DR5.	oridonin	38-46	TNF receptor superfamily member 10b	Homo sapiens	191-194
34681736-5	2021	ROS-induced endoplasmic reticulum (ER) stress by OSMI-1 not only upregulated CHOP-DR5 signaling but also activated Jun-N-terminal kinase (JNK), resulting in a decrease in Bcl2 and the release of cytochrome c from mitochondria.	ros	0-3	TNF receptor superfamily member 10b	Homo sapiens	82-85
34599545-0	2021	CSC-3436 sensitizes triple negative breast cancer cells to TRAIL-induced apoptosis through ROS-mediated p38/CHOP/death receptor 5 signaling pathways.	csc-3436	0-8	TNF receptor superfamily member 10b	Homo sapiens	113-129
34599545-0	2021	CSC-3436 sensitizes triple negative breast cancer cells to TRAIL-induced apoptosis through ROS-mediated p38/CHOP/death receptor 5 signaling pathways.	Reactive Oxygen Species	91-94	TNF receptor superfamily member 10b	Homo sapiens	113-129
34599545-4	2021	We found that CSC-3436 potentiated TRAIL-induced apoptosis in TRAIL-resistant TNBC cells and this correlated with the upregulation of death receptors (DR)-5 and down-regulation of decreased decoy receptor (DcR)-1 expression.	csc-3436	14-22	TNF receptor superfamily member 10b	Homo sapiens	134-156
34599545-7	2021	In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways.	csc-3436	37-45	TNF receptor superfamily member 10b	Homo sapiens	30-33
34599545-7	2021	In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways.	Reactive Oxygen Species	93-116	TNF receptor superfamily member 10b	Homo sapiens	30-33
34599545-7	2021	In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways.	Reactive Oxygen Species	118-121	TNF receptor superfamily member 10b	Homo sapiens	30-33
34599545-8	2021	Overall, our results indicated that CSC-3436 could potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and upregulation of DR5 via the ROS-mediated upregulation of CHOP protein.	csc-3436	36-44	TNF receptor superfamily member 10b	Homo sapiens	163-166
34599545-8	2021	Overall, our results indicated that CSC-3436 could potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and upregulation of DR5 via the ROS-mediated upregulation of CHOP protein.	Reactive Oxygen Species	175-178	TNF receptor superfamily member 10b	Homo sapiens	163-166
34711645-0	2021	Multimeric Anti-DR5 IgM Agonist Antibody IGM-8444 Is a Potent Inducer of Cancer Cell Apoptosis and Synergizes with Chemotherapy and BCL-2 Inhibitor ABT-199.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	148-151	TNF receptor superfamily member 10b	Homo sapiens	16-19
34503423-7	2022	NU 9056 also induced apoptosis by upregulating DR4, DR5, and caspase 8 expressions.	1,2-bis(isothiazol-5-yl)disulfane	0-7	TNF receptor superfamily member 10b	Homo sapiens	52-55
34659909-7	2021	Upon treatment with the imipridones, DIPG cell lines engaged CLpP/CLPX, the integrated stress response with ATF4 activation, and TRAIL death receptor 5 (DR5) induction.	imipridones	24-35	TNF receptor superfamily member 10b	Homo sapiens	153-156
34611476-8	2021	TRAILR2 was down-regulated by oxaliplatin and 5-FU, was not affected by CPT-11, and was increased by cisplatin.	Oxaliplatin	30-41	TNF receptor superfamily member 10b	Homo sapiens	0-7
34611476-8	2021	TRAILR2 was down-regulated by oxaliplatin and 5-FU, was not affected by CPT-11, and was increased by cisplatin.	Fluorouracil	46-50	TNF receptor superfamily member 10b	Homo sapiens	0-7
34611476-8	2021	TRAILR2 was down-regulated by oxaliplatin and 5-FU, was not affected by CPT-11, and was increased by cisplatin.	Cisplatin	101-110	TNF receptor superfamily member 10b	Homo sapiens	0-7
34246076-0	2021	EZH2i EPZ-6438 and HDACi vorinostat synergize with ONC201/TIC10 to activate integrated stress response, DR5, reduce H3K27 methylation, ClpX and promote apoptosis of multiple tumor types including DIPG.	Uridine Diphosphate N-Acetylmuramic Acid	6-9	TNF receptor superfamily member 10b	Homo sapiens	104-107
34575490-5	2021	The aim of the study was to fabricate Amph-PVP-based nanoparticles covalently conjugated with antitumor DR5-specific TRAIL (Tumor necrosis factor-related apoptosis-inducing ligand) variant DR5-B and to evaluate their in vitro cytotoxicity in 3D tumor spheroids.	amph-pvp	38-46	TNF receptor superfamily member 10b	Homo sapiens	104-107
34475055-7	2021	We also found that hyper-acetylation of histone by CBUD-1001 treatment leads to up-regulation of death receptor (DR) 5 in a dose- and time-dependent manner.	cbud-1001	51-60	TNF receptor superfamily member 10b	Homo sapiens	97-118
34475055-8	2021	Furthermore, we identified that enhanced sensitivity to TRAIL by combination with CBUD-1001 depends on the MAPK/CHOP axis, being a key mediator of DR5.	cbud-1001	82-91	TNF receptor superfamily member 10b	Homo sapiens	147-150
34475055-9	2021	CONCLUSION: A novel HDAC inhibitor CBUD-1001 sensitizes TRAIL-induced apoptosis via up-regulation of DR5, and that CBUD-1001 and TRAIL combination treatment offers an effective strategy to overcome TRAIL resistance in CRC cells.	cbud-1001	35-44	TNF receptor superfamily member 10b	Homo sapiens	101-104
34549714-0	2021	(Effect of DR5-mediated docetaxel-loaded lipid microbubble combined with ultrasoundtargeted microbubble destruction on HepG2 cell proliferation and apoptosis).	Docetaxel	24-33	TNF receptor superfamily member 10b	Homo sapiens	11-14
34549714-1	2021	OBJECTIVE: To investigate the effect of DR5-mediated docetaxel-targeted lipid microbubbles (MBs) combined with ultrasound-targeted microbubble destruction on apoptosis and expressions of Bcl-2, nuclear factor-kappaB(NF-kappaB), caspase-8, and DR5 in human HepG2 cells.	Docetaxel	53-62	TNF receptor superfamily member 10b	Homo sapiens	40-43
34549714-1	2021	OBJECTIVE: To investigate the effect of DR5-mediated docetaxel-targeted lipid microbubbles (MBs) combined with ultrasound-targeted microbubble destruction on apoptosis and expressions of Bcl-2, nuclear factor-kappaB(NF-kappaB), caspase-8, and DR5 in human HepG2 cells.	Docetaxel	53-62	TNF receptor superfamily member 10b	Homo sapiens	243-246
34582654-0	2021	Thymoquinone Crosstalks with DR5 to Sensitize TRAIL Resistance and Stimulate ROS-Mediated Cancer Apoptosis.	thymoquinone	0-12	TNF receptor superfamily member 10b	Homo sapiens	29-32
34582654-0	2021	Thymoquinone Crosstalks with DR5 to Sensitize TRAIL Resistance and Stimulate ROS-Mediated Cancer Apoptosis.	Reactive Oxygen Species	77-80	TNF receptor superfamily member 10b	Homo sapiens	29-32
34582654-6	2021	CONCLUSIONS: The synergistic influence between TQ which induced the DR5 and TRAIL, facilitating the connection between TRAIL and its receptors on the cancerous cell membrane.	thymoquinone	47-49	TNF receptor superfamily member 10b	Homo sapiens	68-71
34479917-7	2021	Furthermore, paclitaxel induced ROS-mediated DNA damage that triggered the activation of the extrinsic pathway of apoptosis via the up-regulation of death receptor (DR5) and caspase-8 activation.	Paclitaxel	13-23	TNF receptor superfamily member 10b	Homo sapiens	165-168
34479917-7	2021	Furthermore, paclitaxel induced ROS-mediated DNA damage that triggered the activation of the extrinsic pathway of apoptosis via the up-regulation of death receptor (DR5) and caspase-8 activation.	Reactive Oxygen Species	32-35	TNF receptor superfamily member 10b	Homo sapiens	165-168
34497804-4	2021	For functional analyses, we knocked down one of the cisplatin inducible lncRNAs, death receptor 5 antisense (DR5-AS) lncRNA, which resulted in a morphological change in HeLa cell shape without inducing any cell death.	Cisplatin	52-61	TNF receptor superfamily member 10b	Homo sapiens	81-97
34497804-4	2021	For functional analyses, we knocked down one of the cisplatin inducible lncRNAs, death receptor 5 antisense (DR5-AS) lncRNA, which resulted in a morphological change in HeLa cell shape without inducing any cell death.	Cisplatin	52-61	TNF receptor superfamily member 10b	Homo sapiens	109-112
34246076-0	2021	EZH2i EPZ-6438 and HDACi vorinostat synergize with ONC201/TIC10 to activate integrated stress response, DR5, reduce H3K27 methylation, ClpX and promote apoptosis of multiple tumor types including DIPG.	Vorinostat	25-35	TNF receptor superfamily member 10b	Homo sapiens	104-107
34187946-10	2021	In A549 and NCI-H2170 cells vanillin oxime exposure caused significant (p < 0.05) enhancement in CHOP and DR5 mRNA expression.	Vanillin Oxime	28-42	TNF receptor superfamily member 10b	Homo sapiens	106-109
34903991-6	2021	The result indicated that zebularine and TSA changed the expression level of the Bax, Bak, Bim Bcl-2, Bcl-xL, Mcl-1, DR4, DR5, FAS, FAS-L, TRAIL, DNA methyltransferase 1, 3a, and 3b, histone deacetylase inhibitors 1, 2, and 3 by which induced cell apoptosis and inhibit cell growth in all three cell lines.	pyrimidin-2-one beta-ribofuranoside	26-36	TNF receptor superfamily member 10b	Homo sapiens	122-125
34903991-6	2021	The result indicated that zebularine and TSA changed the expression level of the Bax, Bak, Bim Bcl-2, Bcl-xL, Mcl-1, DR4, DR5, FAS, FAS-L, TRAIL, DNA methyltransferase 1, 3a, and 3b, histone deacetylase inhibitors 1, 2, and 3 by which induced cell apoptosis and inhibit cell growth in all three cell lines.	trichostatin A	41-44	TNF receptor superfamily member 10b	Homo sapiens	122-125
34360606-12	2021	AP-1 also significantly enhanced the apoptotic effect of DOX after 24 h of treatment with significant upregulation of catalase, HTRA2/Omi, FADD together with DR5 and DR4 TRAIL-mediated apoptosis (p < 0.05), contributing to the antiproliferative activity of AP-1.	Doxorubicin	57-60	TNF receptor superfamily member 10b	Homo sapiens	158-161
34080659-6	2021	Genetic inhibitors of DR4 and DR5 significantly reduced amitriptyline-enhanced TRAIL-mediated apoptosis.	Amitriptyline	56-69	TNF receptor superfamily member 10b	Homo sapiens	30-33
34080659-8	2021	Blocking autophagy flux with the final stage autophagy inhibitor chloroquine (CQ) also upregulated DR4 and DR5 expression.	Chloroquine	65-76	TNF receptor superfamily member 10b	Homo sapiens	107-110
34080659-8	2021	Blocking autophagy flux with the final stage autophagy inhibitor chloroquine (CQ) also upregulated DR4 and DR5 expression.	Chloroquine	78-80	TNF receptor superfamily member 10b	Homo sapiens	107-110
34080659-11	2021	Overall, the present results contributed to understanding the mechanism responsible for the synergistic anticancer effect of amitriptyline and TRAIL and also presented a novel mechanism involved in DR4 and DR5 upregulation.	Amitriptyline	125-138	TNF receptor superfamily member 10b	Homo sapiens	206-209
35616096-4	2022	CPT MV could produce ROS in the targeted cells upon laser irradiation to improve death receptor (DR)-5 expression and trigger Cyt c release from mitochondria.	ros	21-24	TNF receptor superfamily member 10b	Homo sapiens	81-102
34195076-0	2021	Fangchinoline Inhibits Human Esophageal Cancer by Transactivating ATF4 to Trigger Both Noxa-Dependent Intrinsic and DR5-Dependent Extrinsic Apoptosis.	fangchinoline	0-13	TNF receptor superfamily member 10b	Homo sapiens	116-119
34195076-6	2021	Moreover, we found that FCL coordinatively triggered Noxa-dependent intrinsic apoptosis and DR5-dependent extrinsic apoptosis by transactivating ATF4, which is a novel mechanism.	fangchinoline	24-27	TNF receptor superfamily member 10b	Homo sapiens	92-95
34141868-6	2021	Metformin-upregulated TRAIL was secreted into conditioned medium (CM) and found to be functional, since the CM promoted TNBC cells undergoing apoptosis, which was abrogated by a recombinant TRAIL-R2-Fc chimera.	Metformin	0-9	TNF receptor superfamily member 10b	Homo sapiens	190-198
34141868-7	2021	Moreover, blockade of TRAIL binding to DR4/DR5 or specific knockdown of TRAIL expression significantly attenuated metformin-induced apoptosis.	Metformin	114-123	TNF receptor superfamily member 10b	Homo sapiens	43-46
34141870-5	2021	Oba01 utilizes anti-DR5 humanized monoclonal antibody (zaptuzumab) coupled via a cleavable linker to monomethyl auristatin E (MMAE).	monomethyl auristatin E	101-124	TNF receptor superfamily member 10b	Homo sapiens	20-23
34141870-5	2021	Oba01 utilizes anti-DR5 humanized monoclonal antibody (zaptuzumab) coupled via a cleavable linker to monomethyl auristatin E (MMAE).	monomethyl auristatin E	126-130	TNF receptor superfamily member 10b	Homo sapiens	20-23
35247515-8	2022	Together, the results herein reveal DDAs as the first small molecule, active site inhibitors of AGR2 and ERp44, and demonstrate roles for AGR2 and ERp44 in regulating the activity, stability, and localization of DR4 and DR5, and activation of Caspase 8.	ddas	36-40	TNF receptor superfamily member 10b	Homo sapiens	220-223
35039880-0	2022	(Corrigendum) 3-Bromopyruvate sensitizes human breast cancer cells to TRAIL-induced apoptosis via the phosphorylated AMPK-mediated upregulation of DR5.	bromopyruvate	14-29	TNF receptor superfamily member 10b	Homo sapiens	147-150
35568793-0	2022	20(s)-ginsenoside Rh2 promotes TRAIL-induced apoptosis by upregulating DR5 in human hepatocellular carcinoma cells.	Ginsenoside Rh2	0-21	TNF receptor superfamily member 10b	Homo sapiens	71-74
35568793-7	2022	At the same time, Rh2 can further enhance TRAIL-induced apoptosis by upregulating the death receptor 5, thereby significantly enhancing its anti-tumor effect.	rh2	18-21	TNF receptor superfamily member 10b	Homo sapiens	86-102
35149588-7	2022	Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TNF-related apoptosis-inducing ligand (TRAIL), 5-fluorouracil (5-FU) chemotherapy, and anti-PD-1 immunotherapy.	Fluorouracil	175-189	TNF receptor superfamily member 10b	Homo sapiens	12-15
35149588-7	2022	Deletion of DR5 in cancer cells in vitro and in vivo abrogated the potentiating effects of CDK4/6 inhibitors on immune cytokine TNF-related apoptosis-inducing ligand (TRAIL), 5-fluorouracil (5-FU) chemotherapy, and anti-PD-1 immunotherapy.	Fluorouracil	191-195	TNF receptor superfamily member 10b	Homo sapiens	12-15
35455398-5	2022	Specifically, dehydrocrenatidine significantly increased the expression of extrinsic pathway components (FAS, DR5, FADD, and TRADD) as well as intrinsic pathway components (Bax and Bim L/S) in liver cancer cells.	dehydrocrenatidine	14-32	TNF receptor superfamily member 10b	Homo sapiens	110-113
35086954-7	2022	Subsequent MEDI3039 combination-screening of TRAIL-R2, caspase-8, FADD and BID knockout models with 60 compounds with varying mechanisms-of-action identified 2 inhibitor of apoptosis proteins (IAPs) that exhibited strong synergy with MEDI3039 that could reverse resistance only in BID-deleted models.	medi3039	234-242	TNF receptor superfamily member 10b	Homo sapiens	45-53
35141009-8	2022	Cariporide treatment also decreased CRC cell shed TRAIL-R2, TRAIL-R3, and PD-L1 which is relevant in the context of immunotherapy.	cariporide	0-10	TNF receptor superfamily member 10b	Homo sapiens	50-58
35077998-13	2022	In conclusion, we identified that the concomitant regulation of both antiapoptotic and proapoptotic factors and DR5 is an essential molecular mechanism for overcoming TRAIL resistance in SH-SY5Y and the combination of ERN-T and AZD5582 potentially constitutes a novel therapeutic strategy, which is highly effective and safe for neuroblastoma.	ern-t	218-223	TNF receptor superfamily member 10b	Homo sapiens	112-115
35077998-13	2022	In conclusion, we identified that the concomitant regulation of both antiapoptotic and proapoptotic factors and DR5 is an essential molecular mechanism for overcoming TRAIL resistance in SH-SY5Y and the combination of ERN-T and AZD5582 potentially constitutes a novel therapeutic strategy, which is highly effective and safe for neuroblastoma.	N,N'-(2,2'-(hexa-2,4-diyne-1,6-diylbis(oxy))bis(2,3-dihydro-1H-indene-2,1-diyl))bis(1-(2-cyclohexyl-2-(2-(methylamino)propanamido)acetyl)pyrrolidine-2-carboxamide)	228-235	TNF receptor superfamily member 10b	Homo sapiens	112-115
35200638-9	2022	(-)-Agelasidine A also increased apoptosis-associated proteins (DR4, DR5, FAS), which are related to extrinsic pathways.	agelasidine A	4-17	TNF receptor superfamily member 10b	Homo sapiens	69-72
35200638-13	2022	Moreover, 4-PBA, an ER stress inhibitor, could also abrogate (-)-agelasidine A-induced cell viability reduction, annexin V+ apoptosis, death receptor (DR4, DR5, FAS) expression, mitochondrial dysfunction, and cytochrome c release.	4-phenylbutylamine	10-15	TNF receptor superfamily member 10b	Homo sapiens	156-159
35200638-13	2022	Moreover, 4-PBA, an ER stress inhibitor, could also abrogate (-)-agelasidine A-induced cell viability reduction, annexin V+ apoptosis, death receptor (DR4, DR5, FAS) expression, mitochondrial dysfunction, and cytochrome c release.	agelasidine A	65-78	TNF receptor superfamily member 10b	Homo sapiens	156-159
35047402-7	2021	We found that the combination of DHA-TF and the death receptor 5-specific TRAIL variant DHER leads to an increase in DR5 expression in all four TNBC cell lines, while higher cytotoxicity was observed in MDA-MB-231, and MDA-MB-436.	artenimol	33-36	TNF receptor superfamily member 10b	Homo sapiens	117-120
35047402-7	2021	We found that the combination of DHA-TF and the death receptor 5-specific TRAIL variant DHER leads to an increase in DR5 expression in all four TNBC cell lines, while higher cytotoxicity was observed in MDA-MB-231, and MDA-MB-436.	dher	88-92	TNF receptor superfamily member 10b	Homo sapiens	48-64
35047402-7	2021	We found that the combination of DHA-TF and the death receptor 5-specific TRAIL variant DHER leads to an increase in DR5 expression in all four TNBC cell lines, while higher cytotoxicity was observed in MDA-MB-231, and MDA-MB-436.	dher	88-92	TNF receptor superfamily member 10b	Homo sapiens	117-120
2715056-7	1989	A comparison of all the available protein sequences of DRB gene products showed that the first hypervariable region of DR3 and DR5 (and DRw6), and no other region, contains the sequence Glu9-Tyr-Ser-Thr-Ser13.	Serine	195-198	TNF receptor superfamily member 10b	Homo sapiens	127-130
2490151-5	1989	We found HLA-DR5 to be significantly overrepresented in the patients with RSA who aborted again after treatment with paternal mononuclear cell immunotherapy, compared with the incidence of this phenotype in a control population.	rabbit sperm membrane autoantigen	74-77	TNF receptor superfamily member 10b	Homo sapiens	13-16
2715056-7	1989	A comparison of all the available protein sequences of DRB gene products showed that the first hypervariable region of DR3 and DR5 (and DRw6), and no other region, contains the sequence Glu9-Tyr-Ser-Thr-Ser13.	Threonine	199-202	TNF receptor superfamily member 10b	Homo sapiens	127-130
2466297-3	1989	The binding of the CS peptides to DR5 or DRw6 proteins was then determined in a proliferation assay using two established DR5 or DRw6-restricted T-cell clones with specificity for the stimulator peptides as responder cells.	Cesium	19-21	TNF receptor superfamily member 10b	Homo sapiens	34-37
2466297-3	1989	The binding of the CS peptides to DR5 or DRw6 proteins was then determined in a proliferation assay using two established DR5 or DRw6-restricted T-cell clones with specificity for the stimulator peptides as responder cells.	Cesium	19-21	TNF receptor superfamily member 10b	Homo sapiens	122-125
2466297-4	1989	One of five CS peptides, comprising together about 50% of the CS protein sequence, was found to compete with the binding of the stimulator peptides to DR5 and DRw6.	Cesium	12-14	TNF receptor superfamily member 10b	Homo sapiens	151-154
2466297-5	1989	The CS peptide CS-(378-398), binding to DR5 and DRw6, was then shown to be able to induce primary in vitro responses of T cells from donors with DR5 and DRw6 haplotypes.	Cesium	4-6	TNF receptor superfamily member 10b	Homo sapiens	40-43
2466297-5	1989	The CS peptide CS-(378-398), binding to DR5 and DRw6, was then shown to be able to induce primary in vitro responses of T cells from donors with DR5 and DRw6 haplotypes.	Cesium	4-6	TNF receptor superfamily member 10b	Homo sapiens	145-148
2466297-5	1989	The CS peptide CS-(378-398), binding to DR5 and DRw6, was then shown to be able to induce primary in vitro responses of T cells from donors with DR5 and DRw6 haplotypes.	Cesium	15-17	TNF receptor superfamily member 10b	Homo sapiens	40-43
2466297-5	1989	The CS peptide CS-(378-398), binding to DR5 and DRw6, was then shown to be able to induce primary in vitro responses of T cells from donors with DR5 and DRw6 haplotypes.	Cesium	15-17	TNF receptor superfamily member 10b	Homo sapiens	145-148
33857626-0	2021	Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo.	Sodium Fluoride	0-15	TNF receptor superfamily member 10b	Homo sapiens	87-90
2445714-2	1987	The population distribution shows that each of the DRw52 associated specificities DR3, DR5, and DRw6 may occur with and without LB-Q1.	lb-q1	128-133	TNF receptor superfamily member 10b	Homo sapiens	87-90
3890265-6	1985	These studies document that the MB1 allodeterminant resides on DS molecules from this DR5 cell line and provide additional evidence that MB1 and MB3 are alleles of the same Class II antigen system.	Deuterium	63-65	TNF receptor superfamily member 10b	Homo sapiens	86-89
3935278-4	1985	This oligonucleotide hybridized only with the DNA from DR3 or DR5 individuals tested, even under stringent conditions of washing.	Oligonucleotides	5-20	TNF receptor superfamily member 10b	Homo sapiens	62-65
3871759-1	1985	Antiserum 8w670 which had been classified as anti-DR5 in the Workshop analysis was found by the direct binding test to react with about 40% of Ia molecules in an Ia preparation from LG38 cells (DR5,5) that was deleted of DR molecules and DR-like molecules we call BR and enriched in DC molecules by pretreatment with a rabbit antiserum raised against alpha-subunits of DR and BR molecules.	Bromine	264-266	TNF receptor superfamily member 10b	Homo sapiens	50-53
3871759-1	1985	Antiserum 8w670 which had been classified as anti-DR5 in the Workshop analysis was found by the direct binding test to react with about 40% of Ia molecules in an Ia preparation from LG38 cells (DR5,5) that was deleted of DR molecules and DR-like molecules we call BR and enriched in DC molecules by pretreatment with a rabbit antiserum raised against alpha-subunits of DR and BR molecules.	Bromine	376-378	TNF receptor superfamily member 10b	Homo sapiens	50-53
6328695-5	1984	The persons with HLA-DR5 had significantly higher anti-EBNA titers than those without DR5.	N-tert-Butyl-N-ethylnitrosamine	55-59	TNF receptor superfamily member 10b	Homo sapiens	21-24
33857626-0	2021	Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo.	Reactive Oxygen Species	70-73	TNF receptor superfamily member 10b	Homo sapiens	87-90
33857626-8	2021	Specifically, NOX4 knockdown inhibited NaF-induced the activation of p53/DR5 axis by reducing NOX4-derived ROS production.	Reactive Oxygen Species	107-110	TNF receptor superfamily member 10b	Homo sapiens	73-76
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	43-46
33942150-18	2021	Multivalent TRAIL polymers bind and activate DR4 and DR5 specifically and exclusively, triggering the signaling pathways with higher potency, and greater efficacy than TRAIL.	Polymers	18-26	TNF receptor superfamily member 10b	Homo sapiens	53-56
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
33898931-6	2021	Consistent with our earlier findings, the BMMSCs protected MM cells against KHYG-1 and DR5-agonistic antibodies by inducing resistance mechanisms that were largely abrogated by the small molecule FL118, an inhibitor of multiple antiapoptotic proteins including Survivin, Mcl-1, and XIAP.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	196-201	TNF receptor superfamily member 10b	Homo sapiens	87-90
33937072-9	2021	Taken together, our study showed that LCT-3d induced apoptosis via DR5-mediated mitochondrial apoptotic pathway in gastric cancer cells.	N-[5-(4-Nitrophenyl)-1,3,4-thiadiazol-2-yl]acetamide	38-41	TNF receptor superfamily member 10b	Homo sapiens	67-70
33894272-8	2021	KEY FINDINGS: Upon treatment with oleuropein, the expression of P21, P53, and TNFRSF10B increased while that of Bcl-2 and Mcl1 decreased.	oleuropein	34-44	TNF receptor superfamily member 10b	Homo sapiens	78-87
33937072-0	2021	LCT-3d Induces Oxidative Stress-Mediated Apoptosis by Upregulating Death Receptor 5 in Gastric Cancer Cells.	N-[5-(4-Nitrophenyl)-1,3,4-thiadiazol-2-yl]acetamide	0-3	TNF receptor superfamily member 10b	Homo sapiens	67-83
33841136-14	2021	DR5 upregulation induced by alternol required the production of reactive oxygen species (ROS).	Alternol	28-36	TNF receptor superfamily member 10b	Homo sapiens	0-3
33937072-4	2021	The up-regulation of Death receptor 5 (DR5) in MGC803 cells was observed with LCT-3d treatment.	N-[5-(4-Nitrophenyl)-1,3,4-thiadiazol-2-yl]acetamide	78-81	TNF receptor superfamily member 10b	Homo sapiens	21-37
33937072-4	2021	The up-regulation of Death receptor 5 (DR5) in MGC803 cells was observed with LCT-3d treatment.	N-[5-(4-Nitrophenyl)-1,3,4-thiadiazol-2-yl]acetamide	78-81	TNF receptor superfamily member 10b	Homo sapiens	39-42
33937072-5	2021	Knockdown of DR5 on MGC803 cells partially reversed the LCT-3d-induced mitochondrial apoptosis.	N-[5-(4-Nitrophenyl)-1,3,4-thiadiazol-2-yl]acetamide	56-59	TNF receptor superfamily member 10b	Homo sapiens	13-16
33937072-7	2021	The results demonstrate that the elevating ROS can up-regulate the expression of DR5, resulting in apoptosis via mitochondrial pathway.	Reactive Oxygen Species	43-46	TNF receptor superfamily member 10b	Homo sapiens	81-84
33916015-0	2021	Death Receptor 5 (TNFRSF10B) Is Upregulated and TRAIL Resistance Is Reversed in Hypoxia and Normoxia in Colorectal Cancer Cell Lines after Treatment with Skyrin, the Active Metabolite of Hypericum spp.	skyrin	154-160	TNF receptor superfamily member 10b	Homo sapiens	0-16
33916015-0	2021	Death Receptor 5 (TNFRSF10B) Is Upregulated and TRAIL Resistance Is Reversed in Hypoxia and Normoxia in Colorectal Cancer Cell Lines after Treatment with Skyrin, the Active Metabolite of Hypericum spp.	skyrin	154-160	TNF receptor superfamily member 10b	Homo sapiens	18-27
33921748-7	2021	Altogether, our findings establish ATF3 as a pro-apoptotic protein in arsenic-induced airway epithelial apoptosis through transcriptionally regulating DR5 and Bcl-xL, highlighting the potential of ATF3 as an early and sensitive biomarker for arsenic-caused lung injury.	Arsenic	70-77	TNF receptor superfamily member 10b	Homo sapiens	151-154
33841136-10	2021	Results: When the mechanisms were investigated, we discovered that alternol increased DR5 expression.	Alternol	67-75	TNF receptor superfamily member 10b	Homo sapiens	86-89
33841136-14	2021	DR5 upregulation induced by alternol required the production of reactive oxygen species (ROS).	Reactive Oxygen Species	64-87	TNF receptor superfamily member 10b	Homo sapiens	0-3
33841136-11	2021	DR5 knockdown by siRNA eliminated the enhanced effect of alternol on TRAIL-mediated apoptosis.	Alternol	57-65	TNF receptor superfamily member 10b	Homo sapiens	0-3
33841136-14	2021	DR5 upregulation induced by alternol required the production of reactive oxygen species (ROS).	Reactive Oxygen Species	89-92	TNF receptor superfamily member 10b	Homo sapiens	0-3
33841136-15	2021	Removing ROS inhibited the induction of DR5 and blocked the antiapoptotic proteins induced by alternol.	Reactive Oxygen Species	9-12	TNF receptor superfamily member 10b	Homo sapiens	40-43
33841136-16	2021	Conclusion: Taken together, our research suggested that alternol increased TRAIL-mediated apoptosis via inhibiting antiapoptotic proteins and upregulating DR5 levels via ROS generation and the CHOP pathway.	Alternol	56-64	TNF receptor superfamily member 10b	Homo sapiens	155-158
33676890-0	2021	Citrus-derived DHCP inhibits mitochondrial complex II to enhance TRAIL sensitivity via ROS-induced DR5 upregulation.	dhcp	15-19	TNF receptor superfamily member 10b	Homo sapiens	99-102
33737574-0	2021	Death agonist antibody against TRAILR2/DR5/TNFRSF10B enhances birinapant anti-tumor activity in HPV-positive head and neck squamous cell carcinomas.	birinapant	62-72	TNF receptor superfamily member 10b	Homo sapiens	31-38
33737574-0	2021	Death agonist antibody against TRAILR2/DR5/TNFRSF10B enhances birinapant anti-tumor activity in HPV-positive head and neck squamous cell carcinomas.	birinapant	62-72	TNF receptor superfamily member 10b	Homo sapiens	39-42
33737574-0	2021	Death agonist antibody against TRAILR2/DR5/TNFRSF10B enhances birinapant anti-tumor activity in HPV-positive head and neck squamous cell carcinomas.	birinapant	62-72	TNF receptor superfamily member 10b	Homo sapiens	43-52
33676890-0	2021	Citrus-derived DHCP inhibits mitochondrial complex II to enhance TRAIL sensitivity via ROS-induced DR5 upregulation.	ros	87-90	TNF receptor superfamily member 10b	Homo sapiens	99-102
33676890-7	2021	ROS significantly increase the expression of TRAIL death receptor 5 (DR5) via the p53 and C/EBP homologous protein pathways.	ros	0-3	TNF receptor superfamily member 10b	Homo sapiens	69-72
33385372-1	2021	In the present study, Death receptor-5 (DR5) antibody conjugated solid lipid nanoparticles (DR5-DAPT-SLNs) has been formulated for effective intracellular of gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) to cancer cells.	dapt	185-254	TNF receptor superfamily member 10b	Homo sapiens	22-38
33385372-1	2021	In the present study, Death receptor-5 (DR5) antibody conjugated solid lipid nanoparticles (DR5-DAPT-SLNs) has been formulated for effective intracellular of gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) to cancer cells.	dapt	185-254	TNF receptor superfamily member 10b	Homo sapiens	40-43
33385372-1	2021	In the present study, Death receptor-5 (DR5) antibody conjugated solid lipid nanoparticles (DR5-DAPT-SLNs) has been formulated for effective intracellular of gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) to cancer cells.	dapt	185-254	TNF receptor superfamily member 10b	Homo sapiens	92-95
33385372-1	2021	In the present study, Death receptor-5 (DR5) antibody conjugated solid lipid nanoparticles (DR5-DAPT-SLNs) has been formulated for effective intracellular of gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) to cancer cells.	dapt	96-100	TNF receptor superfamily member 10b	Homo sapiens	22-38
33385372-1	2021	In the present study, Death receptor-5 (DR5) antibody conjugated solid lipid nanoparticles (DR5-DAPT-SLNs) has been formulated for effective intracellular of gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) to cancer cells.	dapt	96-100	TNF receptor superfamily member 10b	Homo sapiens	40-43
33385372-1	2021	In the present study, Death receptor-5 (DR5) antibody conjugated solid lipid nanoparticles (DR5-DAPT-SLNs) has been formulated for effective intracellular of gamma-secretase inhibitor, N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) to cancer cells.	dapt	96-100	TNF receptor superfamily member 10b	Homo sapiens	92-95
33385372-6	2021	DR5-DAPT-SLNs have higher cytotoxicity in MDA-MB231 cells compared to DAPT-SLNs (non-targeted) and the bulk drug.	dapt	4-8	TNF receptor superfamily member 10b	Homo sapiens	0-3
33385372-8	2021	The above results, therefore, demonstrate DR5 mediated uptake is responsible for improved cytotoxicity of DAPT.	dapt	106-110	TNF receptor superfamily member 10b	Homo sapiens	42-45
33385372-9	2021	In the in vivo anticancer study, DR5-DAPT-SLNs show greater tumor regression when compared to DAPT-SLNs and the bulk drug.	dapt	37-41	TNF receptor superfamily member 10b	Homo sapiens	33-36
33385372-10	2021	In conclusion, the results of the present study demonstrate that the DR5-DAPT-SLNs selectively target cancer cells and potentiate the anticancer efficacy of DAPT against TNBC cells.	dapt	73-77	TNF receptor superfamily member 10b	Homo sapiens	69-72
33385372-10	2021	In conclusion, the results of the present study demonstrate that the DR5-DAPT-SLNs selectively target cancer cells and potentiate the anticancer efficacy of DAPT against TNBC cells.	dapt	157-161	TNF receptor superfamily member 10b	Homo sapiens	69-72
33505114-12	2021	Furthermore, p53 knockdown attenuated the expression of PUMA and DR5 in TRAIL-induced CRC cells treated with encorafenib.	encorafenib	109-120	TNF receptor superfamily member 10b	Homo sapiens	65-68
33469674-5	2021	Combination treatment with VPA and MSCs-TRAIL enhanced the glioma therapeutic effect by increasing death receptor 5 and caspase activation.	Valproic Acid	27-30	TNF receptor superfamily member 10b	Homo sapiens	99-115
33092912-0	2021	Corrigendum to "FLLL12 induces apoptosis in lung cancer cells through a p53/p73-independent but death receptor 5-dependent pathway" [Canc.	flll12	16-22	TNF receptor superfamily member 10b	Homo sapiens	96-112
33505114-10	2021	It was also found that encorafenib exerted its promoting effects on cell apoptosis of CRC cells via the elevation of DR5.	encorafenib	23-34	TNF receptor superfamily member 10b	Homo sapiens	117-120
33037135-0	2021	Selective tumor cell apoptosis and tumor regression in CDH17-positive colorectal cancer models using BI 905711, a novel liver-sparing TRAILR2 agonist.	bi 905711	101-110	TNF receptor superfamily member 10b	Homo sapiens	134-141
33037135-3	2021	BI 905711 is a novel tetravalent bispecific antibody targeting both TRAILR2 and CDH17 and represents a novel liver-sparing TRAILR2 agonist specifically designed to overcome the disadvantages of previous strategies.	bi 905711	0-9	TNF receptor superfamily member 10b	Homo sapiens	68-75
33037135-3	2021	BI 905711 is a novel tetravalent bispecific antibody targeting both TRAILR2 and CDH17 and represents a novel liver-sparing TRAILR2 agonist specifically designed to overcome the disadvantages of previous strategies.	bi 905711	0-9	TNF receptor superfamily member 10b	Homo sapiens	123-130
33352782-5	2020	The G1-blocker hydroxyurea augmented BS-181-induced apoptosis by enhancing TRAIL/DR4/DR5 upregulation and c-FLIP down-regulation.	Hydroxyurea	15-26	TNF receptor superfamily member 10b	Homo sapiens	85-88
33296043-5	2020	Binding of 18F-C2Am to apoptotic and necrotic tumor cells was assessed in vitro, and also in vivo, by dynamic PET and biodistribution measurements in mice bearing human tumor xenografts treated with a TRAILR2 agonist or with conventional chemotherapy.	18f-c2am	11-19	TNF receptor superfamily member 10b	Homo sapiens	201-208
33007289-4	2020	AMC-04 upregulated the expression of activating transcription factor-4 (ATF4)-C/EBP homologous protein (CHOP) and death receptor 5 (DR5) in cancer cells, as revealed by microarray analysis, small-interference RNA assay, and western blotting.	7-amino-4-methylcoumarin	0-3	TNF receptor superfamily member 10b	Homo sapiens	114-130
33007289-4	2020	AMC-04 upregulated the expression of activating transcription factor-4 (ATF4)-C/EBP homologous protein (CHOP) and death receptor 5 (DR5) in cancer cells, as revealed by microarray analysis, small-interference RNA assay, and western blotting.	7-amino-4-methylcoumarin	0-3	TNF receptor superfamily member 10b	Homo sapiens	132-135
32200503-7	2020	Knockdown of DR5 abrogated apoptosis induced by the combination of CUDC-907 and TRAIL in breast cancer cells.	CUDC-907	67-75	TNF receptor superfamily member 10b	Homo sapiens	13-16
32200503-9	2020	JNK inhibitor pretreatment attenuated CUDC-907-induced upregulation of DR5.	CUDC-907	38-46	TNF receptor superfamily member 10b	Homo sapiens	71-74
32200503-0	2020	CUDC-907 enhances TRAIL-induced apoptosis through upregulation of DR5 in breast cancer cells.	CUDC-907	0-8	TNF receptor superfamily member 10b	Homo sapiens	66-69
32200503-10	2020	In summary, CUDC-907 shows potent cytotoxicity against breast cancer cells and facilitates TRAIL-mediated apoptosis through DR5 upregulation.	CUDC-907	12-20	TNF receptor superfamily member 10b	Homo sapiens	124-127
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	TNF receptor superfamily member 10b	Homo sapiens	33-49
33180729-6	2020	We show that the action of the herbal drug, Cryptotanshinone on OS cell lines induces apoptosis by increasing sensitivity to TNF-related apoptosis-inducing ligand (TRAIL) through its multi-pronged action on STAT3, DRP1 and DR5.	cryptotanshinone	44-60	TNF receptor superfamily member 10b	Homo sapiens	223-226
32200503-6	2020	CUDC-907 enhanced expressions of death receptor 5 (DR5), reduced the levels of anti-apoptotic molecules XIAP, Bcl-2 and Bcl-xL.	CUDC-907	0-8	TNF receptor superfamily member 10b	Homo sapiens	51-54
32777260-0	2020	Luteolin enhances TRAIL sensitivity in non-small cell lung cancer cells through increasing DR5 expression and Drp1-mediated mitochondrial fission.	Luteolin	0-8	TNF receptor superfamily member 10b	Homo sapiens	91-94
33122623-7	2020	Moreover, DR5 knockdown or knockout attenuated siRALB-induced apoptosis, confirming the role of the extrinsic apoptotic pathway as a regulator of siRALB-induced cell death.	siralb	47-53	TNF receptor superfamily member 10b	Homo sapiens	10-13
32433558-5	2020	In contrast, oxygen, and nutrient deprivation promote high amounts of TRAILR2 expression in TRAIL-hypersensitive cells in inner spheroid layers.	Oxygen	13-19	TNF receptor superfamily member 10b	Homo sapiens	70-77
32433558-6	2020	COX-II inhibitor celecoxib further enhanced TRAILR2 expression in spheroids, likely resulting from increased ER stress, and thereby re-sensitized TRAIL-resistant cell layers to treatment.	Celecoxib	17-26	TNF receptor superfamily member 10b	Homo sapiens	44-51
32777260-8	2020	Moreover, luteolin treatment alone or in combination with TRAIL increased the phosphorylation of c-Jun N-terminal kinase (JNK), while SP600125 (the JNK inhibitor) significantly abolished the synergistic effect on DR5 expression and Drp1 translocation, indicating that JNK signaling activation was greatly associated with the synergistic effect exerted by luteolin in NSCLC cells.	Luteolin	10-18	TNF receptor superfamily member 10b	Homo sapiens	213-216
32777260-8	2020	Moreover, luteolin treatment alone or in combination with TRAIL increased the phosphorylation of c-Jun N-terminal kinase (JNK), while SP600125 (the JNK inhibitor) significantly abolished the synergistic effect on DR5 expression and Drp1 translocation, indicating that JNK signaling activation was greatly associated with the synergistic effect exerted by luteolin in NSCLC cells.	pyrazolanthrone	134-142	TNF receptor superfamily member 10b	Homo sapiens	213-216
33050333-0	2020	Dexamethasone Inhibits TRAIL-Induced Apoptosis through c-FLIP(L) Upregulation and DR5 Downregulation by GSK3beta Activation in Cancer Cells.	Dexamethasone	0-13	TNF receptor superfamily member 10b	Homo sapiens	82-85
33240775-4	2020	Mechanistically, curcumol directly targets NQO2 to cause reactive oxygen species (ROS) generation, which triggers endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP) death receptor (DR5) signaling, sensitizing NSCLC cell to TRAIL-induced apoptosis.	Reactive Oxygen Species	82-85	TNF receptor superfamily member 10b	Homo sapiens	196-199
33240775-4	2020	Mechanistically, curcumol directly targets NQO2 to cause reactive oxygen species (ROS) generation, which triggers endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP) death receptor (DR5) signaling, sensitizing NSCLC cell to TRAIL-induced apoptosis.	curcumol	17-25	TNF receptor superfamily member 10b	Homo sapiens	196-199
33050333-3	2020	We found that upregulation of c-FLIP(L) and downregulation of death receptor 5 (DR5; receptor for TRAIL ligand) contribute to the anti-apoptotic effect of DEX on TRAIL-induced apoptosis.	Dexamethasone	155-158	TNF receptor superfamily member 10b	Homo sapiens	62-78
33050333-3	2020	We found that upregulation of c-FLIP(L) and downregulation of death receptor 5 (DR5; receptor for TRAIL ligand) contribute to the anti-apoptotic effect of DEX on TRAIL-induced apoptosis.	Dexamethasone	155-158	TNF receptor superfamily member 10b	Homo sapiens	80-83
33050333-7	2020	In addition, DEX decreased protein stability of DR5 via GSK-3beta-mediated upregulation of Cbl, an E3 ligase of DR5.	Dexamethasone	13-16	TNF receptor superfamily member 10b	Homo sapiens	48-51
33050333-7	2020	In addition, DEX decreased protein stability of DR5 via GSK-3beta-mediated upregulation of Cbl, an E3 ligase of DR5.	Dexamethasone	13-16	TNF receptor superfamily member 10b	Homo sapiens	112-115
33050333-8	2020	Knockdown of Cbl by siRNA markedly inhibited DEX-induced DR5 downregulation.	Dexamethasone	45-48	TNF receptor superfamily member 10b	Homo sapiens	57-60
33050333-9	2020	Taken together, these results suggest that DEX inhibits TRAIL-mediated apoptosis via GSK-3beta-mediated DR5 downregulation and c-FLIP(L) upregulation in cancer cells.	Dexamethasone	43-46	TNF receptor superfamily member 10b	Homo sapiens	104-107
33050112-0	2020	Magnolol Enhances the Therapeutic Effects of TRAIL through DR5 Upregulation and Downregulation of c-FLIP and Mcl-1 Proteins in Cancer Cells.	magnolol	0-8	TNF receptor superfamily member 10b	Homo sapiens	59-62
33050112-2	2020	We found that magnolol sensitizes TRAIL-induced apoptotic cell death via upregulation of DR5 and downregulation of cellular FLICE-inhibitory protein (c-FLIP) and Mcl-1 in cancer cells, but not in normal cells.	magnolol	14-22	TNF receptor superfamily member 10b	Homo sapiens	89-92
32941010-1	2020	Fatty acid-induced upregulation of death receptor 5 (DR5) and its cognate ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), promotes hepatocyte lipoapoptosis, which is a key mechanism in the progression of fatty liver disease.	Fatty Acids	0-10	TNF receptor superfamily member 10b	Homo sapiens	35-51
33050112-3	2020	Mechanistically, magnolol increased ATF4-dependent DR5 expression at the transcription level, and knockdown of ATF4 markedly inhibited magnolol-induced DR5 upregulation.	magnolol	17-25	TNF receptor superfamily member 10b	Homo sapiens	51-54
32941010-1	2020	Fatty acid-induced upregulation of death receptor 5 (DR5) and its cognate ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), promotes hepatocyte lipoapoptosis, which is a key mechanism in the progression of fatty liver disease.	Fatty Acids	0-10	TNF receptor superfamily member 10b	Homo sapiens	53-56
33050112-3	2020	Mechanistically, magnolol increased ATF4-dependent DR5 expression at the transcription level, and knockdown of ATF4 markedly inhibited magnolol-induced DR5 upregulation.	magnolol	135-143	TNF receptor superfamily member 10b	Homo sapiens	152-155
33050112-4	2020	Silencing DR5 with siRNA prevented combined treatment with magnolol and TRAIL-induced apoptosis and PARP cleavage.	magnolol	59-67	TNF receptor superfamily member 10b	Homo sapiens	10-13
33050112-6	2020	Our results revealed that magnolol enhanced TRAIL-induced apoptosis via ATF4-dependent DR5 upregulation and downregulation of c-FLIP and Mcl-1 proteins.	magnolol	26-34	TNF receptor superfamily member 10b	Homo sapiens	87-90
32941010-4	2020	To this end, we used yeast display and a designed combinatorial library to identify a synthetic 58-amino acid affibody ligand that specifically binds the DR5.	58-amino acid	96-109	TNF receptor superfamily member 10b	Homo sapiens	154-157
33023194-0	2020	Selinexor Sensitizes TRAIL-R2-Positive TNBC Cells to the Activity of TRAIL-R2xCD3 Bispecific Antibody.	selinexor	0-9	TNF receptor superfamily member 10b	Homo sapiens	21-29
32692906-7	2020	These results represent the first mechanistic insight into how O-glycan structures on cell surface modulate their sensitivity to apoptotic stimuli, suggesting expression of Tn/STn may offer tumor cell survival advantages through altering DR4 and/or DR5 activity.	o-glycan	63-71	TNF receptor superfamily member 10b	Homo sapiens	249-252
32899699-4	2020	ATS/DHA induces the expression of DR5 in a P53 dependent manner in HCT116 and DLD-1 cells.	artenimol	4-7	TNF receptor superfamily member 10b	Homo sapiens	34-37
32899699-5	2020	Both ATS and DHA overcome the resistance to DHER-induced apoptosis in HCT116, mainly through upregulating death receptor 5 (DR5).	artenimol	13-16	TNF receptor superfamily member 10b	Homo sapiens	106-122
32899699-5	2020	Both ATS and DHA overcome the resistance to DHER-induced apoptosis in HCT116, mainly through upregulating death receptor 5 (DR5).	artenimol	13-16	TNF receptor superfamily member 10b	Homo sapiens	124-127
32899699-5	2020	Both ATS and DHA overcome the resistance to DHER-induced apoptosis in HCT116, mainly through upregulating death receptor 5 (DR5).	dher	44-48	TNF receptor superfamily member 10b	Homo sapiens	106-122
32899699-5	2020	Both ATS and DHA overcome the resistance to DHER-induced apoptosis in HCT116, mainly through upregulating death receptor 5 (DR5).	dher	44-48	TNF receptor superfamily member 10b	Homo sapiens	124-127
32899699-6	2020	We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays.	artenimol	25-28	TNF receptor superfamily member 10b	Homo sapiens	97-100
32899699-6	2020	We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays.	dher	56-60	TNF receptor superfamily member 10b	Homo sapiens	97-100
32506763-0	2020	ROS-mediated PERK-eIF2alpha-ATF4 pathway plays an important role in arsenite-induced L-02 cells apoptosis via regulating CHOP-DR5 signaling.	Reactive Oxygen Species	0-3	TNF receptor superfamily member 10b	Homo sapiens	126-129
32506763-0	2020	ROS-mediated PERK-eIF2alpha-ATF4 pathway plays an important role in arsenite-induced L-02 cells apoptosis via regulating CHOP-DR5 signaling.	arsenite	68-76	TNF receptor superfamily member 10b	Homo sapiens	126-129
32506763-5	2020	Results showed that death receptor 5 (DR5) was a mediator of NaAsO2 -induced apoptosis by enhancing construction of the death-inducing signaling complex (DISC).	sodium arsenite	61-67	TNF receptor superfamily member 10b	Homo sapiens	20-36
32506763-5	2020	Results showed that death receptor 5 (DR5) was a mediator of NaAsO2 -induced apoptosis by enhancing construction of the death-inducing signaling complex (DISC).	sodium arsenite	61-67	TNF receptor superfamily member 10b	Homo sapiens	38-41
32506763-8	2020	PERK inhibitor and ATF4 siRNA significantly attenuated NaAsO2 -induced CHOP and DR5 expressions.	sodium arsenite	55-61	TNF receptor superfamily member 10b	Homo sapiens	80-83
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Reactive Oxygen Species	42-45	TNF receptor superfamily member 10b	Homo sapiens	189-192
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	sodium arsenite	96-102	TNF receptor superfamily member 10b	Homo sapiens	189-192
32974652-3	2020	In this work, we present structural insights for the recognition of DR5 and DR0 elements by RXR-RAR heterodimer using x-ray crystallography, small angle x-ray scattering, and hydrogen/deuterium exchange coupled to mass spectrometry.	Hydrogen	175-183	TNF receptor superfamily member 10b	Homo sapiens	68-71
32974652-3	2020	In this work, we present structural insights for the recognition of DR5 and DR0 elements by RXR-RAR heterodimer using x-ray crystallography, small angle x-ray scattering, and hydrogen/deuterium exchange coupled to mass spectrometry.	Deuterium	184-193	TNF receptor superfamily member 10b	Homo sapiens	68-71
32899699-0	2020	Artemisinin Derivatives Stimulate DR5-Specific TRAIL-Induced Apoptosis by Regulating Wildtype P53.	artemisinin	0-11	TNF receptor superfamily member 10b	Homo sapiens	34-37
32878791-0	2020	Up-regulation of Death Receptor 5/TRAIL-R2 Mediates Apoptosis Induced by N,N"-[(3,4-dimethoxyphenyl)methylene] Biscinnamide in Cancer Cells.	n,n"-[(3,4-dimethoxyphenyl)methylene] biscinnamide	73-123	TNF receptor superfamily member 10b	Homo sapiens	17-33
32878791-0	2020	Up-regulation of Death Receptor 5/TRAIL-R2 Mediates Apoptosis Induced by N,N"-[(3,4-dimethoxyphenyl)methylene] Biscinnamide in Cancer Cells.	n,n"-[(3,4-dimethoxyphenyl)methylene] biscinnamide	73-123	TNF receptor superfamily member 10b	Homo sapiens	34-42
32878791-8	2020	RESULTS: DPMBC up-regulated expression levels of DR5 protein and induced apoptosis through the extrinsic apoptotic pathway mediated by DR5 and caspases.	dpmbc	9-14	TNF receptor superfamily member 10b	Homo sapiens	49-52
32878791-8	2020	RESULTS: DPMBC up-regulated expression levels of DR5 protein and induced apoptosis through the extrinsic apoptotic pathway mediated by DR5 and caspases.	dpmbc	9-14	TNF receptor superfamily member 10b	Homo sapiens	135-138
32141025-6	2020	RESULTS: Curcumin augments TRAIL-apoptotic signaling in leukemic cells by upregulating the expression of DR4 and DR5 along with suppression of cFLIP and anti-apoptotic proteins Mcl-1, Bcl-xl, and XIAP.	Curcumin	9-17	TNF receptor superfamily member 10b	Homo sapiens	113-116
32825566-3	2020	In this study, we showed the sub-lethal concentrations of a lysosomotropic autophagy inhibitor, IITZ-01, sensitizes cancer cells (renal, lung, and breast carcinoma) to TRAIL-induced apoptosis through DR5 upregulation and survivin downregulation through ubiquitin-proteasome pathway.	IITZ-01	96-103	TNF receptor superfamily member 10b	Homo sapiens	200-203
32825566-4	2020	Knockdown of DR5 or overexpression of survivin inhibited combined treatment with IITZ-01 and TRAIL-induced apoptosis.	IITZ-01	81-88	TNF receptor superfamily member 10b	Homo sapiens	13-16
32825566-7	2020	Taken together, these results provide the first evidence that IITZ-01 enhances TRAIL-mediated apoptosis through DR5 stabilization by downregulation of Cbl and USP9X-dependent survivin ubiquitination and degradation in renal carcinoma cells.	IITZ-01	62-69	TNF receptor superfamily member 10b	Homo sapiens	112-115
32626921-0	2020	Inhibition of autophagy flux by sertraline attenuates TRAIL resistance in lung cancer via death receptor 5 upregulation.	Sertraline	32-42	TNF receptor superfamily member 10b	Homo sapiens	90-106
32626921-5	2020	To the best of our knowledge, this is the first study to demonstrate that sertraline inhibits autophagic flux and increases the expression of death receptor 5 (DR5) on TRAIL-resistant lung cancer cells.	Sertraline	74-84	TNF receptor superfamily member 10b	Homo sapiens	142-158
32626921-5	2020	To the best of our knowledge, this is the first study to demonstrate that sertraline inhibits autophagic flux and increases the expression of death receptor 5 (DR5) on TRAIL-resistant lung cancer cells.	Sertraline	74-84	TNF receptor superfamily member 10b	Homo sapiens	160-163
32626921-6	2020	Inhibition of autophagy using autophagy inhibitors 3-methyladenine and chloroquine upregulated the expression of DR5 and enhanced TRAIL-induced apoptosis, as confirmed by the increase of pro-apoptotic proteins caspase-8 and caspase-3.	3-methyladenine	51-66	TNF receptor superfamily member 10b	Homo sapiens	113-116
32626921-6	2020	Inhibition of autophagy using autophagy inhibitors 3-methyladenine and chloroquine upregulated the expression of DR5 and enhanced TRAIL-induced apoptosis, as confirmed by the increase of pro-apoptotic proteins caspase-8 and caspase-3.	Chloroquine	71-82	TNF receptor superfamily member 10b	Homo sapiens	113-116
32626921-7	2020	Silencing DR5 expression using DR5 small interfering RNA prevented sertraline-induced TRAIL-mediated apoptosis, indicating the role of DR5 in TRAIL-mediated apoptosis.	Sertraline	67-77	TNF receptor superfamily member 10b	Homo sapiens	10-13
32626921-7	2020	Silencing DR5 expression using DR5 small interfering RNA prevented sertraline-induced TRAIL-mediated apoptosis, indicating the role of DR5 in TRAIL-mediated apoptosis.	Sertraline	67-77	TNF receptor superfamily member 10b	Homo sapiens	31-34
32626921-7	2020	Silencing DR5 expression using DR5 small interfering RNA prevented sertraline-induced TRAIL-mediated apoptosis, indicating the role of DR5 in TRAIL-mediated apoptosis.	Sertraline	67-77	TNF receptor superfamily member 10b	Homo sapiens	31-34
32626921-8	2020	Overall, sertraline enhanced TRAIL-mediated apoptosis via the downregulation of AMP-activated protein kinase phosphorylation, resulting in the inhibition of autophagic flux, upregulation of DR5 expression, and activation of the apoptotic caspase cascade.	Sertraline	9-19	TNF receptor superfamily member 10b	Homo sapiens	190-193
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	TNF receptor superfamily member 10b	Homo sapiens	144-147
32416217-8	2020	Moreover, DT-13 induced the death receptor pathway-dependent apoptosis of HL-60 and Kasumi-1 cells by up-regulating Fas, FasL, DR5 and TRAIL as well as promoted the cleavage of caspase 8, caspase 3 and PARP.	DT-13	10-15	TNF receptor superfamily member 10b	Homo sapiens	127-130
32303681-4	2020	Here, we found that TNFRSF10B, along with a vesicular trafficking regulator protein, YIPF2, were upregulated after treatment with pemetrexed (PEM) in NSCLC cells.	Pemetrexed	130-140	TNF receptor superfamily member 10b	Homo sapiens	20-29
32714568-5	2020	Depletion of the anti-apoptotic protein FLIP, which we identify as a novel mediator of resistance to MLN4924, enhanced apoptosis in a p53-, TRAIL-R2/DR5-, and caspase-8-dependent manner.	pevonedistat	101-108	TNF receptor superfamily member 10b	Homo sapiens	140-148
32714568-5	2020	Depletion of the anti-apoptotic protein FLIP, which we identify as a novel mediator of resistance to MLN4924, enhanced apoptosis in a p53-, TRAIL-R2/DR5-, and caspase-8-dependent manner.	pevonedistat	101-108	TNF receptor superfamily member 10b	Homo sapiens	149-152
32714568-6	2020	Notably, TRAIL-R2 was involved in potentiating the apoptotic response to MLN4924 in the absence of FLIP, in a ligand-independent manner.	pevonedistat	73-80	TNF receptor superfamily member 10b	Homo sapiens	9-17
32319535-8	2020	Overall, the results of the present study revealed that cantharidin effectively sensitized cells to TRAIL-mediated apoptosis and its effects are likely to be mediated by autophagy, the downregulation of c-FLIP and the upregulation of DR-5.	Cantharidin	56-67	TNF receptor superfamily member 10b	Homo sapiens	234-238
32441887-0	2020	Lestaurtinib potentiates TRAIL-induced apoptosis in glioma via CHOP-dependent DR5 induction.	lestaurtinib	0-12	TNF receptor superfamily member 10b	Homo sapiens	78-81
32441887-5	2020	While U87 and U251 cells showed resistance to TRAIL single treatment, they were sensitized to apoptosis induced by TRAIL in the presence of lestaurtinib because of increased death receptor 5 (DR5) levels through CHOP-dependent manner.	lestaurtinib	140-152	TNF receptor superfamily member 10b	Homo sapiens	174-190
32441887-5	2020	While U87 and U251 cells showed resistance to TRAIL single treatment, they were sensitized to apoptosis induced by TRAIL in the presence of lestaurtinib because of increased death receptor 5 (DR5) levels through CHOP-dependent manner.	lestaurtinib	140-152	TNF receptor superfamily member 10b	Homo sapiens	192-195
32559583-11	2020	Moreover, periplocin increased the mRNA expression of NOXA, Bak, Bcl-2, and death receptors such as TRAIL-R1 and TRAIL-R2 and the protein expression of ERK/phospho ERK, p38/phospho p38, and JNK/phospho JNK.	periplocin	10-20	TNF receptor superfamily member 10b	Homo sapiens	113-121
31955141-0	2020	Curcumin-loaded nanostructured lipid carrier induced apoptosis in human HepG2 cells through activation of the DR5/caspase-mediated extrinsic apoptosis pathway.	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	110-113
31955141-5	2020	This study showed that Cur-NLC significantly increased total expression of DR5 protein while simultaneously upregulated cell membrane expression of DR5.	Cur1 compound	23-26	TNF receptor superfamily member 10b	Homo sapiens	75-78
31955141-5	2020	This study showed that Cur-NLC significantly increased total expression of DR5 protein while simultaneously upregulated cell membrane expression of DR5.	Cur1 compound	23-26	TNF receptor superfamily member 10b	Homo sapiens	148-151
31955141-8	2020	Therefore, Cur-NLC induced activation of the extrinsic apoptosis pathway via modulating the DR5/caspase-8/-3 mediated apoptosis pathway in HepG2 cells, suggesting that Cur-NLC is a promising therapeutic agent or supplement for the treatment of hepatocellular carcinoma.	Cur1 compound	11-14	TNF receptor superfamily member 10b	Homo sapiens	92-95
31955141-8	2020	Therefore, Cur-NLC induced activation of the extrinsic apoptosis pathway via modulating the DR5/caspase-8/-3 mediated apoptosis pathway in HepG2 cells, suggesting that Cur-NLC is a promising therapeutic agent or supplement for the treatment of hepatocellular carcinoma.	Cur1 compound	168-171	TNF receptor superfamily member 10b	Homo sapiens	92-95
32156787-6	2020	Therapeutic importin beta1 knockdown, administered via the atelocollagen delivery system, as well as treatment with the importin beta inhibitor, importazole, induced regression and/or eradication of two human TRAIL-resistant tumor cells when combined with agonistic anti-hDR5 antibody treatment.	importazole	145-156	TNF receptor superfamily member 10b	Homo sapiens	271-275
32365976-5	2020	Bortezomib and doxorubicin greatly enhanced the surface expression of the death receptors DR5 and DR4, while panobinostat increased expression of DR5 and suppressed expression of DR4 in both cell lines.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	90-93
32365976-5	2020	Bortezomib and doxorubicin greatly enhanced the surface expression of the death receptors DR5 and DR4, while panobinostat increased expression of DR5 and suppressed expression of DR4 in both cell lines.	Doxorubicin	15-26	TNF receptor superfamily member 10b	Homo sapiens	90-93
32319535-0	2020	Downregulation of c-FLIP and upregulation of DR-5 by cantharidin sensitizes TRAIL-mediated apoptosis in prostate cancer cells via autophagy flux.	Cantharidin	53-64	TNF receptor superfamily member 10b	Homo sapiens	45-49
32319535-5	2020	Notably, it was also identified that cantharidin treatment initiated the downregulation of cellular FLICE-like inhibitory protein (c-FLIP) and upregulation of death receptor 5 (DR-5), and sensitized cells to TRAIL-mediated apoptosis by initiating autophagy flux.	Cantharidin	37-48	TNF receptor superfamily member 10b	Homo sapiens	159-175
32319535-5	2020	Notably, it was also identified that cantharidin treatment initiated the downregulation of cellular FLICE-like inhibitory protein (c-FLIP) and upregulation of death receptor 5 (DR-5), and sensitized cells to TRAIL-mediated apoptosis by initiating autophagy flux.	Cantharidin	37-48	TNF receptor superfamily member 10b	Homo sapiens	177-181
32509779-8	2020	This results in a strongly reduced number of apoptotic cells upon treatment with DR5-specific TRAIL variant DHER in CM.	dher	108-112	TNF receptor superfamily member 10b	Homo sapiens	81-84
32375399-8	2020	Dinaciclib was shown to drastically enhance EV-T killing effects on cancer lines that express good levels of death receptor (DR) 5, which are associated with suppression of CDK1, CDK9 and anti-apoptotic proteins.	dinaciclib	0-10	TNF receptor superfamily member 10b	Homo sapiens	109-130
32303681-4	2020	Here, we found that TNFRSF10B, along with a vesicular trafficking regulator protein, YIPF2, were upregulated after treatment with pemetrexed (PEM) in NSCLC cells.	Pemetrexed	142-145	TNF receptor superfamily member 10b	Homo sapiens	20-29
31812766-5	2020	Moreover, formaldehyde significantly potentiated the induction of death receptor-5, caspase 8/10, cleaved caspase 3/7/9, pro-apoptotic proteins (Bim, Bad and Bax), depolarization of MMP (mitochondrial membrane potential) and AIF (apoptosis-inducing factor) induced by acrolein, and synergistically decreased expressions of pro-survival proteins (Bcl-2 and Bcl-XL) and poly ADP-ribose polymerase.	Formaldehyde	10-22	TNF receptor superfamily member 10b	Homo sapiens	66-82
31923762-0	2020	Oxidative stress-driven DR5 upregulation restores TRAIL/Apo2L sensitivity induced by iron oxide nanoparticles in colorectal cancer.	ferric oxide	85-95	TNF receptor superfamily member 10b	Homo sapiens	24-27
32213959-6	2020	While PGA2 induced apoptosis in HCT116 cells, phosphorylation of p53 and transcriptional induction of p53-target genes such as p21WAF1, PUMA, BAX, NOXA, and DR5 occurred.	prostaglandin A2	6-10	TNF receptor superfamily member 10b	Homo sapiens	157-160
32213959-9	2020	Moreover, among target genes of p53, knockdown of DR5 expression by RNA interference, suppressed PGA2-induced apoptosis.	prostaglandin A2	97-101	TNF receptor superfamily member 10b	Homo sapiens	50-53
32213959-13	2020	PGA2 may induce p53-dependent apoptosis in which DNA-PK activates p53, and DR5, a transcriptional target of p53, plays a pivotal role in HCT116 cells.	prostaglandin A2	0-4	TNF receptor superfamily member 10b	Homo sapiens	75-78
32266096-11	2020	DR5 is one of the upstream receptors of the JNK pathway, and shRNA knockdown of DR5 can partially reverse gossypol-induced apoptosis.	Gossypol	106-114	TNF receptor superfamily member 10b	Homo sapiens	0-3
32266096-11	2020	DR5 is one of the upstream receptors of the JNK pathway, and shRNA knockdown of DR5 can partially reverse gossypol-induced apoptosis.	Gossypol	106-114	TNF receptor superfamily member 10b	Homo sapiens	80-83
31923762-3	2020	Specifically, NanoTRAIL (TRAIL/Apo2L-iron oxide nanoparticles) generated ROS (reactive oxygen species)-triggered JNK (c-Jun N-terminal kinase) activation and induced subsequent autophagy-assisted DR5 upregulation, resulting in a significant enhanced antitumor efficacy of TRAIL/Apo2L, which confirmed in both TRAIL-resistant HT-29, intermediately resistant SW-480 and sensitive HCT-116 cells.	ferric oxide	37-47	TNF receptor superfamily member 10b	Homo sapiens	196-199
31923762-3	2020	Specifically, NanoTRAIL (TRAIL/Apo2L-iron oxide nanoparticles) generated ROS (reactive oxygen species)-triggered JNK (c-Jun N-terminal kinase) activation and induced subsequent autophagy-assisted DR5 upregulation, resulting in a significant enhanced antitumor efficacy of TRAIL/Apo2L, which confirmed in both TRAIL-resistant HT-29, intermediately resistant SW-480 and sensitive HCT-116 cells.	Oxygen	87-93	TNF receptor superfamily member 10b	Homo sapiens	196-199
32124960-13	2020	Overall, the present study provided evidence that ICA sensitized tumor cells to TRAIL-induced apoptosis via ROS-, ERK- and CHOP-mediated upregulation of DR5 and DR4.	icariin	50-53	TNF receptor superfamily member 10b	Homo sapiens	153-156
32124960-13	2020	Overall, the present study provided evidence that ICA sensitized tumor cells to TRAIL-induced apoptosis via ROS-, ERK- and CHOP-mediated upregulation of DR5 and DR4.	Reactive Oxygen Species	108-111	TNF receptor superfamily member 10b	Homo sapiens	153-156
31641820-8	2020	Our study concluded that P5H induced the death receptor, DR5 in HCT-116 and mitochondria-mediated apoptosis pathway in HT-29.	Hydrogen	25-28	TNF receptor superfamily member 10b	Homo sapiens	57-60
31839995-11	2019	Our results indicate that DDAs are unique in causing DR5 accumulation and oligomerization and inducing downstream caspase activation and cancer cell death through mechanisms involving altered DR5 disulfide bonding.	Disulfides	196-205	TNF receptor superfamily member 10b	Homo sapiens	192-195
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	Sirolimus	83-92	TNF receptor superfamily member 10b	Homo sapiens	166-169
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	Sirolimus	94-97	TNF receptor superfamily member 10b	Homo sapiens	166-169
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	ABT-737	108-114	TNF receptor superfamily member 10b	Homo sapiens	166-169
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	temozolomide	119-131	TNF receptor superfamily member 10b	Homo sapiens	166-169
31806377-5	2020	Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation.	temozolomide	133-136	TNF receptor superfamily member 10b	Homo sapiens	166-169
31806377-6	2020	Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death.	ABT-737	23-29	TNF receptor superfamily member 10b	Homo sapiens	60-63
31806377-6	2020	Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death.	temozolomide	34-37	TNF receptor superfamily member 10b	Homo sapiens	60-63
31698509-9	2020	Ecn induced ROS production and GRP78, CHOP, DR5 and DR4 expression as well as depolarized the mitochondria membrane potential.	ecn	0-3	TNF receptor superfamily member 10b	Homo sapiens	44-47
32083004-8	2020	In addition, ZBTB7A transactivates TRAIL-R2, which sensitizes cells to cisplatin-induced apoptosis.	Cisplatin	71-80	TNF receptor superfamily member 10b	Homo sapiens	35-43
32083004-9	2020	The ZBTB7A-TRAIL-R2 cascade is involved in both the extrinsic and intrinsic cisplatin-induced pathways of apoptosis.	Cisplatin	76-85	TNF receptor superfamily member 10b	Homo sapiens	11-19
32187278-8	2020	CASPASE-8 and TNFRSF10B expression levels could predict the response of both the cell lines to rhTRAIL alone or the response to a combination of rhTRAIL and cisplatin.	Cisplatin	157-166	TNF receptor superfamily member 10b	Homo sapiens	14-23
31294850-7	2020	Our modelization results show that TRAIL can bind to DR4 and DR5 when transported by graphene nanoflake, as a proof of concept.	Graphite	85-93	TNF receptor superfamily member 10b	Homo sapiens	61-64
31839995-5	2019	At the protein level, DDAs alter DR5 disulfide bonding to increase steady-state DR5 levels and oligomerization, leading to downstream caspase 8 and 3 activation.	Disulfides	37-46	TNF receptor superfamily member 10b	Homo sapiens	33-36
31839995-5	2019	At the protein level, DDAs alter DR5 disulfide bonding to increase steady-state DR5 levels and oligomerization, leading to downstream caspase 8 and 3 activation.	Disulfides	37-46	TNF receptor superfamily member 10b	Homo sapiens	80-83
31641820-0	2020	Activation of death receptor, DR5 and mitochondria-mediated apoptosis by a 3,4,5-trimethoxybenzyloxy derivative in wild-type and p53 mutant colorectal cancer cell lines.	BW 1069C85	75-100	TNF receptor superfamily member 10b	Homo sapiens	30-33
31987044-0	2020	Cell death induced by the ER stressor thapsigargin involves death receptor 5, a non-autophagic function of MAP1LC3B, and distinct contributions from unfolded protein response components.	Thapsigargin	38-50	TNF receptor superfamily member 10b	Homo sapiens	60-76
31987044-7	2020	RESULTS: In both cell lines, Tg-induced cell death depended on death receptor 5 and caspase-8.	Thapsigargin	29-31	TNF receptor superfamily member 10b	Homo sapiens	63-79
31987044-9	2020	PERK, ATF4 and CHOP were required for Tg-induced cell death, but surprisingly acted in parallel rather than as a linear pathway; ATF4 and CHOP were independently required for Tg-mediated upregulation of death receptor 5 and MAP1LC3B proteins, whereas PERK acted via other pathways.	Thapsigargin	38-40	TNF receptor superfamily member 10b	Homo sapiens	203-219
31987044-9	2020	PERK, ATF4 and CHOP were required for Tg-induced cell death, but surprisingly acted in parallel rather than as a linear pathway; ATF4 and CHOP were independently required for Tg-mediated upregulation of death receptor 5 and MAP1LC3B proteins, whereas PERK acted via other pathways.	Thapsigargin	175-177	TNF receptor superfamily member 10b	Homo sapiens	203-219
31306050-4	2020	In particular, AMP induced caspase-8 dependent apoptosis via upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor (DR5).	ampelopsin	15-18	TNF receptor superfamily member 10b	Homo sapiens	161-164
31306050-5	2020	Knockdown of DR5 by RNA interference blocked AMP-induced apoptosis.	ampelopsin	45-48	TNF receptor superfamily member 10b	Homo sapiens	13-16
31306050-8	2020	These results demonstrate that treatment with AMP induces the apoptosis of EBV-positive cells through upregulation of TRAIL/DR5 and activation of p38 signaling.	ampelopsin	46-49	TNF receptor superfamily member 10b	Homo sapiens	124-127
31206933-0	2019	TRAIL-inspired multivalent dextran conjugates efficiently induce apoptosis upon DR5 receptor clustering.	Dextrans	27-34	TNF receptor superfamily member 10b	Homo sapiens	80-83
31206933-5	2019	Enzyme-catalyzed ligation of a hydrophilic dextran conjugate bearing multiple DR5-targeting sites to a human Fc did not affect potency (EC50 = 2 - 7 nM), providing an option for improved in vivo half-life and prospective conjugation to an antibody of interest in view of bispecific tumor targeting.	Dextrans	43-50	TNF receptor superfamily member 10b	Homo sapiens	78-81
31817791-7	2019	In addition, BITC increased death receptor DR5 expression, and activated the cysteine-aspartic proteases (caspases) cascade.	benzyl isothiocyanate	13-17	TNF receptor superfamily member 10b	Homo sapiens	43-46
33304996-4	2019	We report here on a peptide amphiphile (PA) containing a dimeric, cyclic peptide that self-assembles into cylindrical supramolecular nanofibers and targets DR5.	Peptides, Cyclic	66-80	TNF receptor superfamily member 10b	Homo sapiens	156-159
31004033-7	2019	RG7388 induced a pro-apoptotic gene expression signature with upregulation of p53-target genes involved in the intrinsic (PUMA, BAX) and extrinsic (TNFRSF10B, FAS) pathways of apoptosis, as well as MDM2 Only a slight induction of CDKN1A was observed and upregulation of pro-apoptotic genes dominated, indicating that CLL cells are primed for p53-dependent apoptosis.	RG7388	0-6	TNF receptor superfamily member 10b	Homo sapiens	148-157
33304996-5	2019	Coassembly of the DR5-targeting PA and a pegylated PA creates a supramolecular nanoscale construct with enhanced binding affinity to DR5 relative to a monomeric targeting PA, and was found to be cytotoxic in vitro.	Protactinium	32-34	TNF receptor superfamily member 10b	Homo sapiens	18-21
33304996-5	2019	Coassembly of the DR5-targeting PA and a pegylated PA creates a supramolecular nanoscale construct with enhanced binding affinity to DR5 relative to a monomeric targeting PA, and was found to be cytotoxic in vitro.	Protactinium	32-34	TNF receptor superfamily member 10b	Homo sapiens	133-136
33304996-5	2019	Coassembly of the DR5-targeting PA and a pegylated PA creates a supramolecular nanoscale construct with enhanced binding affinity to DR5 relative to a monomeric targeting PA, and was found to be cytotoxic in vitro.	Protactinium	51-53	TNF receptor superfamily member 10b	Homo sapiens	133-136
33304996-5	2019	Coassembly of the DR5-targeting PA and a pegylated PA creates a supramolecular nanoscale construct with enhanced binding affinity to DR5 relative to a monomeric targeting PA, and was found to be cytotoxic in vitro.	Protactinium	51-53	TNF receptor superfamily member 10b	Homo sapiens	133-136
33304996-6	2019	When combined with the chemotherapy paclitaxel, DR5-targeting carriers showed potent antitumor activity in vivo, demonstrating the multifunctional capabilities of peptide-based supramolecular nanostructures.	Paclitaxel	36-46	TNF receptor superfamily member 10b	Homo sapiens	48-51
31623058-0	2019	Pseudolaric Acid B Induces Growth Inhibition and Caspase-Dependent Apoptosis on Head and Neck Cancer Cell lines through Death Receptor 5.	pseudolaric acid B	0-18	TNF receptor superfamily member 10b	Homo sapiens	120-136
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	Methyloleanolate	9-25	TNF receptor superfamily member 10b	Homo sapiens	121-137
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	Methyloleanolate	9-25	TNF receptor superfamily member 10b	Homo sapiens	139-142
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	Methyloleanolate	9-25	TNF receptor superfamily member 10b	Homo sapiens	240-243
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	28-O-glucopyranosyl-3-O-(O-rhamnopyranosyl-1-3-O-(O-glucopyranosyl)glucopyranosyl)oleanolate	15-25	TNF receptor superfamily member 10b	Homo sapiens	121-137
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	28-O-glucopyranosyl-3-O-(O-rhamnopyranosyl-1-3-O-(O-glucopyranosyl)glucopyranosyl)oleanolate	15-25	TNF receptor superfamily member 10b	Homo sapiens	139-142
31695422-4	2019	Results: Methyloleanolate increased the fraction of Annexin V/PI apoptotic cells and activated caspase-8, caspase-3, and death receptor 5 (DR5) more than oleanolate in A549 and H1299 cells pretreated with pancaspase inhibitor z-VAD-fmk and DR5 depletion.	28-O-glucopyranosyl-3-O-(O-rhamnopyranosyl-1-3-O-(O-glucopyranosyl)glucopyranosyl)oleanolate	15-25	TNF receptor superfamily member 10b	Homo sapiens	240-243
31623058-3	2019	PAB-induced apoptosis is through inducing death receptor 5 (DR5) together with the increase in the expression of cleaved caspase-8.	pseudolaric acid B	0-3	TNF receptor superfamily member 10b	Homo sapiens	42-58
31623058-3	2019	PAB-induced apoptosis is through inducing death receptor 5 (DR5) together with the increase in the expression of cleaved caspase-8.	pseudolaric acid B	0-3	TNF receptor superfamily member 10b	Homo sapiens	60-63
31673231-8	2019	Bortezomib also increased DR5 expression and knockdown of DR5 expression significantly recovered cell viability reduced by the combination treatment.	bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	26-29
31281953-15	2019	Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP.	celastrol	13-22	TNF receptor superfamily member 10b	Homo sapiens	35-51
31281953-15	2019	Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP.	celastrol	13-22	TNF receptor superfamily member 10b	Homo sapiens	53-56
31673231-11	2019	However, upregulation of DR5 by bortezomib was knocked down only by inhibition of ERK1/2 activation significantly, but not by JNK activity inhibition.	bortezomib	32-42	TNF receptor superfamily member 10b	Homo sapiens	25-28
31673231-12	2019	In summary, upregulation of DR5 by bortezomib is of critical significance in the synergy of bortezomib with TRAIL in apoptosis of TRAIL-resistant SNU-216 and that activity of ERK1/2 is required in the bortezomib-induced DR5 overexpression.	bortezomib	35-45	TNF receptor superfamily member 10b	Homo sapiens	28-31
31673231-12	2019	In summary, upregulation of DR5 by bortezomib is of critical significance in the synergy of bortezomib with TRAIL in apoptosis of TRAIL-resistant SNU-216 and that activity of ERK1/2 is required in the bortezomib-induced DR5 overexpression.	bortezomib	35-45	TNF receptor superfamily member 10b	Homo sapiens	220-223
31673231-12	2019	In summary, upregulation of DR5 by bortezomib is of critical significance in the synergy of bortezomib with TRAIL in apoptosis of TRAIL-resistant SNU-216 and that activity of ERK1/2 is required in the bortezomib-induced DR5 overexpression.	bortezomib	92-102	TNF receptor superfamily member 10b	Homo sapiens	28-31
31673231-12	2019	In summary, upregulation of DR5 by bortezomib is of critical significance in the synergy of bortezomib with TRAIL in apoptosis of TRAIL-resistant SNU-216 and that activity of ERK1/2 is required in the bortezomib-induced DR5 overexpression.	bortezomib	92-102	TNF receptor superfamily member 10b	Homo sapiens	220-223
31673231-12	2019	In summary, upregulation of DR5 by bortezomib is of critical significance in the synergy of bortezomib with TRAIL in apoptosis of TRAIL-resistant SNU-216 and that activity of ERK1/2 is required in the bortezomib-induced DR5 overexpression.	bortezomib	92-102	TNF receptor superfamily member 10b	Homo sapiens	28-31
31673231-12	2019	In summary, upregulation of DR5 by bortezomib is of critical significance in the synergy of bortezomib with TRAIL in apoptosis of TRAIL-resistant SNU-216 and that activity of ERK1/2 is required in the bortezomib-induced DR5 overexpression.	bortezomib	92-102	TNF receptor superfamily member 10b	Homo sapiens	220-223
31362889-5	2019	Leptomycin B works synergistically with both TRAIL and death receptor 5 agonistic antibodies to induce apoptosis in TRAIL sensitive cell lines.	leptomycin B	0-12	TNF receptor superfamily member 10b	Homo sapiens	55-71
31322237-6	2019	Western blotting demonstrated that DP induced apoptosis through extrinsic and intrinsic pathways by upregulating death receptor 4 (DR4), DR5, cleaved caspase-3/-7/-9 and cleaved poly (ADP-ribose) polymerase (PARP), and by decreasing total PARP, total caspase-3/7, Bcl-2 and caspase-9/-10.	dracorhodin	35-37	TNF receptor superfamily member 10b	Homo sapiens	137-140
31546731-0	2019	p53-Mediated Oxidative Stress Enhances Indirubin-3"-Monoxime-Induced Apoptosis in HCT116 Colon Cancer Cells by Upregulating Death Receptor 5 and TNF-Related Apoptosis-Inducing Ligand Expression.	indirubin-3'-monoxime	39-60	TNF receptor superfamily member 10b	Homo sapiens	124-140
31546731-2	2019	This study revealed that I3M promotes the expression of death receptor 5 (DR5) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in HCT116 p53+/+ cells, resulting in caspase-mediated apoptosis.	indirubin-3'-monoxime	25-28	TNF receptor superfamily member 10b	Homo sapiens	56-72
31546731-2	2019	This study revealed that I3M promotes the expression of death receptor 5 (DR5) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in HCT116 p53+/+ cells, resulting in caspase-mediated apoptosis.	indirubin-3'-monoxime	25-28	TNF receptor superfamily member 10b	Homo sapiens	74-77
31546731-6	2019	Our results also showed that I3M enhanced transcription factor C/EBP homologous protein (CHOP) expression, resulted in endoplasmic reticulum (ER) stress-mediated DR5 expression, which was upregulated by ROS production in HCT116 p53+/+ cells.	indirubin-3'-monoxime	29-32	TNF receptor superfamily member 10b	Homo sapiens	162-165
31546731-7	2019	Moreover, co-treatment with I3M and TRAIL enhanced DR5 expression, thereby triggering TRAIL-induced apoptosis of HCT116 p53+/+ cells, which was interfered by a DR5-specific blocking chimeric antibody.	indirubin-3'-monoxime	28-31	TNF receptor superfamily member 10b	Homo sapiens	51-54
31546731-7	2019	Moreover, co-treatment with I3M and TRAIL enhanced DR5 expression, thereby triggering TRAIL-induced apoptosis of HCT116 p53+/+ cells, which was interfered by a DR5-specific blocking chimeric antibody.	indirubin-3'-monoxime	28-31	TNF receptor superfamily member 10b	Homo sapiens	160-163
31546731-8	2019	In summary, I3M potently enhances TRAIL-induced apoptosis by upregulating DR5 expression via p53-mediated ROS production in HCT116 p53+/+ cells.	indirubin-3'-monoxime	12-15	TNF receptor superfamily member 10b	Homo sapiens	74-77
31416165-9	2019	Mutation of a putative nuclear export sequence (NES) in TRAIL-R2 or the inhibition of CRM-1 by Leptomycin-B resulted in the nuclear accumulation of TRAIL-R2.	leptomycin B	95-107	TNF receptor superfamily member 10b	Homo sapiens	148-156
30556589-0	2019	Chrysanthemulide A induces apoptosis through DR5 upregulation via JNK-mediated autophagosome accumulation in human osteosarcoma cells.	chrysanthemulide a	0-18	TNF receptor superfamily member 10b	Homo sapiens	45-48
30556589-8	2019	Furthermore, CA activated the c-Jun N-terminal kinase (JNK) signaling pathway, and treatment with JNK siRNAs or inhibitor SP600125 significantly attenuated CA-mediated autophagosome accumulation and DR5-mediated cell apoptosis.	pyrazolanthrone	122-130	TNF receptor superfamily member 10b	Homo sapiens	199-202
30958996-4	2019	Transfection of DR5 siRNA into H1299 cells significantly diminished the enhancing effects of Q on TSA-induced apoptosis.	Quercetin	93-94	TNF receptor superfamily member 10b	Homo sapiens	16-19
31233200-8	2019	However, in the resistant cells, the oxaliplatin-triggered extrinsic apoptotic pathway appeared to be suppressed by decreased lipid raft formation, and recruitment of death receptor 5 and FADD into lipid rafts.	Oxaliplatin	37-48	TNF receptor superfamily member 10b	Homo sapiens	167-183
30958996-4	2019	Transfection of DR5 siRNA into H1299 cells significantly diminished the enhancing effects of Q on TSA-induced apoptosis.	trichostatin A	98-101	TNF receptor superfamily member 10b	Homo sapiens	16-19
30958996-8	2019	These data suggest that the up-regulation of p300 expression, which in turn increases histone acetylation and DR5 expression, plays an important role in the enhancing effect of Q on TSA/vorinostat- induced apoptosis in H1299 cells.	Quercetin	177-178	TNF receptor superfamily member 10b	Homo sapiens	110-113
30958996-8	2019	These data suggest that the up-regulation of p300 expression, which in turn increases histone acetylation and DR5 expression, plays an important role in the enhancing effect of Q on TSA/vorinostat- induced apoptosis in H1299 cells.	trichostatin A	182-185	TNF receptor superfamily member 10b	Homo sapiens	110-113
30958996-8	2019	These data suggest that the up-regulation of p300 expression, which in turn increases histone acetylation and DR5 expression, plays an important role in the enhancing effect of Q on TSA/vorinostat- induced apoptosis in H1299 cells.	Vorinostat	186-196	TNF receptor superfamily member 10b	Homo sapiens	110-113
30730256-8	2019	These results indicated that ERK1/2-mediated ELK1/CHOP/DR5 pathway is involved in 6-MSITC-induced apoptosis in colorectal cancer cells.	6-(Methylsulfinyl)hexyl isothiocyanate	82-89	TNF receptor superfamily member 10b	Homo sapiens	55-58
30737960-5	2019	Through upregulating the expression of DR4 and DR5 at transcriptional and protein levels, Periplocin enhanced the sensitivity of gastric cancer cells to TRAIL.	periplocin	90-100	TNF receptor superfamily member 10b	Homo sapiens	47-50
30724400-3	2019	RESULTS: Cisplatin treatment in IMR-32 cells increased the expression of death receptor 5 (DR5; TRAIL-R2), but not other receptors, via downregulation of NF-kappaB activity.	Cisplatin	9-18	TNF receptor superfamily member 10b	Homo sapiens	73-89
30724400-3	2019	RESULTS: Cisplatin treatment in IMR-32 cells increased the expression of death receptor 5 (DR5; TRAIL-R2), but not other receptors, via downregulation of NF-kappaB activity.	Cisplatin	9-18	TNF receptor superfamily member 10b	Homo sapiens	91-94
30724400-3	2019	RESULTS: Cisplatin treatment in IMR-32 cells increased the expression of death receptor 5 (DR5; TRAIL-R2), but not other receptors, via downregulation of NF-kappaB activity.	Cisplatin	9-18	TNF receptor superfamily member 10b	Homo sapiens	96-104
30724400-4	2019	However, the cisplatin-mediated increase in DR5 failed to induce cell death following TRAIL treatment.	Cisplatin	13-22	TNF receptor superfamily member 10b	Homo sapiens	44-47
30724400-9	2019	Concurrent treatment with cisplatin enhanced TRAIL-mediated cytotoxicity, which was abrogated by an additional pretreatment with DR5:Fc chimera protein.	Cisplatin	26-35	TNF receptor superfamily member 10b	Homo sapiens	129-132
30730256-0	2019	Involvement of ERK1/2-mediated ELK1/CHOP/DR5 pathway in 6-(methylsulfinyl)hexyl isothiocyanate-induced apoptosis of colorectal cancer cells.	6-(Methylsulfinyl)hexyl isothiocyanate	56-94	TNF receptor superfamily member 10b	Homo sapiens	41-44
30765502-8	2019	Furthermore, intracellular cholesterol regulates temozolomide-induced cell death in glioblastoma cells via accumulation and activation of death receptor 5 in plasma membrane lipid rafts.	Cholesterol	27-38	TNF receptor superfamily member 10b	Homo sapiens	138-154
30730256-6	2019	6-MSITC stimulated ERK1/2 phosphorylation, and then activated ERK1/2 signaling including ELK1 phosphorylation, and upregulation of C/EBP homologous protein (CHOP) and death receptor 5 (DR5).	6-(Methylsulfinyl)hexyl isothiocyanate	0-7	TNF receptor superfamily member 10b	Homo sapiens	167-183
30730256-6	2019	6-MSITC stimulated ERK1/2 phosphorylation, and then activated ERK1/2 signaling including ELK1 phosphorylation, and upregulation of C/EBP homologous protein (CHOP) and death receptor 5 (DR5).	6-(Methylsulfinyl)hexyl isothiocyanate	0-7	TNF receptor superfamily member 10b	Homo sapiens	185-188
30864676-0	2019	Reversine induces cell cycle arrest and apoptosis via upregulation of the Fas and DR5 signaling pathways in human colorectal cancer cells.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	0-9	TNF receptor superfamily member 10b	Homo sapiens	82-85
30864676-10	2019	Reversine-induced apoptosis and cell cycle arrest were suppressed by inhibition of Fas and DR5 expression via siRNA.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	0-9	TNF receptor superfamily member 10b	Homo sapiens	91-94
30642878-7	2019	We used this assay to screen compounds from three commercially available libraries, and identified 1-benzyl-3-cetyl-2-methylimidazolium iodide (NH125) as a potent inducer of DR5 expression.	NH 125	99-142	TNF receptor superfamily member 10b	Homo sapiens	174-177
30642878-7	2019	We used this assay to screen compounds from three commercially available libraries, and identified 1-benzyl-3-cetyl-2-methylimidazolium iodide (NH125) as a potent inducer of DR5 expression.	NH 125	144-149	TNF receptor superfamily member 10b	Homo sapiens	174-177
30817944-5	2019	The sensitizing effect of AC to TRAIL was well correlated with inhibition of death receptor 5 (DR5) CHOP, and p53 expression.	auriculasin	26-28	TNF receptor superfamily member 10b	Homo sapiens	77-93
30692634-5	2019	Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP.	Reactive Oxygen Species	70-93	TNF receptor superfamily member 10b	Homo sapiens	34-37
30692634-5	2019	Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP.	Reactive Oxygen Species	95-98	TNF receptor superfamily member 10b	Homo sapiens	34-37
30817944-5	2019	The sensitizing effect of AC to TRAIL was well correlated with inhibition of death receptor 5 (DR5) CHOP, and p53 expression.	auriculasin	26-28	TNF receptor superfamily member 10b	Homo sapiens	95-98
30817944-7	2019	These results suggest that non-toxic concentrations of AC sensitize TRAIL-resistant primary prostate cancer cells to TRAIL-mediated apoptosis via up-regulation of DR5 and downstream signaling pathways.	auriculasin	55-57	TNF receptor superfamily member 10b	Homo sapiens	163-166
31032087-0	2019	Artonin E sensitizes TRAIL-induced apoptosis by DR5 upregulation and cFLIP downregulation in TRAIL-refractory colorectal cancer LoVo cells.	artonin E	0-9	TNF receptor superfamily member 10b	Homo sapiens	48-51
31032087-3	2019	In an effort to overcome TRAIL-refractory cancer, we investigated the effect of artonin E in regulating death receptor 5 (DR5) and cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (cFLIP), two major mediators regulate TRAIL-induced apoptosis, in LoVo cells as a model of TRAIL refractory CRC.	artonin E	80-89	TNF receptor superfamily member 10b	Homo sapiens	104-120
31032087-3	2019	In an effort to overcome TRAIL-refractory cancer, we investigated the effect of artonin E in regulating death receptor 5 (DR5) and cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (cFLIP), two major mediators regulate TRAIL-induced apoptosis, in LoVo cells as a model of TRAIL refractory CRC.	artonin E	80-89	TNF receptor superfamily member 10b	Homo sapiens	122-125
31032087-9	2019	Artonin E enhanced both mRNA and protein expression of DR5.	artonin E	0-9	TNF receptor superfamily member 10b	Homo sapiens	55-58
31032087-11	2019	All together we showed that artonin E enhanced TRAIL-induced apoptosis in LoVo cells through DR5 upregulation and cFLIP downregulation.	artonin E	28-37	TNF receptor superfamily member 10b	Homo sapiens	93-96
31032087-12	2019	Conclusions: Artonin E was able to increase DR5 expression and decrease cFLIP expression in LoVo cells.	artonin E	13-22	TNF receptor superfamily member 10b	Homo sapiens	44-47
30765502-8	2019	Furthermore, intracellular cholesterol regulates temozolomide-induced cell death in glioblastoma cells via accumulation and activation of death receptor 5 in plasma membrane lipid rafts.	Temozolomide	49-61	TNF receptor superfamily member 10b	Homo sapiens	138-154
30689998-0	2019	Galbanic acid potentiates TRAIL induced apoptosis in resistant non-small cell lung cancer cells via inhibition of MDR1 and activation of caspases and DR5.	galbanic acid	0-13	TNF receptor superfamily member 10b	Homo sapiens	150-153
31019655-12	2019	The blockage of autophagy by bafilomycin A1 or Atg7 siRNA abolished SNX-2112-induced upregulation of DR5.	SNX 2112	68-76	TNF receptor superfamily member 10b	Homo sapiens	101-104
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	Reactive Oxygen Species	11-14	TNF receptor superfamily member 10b	Homo sapiens	141-144
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	pyrazolanthrone	44-52	TNF receptor superfamily member 10b	Homo sapiens	141-144
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	pifithrin	72-80	TNF receptor superfamily member 10b	Homo sapiens	141-144
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	SNX 2112	166-174	TNF receptor superfamily member 10b	Homo sapiens	141-144
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	Reactive Oxygen Species	204-207	TNF receptor superfamily member 10b	Homo sapiens	141-144
30689998-10	2019	Overall, our findings suggest that galbanic acid enhances TRAIL induced apoptosis via inhibition of MDR1 and activation of caspases and DR5 in H460/R cells as a potent TRAIL sensitizer.	galbanic acid	35-48	TNF receptor superfamily member 10b	Homo sapiens	136-139
31019655-0	2019	Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway.	SNX 2112	16-24	TNF receptor superfamily member 10b	Homo sapiens	128-131
31019655-0	2019	Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway.	Reactive Oxygen Species	97-100	TNF receptor superfamily member 10b	Homo sapiens	128-131
31019655-9	2019	Moreover, SNX-2112 induced the upregulation of death-receptor DR5 in HeLa cells.	SNX 2112	10-18	TNF receptor superfamily member 10b	Homo sapiens	62-65
31019655-10	2019	The silencing of DR5 by siRNA significantly decreased cell apoptosis by the combined effect of SNX-2112 and TRAIL.	SNX 2112	95-103	TNF receptor superfamily member 10b	Homo sapiens	17-20
30674532-5	2019	In this study, we report that death receptor 5 (DR5), a key component of the extrinsic apoptotic pathway, is markedly induced in response to BRD4 depletion and BETi treatment in colorectal cancer cells.	beti	160-164	TNF receptor superfamily member 10b	Homo sapiens	30-46
30674532-5	2019	In this study, we report that death receptor 5 (DR5), a key component of the extrinsic apoptotic pathway, is markedly induced in response to BRD4 depletion and BETi treatment in colorectal cancer cells.	beti	160-164	TNF receptor superfamily member 10b	Homo sapiens	48-51
30674532-7	2019	Enhanced DR5 induction was necessary for the chemosensitization and apoptotic effects of BETi and was responsible for increased BETi sensitivity in colorectal cancer cells containing a mutation in speckle-type POZ protein (SPOP), a subunit of BRD4 E3 ubiquitin ligase.	beti	89-93	TNF receptor superfamily member 10b	Homo sapiens	9-12
30674532-7	2019	Enhanced DR5 induction was necessary for the chemosensitization and apoptotic effects of BETi and was responsible for increased BETi sensitivity in colorectal cancer cells containing a mutation in speckle-type POZ protein (SPOP), a subunit of BRD4 E3 ubiquitin ligase.	beti	128-132	TNF receptor superfamily member 10b	Homo sapiens	9-12
30674532-8	2019	In a colorectal cancer xenograft model, BETi combined with chemotherapy suppressed the tumor growth in a DR5-dependent manner and potently inhibited patient-derived xenograft tumor growth with enhanced DR5 induction and apoptosis.	beti	40-44	TNF receptor superfamily member 10b	Homo sapiens	105-108
30674532-8	2019	In a colorectal cancer xenograft model, BETi combined with chemotherapy suppressed the tumor growth in a DR5-dependent manner and potently inhibited patient-derived xenograft tumor growth with enhanced DR5 induction and apoptosis.	beti	40-44	TNF receptor superfamily member 10b	Homo sapiens	202-205
30674532-9	2019	These findings suggest that BETi alone or in combination with chemotherapy is effective against colorectal cancer due to enhanced DR5 induction and apoptosis.	beti	28-32	TNF receptor superfamily member 10b	Homo sapiens	130-133
30870485-13	2019	This is the first study to demonstrate that XN alters the expression of DR5 as well as the synergistic effect of XN on TRAIL in NB and provides a strong rationale for further preclinical analysis.	xanthohumol	44-46	TNF receptor superfamily member 10b	Homo sapiens	72-75
30647121-7	2019	NEO214-induced cytotoxicity involves apoptosis triggered by endoplasmic reticulum (ER) stress, as well as activating the Death Receptor 5 (DR5)/TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) pathway.	neo214	0-6	TNF receptor superfamily member 10b	Homo sapiens	121-137
29916141-11	2019	R-CRT overexpression in the cytoplasm of MO59K rendered the cells susceptible to BT-induced, DR5-mediated cell death.	Bortezomib	81-83	TNF receptor superfamily member 10b	Homo sapiens	93-96
30647121-7	2019	NEO214-induced cytotoxicity involves apoptosis triggered by endoplasmic reticulum (ER) stress, as well as activating the Death Receptor 5 (DR5)/TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) pathway.	neo214	0-6	TNF receptor superfamily member 10b	Homo sapiens	139-142
30431076-5	2019	The attenuation of the autophagic flux by applying the specific inhibitor of autophagy, chloroquine, significantly suppressed DR5 expression.	Chloroquine	88-99	TNF receptor superfamily member 10b	Homo sapiens	126-129
30589515-9	2019	Interestingly, we observed that induction of the salvage pathway by external administration of l-fucose restores DR5-mediated apoptosis in both DLD-1 and HCT 116 cells.	Fucose	95-103	TNF receptor superfamily member 10b	Homo sapiens	113-116
30431076-7	2019	Furthermore, pre-treatment with the c-Jun N-terminal kinase (JNK) inhibitor, SP600125, significantly attenuated the luteolin-induced upregulation of DR5 expression, thereby suggesting that JNK activation promotes DR5 expression.	pyrazolanthrone	77-85	TNF receptor superfamily member 10b	Homo sapiens	149-152
30431076-7	2019	Furthermore, pre-treatment with the c-Jun N-terminal kinase (JNK) inhibitor, SP600125, significantly attenuated the luteolin-induced upregulation of DR5 expression, thereby suggesting that JNK activation promotes DR5 expression.	pyrazolanthrone	77-85	TNF receptor superfamily member 10b	Homo sapiens	213-216
30359552-0	2019	Ixazomib promotes CHOP-dependent DR5 induction and apoptosis in colorectal cancer cells.	ixazomib	0-8	TNF receptor superfamily member 10b	Homo sapiens	33-36
30359552-4	2019	Western blotting and real-time RT-PCR were performed to detect ixazomib-induced DR5 upregulation.	ixazomib	63-71	TNF receptor superfamily member 10b	Homo sapiens	80-83
30991885-6	2019	We found that MS-444 treatment of glioblastoma cells resulted in loss of viability and induction of apoptosis, with evidence implicating death receptor 5.	5,8-dihydroxy-3-methyl-4-(9H)-naphtho(2,3-c)furanone	14-20	TNF receptor superfamily member 10b	Homo sapiens	137-153
30359552-8	2019	Our findings indicated that ixazomib treatment induces CHOP-dependent DR5 induction, irrespective of p53 status.	ixazomib	28-36	TNF receptor superfamily member 10b	Homo sapiens	70-73
30359552-9	2019	Furthermore, DR5 is necessary for ixazomib-mediated apoptosis.	ixazomib	34-42	TNF receptor superfamily member 10b	Homo sapiens	13-16
30359552-10	2019	Ixazomib also synergized with TRAIL to induce marked apoptosis via DR5 in CRC cells.	ixazomib	0-8	TNF receptor superfamily member 10b	Homo sapiens	67-70
30359552-11	2019	CONCLUSIONS: Our findings further suggested that ixazomib sensitizes TRAIL/death receptor signaling pathway-targeted CRC and suggested that DR5 induction could be a valuable indicator of ixazomib sensitivity.	ixazomib	187-195	TNF receptor superfamily member 10b	Homo sapiens	140-143
30423122-7	2019	Pretreatment with flutamide, as well as knockdown of androgen receptor, decreased testosterone-induced DR5 and CHOP expression, as well as apoptosis.	Flutamide	18-27	TNF receptor superfamily member 10b	Homo sapiens	103-106
30423122-7	2019	Pretreatment with flutamide, as well as knockdown of androgen receptor, decreased testosterone-induced DR5 and CHOP expression, as well as apoptosis.	Testosterone	82-94	TNF receptor superfamily member 10b	Homo sapiens	103-106
30423122-4	2019	In this study, we found that testosterone induced expression of various UPR genes, including CHOP, as well as DR5, in cultured human granulosa-lutein cells (GLCs).	Testosterone	29-41	TNF receptor superfamily member 10b	Homo sapiens	110-113
30423122-8	2019	Expression of DR5 and CHOP was upregulated in GLCs obtained from patients with PCOS, as well as in granulosa cells of antral follicles in ovarian sections obtained from patients with PCOS and dehydroepiandrosterone-induced PCOS mice.	Dehydroepiandrosterone	192-214	TNF receptor superfamily member 10b	Homo sapiens	14-17
30423122-5	2019	Pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) inhibited testosterone-induced apoptosis and expression of DR5 and CHOP.	ursodoxicoltaurine	42-67	TNF receptor superfamily member 10b	Homo sapiens	135-138
30423122-5	2019	Pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) inhibited testosterone-induced apoptosis and expression of DR5 and CHOP.	ursodoxicoltaurine	69-74	TNF receptor superfamily member 10b	Homo sapiens	135-138
30202993-3	2019	In this study, we investigated the hepatotoxicity caused by KMTR2, an anti-human TRAIL-R2 monoclonal antibody, in chimeric mice with humanized livers (PXB-mice).	kmtr2	60-65	TNF receptor superfamily member 10b	Homo sapiens	81-89
30423122-5	2019	Pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) inhibited testosterone-induced apoptosis and expression of DR5 and CHOP.	Testosterone	86-98	TNF receptor superfamily member 10b	Homo sapiens	135-138
30423122-6	2019	Knockdown of CHOP inhibited testosterone-induced DR5 expression and apoptosis, and knockdown of DR5 inhibited testosterone-induced apoptosis.	Testosterone	28-40	TNF receptor superfamily member 10b	Homo sapiens	49-52
30423122-6	2019	Knockdown of CHOP inhibited testosterone-induced DR5 expression and apoptosis, and knockdown of DR5 inhibited testosterone-induced apoptosis.	Testosterone	110-122	TNF receptor superfamily member 10b	Homo sapiens	96-99
30486888-9	2018	We show here for the first time that (a) olaparib significantly increased tumor cell sensitivity to NK killing and ADCC in both BRCA WT and BRCA mutant prostate carcinoma cells, independent of PD-L1 or EGFR modulation; (b) mechanistically, treatment with olaparib upregulated death receptor TRAIL-R2; and (c) olaparib significantly enhanced NK killing of additional tumor types, including breast, non-small cell lung carcinoma, and chordoma.	olaparib	41-49	TNF receptor superfamily member 10b	Homo sapiens	291-299
30359578-0	2018	C-27-carboxylated oleanane triterpenoids up-regulate TRAIL DISC assembly via p38 MAPK and CHOP-mediated DR5 expression in human glioblastoma cells.	c-27-carboxylated oleanane	0-26	TNF receptor superfamily member 10b	Homo sapiens	104-107
30359578-0	2018	C-27-carboxylated oleanane triterpenoids up-regulate TRAIL DISC assembly via p38 MAPK and CHOP-mediated DR5 expression in human glioblastoma cells.	triterpenoids	27-40	TNF receptor superfamily member 10b	Homo sapiens	104-107
30359578-5	2018	The upregulation of DR5 expression by C27OAs strictly depends on transactivation of C/EBP homology protein, which is regulated through the p38 MAPK pathway, rather than p53 and intracellular reactive oxygen species status.	Reactive Oxygen Species	191-214	TNF receptor superfamily member 10b	Homo sapiens	20-23
30713790-0	2019	Bortezomib sensitizes multiple myeloma to NK cells via ER-stress-induced suppression of HLA-E and upregulation of DR5.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	114-117
30463333-5	2018	Maritoclax-induced DR5 upregulation was regulated by induction of C/EBP homologous protein (CHOP) expression.	marinopyrrole A	0-10	TNF receptor superfamily member 10b	Homo sapiens	19-22
29964331-5	2018	BIX-01294 markedly increased death receptor 5 (DR5) expression, while silencing of DR5 using small interfering RNAs abolished the TRAIL-sensitizing effect of BIX-01294.	BIX 01294	158-167	TNF receptor superfamily member 10b	Homo sapiens	83-86
30132536-0	2018	3-Bromopyruvate sensitizes human breast cancer cells to TRAIL-induced apoptosis via the phosphorylated AMPK-mediated upregulation of DR5.	bromopyruvate	0-15	TNF receptor superfamily member 10b	Homo sapiens	133-136
30132536-5	2018	In the present study, it was demonstrated that 3-BP synergistically sensitized breast cancer cells to TRAIL-induced apoptosis via the upregulation of death receptor 5 (DR5).	bromopyruvate	47-51	TNF receptor superfamily member 10b	Homo sapiens	150-166
30132536-5	2018	In the present study, it was demonstrated that 3-BP synergistically sensitized breast cancer cells to TRAIL-induced apoptosis via the upregulation of death receptor 5 (DR5).	bromopyruvate	47-51	TNF receptor superfamily member 10b	Homo sapiens	168-171
30132536-12	2018	In conclusion, these results indicated that 3-BP sensitized breast cancer cells to TRAIL via the AMPK-mediated upregulation of DR5.	bromopyruvate	44-48	TNF receptor superfamily member 10b	Homo sapiens	127-130
29964331-0	2018	Inhibition of euchromatin histone-lysine N-methyltransferase 2 sensitizes breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through reactive oxygen species-mediated activating transcription factor 4-C/EBP homologous protein-death receptor 5 pathway activation.	Reactive Oxygen Species	161-184	TNF receptor superfamily member 10b	Homo sapiens	253-269
29964331-6	2018	Specifically, BIX-01294 induced C/EBP homologous protein (CHOP)-mediated DR5 gene transcriptional activation and DR5 promoter activation was induced by upregulation of the protein kinase R-like endoplasmic reticulum kinase-mediated activating transcription factor 4 (ATF4).	BIX 01294	14-23	TNF receptor superfamily member 10b	Homo sapiens	73-76
29964331-5	2018	BIX-01294 markedly increased death receptor 5 (DR5) expression, while silencing of DR5 using small interfering RNAs abolished the TRAIL-sensitizing effect of BIX-01294.	BIX 01294	0-9	TNF receptor superfamily member 10b	Homo sapiens	29-45
29964331-5	2018	BIX-01294 markedly increased death receptor 5 (DR5) expression, while silencing of DR5 using small interfering RNAs abolished the TRAIL-sensitizing effect of BIX-01294.	BIX 01294	0-9	TNF receptor superfamily member 10b	Homo sapiens	47-50
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Reactive Oxygen Species	24-47	TNF receptor superfamily member 10b	Homo sapiens	109-112
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Acetylcysteine	51-70	TNF receptor superfamily member 10b	Homo sapiens	109-112
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	BIX 01294	91-100	TNF receptor superfamily member 10b	Homo sapiens	109-112
29964331-8	2018	These findings suggest that BIX-01294 sensitizes breast cancer cells to TRAIL by upregulating ATF4/CHOP-dependent DR5 expression with a reactive oxygen species-dependent manner.	BIX 01294	28-37	TNF receptor superfamily member 10b	Homo sapiens	114-117
29964331-8	2018	These findings suggest that BIX-01294 sensitizes breast cancer cells to TRAIL by upregulating ATF4/CHOP-dependent DR5 expression with a reactive oxygen species-dependent manner.	Reactive Oxygen Species	136-159	TNF receptor superfamily member 10b	Homo sapiens	114-117
29869749-0	2018	1H, 13C, 15N NMR resonance assignments and secondary structure determination of the extra-cellular domain from the human proapoptotic TRAIL-R2 death receptor 5 (DR5-ECD).	Hydrogen	0-2	TNF receptor superfamily member 10b	Homo sapiens	143-159
29869749-0	2018	1H, 13C, 15N NMR resonance assignments and secondary structure determination of the extra-cellular domain from the human proapoptotic TRAIL-R2 death receptor 5 (DR5-ECD).	Hydrogen	0-2	TNF receptor superfamily member 10b	Homo sapiens	161-164
30177492-5	2018	The results of MTT assay of Jurkat, K562 and Molt-4 cells with IPH and co-staining experiments with IPH and an anti-DR5 antibody indicate that IPH binds to DR5 and induces apoptosis in a manner parallel to the DR5 expression level.	monooxyethylene trimethylolpropane tristearate	15-18	TNF receptor superfamily member 10b	Homo sapiens	156-159
30177492-5	2018	The results of MTT assay of Jurkat, K562 and Molt-4 cells with IPH and co-staining experiments with IPH and an anti-DR5 antibody indicate that IPH binds to DR5 and induces apoptosis in a manner parallel to the DR5 expression level.	monooxyethylene trimethylolpropane tristearate	15-18	TNF receptor superfamily member 10b	Homo sapiens	156-159
30177492-5	2018	The results of MTT assay of Jurkat, K562 and Molt-4 cells with IPH and co-staining experiments with IPH and an anti-DR5 antibody indicate that IPH binds to DR5 and induces apoptosis in a manner parallel to the DR5 expression level.	iph	100-103	TNF receptor superfamily member 10b	Homo sapiens	156-159
30177492-5	2018	The results of MTT assay of Jurkat, K562 and Molt-4 cells with IPH and co-staining experiments with IPH and an anti-DR5 antibody indicate that IPH binds to DR5 and induces apoptosis in a manner parallel to the DR5 expression level.	iph	100-103	TNF receptor superfamily member 10b	Homo sapiens	156-159
30177492-5	2018	The results of MTT assay of Jurkat, K562 and Molt-4 cells with IPH and co-staining experiments with IPH and an anti-DR5 antibody indicate that IPH binds to DR5 and induces apoptosis in a manner parallel to the DR5 expression level.	iph	100-103	TNF receptor superfamily member 10b	Homo sapiens	156-159
30177492-5	2018	The results of MTT assay of Jurkat, K562 and Molt-4 cells with IPH and co-staining experiments with IPH and an anti-DR5 antibody indicate that IPH binds to DR5 and induces apoptosis in a manner parallel to the DR5 expression level.	iph	100-103	TNF receptor superfamily member 10b	Homo sapiens	156-159
30189637-5	2018	Niclosamide markedly increased DR5 protein levels, including cell-surface DR5, and decreased c-FLIP protein levels.	Niclosamide	0-11	TNF receptor superfamily member 10b	Homo sapiens	31-34
30189637-5	2018	Niclosamide markedly increased DR5 protein levels, including cell-surface DR5, and decreased c-FLIP protein levels.	Niclosamide	0-11	TNF receptor superfamily member 10b	Homo sapiens	74-77
30189637-6	2018	Down-regulation of DR5 by specific small interfering RNA (siRNA) and ectopic expression of c-FLIP markedly blocked niclosamide plus TRAIL-induced apoptosis.	Niclosamide	115-126	TNF receptor superfamily member 10b	Homo sapiens	19-22
30189637-7	2018	Our findings provide that niclosamide could overcome resistance to TRAIL through up-regulating DR5 on the cell surface and down-regulating c-FLIP in cancer cells.	Niclosamide	26-37	TNF receptor superfamily member 10b	Homo sapiens	95-98
29957841-7	2018	The cholesterol-sequestering agent nystatin partially reversed DR5 clustering and DISC formation, preventing apoptosis triggered by the combination of beta-elemene and TRAIL.	Cholesterol	4-15	TNF receptor superfamily member 10b	Homo sapiens	63-66
29957841-7	2018	The cholesterol-sequestering agent nystatin partially reversed DR5 clustering and DISC formation, preventing apoptosis triggered by the combination of beta-elemene and TRAIL.	Nystatin	35-43	TNF receptor superfamily member 10b	Homo sapiens	63-66
29957841-5	2018	Compared to beta-elemene or TRAIL alone, treatment with beta-elemene and TRAIL obviously promoted DR5 clustering as well as translocation of Caspase-8, DR5 and FADD into lipid rafts.	beta-elemene	56-68	TNF receptor superfamily member 10b	Homo sapiens	98-101
29929000-0	2018	Telmisartan generates ROS-dependent upregulation of death receptor 5 to sensitize TRAIL in lung cancer via inhibition of autophagy flux.	Telmisartan	0-11	TNF receptor superfamily member 10b	Homo sapiens	52-68
29957841-5	2018	Compared to beta-elemene or TRAIL alone, treatment with beta-elemene and TRAIL obviously promoted DR5 clustering as well as translocation of Caspase-8, DR5 and FADD into lipid rafts.	beta-elemene	56-68	TNF receptor superfamily member 10b	Homo sapiens	152-155
29929000-0	2018	Telmisartan generates ROS-dependent upregulation of death receptor 5 to sensitize TRAIL in lung cancer via inhibition of autophagy flux.	ros	22-25	TNF receptor superfamily member 10b	Homo sapiens	52-68
29929000-4	2018	In this study, we evaluated telmisartan as a novel TRAIL-DR5-targeting agent with the aim of rendering TRAIL-based cancer therapies more active.	Telmisartan	28-39	TNF receptor superfamily member 10b	Homo sapiens	57-60
29929000-6	2018	The molecular mechanism includes the blocking of AMPK phosphorylation causes inhibition of autophagy flux by telmisartan resulting in ROS generation leading to death receptor (DR5) upregulation and subsequent activation of the caspase cascade by TRAIL treatment.	ros	134-137	TNF receptor superfamily member 10b	Homo sapiens	176-179
29929000-7	2018	Furthermore, using chloroquine and siATG5 significantly enhances ROS production and application of the ROS scavenger N-acetyl-cysteine (NAC) rescues the cells undergoing apoptosis by abrogating the expression of DR5 and finally the caspase cascade.	Chloroquine	19-30	TNF receptor superfamily member 10b	Homo sapiens	212-215
29929000-7	2018	Furthermore, using chloroquine and siATG5 significantly enhances ROS production and application of the ROS scavenger N-acetyl-cysteine (NAC) rescues the cells undergoing apoptosis by abrogating the expression of DR5 and finally the caspase cascade.	ros	103-106	TNF receptor superfamily member 10b	Homo sapiens	212-215
29929000-7	2018	Furthermore, using chloroquine and siATG5 significantly enhances ROS production and application of the ROS scavenger N-acetyl-cysteine (NAC) rescues the cells undergoing apoptosis by abrogating the expression of DR5 and finally the caspase cascade.	Acetylcysteine	117-134	TNF receptor superfamily member 10b	Homo sapiens	212-215
29929000-7	2018	Furthermore, using chloroquine and siATG5 significantly enhances ROS production and application of the ROS scavenger N-acetyl-cysteine (NAC) rescues the cells undergoing apoptosis by abrogating the expression of DR5 and finally the caspase cascade.	Acetylcysteine	136-139	TNF receptor superfamily member 10b	Homo sapiens	212-215
30061216-6	2018	Nelfinavir induced ER stress and increased the expression of TRAIL death receptor (DR) 4 and DR5, sensitizing the cancer cells to TRAIL.	Nelfinavir	0-10	TNF receptor superfamily member 10b	Homo sapiens	93-96
30157799-4	2018	We show that due to to its dual action on DR5, a death receptor for TRAIL and on STAT3, Cryptotanshinone can be used to increase sensitivity to TRAIL.	cryptotanshinone	88-104	TNF receptor superfamily member 10b	Homo sapiens	42-45
30120241-0	2018	Author Correction: Bisphosphonate enhances TRAIL sensitivity to human osteosarcoma cells via death receptor 5 upregulation.	Diphosphonates	19-33	TNF receptor superfamily member 10b	Homo sapiens	93-109
29800641-0	2018	Isoalantolactone induces apoptosis through reactive oxygen species-dependent upregulation of death receptor 5 in human esophageal cancer cells.	isoalantolactone	0-16	TNF receptor superfamily member 10b	Homo sapiens	93-109
29596115-7	2018	Quercetin action is manifested by the upregulation of rhTRAIL-binding receptors DR4 and DR5 on the surface of cancer cells and by increased rate of the proteasome-mediated degradation of the antiapoptotic protein FLIP.	Quercetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	88-91
29792947-4	2018	Combined treatment with SFN and TRAIL (SFN/TRAIL) significantly induced apoptosis concomitant with activation of caspases, loss of mitochondrial membrane potential (MMP), Bid truncation, and induction of death receptor 5.	sulforaphane	24-27	TNF receptor superfamily member 10b	Homo sapiens	204-220
29800641-0	2018	Isoalantolactone induces apoptosis through reactive oxygen species-dependent upregulation of death receptor 5 in human esophageal cancer cells.	Reactive Oxygen Species	43-66	TNF receptor superfamily member 10b	Homo sapiens	93-109
29792947-4	2018	Combined treatment with SFN and TRAIL (SFN/TRAIL) significantly induced apoptosis concomitant with activation of caspases, loss of mitochondrial membrane potential (MMP), Bid truncation, and induction of death receptor 5.	sulforaphane	39-42	TNF receptor superfamily member 10b	Homo sapiens	204-220
29800641-5	2018	Treatment with isoalantolactone activated caspases-3, -7, and -10, and upregulated death receptor (DR)5.	isoalantolactone	15-31	TNF receptor superfamily member 10b	Homo sapiens	83-103
29800641-6	2018	Furthermore, DR5 knockdown partially reversed the effect of isoalantolactone.	isoalantolactone	60-76	TNF receptor superfamily member 10b	Homo sapiens	13-16
29800641-12	2018	In conclusion, our results revealed that isoalantolactone induced apoptosis through the extrinsic pathway via upregulation of DR5 and elevation of ROS in human esophageal cancer cells.	isoalantolactone	41-57	TNF receptor superfamily member 10b	Homo sapiens	126-129
30111400-6	2018	CONCLUSION: Osthole can sensitize HL-60 cells to TRAIL-induced apoptosis, which may be related with the activation of mitochondrial pathways and up-regulation of DR5.	osthol	12-19	TNF receptor superfamily member 10b	Homo sapiens	162-165
30004456-0	2018	Garcinol Enhances TRAIL-Induced Apoptotic Cell Death through Up-Regulation of DR5 and Down-Regulation of c-FLIP Expression.	garcinol	0-8	TNF receptor superfamily member 10b	Homo sapiens	78-81
30111400-5	2018	RESULTS: The combined treatment (100micromol/L Osthole + 40 ng/ml TRAIL) of HL-60 cells for 48 h induced an apoptotic rate of (33.9+-2.7) %, which was significantly higher than that of cells treated with Osthole or TRAIL alone (P&lt;0.05); at the same time, the combined treatment promoted the decrease of MMP and the expression rate of BCL-2/BAX, and potentiated the expression of DR5 and Caspase-3,-8,-9 activity.	osthol	47-54	TNF receptor superfamily member 10b	Homo sapiens	382-385
29970185-14	2018	Knockdown of DR4 and DR5 with siRNAs increased cell survival rate and decreased the expression of cleaved-PARP induced by the combination of azithromycin and TRAIL.	Azithromycin	141-153	TNF receptor superfamily member 10b	Homo sapiens	21-24
29970185-16	2018	CONCLUSION: The synergistic antitumor effect of azithromycin and TRAIL mainly relies on the up-regulations of DR4 and DR5, which in turn result from LC-3B-involved autophagy inhibition.	Azithromycin	48-60	TNF receptor superfamily member 10b	Homo sapiens	118-121
29970185-13	2018	Azithromycin increased the expressions of DR4, DR5, p62 and LC-3B proteins and potentiated induction of apoptosis by TRAIL.	Azithromycin	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
30004456-6	2018	Garcinol plus TRAIL induced up-regulation of DR5 and down-regulation of c-FLIP expression at post-translational levels.	garcinol	0-8	TNF receptor superfamily member 10b	Homo sapiens	45-48
30004456-7	2018	Furthermore, knock-down of DR5 by siRNA and ectopic expression of c-FLIP blocked apoptotic cell death induced by garcinol plus TRAIL.	garcinol	113-121	TNF receptor superfamily member 10b	Homo sapiens	27-30
29694835-3	2018	In this research, we showed for the first time that candesartan treatment significantly sensitized human lung adenocarcinoma cells to Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis by targeting TRAIL-DR5.	candesartan	52-63	TNF receptor superfamily member 10b	Homo sapiens	236-239
29694835-6	2018	The molecular mechanisms underlying candesartan-induced TRAIL-mediated apoptosis involved the downstream of AMPK phosphorylation resulting inhibition of autophagy flux, recruitment of death receptor 5 (DR5) and activation of apoptotic caspase cascade.	candesartan	36-47	TNF receptor superfamily member 10b	Homo sapiens	184-200
29694835-6	2018	The molecular mechanisms underlying candesartan-induced TRAIL-mediated apoptosis involved the downstream of AMPK phosphorylation resulting inhibition of autophagy flux, recruitment of death receptor 5 (DR5) and activation of apoptotic caspase cascade.	candesartan	36-47	TNF receptor superfamily member 10b	Homo sapiens	202-205
29615720-0	2018	Involvement of AMP-activated protein kinase and Death Receptor 5 in TRAIL-Berberine-induced apoptosis of cancer cells.	Berberine	74-83	TNF receptor superfamily member 10b	Homo sapiens	48-64
29891932-4	2018	We demonstrate that in vivo accumulation or exogenous application of MEcPP alters the expression of two auxin reporters, DR5:GFP and DII-VENUS, and reduces the abundance of the auxin-efflux carrier PIN-FORMED1 (PIN1) at the plasma membrane.	methyl-D-erythritol 2,4-cyclodiphosphate	69-74	TNF receptor superfamily member 10b	Homo sapiens	121-124
29768226-3	2018	Three conserved domains of Death receptor (DR5) protein extracellular domain, which are fortified cysteine, were chosen and chemically synthesised.	Cysteine	98-106	TNF receptor superfamily member 10b	Homo sapiens	43-46
29764340-4	2018	A human apoptosis protein array kit showed that death receptor 5 may be involved in silymarin-induced apoptosis, which was also shown through western blotting, immunocytochemistry, and reverse transcription-polymerase chain reaction.	Silymarin	84-93	TNF receptor superfamily member 10b	Homo sapiens	48-64
29615720-7	2018	These showed induction of several genes including TNFRSF10B (expresses DR5) and Harakiri following BBR treatment, which were further validated by qPCR analysis.	Berberine	99-102	TNF receptor superfamily member 10b	Homo sapiens	50-59
29549167-0	2018	Tetrandrine (TET) Induces Death Receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5) and Sensitizes Prostate Cancer Cells to TRAIL-Induced Apoptosis.	tetrandrine	0-11	TNF receptor superfamily member 10b	Homo sapiens	69-77
29549167-0	2018	Tetrandrine (TET) Induces Death Receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5) and Sensitizes Prostate Cancer Cells to TRAIL-Induced Apoptosis.	tetrandrine	0-11	TNF receptor superfamily member 10b	Homo sapiens	79-82
29549167-0	2018	Tetrandrine (TET) Induces Death Receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5) and Sensitizes Prostate Cancer Cells to TRAIL-Induced Apoptosis.	tetrandrine	13-16	TNF receptor superfamily member 10b	Homo sapiens	69-77
29549167-0	2018	Tetrandrine (TET) Induces Death Receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5) and Sensitizes Prostate Cancer Cells to TRAIL-Induced Apoptosis.	tetrandrine	13-16	TNF receptor superfamily member 10b	Homo sapiens	79-82
29549167-4	2018	We demonstrate here that small-molecule tetrandrine (TET) potentially sensitizes previously resistant (LNCaP and C4-2B cells) and mildly sensitive (PC3 cells) prostate cancer cells to TRAIL-induced apoptosis, and they do so by upregulating mRNA expression and protein levels of death receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5).	tetrandrine	40-51	TNF receptor superfamily member 10b	Homo sapiens	321-329
29549167-4	2018	We demonstrate here that small-molecule tetrandrine (TET) potentially sensitizes previously resistant (LNCaP and C4-2B cells) and mildly sensitive (PC3 cells) prostate cancer cells to TRAIL-induced apoptosis, and they do so by upregulating mRNA expression and protein levels of death receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5).	tetrandrine	40-51	TNF receptor superfamily member 10b	Homo sapiens	331-334
29549167-4	2018	We demonstrate here that small-molecule tetrandrine (TET) potentially sensitizes previously resistant (LNCaP and C4-2B cells) and mildly sensitive (PC3 cells) prostate cancer cells to TRAIL-induced apoptosis, and they do so by upregulating mRNA expression and protein levels of death receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5).	tetrandrine	53-56	TNF receptor superfamily member 10b	Homo sapiens	321-329
29549167-4	2018	We demonstrate here that small-molecule tetrandrine (TET) potentially sensitizes previously resistant (LNCaP and C4-2B cells) and mildly sensitive (PC3 cells) prostate cancer cells to TRAIL-induced apoptosis, and they do so by upregulating mRNA expression and protein levels of death receptors Apo Trail R1 (DR4) and Apo Trail R2 (DR5).	tetrandrine	53-56	TNF receptor superfamily member 10b	Homo sapiens	331-334
29549167-6	2018	We show that double knockdown of DR4 and DR5 abrogated the apoptotic effects of TET and TRAIL.	tetrandrine	80-83	TNF receptor superfamily member 10b	Homo sapiens	41-44
29549167-7	2018	We also demonstrate that TET-induced DR4 and DR5 expression is independent of p53 status.	tetrandrine	25-28	TNF receptor superfamily member 10b	Homo sapiens	45-48
29615720-7	2018	These showed induction of several genes including TNFRSF10B (expresses DR5) and Harakiri following BBR treatment, which were further validated by qPCR analysis.	Berberine	99-102	TNF receptor superfamily member 10b	Homo sapiens	71-74
29599323-6	2018	To determine the pathway and relevant components by which gallic acid-induced apoptosis is mediated through, cells were transfected with siRNA (Fas, FasL, DR5, p53) using Lipofectamine 2000.	Gallic Acid	58-69	TNF receptor superfamily member 10b	Homo sapiens	155-158
29599323-8	2018	Gallic acid induced up-regulation of Fas, FasL, and DR5 expression in AGS cells.	Gallic Acid	0-11	TNF receptor superfamily member 10b	Homo sapiens	52-55
29599323-9	2018	Transfection of cells with Fas, FasL, or DR5 siRNA reduced gallic acid-induced cell death.	Gallic Acid	59-70	TNF receptor superfamily member 10b	Homo sapiens	41-44
29599323-10	2018	In addition, p53 was shown to be involved in gallic acid-mediated Fas, FasL, and DR5 expression as well as cell apoptosis in AGS cells.	Gallic Acid	45-56	TNF receptor superfamily member 10b	Homo sapiens	81-84
29556305-6	2018	The present data indicate that Taxol may enhance the pro-apoptotic effects of TRAIL overexpression in HeLa cells by increasing cleaved caspase-3 and DR5 expression levels and decreasing Bcl-2 expression levels.	Paclitaxel	31-36	TNF receptor superfamily member 10b	Homo sapiens	149-152
29300929-8	2018	Furthermore, bortezomib and TRAIL synergistically induced reactive oxygen species (ROS) generation and caused death receptor 5 upregulation through activation of the extracellular signal-regulated kinase-C/EBP homologous protein signaling cascade.	Bortezomib	13-23	TNF receptor superfamily member 10b	Homo sapiens	110-126
29744288-0	2018	Dasatinib promotes TRAIL-mediated apoptosis by upregulating CHOP-dependent death receptor 5 in gastric cancer.	Dasatinib	0-9	TNF receptor superfamily member 10b	Homo sapiens	75-91
29744288-7	2018	Moreover, increased DR5 expression facilitated dasatinib-induced apoptosis; the dasatinib-induced increase in DR5 expression was mediated by CCAAT/enhancer-binding protein homologous protein (CHOP).	Dasatinib	47-56	TNF receptor superfamily member 10b	Homo sapiens	20-23
29744288-5	2018	In addition, we found that dasatinib increased the expression of death receptor 5 (DR5) in GC cells.	Dasatinib	27-36	TNF receptor superfamily member 10b	Homo sapiens	65-81
29744288-7	2018	Moreover, increased DR5 expression facilitated dasatinib-induced apoptosis; the dasatinib-induced increase in DR5 expression was mediated by CCAAT/enhancer-binding protein homologous protein (CHOP).	Dasatinib	80-89	TNF receptor superfamily member 10b	Homo sapiens	110-113
29744288-5	2018	In addition, we found that dasatinib increased the expression of death receptor 5 (DR5) in GC cells.	Dasatinib	27-36	TNF receptor superfamily member 10b	Homo sapiens	83-86
29744288-8	2018	Furthermore, dasatinib also synergized with TRAIL to induce apoptosis via DR5 in GC cells.	Dasatinib	13-22	TNF receptor superfamily member 10b	Homo sapiens	74-77
29158005-9	2018	In the 1,25(OH)2D3 + HDAC2 overexpression group, the expressions of p53, Bax, DR5 and caspase 8 were significantly lower but the expression of Bcl-2 was significantly higher than those of the 1,25(OH)2D3 treatment group (P &lt; 0.05).	25(oh)	9-15	TNF receptor superfamily member 10b	Homo sapiens	78-81
29744288-9	2018	Our results show that dasatinib promoted TRAIL-mediated apoptosis via upregulation of CHOP-dependent DR5 expression in GC, suggesting that DR5 induction can be used as an indicator of dasatinib sensitivity.	Dasatinib	22-31	TNF receptor superfamily member 10b	Homo sapiens	101-104
29744288-9	2018	Our results show that dasatinib promoted TRAIL-mediated apoptosis via upregulation of CHOP-dependent DR5 expression in GC, suggesting that DR5 induction can be used as an indicator of dasatinib sensitivity.	Dasatinib	22-31	TNF receptor superfamily member 10b	Homo sapiens	139-142
29498673-4	2018	Remarkably, though, despite the fact that all membrane-bound TRAIL receptors harbor putative glycosylation sites, only pro-apoptotic signaling through DR4 and DR5 has, so far, been found to be regulated by N- and O-glycosylation, respectively.	Nitrogen	206-207	TNF receptor superfamily member 10b	Homo sapiens	159-162
29278689-7	2018	TRAIL-induced apoptosis, enhanced by the inhibitor of the Bcl-2 family ABT-737, or by the translation inhibitor homoharringtonine, proceeded in both cell lines predominantly via the DR5 receptor.	Homoharringtonine	112-129	TNF receptor superfamily member 10b	Homo sapiens	182-185
29158005-9	2018	In the 1,25(OH)2D3 + HDAC2 overexpression group, the expressions of p53, Bax, DR5 and caspase 8 were significantly lower but the expression of Bcl-2 was significantly higher than those of the 1,25(OH)2D3 treatment group (P &lt; 0.05).	Calcitriol	7-18	TNF receptor superfamily member 10b	Homo sapiens	78-81
29435013-0	2018	Enhancement of cisplatin cytotoxicity by Retigeric acid B involves blocking DNA repair and activating DR5 in prostate cancer cells.	Cisplatin	15-24	TNF receptor superfamily member 10b	Homo sapiens	102-105
29435013-6	2018	Concurrently, the proapoptotic protein death receptor 5 (DR5) was activated by RAB, which also enhanced the chemotherapeutic response of CDDP.	Cisplatin	137-141	TNF receptor superfamily member 10b	Homo sapiens	39-55
29435013-8	2018	The results of the present study identified that RAB functioned synergistically with CDDP to increase the efficacy of CDDP by inhibiting DNA damage repair and activating DR5, suggesting the mechanistic basis for the antitumor effect of RAB in combination with current chemotherapeutics.	retigeric acid B	49-52	TNF receptor superfamily member 10b	Homo sapiens	170-173
29435013-6	2018	Concurrently, the proapoptotic protein death receptor 5 (DR5) was activated by RAB, which also enhanced the chemotherapeutic response of CDDP.	Cisplatin	137-141	TNF receptor superfamily member 10b	Homo sapiens	57-60
29435013-7	2018	Knockdown of DR5 partially blocked RAB-CDDP synergism, suggesting the crucial involvement of DR5 in this event.	retigeric acid B	35-38	TNF receptor superfamily member 10b	Homo sapiens	13-16
29435013-7	2018	Knockdown of DR5 partially blocked RAB-CDDP synergism, suggesting the crucial involvement of DR5 in this event.	retigeric acid B	35-38	TNF receptor superfamily member 10b	Homo sapiens	93-96
29435013-7	2018	Knockdown of DR5 partially blocked RAB-CDDP synergism, suggesting the crucial involvement of DR5 in this event.	Cisplatin	39-43	TNF receptor superfamily member 10b	Homo sapiens	13-16
29435013-7	2018	Knockdown of DR5 partially blocked RAB-CDDP synergism, suggesting the crucial involvement of DR5 in this event.	Cisplatin	39-43	TNF receptor superfamily member 10b	Homo sapiens	93-96
29435013-8	2018	The results of the present study identified that RAB functioned synergistically with CDDP to increase the efficacy of CDDP by inhibiting DNA damage repair and activating DR5, suggesting the mechanistic basis for the antitumor effect of RAB in combination with current chemotherapeutics.	Cisplatin	85-89	TNF receptor superfamily member 10b	Homo sapiens	170-173
29435013-8	2018	The results of the present study identified that RAB functioned synergistically with CDDP to increase the efficacy of CDDP by inhibiting DNA damage repair and activating DR5, suggesting the mechanistic basis for the antitumor effect of RAB in combination with current chemotherapeutics.	Cisplatin	118-122	TNF receptor superfamily member 10b	Homo sapiens	170-173
29531826-14	2018	Upregulation of DR5 is involved in BIX plus TRAIL-mediated apoptosis.	2-(3,4-dihydroxyphenyl)-2-oxoethyl thiocyanate	35-38	TNF receptor superfamily member 10b	Homo sapiens	16-19
29531826-0	2018	BIX-01294 sensitizes renal cancer Caki cells to TRAIL-induced apoptosis through downregulation of survivin expression and upregulation of DR5 expression.	BIX 01294	0-9	TNF receptor superfamily member 10b	Homo sapiens	138-141
29272788-0	2018	Combination of novel DR5 targeting agonistic scFv antibody TR2-3 with cisplatin shows enhanced synergistic antitumor activity in vitro and in vivo.	Cisplatin	70-79	TNF receptor superfamily member 10b	Homo sapiens	21-24
29531826-7	2018	Furthermore, BIX induced upregulation of DR5 expression at the transcriptional levels, and knockdown of DR5 expression using small interfering RNAs (siRNAs) markedly attenuated BIX and TRAIL-induced apoptosis.	2-(3,4-dihydroxyphenyl)-2-oxoethyl thiocyanate	13-16	TNF receptor superfamily member 10b	Homo sapiens	41-44
29531826-7	2018	Furthermore, BIX induced upregulation of DR5 expression at the transcriptional levels, and knockdown of DR5 expression using small interfering RNAs (siRNAs) markedly attenuated BIX and TRAIL-induced apoptosis.	2-(3,4-dihydroxyphenyl)-2-oxoethyl thiocyanate	177-180	TNF receptor superfamily member 10b	Homo sapiens	104-107
29531826-11	2018	Taken together, these results suggest that BIX facilitates TRAIL-mediated apoptosis via downregulation of survivin and upregulation of DR5 expression in renal carcinoma Caki cells.	2-(3,4-dihydroxyphenyl)-2-oxoethyl thiocyanate	43-46	TNF receptor superfamily member 10b	Homo sapiens	135-138
29434187-6	2018	Activation of the amino-acid-sensing kinase general control nonderepressible 2 (GCN2) upon glutamine deprivation is responsible for TRAIL-R2 upregulation through a signaling pathway involving ATF4 and CHOP transcription factors.	Glutamine	91-100	TNF receptor superfamily member 10b	Homo sapiens	132-140
29272788-8	2018	In addition, treatment with cisplatin alone for 24 h resulted in significantly up-regulating the mRNA and protein levels of DR5 in both COLO205 and MDA-MB-231 cell lines by q-PCR and Western blot assay.	Cisplatin	28-37	TNF receptor superfamily member 10b	Homo sapiens	124-127
29272788-10	2018	These results indicated that cisplatin sensitized COLO205 and MDA-MB-231 cancer cells to TR2-3-mediated apoptosis by up-regulation of DR5 expression.	Cisplatin	29-38	TNF receptor superfamily member 10b	Homo sapiens	134-137
29434473-6	2018	Quercetin was able to sensitize rhTRAIL-resistant breast cancers to rhTRAIL-induced apoptosis as detected by Western blotting through the proteasome-mediated degradation of c-FLIPL and through the upregulation of DR5 expression transcriptionally.	Quercetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	213-216
29272788-12	2018	CONCLUSIONS: Our findings suggest that cisplatin enhanced the antitumor activity of TR2-3 in COLO205 and MDA-MB-231 cancer cells through up-regulation of DR5 expression.	Cisplatin	39-48	TNF receptor superfamily member 10b	Homo sapiens	154-157
29535810-13	2018	Our results showed that silibinin enhanced TRAIL-induced apoptosis by upregulating DR5 expression through the ROS-ER stress-CaMKII-Sp1 axis.	Silybin	24-33	TNF receptor superfamily member 10b	Homo sapiens	83-86
29162448-0	2018	Intracellular cholesterol level regulates sensitivity of glioblastoma cells against temozolomide-induced cell death by modulation of caspase-8 activation via death receptor 5-accumulation and activation in the plasma membrane lipid raft.	Cholesterol	14-25	TNF receptor superfamily member 10b	Homo sapiens	158-174
29162448-0	2018	Intracellular cholesterol level regulates sensitivity of glioblastoma cells against temozolomide-induced cell death by modulation of caspase-8 activation via death receptor 5-accumulation and activation in the plasma membrane lipid raft.	Temozolomide	84-96	TNF receptor superfamily member 10b	Homo sapiens	158-174
29162448-7	2018	TMZ without or with MbetaCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death.	Temozolomide	0-3	TNF receptor superfamily member 10b	Homo sapiens	63-66
29162448-7	2018	TMZ without or with MbetaCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death.	methyl-beta-cyclodextrin	20-27	TNF receptor superfamily member 10b	Homo sapiens	63-66
29162448-7	2018	TMZ without or with MbetaCD and/or Chol caused accumulation of DR5 into the plasma membrane lipid raft and formed a complex with caspase-8, an extrinsic caspase cascade inducer, reflected in the induction of cell death.	Cholesterol	35-39	TNF receptor superfamily member 10b	Homo sapiens	63-66
29162448-8	2018	In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MbetaCD, and Chol.	Temozolomide	150-153	TNF receptor superfamily member 10b	Homo sapiens	64-67
29162448-8	2018	In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MbetaCD, and Chol.	methyl-beta-cyclodextrin	155-162	TNF receptor superfamily member 10b	Homo sapiens	64-67
29162448-8	2018	In addition, treatment with caspase-8 inhibitor or knockdown of DR5 dramatically suppressed U251-Con cell death induced by combination treatment with TMZ, MbetaCD, and Chol.	Cholesterol	168-172	TNF receptor superfamily member 10b	Homo sapiens	64-67
29535810-0	2018	Silibinin sensitizes TRAIL-mediated apoptosis by upregulating DR5 through ROS-induced endoplasmic reticulum stress-Ca2+-CaMKII-Sp1 pathway.	Silybin	0-9	TNF receptor superfamily member 10b	Homo sapiens	62-65
29535810-0	2018	Silibinin sensitizes TRAIL-mediated apoptosis by upregulating DR5 through ROS-induced endoplasmic reticulum stress-Ca2+-CaMKII-Sp1 pathway.	Reactive Oxygen Species	74-77	TNF receptor superfamily member 10b	Homo sapiens	62-65
29535810-4	2018	Silibinin also triggered TRAIL-induced apoptosis in A549 cells through upregulation of death receptor 5 (DR5).	Silybin	0-9	TNF receptor superfamily member 10b	Homo sapiens	87-103
29535810-4	2018	Silibinin also triggered TRAIL-induced apoptosis in A549 cells through upregulation of death receptor 5 (DR5).	Silybin	0-9	TNF receptor superfamily member 10b	Homo sapiens	105-108
29535810-5	2018	Pretreatment with DR5/Fc chimeric protein and DR5-targeted small interfering RNA (siRNA) significantly blocked silibinin/TRAIL-mediated apoptosis in A549 cells.	Silybin	111-120	TNF receptor superfamily member 10b	Homo sapiens	18-21
29535810-5	2018	Pretreatment with DR5/Fc chimeric protein and DR5-targeted small interfering RNA (siRNA) significantly blocked silibinin/TRAIL-mediated apoptosis in A549 cells.	Silybin	111-120	TNF receptor superfamily member 10b	Homo sapiens	46-49
29535810-6	2018	Furthermore, silibinin increased the production of reactive oxygen species (ROS), which led to the induction of TRAIL-mediated apoptosis through DR5 upregulation.	Silybin	13-22	TNF receptor superfamily member 10b	Homo sapiens	145-148
29162448-10	2018	These findings suggest that intracellular cholesterol level affects TMZ treatment of GBM mediated via a DR5-caspase-8 mechanism.	Cholesterol	42-53	TNF receptor superfamily member 10b	Homo sapiens	104-107
29162448-10	2018	These findings suggest that intracellular cholesterol level affects TMZ treatment of GBM mediated via a DR5-caspase-8 mechanism.	Temozolomide	68-71	TNF receptor superfamily member 10b	Homo sapiens	104-107
30257253-0	2018	miR-128 Targets the SIRT1/ROS/DR5 Pathway to Sensitize Colorectal Cancer to TRAIL-Induced Apoptosis.	mir-128	0-7	TNF receptor superfamily member 10b	Homo sapiens	30-33
30257253-12	2018	This increase of ROS subsequently induced DR5 expression, and thus increased TRAIL-induced apoptosis in CRC cells.	Reactive Oxygen Species	17-20	TNF receptor superfamily member 10b	Homo sapiens	42-45
29164887-9	2017	Moreover, we found that PTER induced the expression of DR4 and DR5 through the reactive oxygen species (ROS)/ endoplasmic reticulum (ER) stress/ERK 1/2 and p38/C/EBP-homologous protein (CHOP) signaling pathways.	Reactive Oxygen Species	79-102	TNF receptor superfamily member 10b	Homo sapiens	63-66
29164887-9	2017	Moreover, we found that PTER induced the expression of DR4 and DR5 through the reactive oxygen species (ROS)/ endoplasmic reticulum (ER) stress/ERK 1/2 and p38/C/EBP-homologous protein (CHOP) signaling pathways.	Reactive Oxygen Species	104-107	TNF receptor superfamily member 10b	Homo sapiens	63-66
29164887-10	2017	Overall, our results showed that PTER potentiated TRAIL-induced apoptosis via ROS-mediated CHOP activation leading to the expression of DR4 and DR5.	Reactive Oxygen Species	78-81	TNF receptor superfamily member 10b	Homo sapiens	144-147
29535810-6	2018	Furthermore, silibinin increased the production of reactive oxygen species (ROS), which led to the induction of TRAIL-mediated apoptosis through DR5 upregulation.	Reactive Oxygen Species	51-74	TNF receptor superfamily member 10b	Homo sapiens	145-148
29535810-13	2018	Our results showed that silibinin enhanced TRAIL-induced apoptosis by upregulating DR5 expression through the ROS-ER stress-CaMKII-Sp1 axis.	Reactive Oxygen Species	110-113	TNF receptor superfamily member 10b	Homo sapiens	83-86
29535810-6	2018	Furthermore, silibinin increased the production of reactive oxygen species (ROS), which led to the induction of TRAIL-mediated apoptosis through DR5 upregulation.	Reactive Oxygen Species	76-79	TNF receptor superfamily member 10b	Homo sapiens	145-148
29072615-8	2017	Collectively, our data show that LSS-11 is a potent naphthalimide-based chemosensitizer that could enhance cell death in paclitaxel-resistant lung cancer cells through the DR5/PARP1 pathway and STAT3/MDR1/MRP1 STAT3 inhibition.	LSS-11	33-39	TNF receptor superfamily member 10b	Homo sapiens	172-175
29535810-11	2018	Ca2+/calmodulin-dependent protein kinase (CaMKII) inhibitor, K252a, blocked silibinin/TRAIL-induced DR5 expression along with TRAIL-mediated apoptosis.	Silybin	76-85	TNF receptor superfamily member 10b	Homo sapiens	100-103
29535810-12	2018	Accordingly, we showed that ROS/ER stress-induced CaMKII activated Sp1, which is an important transcription factor for DR5 expression.	Reactive Oxygen Species	28-31	TNF receptor superfamily member 10b	Homo sapiens	119-122
29296202-5	2017	Ciglitazone kills cervical cancer cells by activating death receptor signalling pathway, caspase cascade and BH3 interacting-domain death agonist (Bid) cleavage through the up-regulation of Death Receptor 4 (DR4)/DR5 and soluble and membrane-bound TNF related apoptosis inducing ligand (TRAIL).	ciglitazone	0-11	TNF receptor superfamily member 10b	Homo sapiens	213-216
29070784-10	2017	RESULTS Kaempferol enhanced apoptosis and drastically up-regulated DR4, DR5, CHOP, JNK, ERK1/2, p38 and apoptotic protein expression with decline in the expression of anti-apoptotic proteins.	kaempferol	8-18	TNF receptor superfamily member 10b	Homo sapiens	72-75
29070784-12	2017	CONCLUSIONS Kaempferol sensitized ovarian cancer cells to TRAIL-induced apoptosis via up-regulation of DR4 and DR5 through ERK/JNK/CHOP pathways.	kaempferol	12-22	TNF receptor superfamily member 10b	Homo sapiens	111-114
29297126-6	2017	The cytotoxicity of DR5-B variant is significantly higher compared to wild-type TRAIL in combination with cisplatin in 9 of 12 tumor cell lines.	Cisplatin	106-115	TNF receptor superfamily member 10b	Homo sapiens	20-23
29072615-8	2017	Collectively, our data show that LSS-11 is a potent naphthalimide-based chemosensitizer that could enhance cell death in paclitaxel-resistant lung cancer cells through the DR5/PARP1 pathway and STAT3/MDR1/MRP1 STAT3 inhibition.	Naphthalimides	52-65	TNF receptor superfamily member 10b	Homo sapiens	172-175
29072615-8	2017	Collectively, our data show that LSS-11 is a potent naphthalimide-based chemosensitizer that could enhance cell death in paclitaxel-resistant lung cancer cells through the DR5/PARP1 pathway and STAT3/MDR1/MRP1 STAT3 inhibition.	Paclitaxel	121-131	TNF receptor superfamily member 10b	Homo sapiens	172-175
28702823-0	2017	Etoposide and doxorubicin enhance the sensitivity of triple negative breast cancers through modulation of TRAIL-DR5 axis.	Doxorubicin	14-25	TNF receptor superfamily member 10b	Homo sapiens	112-115
28702823-7	2017	The binding energy for TRAIL-DR5 complexation in the ternary complexes containing ET (-111.08 kcal/mol) and DOX (-76.35 kcal/mol) were higher than reported binding energy of binary complex (-53.70 kcal/mol).	Doxorubicin	108-111	TNF receptor superfamily member 10b	Homo sapiens	29-32
28702823-0	2017	Etoposide and doxorubicin enhance the sensitivity of triple negative breast cancers through modulation of TRAIL-DR5 axis.	Etoposide	0-9	TNF receptor superfamily member 10b	Homo sapiens	112-115
28702823-12	2017	Thus, data suggests ET and DOX act as DR5 agonistic ligands and enhance the cellular apoptosis in TNBC.	Doxorubicin	27-30	TNF receptor superfamily member 10b	Homo sapiens	38-41
28702823-2	2017	Recently, we reported the molecular level details for the modulation of TRAIL-DR5 axis by quinacrine (QC) in breast cancer cells.	Quinacrine	90-100	TNF receptor superfamily member 10b	Homo sapiens	78-81
28702823-3	2017	In this work, the DR5 mediated anticancer potential of topoisomerase inhibitor etoposide (ET) and doxorubicin (DOX) against TNBC has been evaluated.	Etoposide	79-88	TNF receptor superfamily member 10b	Homo sapiens	18-21
28702823-3	2017	In this work, the DR5 mediated anticancer potential of topoisomerase inhibitor etoposide (ET) and doxorubicin (DOX) against TNBC has been evaluated.	Etoposide	90-92	TNF receptor superfamily member 10b	Homo sapiens	18-21
28702823-3	2017	In this work, the DR5 mediated anticancer potential of topoisomerase inhibitor etoposide (ET) and doxorubicin (DOX) against TNBC has been evaluated.	Doxorubicin	98-109	TNF receptor superfamily member 10b	Homo sapiens	18-21
28702823-3	2017	In this work, the DR5 mediated anticancer potential of topoisomerase inhibitor etoposide (ET) and doxorubicin (DOX) against TNBC has been evaluated.	Doxorubicin	111-114	TNF receptor superfamily member 10b	Homo sapiens	18-21
28702823-4	2017	ET and DOX enhanced the DR5 expression in TNBC cells, whereas non-topoisomerase inhibitors pifithrin-alpha (PIF) and dexamethasone (DEX) failed to do so.	Etoposide	0-2	TNF receptor superfamily member 10b	Homo sapiens	24-27
28702823-4	2017	ET and DOX enhanced the DR5 expression in TNBC cells, whereas non-topoisomerase inhibitors pifithrin-alpha (PIF) and dexamethasone (DEX) failed to do so.	Doxorubicin	7-10	TNF receptor superfamily member 10b	Homo sapiens	24-27
28467689-5	2017	Vernodalol increased the expression of death receptor (DR) 5, and silencing of DR5 with a small interfering RNA (siRNA) reduced the effect of vernodalol on TRAIL-mediated apoptosis.	vernodalol	0-10	TNF receptor superfamily member 10b	Homo sapiens	39-60
28631177-6	2017	The expression of TRAIL and TRAIL-R2 in SAA patients was significantly decreased compared with controls; however, there was no statistical difference in TRAIL mRNA expression between the two groups.	saa	40-43	TNF receptor superfamily member 10b	Homo sapiens	28-36
28467689-5	2017	Vernodalol increased the expression of death receptor (DR) 5, and silencing of DR5 with a small interfering RNA (siRNA) reduced the effect of vernodalol on TRAIL-mediated apoptosis.	vernodalol	142-152	TNF receptor superfamily member 10b	Homo sapiens	79-82
28467689-8	2017	In addition, a c-Jun N-terminal kinase (JNK) inhibitor blocked the vernodalol-induced up-regulation of DR5, indicating that the effect depended on JNK activation.	vernodalol	67-77	TNF receptor superfamily member 10b	Homo sapiens	103-106
28467689-11	2017	Based on our results, vernodalol enhanced TRAIL-induced apoptosis by down-regulating Mcl-1 and up-regulating DR5, and the effects of DR5 depended on JNK activation and CHOP induction.	vernodalol	22-32	TNF receptor superfamily member 10b	Homo sapiens	109-112
28467689-11	2017	Based on our results, vernodalol enhanced TRAIL-induced apoptosis by down-regulating Mcl-1 and up-regulating DR5, and the effects of DR5 depended on JNK activation and CHOP induction.	vernodalol	22-32	TNF receptor superfamily member 10b	Homo sapiens	133-136
28918048-0	2017	miR-133a Promotes TRAIL Resistance in Glioblastoma via Suppressing Death Receptor 5 and Activating NF-kappaB Signaling.	mir-133a	0-8	TNF receptor superfamily member 10b	Homo sapiens	67-83
28918048-3	2017	In this study, a negative correlation between DR5 expression and TRAIL resistance was observed, and miR-133a was predicted to be the most promising candidate to suppress DR5 expression.	mir-133a	100-108	TNF receptor superfamily member 10b	Homo sapiens	170-173
28918048-7	2017	In conclusion, our data demonstrate that miR-133a promotes TRAIL resistance in glioblastoma by suppressing DR5 expression and activating NF-kappaB signaling.	mir-133a	41-49	TNF receptor superfamily member 10b	Homo sapiens	107-110
28793767-3	2017	In our study, 20(S)-Rh2 induced the expression of orphan nuclear receptor Nur77 and death receptor proteins Fas, FasL, DR5, and TRAIL, as well as the cleavage of caspase 8 and caspase 3 in HL-60 cells.	rh2	20-23	TNF receptor superfamily member 10b	Homo sapiens	119-122
28092099-6	2017	Results show that upon DR5 activation, CaM was recruited into DR5-mediated DISC in a calcium dependent manner.	Calcium	85-92	TNF receptor superfamily member 10b	Homo sapiens	23-26
28899403-8	2017	Additionally, DR5 in patients with AOSD are associated with macrophage activation syndrome (MAS) and steroid pulse therapy.	Steroids	101-108	TNF receptor superfamily member 10b	Homo sapiens	14-17
28767099-0	2017	Fisetin Induces Apoptosis Through p53-Mediated Up-Regulation of DR5 Expression in Human Renal Carcinoma Caki Cells.	fisetin	0-7	TNF receptor superfamily member 10b	Homo sapiens	64-67
28471808-0	2017	3-Bromopyruvate enhances TRAIL-induced apoptosis in human nasopharyngeal carcinoma cells through CHOP-dependent upregulation of TRAIL-R2.	bromopyruvate	0-15	TNF receptor superfamily member 10b	Homo sapiens	128-136
29018571-1	2017	To investigate the ability of SAHA-induced TRAIL DR5-CTSB crosstalk to initiate the breast cancer autophagy, RTCA assay was performed to assess the effect of SAHA on breast cancer cells, and western blot and ELISA were used to verify the inductive effects on expression of CTSB.	Vorinostat	30-34	TNF receptor superfamily member 10b	Homo sapiens	49-52
29018571-4	2017	The distribution of LC3-II in TRAIL DR5-silenced breast cancer cells treated with SAHA was observed by immunofluorescence microscopy, the mRNA levels of autophagy-related genes were detected by RNA microarray, and the activity of autophagy-related signaling pathways was screened by MAPK antibody array.	Vorinostat	82-86	TNF receptor superfamily member 10b	Homo sapiens	36-39
29018571-6	2017	Western blot and ELISA results indicated that TRAIL DR5 was involved in the expression of CTSB in SAHA-induced breast cancer cells.	Vorinostat	98-102	TNF receptor superfamily member 10b	Homo sapiens	52-55
29018571-7	2017	Cell viability and apoptosis assays showed that the inactivation of TRAIL DR5 can significantly inhibit the effects of SAHA.	Vorinostat	119-123	TNF receptor superfamily member 10b	Homo sapiens	74-77
29018571-9	2017	While SAHA was added in the TRAIL-DR5 blocked cells, the distribution of LC3-II signal was dispersed, the intensity of fluorescence signal was weaker than that of SAHA alone.	Vorinostat	6-10	TNF receptor superfamily member 10b	Homo sapiens	34-37
29018571-12	2017	These results provide more evidence that SAHA may stimulate TRAIL DR5-CTSB crosstalk, influence the activity of downstream TOR signalling pathway mainly through the AKTs pathway, and initiate the autophagy of breast cancer cells.	Vorinostat	41-45	TNF receptor superfamily member 10b	Homo sapiens	66-69
28571773-0	2017	DATS sensitizes glioma cells to TRAIL-mediated apoptosis by up-regulation of death receptor 5 via ROS.	ros	98-101	TNF receptor superfamily member 10b	Homo sapiens	77-93
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	diallyl trisulfide	13-17	TNF receptor superfamily member 10b	Homo sapiens	136-139
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	ros	173-176	TNF receptor superfamily member 10b	Homo sapiens	136-139
28624529-0	2017	Cyclopamine sensitizes TRAIL-resistant gastric cancer cells to TRAIL-induced apoptosis via endoplasmic reticulum stress-mediated increase of death receptor 5 and survivin degradation.	cyclopamine	0-11	TNF receptor superfamily member 10b	Homo sapiens	141-157
28624529-3	2017	In this study, we show that cyclopamine sensitizes gastric cancer cells to TRAIL-induced apoptosis by elevating the expression of DR5.	cyclopamine	28-39	TNF receptor superfamily member 10b	Homo sapiens	130-133
28092099-6	2017	Results show that upon DR5 activation, CaM was recruited into DR5-mediated DISC in a calcium dependent manner.	Calcium	85-92	TNF receptor superfamily member 10b	Homo sapiens	62-65
28092099-11	2017	These results demonstrated CaM binding to DR5-mediated DISC in a calcium dependent manner and may identify CaM as a key regulator of DR5-mediated DISC formation for apoptosis in breast cancer.	Calcium	65-72	TNF receptor superfamily member 10b	Homo sapiens	42-45
28092099-11	2017	These results demonstrated CaM binding to DR5-mediated DISC in a calcium dependent manner and may identify CaM as a key regulator of DR5-mediated DISC formation for apoptosis in breast cancer.	Calcium	65-72	TNF receptor superfamily member 10b	Homo sapiens	133-136
28758908-9	2017	We discovered also that taxanes can increase the expression of death receptor TRAIL-R2 in PC3 prostate cancer cells.	Taxoids	24-31	TNF receptor superfamily member 10b	Homo sapiens	78-86
28511296-5	2017	In particular, the expression of the death receptors DR5 and FAS was significantly increased by MMPP treatment.	2-methoxy-4-(3-(4-methoxyphenyl)prop-1-en-1-yl)phenol	96-100	TNF receptor superfamily member 10b	Homo sapiens	53-56
28067150-0	2017	Low-dose 5-fluorouracil sensitizes HepG2 cells to TRAIL through TRAIL receptor DR5 and survivin-dependent mechanisms.	Fluorouracil	9-23	TNF receptor superfamily member 10b	Homo sapiens	79-82
28414160-0	2017	Paraquat induces extrinsic pathway of apoptosis in A549 cells by induction of DR5 and repression of anti-apoptotic proteins, DDX3 and GSK3 expression.	Paraquat	0-8	TNF receptor superfamily member 10b	Homo sapiens	78-81
28746849-2	2017	Recent studies have proposed that activation of several tumor necrosis factor receptors, including Death Receptor 5, involves a scissorlike opening of the disulfide-linked transmembrane (TM) dimer.	Disulfides	155-164	TNF receptor superfamily member 10b	Homo sapiens	99-115
28120533-2	2017	We have recently demonstrated that nanovectorization of TRAIL with single-walled carbon nanotubes enhanced TRAIL affinity to DR5.	Carbon	81-87	TNF receptor superfamily member 10b	Homo sapiens	125-128
28476883-10	2017	We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene.	Lysine	159-165	TNF receptor superfamily member 10b	Homo sapiens	191-194
28414160-4	2017	Additionally, PQ treatment caused an increase in DR5 (death receptor-5) and caspase-8 interaction, indicating formation of DISC (death-inducing signaling complex).	Paraquat	14-16	TNF receptor superfamily member 10b	Homo sapiens	49-52
28414160-4	2017	Additionally, PQ treatment caused an increase in DR5 (death receptor-5) and caspase-8 interaction, indicating formation of DISC (death-inducing signaling complex).	Paraquat	14-16	TNF receptor superfamily member 10b	Homo sapiens	54-70
28414160-6	2017	Moreover, PQ drastically increased DR5 expression and membrane localization.	Paraquat	10-12	TNF receptor superfamily member 10b	Homo sapiens	35-38
28414160-7	2017	Furthermore, PQ caused prominent concentration dependent reductions of DDX3 (the DEAD box protein-3) and GSK3 (glycogen synthase kinase-3) which can associate with DR5 and prevent DISC formation.	Paraquat	13-15	TNF receptor superfamily member 10b	Homo sapiens	164-167
28414160-8	2017	Additionally, PQ decreased DR5-DDX3 interaction, suggesting a reduction of DDX3/GSK3 anti-apoptotic complex.	Paraquat	14-16	TNF receptor superfamily member 10b	Homo sapiens	27-30
28414160-11	2017	Taken together, these results suggest that PQ may induce extrinsic pathway of apoptosis in A549 cells through upregulation of DR5 and repression of anti-apoptotic proteins, DDX3/GSK3 leading to reduction of anti-apoptotic complex.	Paraquat	43-45	TNF receptor superfamily member 10b	Homo sapiens	126-129
27965309-0	2017	Selective Targeting of Myeloid-Derived Suppressor Cells in Cancer Patients Using DS-8273a, an Agonistic TRAIL-R2 Antibody.	DS-8273a	81-89	TNF receptor superfamily member 10b	Homo sapiens	104-112
28067150-5	2017	The enhanced induction of cell death by the 5-FU/TRAIL combination was mediated by DR5 up-regulation and survivin down-regulation.	Fluorouracil	44-48	TNF receptor superfamily member 10b	Homo sapiens	83-86
28498435-6	2017	The effects of plumbagin on the expression of DR5, Bax and cFLIP could be partially abolished by the reactive oxygen species (ROS) scavenger NAC.	Reactive Oxygen Species	101-124	TNF receptor superfamily member 10b	Homo sapiens	46-49
28498435-6	2017	The effects of plumbagin on the expression of DR5, Bax and cFLIP could be partially abolished by the reactive oxygen species (ROS) scavenger NAC.	Reactive Oxygen Species	126-129	TNF receptor superfamily member 10b	Homo sapiens	46-49
28593135-5	2017	Gene expression studies revealed that cotreatment with melatonin and VPA triggered the up-regulation of certain genes related to apoptosis (TNFRSF10A and TNFRSF10B), autophagy (BECN, ATG3 and ATG5) and necrosis (MLKL, PARP-1 and RIPK1).	Melatonin	55-64	TNF receptor superfamily member 10b	Homo sapiens	154-163
28498480-0	2017	Miconazole induces apoptosis via the death receptor 5-dependent and mitochondrial-mediated pathways in human bladder cancer cells.	Miconazole	0-10	TNF receptor superfamily member 10b	Homo sapiens	37-53
28529596-6	2017	It was demonstrated that activity of the TRAIL-R2 (DR5) pathway was critical in the development of andrographolide-mediated rhTRAIL sensitization, since its inhibition significantly reduced the extent of apoptosis induced by the combination of rhTRAIL and andrographolide.	andrographolide	99-114	TNF receptor superfamily member 10b	Homo sapiens	41-49
28529596-6	2017	It was demonstrated that activity of the TRAIL-R2 (DR5) pathway was critical in the development of andrographolide-mediated rhTRAIL sensitization, since its inhibition significantly reduced the extent of apoptosis induced by the combination of rhTRAIL and andrographolide.	andrographolide	99-114	TNF receptor superfamily member 10b	Homo sapiens	51-54
28529596-6	2017	It was demonstrated that activity of the TRAIL-R2 (DR5) pathway was critical in the development of andrographolide-mediated rhTRAIL sensitization, since its inhibition significantly reduced the extent of apoptosis induced by the combination of rhTRAIL and andrographolide.	andrographolide	256-271	TNF receptor superfamily member 10b	Homo sapiens	41-49
28529596-6	2017	It was demonstrated that activity of the TRAIL-R2 (DR5) pathway was critical in the development of andrographolide-mediated rhTRAIL sensitization, since its inhibition significantly reduced the extent of apoptosis induced by the combination of rhTRAIL and andrographolide.	andrographolide	256-271	TNF receptor superfamily member 10b	Homo sapiens	51-54
28529596-8	2017	N-acetyl cysteine prevented andrographolide-mediated DR5 induction and the apoptotic effect induced by the combination of rhTRAIL and andrographolide.	Acetylcysteine	0-17	TNF receptor superfamily member 10b	Homo sapiens	53-56
28529596-8	2017	N-acetyl cysteine prevented andrographolide-mediated DR5 induction and the apoptotic effect induced by the combination of rhTRAIL and andrographolide.	andrographolide	28-43	TNF receptor superfamily member 10b	Homo sapiens	53-56
28529596-9	2017	Collectively, the present study demonstrated that andrographolide enhances TRAIL-induced apoptosis through induction of DR5 expression.	andrographolide	50-65	TNF receptor superfamily member 10b	Homo sapiens	120-123
28482915-0	2017	DR5 suppression induces sphingosine-1-phosphate-dependent TRAF2 polyubiquitination, leading to activation of JNK/AP-1 and promotion of cancer cell invasion.	sphingosine 1-phosphate	24-47	TNF receptor superfamily member 10b	Homo sapiens	0-3
28529565-8	2017	The knockdown of p53 by specific small interfering RNA resulted in the depletion of p53, and inhibited the OPA and PPA treatment-induced increases in p53, which led to a decrease in the expression of p21, DR5, Fas, PUMA and phosphatase and tensin homolog proteins.	ppa	115-118	TNF receptor superfamily member 10b	Homo sapiens	205-208
28459212-3	2017	Our previous article reported that small molecule YM155 induced apoptosis in pancreatic cancer cells via activation of death receptor 5.	YM 155	50-55	TNF receptor superfamily member 10b	Homo sapiens	119-135
28459212-7	2017	Western blotting analysis revealed that lexatumumab and PF573228 combination treatment increased death receptor 5 but decreased Bcl-xL expression.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	56-64	TNF receptor superfamily member 10b	Homo sapiens	97-113
28387244-6	2017	MT-6 treatment also induced mitochondrial membrane potential loss, JNK activation, and DR5 expression.	Melatonin	0-4	TNF receptor superfamily member 10b	Homo sapiens	87-90
28487767-0	2017	Inducement of apoptosis by cucurbitacin E, a tetracyclic triterpenes, through death receptor 5 in human cervical cancer cell lines.	cucurbitacin E	27-41	TNF receptor superfamily member 10b	Homo sapiens	78-94
28487767-0	2017	Inducement of apoptosis by cucurbitacin E, a tetracyclic triterpenes, through death receptor 5 in human cervical cancer cell lines.	Triterpenes	57-68	TNF receptor superfamily member 10b	Homo sapiens	78-94
28387244-7	2017	Cotreatment of cells with the JNK inhibitor SP600125 considerably attenuated MT-6-induced apoptosis, mitochondria membrane potential loss, DR5 upregulation, and suppression of cell viability.	pyrazolanthrone	44-52	TNF receptor superfamily member 10b	Homo sapiens	139-142
28202415-10	2017	Accordingly, TRAIL/Gln deprivation enhanced the expression of death receptor 5 (DR5) and transient knockdown of DR5 completely restored TRAIL/Gln deprivation-mediated apoptosis.	Glutamine	19-22	TNF receptor superfamily member 10b	Homo sapiens	62-78
28202415-10	2017	Accordingly, TRAIL/Gln deprivation enhanced the expression of death receptor 5 (DR5) and transient knockdown of DR5 completely restored TRAIL/Gln deprivation-mediated apoptosis.	Glutamine	19-22	TNF receptor superfamily member 10b	Homo sapiens	80-83
28202415-10	2017	Accordingly, TRAIL/Gln deprivation enhanced the expression of death receptor 5 (DR5) and transient knockdown of DR5 completely restored TRAIL/Gln deprivation-mediated apoptosis.	Glutamine	142-145	TNF receptor superfamily member 10b	Homo sapiens	62-78
28202415-10	2017	Accordingly, TRAIL/Gln deprivation enhanced the expression of death receptor 5 (DR5) and transient knockdown of DR5 completely restored TRAIL/Gln deprivation-mediated apoptosis.	Glutamine	142-145	TNF receptor superfamily member 10b	Homo sapiens	112-115
28270124-0	2017	Cyproterone acetate enhances TRAIL-induced androgen-independent prostate cancer cell apoptosis via up-regulation of death receptor 5.	Cyproterone Acetate	0-19	TNF receptor superfamily member 10b	Homo sapiens	116-132
28126677-4	2017	Furthermore, ATS exposure in TRAIL resistant cells resulted in significant increase of both DR4/DR5 expression and STAT3 inhibition thereby arbitrating TRAIL mediated apoptosis in HepG2 cells.	Artesunate	13-16	TNF receptor superfamily member 10b	Homo sapiens	96-99
28553347-6	2017	Mitomycin C upregulated the expression levels of Fas, DR4, DR5, cleaved caspase-8/9, Bax, Bim and cleaved caspase-3 proteins, and it downregulated Bcl-2 and Bcl-xL expression.	Mitomycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	59-62
28300219-4	2017	We found that doxorubicin and related anthracycline agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both protein and mRNA levels.	Doxorubicin	14-25	TNF receptor superfamily member 10b	Homo sapiens	195-198
28300219-4	2017	We found that doxorubicin and related anthracycline agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both protein and mRNA levels.	Anthracyclines	38-51	TNF receptor superfamily member 10b	Homo sapiens	195-198
28300219-4	2017	We found that doxorubicin and related anthracycline agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both protein and mRNA levels.	Daunorubicin	66-78	TNF receptor superfamily member 10b	Homo sapiens	195-198
28300219-4	2017	We found that doxorubicin and related anthracycline agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both protein and mRNA levels.	Idarubicin	80-90	TNF receptor superfamily member 10b	Homo sapiens	195-198
28300219-4	2017	We found that doxorubicin and related anthracycline agents (e.g., daunorubicin, idarubicin, and epirubicin) significantly upregulated the expression of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both protein and mRNA levels.	Epirubicin	96-106	TNF receptor superfamily member 10b	Homo sapiens	195-198
28103535-3	2017	Our experiments showed that the combination of EGCG and Am80 synergistically induced both apoptosis in human lung cancer cell line PC-9 and up-regulated expressions of growth arrest and DNA damage-inducible gene 153 (GADD153), death receptor 5, and p21waf1 genes in the cells.	epigallocatechin gallate	47-51	TNF receptor superfamily member 10b	Homo sapiens	227-243
28103535-3	2017	Our experiments showed that the combination of EGCG and Am80 synergistically induced both apoptosis in human lung cancer cell line PC-9 and up-regulated expressions of growth arrest and DNA damage-inducible gene 153 (GADD153), death receptor 5, and p21waf1 genes in the cells.	tamibarotene	56-60	TNF receptor superfamily member 10b	Homo sapiens	227-243
28270124-9	2017	Further investigation of the TRAIL-induced apoptosis pathway revealed that cyproterone acetate exerted its effect by selectively increasing death receptor 5 (DR5) mRNA and protein expression.	Cyproterone Acetate	75-94	TNF receptor superfamily member 10b	Homo sapiens	140-156
28270124-9	2017	Further investigation of the TRAIL-induced apoptosis pathway revealed that cyproterone acetate exerted its effect by selectively increasing death receptor 5 (DR5) mRNA and protein expression.	Cyproterone Acetate	75-94	TNF receptor superfamily member 10b	Homo sapiens	158-161
28270124-10	2017	Cyproterone acetate treatment also increased DR5 gene promoter activity, which could be abolished by mutation of a consensus binding domain of transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP) in the DR5 gene promoter.	Cyproterone Acetate	0-19	TNF receptor superfamily member 10b	Homo sapiens	45-48
28270124-10	2017	Cyproterone acetate treatment also increased DR5 gene promoter activity, which could be abolished by mutation of a consensus binding domain of transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP) in the DR5 gene promoter.	Cyproterone Acetate	0-19	TNF receptor superfamily member 10b	Homo sapiens	228-231
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	Cyproterone Acetate	0-19	TNF receptor superfamily member 10b	Homo sapiens	198-201
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	4-phenylbutyric acid	132-148	TNF receptor superfamily member 10b	Homo sapiens	198-201
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	Cyproterone Acetate	161-180	TNF receptor superfamily member 10b	Homo sapiens	198-201
28270124-12	2017	More importantly, siRNA silencing of CHOP significantly reduced cyproterone acetate-induced DR5 up-regulation and TRAIL sensitivity in prostate cancer cells.	Cyproterone Acetate	64-83	TNF receptor superfamily member 10b	Homo sapiens	92-95
27993669-6	2017	Suppression of etoposide-induced cell death correlated with a downregulation of p53 expression, which, among other functions, regulates the expression of death receptor 5, one of the activators of caspase-8.	Etoposide	15-24	TNF receptor superfamily member 10b	Homo sapiens	154-170
27903966-3	2017	[Pemetrexed + sildenafil] activated an eIF2alpha - ATF4 - CHOP - Beclin1 pathway causing formation of toxic autophagosomes; activated a protective IRE1 - XBP-1 - chaperone induction pathway; and activated a toxic eIF2alpha - CHOP - DR4 / DR5 / CD95 induction pathway.	Pemetrexed	1-11	TNF receptor superfamily member 10b	Homo sapiens	238-241
28209994-4	2017	The underlying apoptotic mechanisms involved upregulation of death receptor 5 (DR5) and CCAAT/enhancer binding protein homologous protein, which is related to the endoplasmic reticulum stress response, and is further associated with reactive oxygen species generation and Ca2+ accumulation.	Reactive Oxygen Species	233-256	TNF receptor superfamily member 10b	Homo sapiens	61-77
28209994-4	2017	The underlying apoptotic mechanisms involved upregulation of death receptor 5 (DR5) and CCAAT/enhancer binding protein homologous protein, which is related to the endoplasmic reticulum stress response, and is further associated with reactive oxygen species generation and Ca2+ accumulation.	Reactive Oxygen Species	233-256	TNF receptor superfamily member 10b	Homo sapiens	79-82
28098861-8	2017	Triptolide treatment of HepG2 cells caused a significant increase in the expression of p21, Bax and DR5 genes in HepG2 cells.	triptolide	0-10	TNF receptor superfamily member 10b	Homo sapiens	100-103
28076753-2	2017	LSCs isolated from methotrexate resistant side population (SP) of leukemic cell lines HL60 and MOLT4 exhibited high levels of CD25 and TRAIL R2/DR5 which are potential targets.	Methotrexate	19-31	TNF receptor superfamily member 10b	Homo sapiens	135-143
28076753-2	2017	LSCs isolated from methotrexate resistant side population (SP) of leukemic cell lines HL60 and MOLT4 exhibited high levels of CD25 and TRAIL R2/DR5 which are potential targets.	Methotrexate	19-31	TNF receptor superfamily member 10b	Homo sapiens	144-147
28228218-0	2017	[Thioridazine Sensitizes Apoptotic Effect of TRAIL in Human Lung Cancer PC9 Cells Through ER Stress Mediated Up-regulation of DR5].	Thioridazine	1-13	TNF receptor superfamily member 10b	Homo sapiens	126-129
28228218-2	2017	This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplasmic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.	Thioridazine	84-96	TNF receptor superfamily member 10b	Homo sapiens	178-194
28228218-2	2017	This study is to observe the proliferation inhibition effect of TRAIL sensitized by thioridazine on PC9 cells through endoplasmic reticulum (ER) stress mediated up-regulation of death receptor 5 (DR5) and investigate its mechanism.	Thioridazine	84-96	TNF receptor superfamily member 10b	Homo sapiens	196-199
28228218-7	2017	Thioridazine increased the inhibition and apoptosis of PC9 cells and up-regulated the expression of cell-surface DR5 induced by TRAIL.	Thioridazine	0-12	TNF receptor superfamily member 10b	Homo sapiens	113-116
28228218-9	2017	Western blotting indicated that compared with TRAIL group, expressions of Cleaved-caspase-8, Cleaved-PARP and DR5 increased significantly in combination group of TRAIL and thioridazine.	Thioridazine	172-184	TNF receptor superfamily member 10b	Homo sapiens	110-113
28228218-10	2017	The induction of DR5 and pro-apoptotic effect were mediated through activation of ER stress accompanying by increased synthesis of GRP78 and CHOP, which can be blocked by adding of ER stress inhibitor 4-PBA.	4-phenylbutylamine	201-206	TNF receptor superfamily member 10b	Homo sapiens	17-20
28228218-11	2017	CONCLUSIONS: Thioridazine enhanced proliferation inhibition effect of TRAIL in PC9 cells may be facilitated through ER stress mediated upregulation of DR5.	Thioridazine	13-25	TNF receptor superfamily member 10b	Homo sapiens	151-154
28182009-10	2017	Expression of the extracellular domains of Fas or TRAILR2 with a glycolipid membrane anchor specifically reduced the intrinsic signalling pathway of CD40 in 293T cells.	Glycolipids	65-75	TNF receptor superfamily member 10b	Homo sapiens	50-57
28135339-8	2017	These results suggest that lovastatin sensitizes TRAIL-induced apoptosis by up-regulation of DR5 level via NF-kappaB inactivation, but also directly induces apoptosis by dysregulation of MAPK pathway.	Lovastatin	27-37	TNF receptor superfamily member 10b	Homo sapiens	93-96
27903966-3	2017	[Pemetrexed + sildenafil] activated an eIF2alpha - ATF4 - CHOP - Beclin1 pathway causing formation of toxic autophagosomes; activated a protective IRE1 - XBP-1 - chaperone induction pathway; and activated a toxic eIF2alpha - CHOP - DR4 / DR5 / CD95 induction pathway.	Sildenafil Citrate	14-24	TNF receptor superfamily member 10b	Homo sapiens	238-241
27192488-6	2016	We demonstrated that 3-HTMC treatment on both cell lines induced apoptotic process associated with overexpression of death receptor DR5, activation of caspase-8 and -3, PARP cleavage, and DNA fragmentation.	3-hydroxy-3',4,4',5'-tetramethoxychalcone	21-27	TNF receptor superfamily member 10b	Homo sapiens	132-135
28662515-9	2017	CONCLUSIONS: Our results revealed that shikonin could inhibit cells viability and induce apoptosis of CCA cells, effects enhanced by TRAIL treatment via ROS mediated JNK signalling pathways, involving up-regulation of DR5 expression.	shikonin	39-47	TNF receptor superfamily member 10b	Homo sapiens	218-221
27978543-7	2016	Furthermore, bortezomib treatment significantly increased expression of the death receptors TRAILR-1 and TRAILR-2 in chondrosarcoma cells.	Bortezomib	13-23	TNF receptor superfamily member 10b	Homo sapiens	105-113
27720987-0	2016	Death Receptor 5 Networks Require Membrane Cholesterol for Proper Structure and Function.	Cholesterol	43-54	TNF receptor superfamily member 10b	Homo sapiens	0-16
27720987-1	2016	Death receptor 5 (DR5) is an apoptosis-inducing member of the tumor necrosis factor receptor superfamily, whose activity has been linked to membrane cholesterol content.	Cholesterol	149-160	TNF receptor superfamily member 10b	Homo sapiens	0-16
27720987-1	2016	Death receptor 5 (DR5) is an apoptosis-inducing member of the tumor necrosis factor receptor superfamily, whose activity has been linked to membrane cholesterol content.	Cholesterol	149-160	TNF receptor superfamily member 10b	Homo sapiens	18-21
27720987-2	2016	Upon ligand binding, DR5 forms large clusters within the plasma membrane that have often been assumed to be manifestations of receptor co-localization in cholesterol-rich membrane domains.	Cholesterol	154-165	TNF receptor superfamily member 10b	Homo sapiens	21-24
27720987-11	2016	As evidence, we show that cholesterol is necessary for the covalent dimerization of DR5 transmembrane domains.	Cholesterol	26-37	TNF receptor superfamily member 10b	Homo sapiens	84-87
27603596-0	2017	Tunicamycin enhances human colon cancer cells to TRAIL-induced apoptosis by JNK-CHOP-mediated DR5 upregulation and the inhibition of the EGFR pathway.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	94-97
27603596-4	2017	Knockdown of DR5 but not DR4 expression by specific shRNAs or siRNAs significantly increased tunicamycin-mediated and TRAIL-mediated cell viability.	Tunicamycin	93-104	TNF receptor superfamily member 10b	Homo sapiens	13-16
27603596-5	2017	DR5 induction was regulated by C/EBP homologous protein (CHOP) and JNK as CHOP siRNA or JNK inhibitor SP600125 considerably abolished the DR5 induction.	pyrazolanthrone	102-110	TNF receptor superfamily member 10b	Homo sapiens	0-3
27603596-5	2017	DR5 induction was regulated by C/EBP homologous protein (CHOP) and JNK as CHOP siRNA or JNK inhibitor SP600125 considerably abolished the DR5 induction.	pyrazolanthrone	102-110	TNF receptor superfamily member 10b	Homo sapiens	138-141
27603596-7	2017	In summary, tunicamycin effectively enhanced TRAIL-induced apoptosis might through JNK-CHOP-mediated DR5 upregulation and the inhibition of the epidermal growth factor receptor pathway.	Tunicamycin	12-23	TNF receptor superfamily member 10b	Homo sapiens	101-104
28028438-11	2016	Unfortunately, the initial increased reduction in tumor growth compared with hvTRA mono treatment was not sustained, and this was related to downregulation of the DR5 level by vemurafenib.	Vemurafenib	176-187	TNF receptor superfamily member 10b	Homo sapiens	163-166
26822174-6	2016	Antioxidant N-acetyl-L-cysteine (NAC) and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 inhibited PEITC-induced DR4 and DR5 expression.	Acetylcysteine	33-36	TNF receptor superfamily member 10b	Homo sapiens	125-128
26822174-6	2016	Antioxidant N-acetyl-L-cysteine (NAC) and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 inhibited PEITC-induced DR4 and DR5 expression.	pyrazolanthrone	84-92	TNF receptor superfamily member 10b	Homo sapiens	125-128
26822174-6	2016	Antioxidant N-acetyl-L-cysteine (NAC) and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 inhibited PEITC-induced DR4 and DR5 expression.	phenethyl isothiocyanate	103-108	TNF receptor superfamily member 10b	Homo sapiens	125-128
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	Polyethyleneimine	72-75	TNF receptor superfamily member 10b	Homo sapiens	146-149
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	Polyethyleneimine	72-75	TNF receptor superfamily member 10b	Homo sapiens	190-193
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	Polyethyleneimine	258-274	TNF receptor superfamily member 10b	Homo sapiens	146-149
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	lmw-pei	276-283	TNF receptor superfamily member 10b	Homo sapiens	146-149
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	lmw-pei	350-357	TNF receptor superfamily member 10b	Homo sapiens	146-149
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	pluronic-pei	163-175	TNF receptor superfamily member 10b	Homo sapiens	146-149
26932761-2	2016	To solve the toxicity versus efficacy and tumor-targeting challenges of PEI used as gene delivery vector, we constructed a novel non-viral vector DR5-TAT-modified Pluronic-PEI (Pluronic-PEI-DR5-TAT), which was based on the attachment of low-molecular-weight polyethylenimine (LMW-PEI) to the amphiphilic polymer Pluronic to prepare Pluronic-modified LMW-PEI (Pluronic-PEI).	pluronic-pei	163-175	TNF receptor superfamily member 10b	Homo sapiens	190-193
27933820-2	2016	Here, hyaluronate-gold nanorod/death receptor 5 antibody (HA-AuNR/DR5 Ab) complex was developed for transdermal theranosis of skin cancer.	hyaluronate	6-17	TNF receptor superfamily member 10b	Homo sapiens	31-47
27933820-2	2016	Here, hyaluronate-gold nanorod/death receptor 5 antibody (HA-AuNR/DR5 Ab) complex was developed for transdermal theranosis of skin cancer.	hyaluronate	6-17	TNF receptor superfamily member 10b	Homo sapiens	66-69
27629794-3	2016	Interestingly, gefitinib increases the expression of cell surface receptors DR4 and DR5, possibly explaining the synergistic effect.	Gefitinib	15-24	TNF receptor superfamily member 10b	Homo sapiens	84-87
27750195-2	2016	Our working group has recently demonstrated that nanovectorization of TRAIL with single wall carbon nanotubes (abbreviated NPT) enhanced TRAIL affinity to the high affinity site DR5 and increased pro apoptotic potential in different human tumor cell lines.	Carbon	93-99	TNF receptor superfamily member 10b	Homo sapiens	178-181
27750195-13	2016	As well, it was shown that the extra cellular acidosis led to the protonation of the TRAIL residue histidine by flipping the His switch to the on position with a concomitant decrease in affinity for DR4 and DR5 receptors.	Histidine	99-108	TNF receptor superfamily member 10b	Homo sapiens	207-210
27629794-4	2016	Knockdown of DR4 and DR5 by siRNA significantly decreases gefitinib- and TRAIL-mediated cell apoptosis, supporting this idea.	Gefitinib	58-67	TNF receptor superfamily member 10b	Homo sapiens	21-24
27629794-5	2016	Because the inhibition of gefitinib-induced autophagy by 3-MA significantly decreases DR4 and DR5 upregulation, as well as reduces gefitinib- and TRAIL-induced apoptosis, we conclude that death receptor upregulation is autophagy mediated.	Gefitinib	26-35	TNF receptor superfamily member 10b	Homo sapiens	94-97
27295176-0	2016	Improved anti-tumor activity of oxaliplatin by encapsulating in anti-DR5 targeted gold nanoparticles.	Oxaliplatin	32-43	TNF receptor superfamily member 10b	Homo sapiens	69-72
27543608-6	2016	Collectively, we identified CPI-7c as a novel small-molecule inhibitor of MDM2 with a unique two-prong mechanism of action that sensitized TRAIL-resistant cancer cells to apoptosis by modulating the MDM2-p53-DR4/DR5 pathway.	cpi-7c	28-34	TNF receptor superfamily member 10b	Homo sapiens	212-215
27515963-7	2016	Yet, AZD1152 treatment enhanced death receptor TRAIL-R2 levels in all tumor cell lines investigated.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	5-12	TNF receptor superfamily member 10b	Homo sapiens	47-55
27731378-3	2016	In this study, we show that ER stress mediated by thapsigargin promoted CHOP and DR5 synthesis thus sensitizing TRAIL treatment, which induced ESCC cells apoptosis.	Thapsigargin	50-62	TNF receptor superfamily member 10b	Homo sapiens	81-84
27594528-0	2016	A new brominated chalcone derivative suppresses the growth of gastric cancer cells in vitro and in vivo involving ROS mediated up-regulation of DR5 and 4 expression and apoptosis.	Chalcone	17-25	TNF receptor superfamily member 10b	Homo sapiens	144-153
27594528-0	2016	A new brominated chalcone derivative suppresses the growth of gastric cancer cells in vitro and in vivo involving ROS mediated up-regulation of DR5 and 4 expression and apoptosis.	Reactive Oxygen Species	114-117	TNF receptor superfamily member 10b	Homo sapiens	144-153
27387452-0	2016	A new oridonin analog suppresses triple-negative breast cancer cells and tumor growth via the induction of death receptor 5.	oridonin	6-14	TNF receptor superfamily member 10b	Homo sapiens	107-123
27698877-5	2016	The present study demonstrated, using immunofluorescence and western blotting, that blocking gamma-secretase activity in T-ALL cells with N-[(3,5-difluorophenyl) acetyl]-L-alanyl-2-phenyl] glycine-1,1-dimethylethyl ester (DAPT) downregulated NCID and upregulated the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor 5 (DR5).	n-[(3,5-difluorophenyl) acetyl]-l-alanyl-2-phenyl] glycine-1,1-dimethylethyl ester	138-220	TNF receptor superfamily member 10b	Homo sapiens	332-348
27698877-5	2016	The present study demonstrated, using immunofluorescence and western blotting, that blocking gamma-secretase activity in T-ALL cells with N-[(3,5-difluorophenyl) acetyl]-L-alanyl-2-phenyl] glycine-1,1-dimethylethyl ester (DAPT) downregulated NCID and upregulated the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor 5 (DR5).	n-[(3,5-difluorophenyl) acetyl]-l-alanyl-2-phenyl] glycine-1,1-dimethylethyl ester	138-220	TNF receptor superfamily member 10b	Homo sapiens	350-353
27565731-5	2016	Meanwhile, ONC201-induced TRAIL/death receptor-5 (DR-5) expression, caspase-8 activation and CRC cell apoptosis were also potentiated with AZD-8055 co-treatment.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	139-147	TNF receptor superfamily member 10b	Homo sapiens	26-48
27648301-3	2016	We demonstrate TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) resistance in the majority of human colon cancers tested and utilize the glucose analog 2-deoxy-d-glucose to sensitize TRAIL-resistant gastrointestinal adenocarcinoma cells, and not normal gastrointestinal epithelial cells, to TRAIL-induced apoptosis through enhanced death receptor 5 expression, downstream modulation of MAPK signaling and subsequent miRNA expression modulation by increasing the expression of miR-494 via MEK activation.	Glucose	152-159	TNF receptor superfamily member 10b	Homo sapiens	347-363
27924159-0	2016	In Vitro and In Vivo Evaluation of 89Zr-DS-8273a as a Theranostic for Anti-Death Receptor 5 Therapy.	Deuterium	40-42	TNF receptor superfamily member 10b	Homo sapiens	75-91
27924159-1	2016	Background: DS-8273a, an anti-human death receptor 5 (DR5) agonistic antibody, has cytotoxic activity against human cancer cells and induces apoptosis after specific binding to DR5.	DS-8273a	12-20	TNF receptor superfamily member 10b	Homo sapiens	36-52
27924159-1	2016	Background: DS-8273a, an anti-human death receptor 5 (DR5) agonistic antibody, has cytotoxic activity against human cancer cells and induces apoptosis after specific binding to DR5.	DS-8273a	12-20	TNF receptor superfamily member 10b	Homo sapiens	54-57
27924159-1	2016	Background: DS-8273a, an anti-human death receptor 5 (DR5) agonistic antibody, has cytotoxic activity against human cancer cells and induces apoptosis after specific binding to DR5.	DS-8273a	12-20	TNF receptor superfamily member 10b	Homo sapiens	177-180
27569287-4	2016	Unexpectedly, DR5 is upregulated in the cells treated with DCA/metformin, and sustained under hypoxia.	Dichloroacetic Acid	59-62	TNF receptor superfamily member 10b	Homo sapiens	14-17
27569287-4	2016	Unexpectedly, DR5 is upregulated in the cells treated with DCA/metformin, and sustained under hypoxia.	Metformin	63-72	TNF receptor superfamily member 10b	Homo sapiens	14-17
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Dichloroacetic Acid	32-35	TNF receptor superfamily member 10b	Homo sapiens	9-12
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Dichloroacetic Acid	32-35	TNF receptor superfamily member 10b	Homo sapiens	88-91
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Metformin	36-45	TNF receptor superfamily member 10b	Homo sapiens	9-12
27569287-5	2016	Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death.	Metformin	36-45	TNF receptor superfamily member 10b	Homo sapiens	88-91
27569287-6	2016	Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin.	Dichloroacetic Acid	105-108	TNF receptor superfamily member 10b	Homo sapiens	90-93
27569287-6	2016	Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin.	Metformin	109-118	TNF receptor superfamily member 10b	Homo sapiens	90-93
27648301-3	2016	We demonstrate TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) resistance in the majority of human colon cancers tested and utilize the glucose analog 2-deoxy-d-glucose to sensitize TRAIL-resistant gastrointestinal adenocarcinoma cells, and not normal gastrointestinal epithelial cells, to TRAIL-induced apoptosis through enhanced death receptor 5 expression, downstream modulation of MAPK signaling and subsequent miRNA expression modulation by increasing the expression of miR-494 via MEK activation.	Deoxyglucose	167-184	TNF receptor superfamily member 10b	Homo sapiens	347-363
26952193-11	2016	Moreover, because of negative values of  H  and  S * quantities, we demonstrated that van der Waals and hydrogen bonds governed the strong NPT-DR5 association for pH &gt; 7.4 (as for TRAIL alone).	Sulfur	49-50	TNF receptor superfamily member 10b	Homo sapiens	143-146
27506940-4	2016	DR5, which is essential for 5-FU-induced apoptosis, accumulated in lysosomes and autophagosomes upon chloroquine treatment.	Fluorouracil	28-32	TNF receptor superfamily member 10b	Homo sapiens	0-3
27506940-4	2016	DR5, which is essential for 5-FU-induced apoptosis, accumulated in lysosomes and autophagosomes upon chloroquine treatment.	Chloroquine	101-112	TNF receptor superfamily member 10b	Homo sapiens	0-3
27506940-8	2016	We conclude that targeting of lysosomes by chloroquine deregulates DR5 trafficking and abrogates 5-FU- but not TRAIL-stimulated cell elimination, hence suggesting a novel mechanism for receptor activation.	Chloroquine	43-54	TNF receptor superfamily member 10b	Homo sapiens	67-70
27406983-0	2016	A Histone Deacetylase Inhibitor, OBP-801, and Celecoxib Synergistically Inhibit the Cell Growth with Apoptosis via a DR5-Dependent Pathway in Bladder Cancer Cells.	Celecoxib	46-55	TNF receptor superfamily member 10b	Homo sapiens	117-120
27406983-7	2016	Therefore, we conjectured that the apoptosis induced by OBP-801 and celecoxib is at least partially dependent on DR5.	Celecoxib	68-77	TNF receptor superfamily member 10b	Homo sapiens	113-116
26952193-11	2016	Moreover, because of negative values of  H  and  S * quantities, we demonstrated that van der Waals and hydrogen bonds governed the strong NPT-DR5 association for pH &gt; 7.4 (as for TRAIL alone).	Hydrogen	104-112	TNF receptor superfamily member 10b	Homo sapiens	143-146
27461934-4	2016	In addition, by using caspase-3, caspase-8 and caspase-9 activity assays and western blot analysis, the anticancer effects of triptolide against osteosarcoma growth were found to involve activation of the DR-5/p53/Bax/caspase-9/ caspase-3 signaling pathway and the DR-5/FADD/caspase-8/lysosomal/cathepsin B/caspase-3 signaling pathway in the MG-63 cells.	triptolide	126-136	TNF receptor superfamily member 10b	Homo sapiens	205-209
27461934-4	2016	In addition, by using caspase-3, caspase-8 and caspase-9 activity assays and western blot analysis, the anticancer effects of triptolide against osteosarcoma growth were found to involve activation of the DR-5/p53/Bax/caspase-9/ caspase-3 signaling pathway and the DR-5/FADD/caspase-8/lysosomal/cathepsin B/caspase-3 signaling pathway in the MG-63 cells.	triptolide	126-136	TNF receptor superfamily member 10b	Homo sapiens	265-269
27461934-5	2016	An important factor in the anticancer effects of triptolide against osteosarcoma was TRAIL-DR-5.	triptolide	49-59	TNF receptor superfamily member 10b	Homo sapiens	91-95
27461934-6	2016	The data suggest that triptolide may be a potential novel chemotherapeutic agent for osteosarcoma and acts through the TRAIL-DR-5 signaling pathway.	triptolide	22-32	TNF receptor superfamily member 10b	Homo sapiens	125-129
27581364-4	2016	Physapubescin decreases the expression of HIF-2alpha and increases the expression of CCAAT/enhancer-binding protein homologus protein (CHOP), which leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3, cleavage of poly (ADP-Ribose) polymerase (PARP) and apoptosis.	physapubescin	0-13	TNF receptor superfamily member 10b	Homo sapiens	174-190
27268146-6	2016	In A549 and H1299 cells, magnolol and PM remarkably induced cell apoptosis by arresting the cell cycle in the G0/G1 phase while simultaneously activating various pro-apoptotic signals, including TRAIL-R2 (DR5), Bax, caspase 3, cleaved caspase 3, and cleaved PARP.	magnolol	25-33	TNF receptor superfamily member 10b	Homo sapiens	195-203
27268146-6	2016	In A549 and H1299 cells, magnolol and PM remarkably induced cell apoptosis by arresting the cell cycle in the G0/G1 phase while simultaneously activating various pro-apoptotic signals, including TRAIL-R2 (DR5), Bax, caspase 3, cleaved caspase 3, and cleaved PARP.	magnolol	25-33	TNF receptor superfamily member 10b	Homo sapiens	205-208
27268146-8	2016	ChIP assays also demonstrated that magnolol and PM significantly enriched the histone acetyl mark (H3K27ac) in the promoter region of DR5.	magnolol	35-43	TNF receptor superfamily member 10b	Homo sapiens	134-137
27268146-10	2016	Therefore, magnolol and PM, as potential inhibitors of class I HDACs, induced tumor cell apoptosis and suppressed tumor growth partially by epigenetically activating DR5, which is a key protein in death receptor signaling pathway.	magnolol	11-19	TNF receptor superfamily member 10b	Homo sapiens	166-169
27268146-10	2016	Therefore, magnolol and PM, as potential inhibitors of class I HDACs, induced tumor cell apoptosis and suppressed tumor growth partially by epigenetically activating DR5, which is a key protein in death receptor signaling pathway.	pipermethystine	24-26	TNF receptor superfamily member 10b	Homo sapiens	166-169
27581364-4	2016	Physapubescin decreases the expression of HIF-2alpha and increases the expression of CCAAT/enhancer-binding protein homologus protein (CHOP), which leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3, cleavage of poly (ADP-Ribose) polymerase (PARP) and apoptosis.	physapubescin	0-13	TNF receptor superfamily member 10b	Homo sapiens	192-195
27277541-0	2016	Proteasome inhibitor MG132 potentiates TRAIL-induced apoptosis in gallbladder carcinoma GBC-SD cells via DR5-dependent pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	TNF receptor superfamily member 10b	Homo sapiens	105-108
27512955-7	2016	Importantly, our results indicate, for the first time, that DR5 upregulation is mediated by autophagy, as blockade of CK-induced autophagy by 3-MA, LY294002 or Atg7 siRNAs substantially decreases DR5 upregulation and reduces the synergistic effect.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	148-156	TNF receptor superfamily member 10b	Homo sapiens	60-63
27363951-3	2016	Sanguinarine treatment increased DR5/TRAILR2 (death receptor 5/TRAIL receptor 2) expression and enhanced the activation of caspase-8 and cleavage of its substrate, Bid.	sanguinarine	0-12	TNF receptor superfamily member 10b	Homo sapiens	33-36
27363951-3	2016	Sanguinarine treatment increased DR5/TRAILR2 (death receptor 5/TRAIL receptor 2) expression and enhanced the activation of caspase-8 and cleavage of its substrate, Bid.	sanguinarine	0-12	TNF receptor superfamily member 10b	Homo sapiens	37-44
27363951-3	2016	Sanguinarine treatment increased DR5/TRAILR2 (death receptor 5/TRAIL receptor 2) expression and enhanced the activation of caspase-8 and cleavage of its substrate, Bid.	sanguinarine	0-12	TNF receptor superfamily member 10b	Homo sapiens	46-62
27277541-8	2016	Taken together, these findings indicate that MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway, and suggest that MG132 may be a promising agent for sensitizing GBC-SD cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-50	TNF receptor superfamily member 10b	Homo sapiens	129-132
27277541-8	2016	Taken together, these findings indicate that MG132 possesses anti-gallbladder cancer potential that correlate with regulation of DR5-dependent pathway, and suggest that MG132 may be a promising agent for sensitizing GBC-SD cells to TRAIL-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	169-174	TNF receptor superfamily member 10b	Homo sapiens	129-132
27453990-7	2016	Tumor cell selective apoptotic action of UA was mainly attributed due to the activation of extrinsic apoptosis pathway via up regulation of DR4, DR5 and PARP cleavage in MCF-7 cells over non-tumorigenic MCF-10A cells.	ursolic acid	41-43	TNF receptor superfamily member 10b	Homo sapiens	145-148
27176604-9	2016	Manu A caused depolarization of the mitochondrial membrane with induction of CHOP, DR4 and DR5.	manumycin	0-6	TNF receptor superfamily member 10b	Homo sapiens	91-94
27053682-8	2016	Pre-treatment of PDA cells with MS-444 (Novartis), an established small molecule inhibitor of HuR, substantially increased DR4 and DR5 cell surface levels and enhanced TRAIL sensitivity, further validating HuR"s role in affecting TRAIL apoptotic resistance.	5,8-dihydroxy-3-methyl-4-(9H)-naphtho(2,3-c)furanone	32-38	TNF receptor superfamily member 10b	Homo sapiens	131-134
27260301-7	2016	Additionally, we found that CAPE stimulated the expression of death receptor 5 (DR5) and treatment with DR5/Fc chimera protein significantly blocked CAPE/TRAIL-induced apoptosis, which indicates that CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5.	caffeic acid phenethyl ester	149-153	TNF receptor superfamily member 10b	Homo sapiens	104-107
27260301-7	2016	Additionally, we found that CAPE stimulated the expression of death receptor 5 (DR5) and treatment with DR5/Fc chimera protein significantly blocked CAPE/TRAIL-induced apoptosis, which indicates that CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5.	caffeic acid phenethyl ester	149-153	TNF receptor superfamily member 10b	Homo sapiens	104-107
27176505-0	2016	The pyrrolo-1,5-benzoxazepine, PBOX-15, enhances TRAIL-induced apoptosis by upregulation of DR5 and downregulation of core cell survival proteins in acute lymphoblastic leukaemia cells.	pyrrolo-1,5-benzoxazepine	4-29	TNF receptor superfamily member 10b	Homo sapiens	92-95
27176505-0	2016	The pyrrolo-1,5-benzoxazepine, PBOX-15, enhances TRAIL-induced apoptosis by upregulation of DR5 and downregulation of core cell survival proteins in acute lymphoblastic leukaemia cells.	PBOX-15	31-38	TNF receptor superfamily member 10b	Homo sapiens	92-95
27176505-7	2016	PBOX-15 synergistically enhanced apoptosis induced by TRAIL and a DR5-selective TRAIL variant in ALL-derived cells.	PBOX-15	0-7	TNF receptor superfamily member 10b	Homo sapiens	66-69
27176505-10	2016	We demonstrate that PBOX-15 can enhance TRAIL-induced apoptosis by upregulation of DR5, reduction of cellular mitochondrial potential, activation of the caspase cascade and downregulation of PI3K/Akt, c-FLIP, Mcl-1 and IAP survival pathways.	PBOX-15	20-27	TNF receptor superfamily member 10b	Homo sapiens	83-86
27260301-0	2016	Caffeic acid phenethyl ester enhances TRAIL-mediated apoptosis via CHOP-induced death receptor 5 upregulation in hepatocarcinoma Hep3B cells.	caffeic acid phenethyl ester	0-28	TNF receptor superfamily member 10b	Homo sapiens	80-96
27260301-7	2016	Additionally, we found that CAPE stimulated the expression of death receptor 5 (DR5) and treatment with DR5/Fc chimera protein significantly blocked CAPE/TRAIL-induced apoptosis, which indicates that CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5.	caffeic acid phenethyl ester	28-32	TNF receptor superfamily member 10b	Homo sapiens	62-78
27260301-7	2016	Additionally, we found that CAPE stimulated the expression of death receptor 5 (DR5) and treatment with DR5/Fc chimera protein significantly blocked CAPE/TRAIL-induced apoptosis, which indicates that CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5.	caffeic acid phenethyl ester	28-32	TNF receptor superfamily member 10b	Homo sapiens	80-83
26984266-10	2016	We further investigated the upstream extrinsic pathway and showed that kaempferol stimulated death receptor signals [Fas/CD95, death receptor 4 (DR4) and DR5] through increasing the levels of phosphorylated p53 and phosphorylated ATM pathways in HUVECs, which can be individually confirmed by N-acetylcysteine (NAC), ATM specific inhibitor (caffeine) and p53 siRNA.	kaempferol	71-81	TNF receptor superfamily member 10b	Homo sapiens	154-157
26669750-7	2016	Aotaphenazine (1) enhanced the levels of apoptosis inducing proteins DR4, DR5, p53 and also decreased the levels of cell survival protein Bcl-2 in TRAIL-resistant human gastric adenocarcinoma (AGS) cells in a dose-dependent manner.	Aotaphenazine	0-13	TNF receptor superfamily member 10b	Homo sapiens	74-77
27029345-9	2016	We investigated the downstream changes in apoptosis pathway components upon Mitoxantrone treatment, and observed that Death Receptors (DR4 and DR5) expression was upregulated, and pro-apoptotic and anti-apoptotic gene expression patterns were altered in favor of apoptosis.	Mitoxantrone	76-88	TNF receptor superfamily member 10b	Homo sapiens	143-146
26983803-6	2016	Furthermore, DR5 knockdown attenuated the combination treatment of tanshinone IIA with TRAIL-mediated cell death in human NSCLC cells.	tanshinone	67-81	TNF receptor superfamily member 10b	Homo sapiens	13-16
27129269-5	2016	Results show that CaM directly binds to DR5 in a calcium dependent manner in breast cancer cells.	Calcium	49-56	TNF receptor superfamily member 10b	Homo sapiens	40-43
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Tryptophan	16-19	TNF receptor superfamily member 10b	Homo sapiens	67-70
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Tryptophan	16-19	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Tryptophan	16-19	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Arginine	25-28	TNF receptor superfamily member 10b	Homo sapiens	67-70
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Arginine	25-28	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Arginine	25-28	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	34-37	TNF receptor superfamily member 10b	Homo sapiens	67-70
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	34-37	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	34-37	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Leucine	43-46	TNF receptor superfamily member 10b	Homo sapiens	67-70
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Leucine	43-46	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Leucine	43-46	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	56-59	TNF receptor superfamily member 10b	Homo sapiens	67-70
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	56-59	TNF receptor superfamily member 10b	Homo sapiens	107-110
27129269-8	2016	The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation to signal apoptosis also play an important role for CaM-DR5 binding.	Glutamic Acid	56-59	TNF receptor superfamily member 10b	Homo sapiens	107-110
27222248-5	2016	Using chemical and genetic approaches, we have demonstrated that the B-Raf inhibitor PLX4032 induces DR5 upregulation exclusively in Ras-mutant cancer cells; this effect is dependent on Ras/c-Raf/MEK/ERK signaling activation.	Vemurafenib	85-92	TNF receptor superfamily member 10b	Homo sapiens	101-104
27222248-6	2016	PLX4032 induces DR5 expression at transcriptional levels, largely due to enhancing CHOP/Elk1-mediated DR5 transcription.	Vemurafenib	0-7	TNF receptor superfamily member 10b	Homo sapiens	16-19
27222248-6	2016	PLX4032 induces DR5 expression at transcriptional levels, largely due to enhancing CHOP/Elk1-mediated DR5 transcription.	Vemurafenib	0-7	TNF receptor superfamily member 10b	Homo sapiens	102-105
26983803-7	2016	Tanshinone IIA also increased CHOP and activated the PERK-ATF4 pathway suggesting that tanshinone IIA increased DR5 and CHOP by activating the PERK-ATF4 pathway.	tanshinone	87-97	TNF receptor superfamily member 10b	Homo sapiens	112-115
26983803-9	2016	Taken together, these results indicate that tanshinone IIA increases TRAIL-induced cell death via upregulating DR5 and downregulating survivin mediated by, respectively, selective activation of PERK/ATF4 and inhibition of STAT3, suggesting combinatorial intervention of tanshinone IIA and TRAIL as a new therapeutic strategy for human NSCLC.	tanshinone	44-58	TNF receptor superfamily member 10b	Homo sapiens	111-114
26662956-0	2016	Synergistic effect of fisetin combined with sorafenib in human cervical cancer HeLa cells through activation of death receptor-5 mediated caspase-8/caspase-3 and the mitochondria-dependent apoptotic pathway.	fisetin	22-29	TNF receptor superfamily member 10b	Homo sapiens	112-128
26615420-0	2016	The alkyllysophospholipid edelfosine enhances TRAIL-mediated apoptosis in gastric cancer cells through death receptor 5 and the mitochondrial pathway.	alkyllysophospholipid edelfosine	4-36	TNF receptor superfamily member 10b	Homo sapiens	103-119
27037412-9	2016	In combination with irinotecan or doxorubicin, FAP-DR5 treatment resulted in substantial tumor regression in patient-derived xenograft models.	Irinotecan	20-30	TNF receptor superfamily member 10b	Homo sapiens	51-54
27037412-9	2016	In combination with irinotecan or doxorubicin, FAP-DR5 treatment resulted in substantial tumor regression in patient-derived xenograft models.	Doxorubicin	34-45	TNF receptor superfamily member 10b	Homo sapiens	51-54
26662956-0	2016	Synergistic effect of fisetin combined with sorafenib in human cervical cancer HeLa cells through activation of death receptor-5 mediated caspase-8/caspase-3 and the mitochondria-dependent apoptotic pathway.	Sorafenib	44-53	TNF receptor superfamily member 10b	Homo sapiens	112-128
26662956-7	2016	Our study showed that the combination of fisetin and sorafenib exerted better synergistic effects in vitro and in vivo than either agent used alone against human cervical cancer, and this synergism was based on apoptotic potential through a mitochondrial- and DR5-dependent caspase-8/caspase-3 signaling pathway.	fisetin	41-48	TNF receptor superfamily member 10b	Homo sapiens	260-263
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	44-60
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	62-65
26662956-7	2016	Our study showed that the combination of fisetin and sorafenib exerted better synergistic effects in vitro and in vivo than either agent used alone against human cervical cancer, and this synergism was based on apoptotic potential through a mitochondrial- and DR5-dependent caspase-8/caspase-3 signaling pathway.	Sorafenib	53-62	TNF receptor superfamily member 10b	Homo sapiens	260-263
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	66-75
26942880-9	2016	The induction of DR5 also sensitized NPC cells to radiotherapy, and the SER was 1.195.	Serine	72-75	TNF receptor superfamily member 10b	Homo sapiens	17-20
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	94-97
26615420-6	2016	In addition, edelfosine-mediated rhTRAIL sensitization was regulated by the DR5 pathway.	edelfosine	13-23	TNF receptor superfamily member 10b	Homo sapiens	76-79
27033605-6	2016	Depletion of DR4 or DR5 by small interfering RNA significantly reversed the cell growth inhibitory effects of bakuchiol in HCT116 and HT-29 cells.	bakuchiol	110-119	TNF receptor superfamily member 10b	Homo sapiens	20-23
27033605-8	2016	The collective results suggest that bakuchiol facilitates TRAIL-induced apoptosis in colon cancer cells through up-regulation of the TRAIL receptors; DR4 and DR5 via ROS/JNK pathway signals.	bakuchiol	36-45	TNF receptor superfamily member 10b	Homo sapiens	158-161
26971531-3	2016	Baicalein stimulated the expression of DR5, FasL, and FADD, and activated caspase-8 by reducing the levels of FLIPs (FLICE-inhibitory proteins).	baicalein	0-9	TNF receptor superfamily member 10b	Homo sapiens	39-42
26991930-2	2016	Herein, we present a modular approach to generate death receptor 5 (DR5) binding constructs comprising multiple copies of DR5 targeting peptide (DR5TP) covalently bound to biomolecular scaffolds of peptidic nature.	dr5tp	145-150	TNF receptor superfamily member 10b	Homo sapiens	50-66
26991930-2	2016	Herein, we present a modular approach to generate death receptor 5 (DR5) binding constructs comprising multiple copies of DR5 targeting peptide (DR5TP) covalently bound to biomolecular scaffolds of peptidic nature.	dr5tp	145-150	TNF receptor superfamily member 10b	Homo sapiens	68-71
26991930-2	2016	Herein, we present a modular approach to generate death receptor 5 (DR5) binding constructs comprising multiple copies of DR5 targeting peptide (DR5TP) covalently bound to biomolecular scaffolds of peptidic nature.	dr5tp	145-150	TNF receptor superfamily member 10b	Homo sapiens	122-125
26769704-6	2016	Moreover, the expression of tBid, DR5, and Fas proteins was enhanced by FBRA extract, and the pretreatment with caspase-8 inhibitor, but not caspase-9 inhibitor, restored the reduction of the cell viability induced by FBRA extract.	fbra	72-76	TNF receptor superfamily member 10b	Homo sapiens	34-37
26995783-4	2016	This study sought to provide structural and molecular insight for the roles of four selected DR5 DD mutations (E355K, E367K, K415N, and L363F) in the oligomerization of DR5 DD-FADD complex during the DISC formation.	dd-fadd	173-180	TNF receptor superfamily member 10b	Homo sapiens	93-96
26995783-4	2016	This study sought to provide structural and molecular insight for the roles of four selected DR5 DD mutations (E355K, E367K, K415N, and L363F) in the oligomerization of DR5 DD-FADD complex during the DISC formation.	dd-fadd	173-180	TNF receptor superfamily member 10b	Homo sapiens	169-172
26956619-0	2016	ERK mediated upregulation of death receptor 5 overcomes the lack of p53 functionality in the diaminothiazole DAT1 induced apoptosis in colon cancer models: efficiency of DAT1 in Ras-Raf mutated cells.	Thiazole-2,4-diamine	93-108	TNF receptor superfamily member 10b	Homo sapiens	29-45
26679052-5	2016	This study showed that treatment with cytotoxic concentration of antrocin induced both intrinsic and extrinsic apoptotic pathways in human bladder cancer 5637 cells, evidenced by increase of Fas, DR5, Bax expression and caspase-3, -8 and -9 activation.	antrocin	65-73	TNF receptor superfamily member 10b	Homo sapiens	196-199
26679052-13	2016	Both antrocin-induced intrinsic and extrinsic apoptosis is through upregulation of pro-apoptotic proteins, including Bax, Fas, and DR5.	antrocin	5-13	TNF receptor superfamily member 10b	Homo sapiens	131-134
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	157-164	TNF receptor superfamily member 10b	Homo sapiens	153-156
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	157-164	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	157-164	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	160-164	TNF receptor superfamily member 10b	Homo sapiens	153-156
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	160-164	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	160-164	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	344-351	TNF receptor superfamily member 10b	Homo sapiens	153-156
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	344-351	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	dd-fadd	344-351	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	255-259	TNF receptor superfamily member 10b	Homo sapiens	153-156
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	255-259	TNF receptor superfamily member 10b	Homo sapiens	340-343
26995783-5	2016	Results from the molecular dynamics simulations show that the simulated mutants induce conformational, dynamical motions and interactions changes in the DR5 DD-FADD tetramer complex, including changes in a protein"s backbone flexibility, less exposure of FADD DED"s caspase-8 binding site, reduced H-bonding and hydrophobic contacts at the DR5 DD-FADD DD binding, altered distribution of the electrostatic potentials and correlated motions of residues, and reduced binding affinity of DR5 DD binding to FADD.	fadd	255-259	TNF receptor superfamily member 10b	Homo sapiens	340-343
26964637-0	2016	Chloroquine enhances TRAIL-mediated apoptosis through up-regulation of DR5 by stabilization of mRNA and protein in cancer cells.	Chloroquine	0-11	TNF receptor superfamily member 10b	Homo sapiens	71-74
26964637-4	2016	CQ up-regulates DR5 mRNA and protein expression in a dose- and time- dependent manner.	Chloroquine	0-2	TNF receptor superfamily member 10b	Homo sapiens	16-19
26964637-6	2016	Moreover, we found that CQ decreased the expression of Cbl, an E3 ligase of DR5, and knock-down of Cbl markedly enhanced DR5 up-regulation.	Chloroquine	24-26	TNF receptor superfamily member 10b	Homo sapiens	76-79
26964637-7	2016	Other lysosomal inhibitors, including monensin and nigericin, also up-regulated DR5 and sensitized TRAIL-mediated apoptosis.	Nigericin	51-60	TNF receptor superfamily member 10b	Homo sapiens	80-83
26964637-8	2016	Therefore, this study demonstrates that lysosomal inhibition by CQ may sensitize TRAIL-mediated apoptosis in human renal cancer Caki cells via DR5 up-regulation.	Chloroquine	64-66	TNF receptor superfamily member 10b	Homo sapiens	143-146
26661339-12	2016	CONCLUSIONS AND IMPLICATIONS: ROS generation by decursin selectively activated the PERK/ATF4 axis of the endoplasmic reticulum stress signalling pathway, leading to enhanced TRAIL sensitivity in TRAIL-resistant NSCLC cell lines, partly via up-regulation of DR5.	Reactive Oxygen Species	30-33	TNF receptor superfamily member 10b	Homo sapiens	257-260
26771233-8	2016	Whole transcriptomic analysis demonstrated that propionibacterial supernatant or propionibacterial metabolites (propionate and acetate), in combination with TRAIL, increased pro-apoptotic gene expression (TRAIL-R2/DR5) and decreased anti-apoptotic gene expression (FLIP, XIAP) in HT29 human colon cancer cells.	Propionates	112-122	TNF receptor superfamily member 10b	Homo sapiens	205-213
26332363-7	2016	MEAG also caused an increase in truncated Bid (t-Bid), cleaved caspase-8, and death receptor 5 (DR5).	meag	0-4	TNF receptor superfamily member 10b	Homo sapiens	78-94
26332363-7	2016	MEAG also caused an increase in truncated Bid (t-Bid), cleaved caspase-8, and death receptor 5 (DR5).	meag	0-4	TNF receptor superfamily member 10b	Homo sapiens	96-99
26332363-8	2016	Interestingly, withaferin A (WA), a bioactive component of MEAG, clearly induced apoptosis accompanied by upregulation of Bim, t-Bid, caspase-8, and DR5 similar to the effects of MEAG.	withaferin A	15-27	TNF receptor superfamily member 10b	Homo sapiens	149-152
26843620-3	2016	Importantly, treatment with AD5-10, a DR5-specific agonistic monoclonal antibody, was able to mimic TRAIL-induced apoptosis in CABYR-a/b-silenced cells.	ad5-10	28-34	TNF receptor superfamily member 10b	Homo sapiens	38-41
26771233-8	2016	Whole transcriptomic analysis demonstrated that propionibacterial supernatant or propionibacterial metabolites (propionate and acetate), in combination with TRAIL, increased pro-apoptotic gene expression (TRAIL-R2/DR5) and decreased anti-apoptotic gene expression (FLIP, XIAP) in HT29 human colon cancer cells.	Propionates	112-122	TNF receptor superfamily member 10b	Homo sapiens	214-217
26771233-8	2016	Whole transcriptomic analysis demonstrated that propionibacterial supernatant or propionibacterial metabolites (propionate and acetate), in combination with TRAIL, increased pro-apoptotic gene expression (TRAIL-R2/DR5) and decreased anti-apoptotic gene expression (FLIP, XIAP) in HT29 human colon cancer cells.	Acetates	127-134	TNF receptor superfamily member 10b	Homo sapiens	205-213
26771233-8	2016	Whole transcriptomic analysis demonstrated that propionibacterial supernatant or propionibacterial metabolites (propionate and acetate), in combination with TRAIL, increased pro-apoptotic gene expression (TRAIL-R2/DR5) and decreased anti-apoptotic gene expression (FLIP, XIAP) in HT29 human colon cancer cells.	Acetates	127-134	TNF receptor superfamily member 10b	Homo sapiens	214-217
26859847-6	2016	Our results also revealed that FKC induced intrinsic and extrinsic apoptosis via upregulation of the levels of pro-apoptotic proteins (Bak) and death receptors (DR5), while downregulation of the levels of anti-apoptotic proteins (XIAP, cIAP-1, c-FlipL, Bcl-xL and survivin), resulting in the activation of caspase-3, -8 and -9 and cleavage of poly(ADP-ribose) polymerase (PARP).	flavokawain C	31-34	TNF receptor superfamily member 10b	Homo sapiens	161-164
26959625-11	2016	CONCLUSION: Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38).	Ellagic Acid	12-24	TNF receptor superfamily member 10b	Homo sapiens	55-58
25417048-7	2016	Exploration of NF-kappaB inhibitor (Phenylarsine oxide, 0.1 muM) synergistically further increased SVT-induced DR3 and DR5 expressions accompanied with further inhibition of cancer cells growth.	oxophenylarsine	36-54	TNF receptor superfamily member 10b	Homo sapiens	119-122
27268643-0	2016	Combination of Nimbolide and TNF-alpha-Increases Human Colon Adenocarcinoma Cell Death through JNK-mediated DR5 Up- regulation.	nimbolide	15-24	TNF receptor superfamily member 10b	Homo sapiens	108-111
25867072-6	2016	ATP-competitive mTOR/PI3K inhibitors also promote DR5 induction and FADD-dependent apoptosis in colon cancer cells.	Adenosine Triphosphate	0-3	TNF receptor superfamily member 10b	Homo sapiens	50-53
25867065-7	2016	We found that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cells.	Vemurafenib	39-46	TNF receptor superfamily member 10b	Homo sapiens	161-164
25867065-7	2016	We found that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cells.	AZD 6244	81-88	TNF receptor superfamily member 10b	Homo sapiens	161-164
25867065-7	2016	We found that both B-Raf (for example, PLX4032) and MEK inhibitors (for example, AZD6244 and PD0325901) effectively inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cells.	mirdametinib	93-102	TNF receptor superfamily member 10b	Homo sapiens	161-164
26711147-4	2016	Furthermore, ASA could up-regulate TNF-R1 and DR5 via activation of p38 MAPK, thereby activating caspase 8, revealing the death receptor pathway was also involved in this process.	Aspirin	13-16	TNF receptor superfamily member 10b	Homo sapiens	46-49
27268643-8	2016	In apoptotic pathway, nimbolide activated c-Jun N-terminal kinase (JNK) phosphorylation, BH3 interacting-domain death agonist (Bid) and up-regulated the death receptor 5 (DR5) level.	nimbolide	22-31	TNF receptor superfamily member 10b	Homo sapiens	153-169
27268643-8	2016	In apoptotic pathway, nimbolide activated c-Jun N-terminal kinase (JNK) phosphorylation, BH3 interacting-domain death agonist (Bid) and up-regulated the death receptor 5 (DR5) level.	nimbolide	22-31	TNF receptor superfamily member 10b	Homo sapiens	171-174
27268643-9	2016	In the combination group, nimbolide markedly sensitized TNF-alpha-induced JNK, Bid, caspase-3 activation and the up-regulation of DR5.	nimbolide	26-35	TNF receptor superfamily member 10b	Homo sapiens	130-133
27268643-10	2016	Our findings overall indicate that nimbolide may enhance TNF-alpha-mediated cellular proliferation inhibition through increasing cell apoptosis of HT-29 cells by up-reglation of DR5 expression via the JNK pathway.	nimbolide	35-44	TNF receptor superfamily member 10b	Homo sapiens	178-181
26499766-7	2015	In addition, goniothalamin enhanced TRAIL-induced apoptosis through increased death receptor DR5 expression and decreased anti-apoptotic regulator cFLIP.	goniothalamin	13-26	TNF receptor superfamily member 10b	Homo sapiens	93-96
26798390-0	2016	Isoproterenol Enhances Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand-Induced Apoptosis in Human Embryonic Kidney Cells through Death Receptor 5 up-Regulation.	Isoproterenol	0-13	TNF receptor superfamily member 10b	Homo sapiens	137-153
27822364-6	2016	Molecular docking analysis revealed that compound 1 could bind stably to the TRAIL/DR5 complex through hydrogen bonds.	Hydrogen	103-111	TNF receptor superfamily member 10b	Homo sapiens	83-86
26381901-6	2015	We discovered that doxorubicin (DOX) sensitizes TRAIL-resistant HT-29 colon cancer cells to TRAIL by upregulating mRNA expression of DR5 by 60% in vitro.	Doxorubicin	19-30	TNF receptor superfamily member 10b	Homo sapiens	133-136
26381901-6	2015	We discovered that doxorubicin (DOX) sensitizes TRAIL-resistant HT-29 colon cancer cells to TRAIL by upregulating mRNA expression of DR5 by 60% in vitro.	Doxorubicin	32-35	TNF receptor superfamily member 10b	Homo sapiens	133-136
26381901-8	2015	Alternatively, when DOX was encapsulated in hyaluronic acid-based nanoparticles (HAC/DOX) and intravenously administered with TRAILPEG, DR-mediated apoptosis was potentiated in HT-29 tumors by upregulating DR5 protein expression by 70% and initiating both extrinsic and intrinsic apoptotic pathways with reduced systemic toxicity compared to HAC/DOX or free DOX combined with TRAILPEG (80% vs. 40% survival rate; 75% vs. 34% tumor growth inhibition).	Doxorubicin	20-23	TNF receptor superfamily member 10b	Homo sapiens	206-209
26381901-8	2015	Alternatively, when DOX was encapsulated in hyaluronic acid-based nanoparticles (HAC/DOX) and intravenously administered with TRAILPEG, DR-mediated apoptosis was potentiated in HT-29 tumors by upregulating DR5 protein expression by 70% and initiating both extrinsic and intrinsic apoptotic pathways with reduced systemic toxicity compared to HAC/DOX or free DOX combined with TRAILPEG (80% vs. 40% survival rate; 75% vs. 34% tumor growth inhibition).	Hyaluronic Acid	44-59	TNF receptor superfamily member 10b	Homo sapiens	206-209
26381901-8	2015	Alternatively, when DOX was encapsulated in hyaluronic acid-based nanoparticles (HAC/DOX) and intravenously administered with TRAILPEG, DR-mediated apoptosis was potentiated in HT-29 tumors by upregulating DR5 protein expression by 70% and initiating both extrinsic and intrinsic apoptotic pathways with reduced systemic toxicity compared to HAC/DOX or free DOX combined with TRAILPEG (80% vs. 40% survival rate; 75% vs. 34% tumor growth inhibition).	hac	81-84	TNF receptor superfamily member 10b	Homo sapiens	206-209
26506422-9	2015	In Panc-1 cells, ABT-263 increased the surface expression of death receptor (DR) 5; the NF-kappaB pathway, but not endoplasmic reticulum stress, participated in the increase.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	17-20	TNF receptor superfamily member 10b	Homo sapiens	61-82
26426449-7	2015	The triptolide-induced sensitization was accompanied by increased TRAIL-R2 (DR5) and decreased heat shock protein 70 expression.	triptolide	4-14	TNF receptor superfamily member 10b	Homo sapiens	66-74
26426449-7	2015	The triptolide-induced sensitization was accompanied by increased TRAIL-R2 (DR5) and decreased heat shock protein 70 expression.	triptolide	4-14	TNF receptor superfamily member 10b	Homo sapiens	76-79
26499766-0	2015	Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation.	goniothalamin	0-13	TNF receptor superfamily member 10b	Homo sapiens	82-85
26692822-13	2015	In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4.	Arsenic Trioxide	13-18	TNF receptor superfamily member 10b	Homo sapiens	78-81
26692822-13	2015	In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4.	Fluorouracil	39-43	TNF receptor superfamily member 10b	Homo sapiens	78-81
26499766-8	2015	Interestingly, goniothalamin increased translocation of DR5 to cell surface and consequently contributed to the enhancement of TRAIL-induced apoptosis.	goniothalamin	15-28	TNF receptor superfamily member 10b	Homo sapiens	56-59
26349783-5	2015	We demonstrated here that chaetocin effectively suppressed the growth of multiple lung cancer cells through inducing apoptosis in a death receptor 5 (DR5)-dependent manner.	chaetocin	26-35	TNF receptor superfamily member 10b	Homo sapiens	132-148
25640641-6	2015	Phenylacetylamide triggered the expression of C/EBP homologous protein at the early treatment stage, followed by death receptor-5 upregulation, caspase activation, and beta-actin/tubulin degradation.	phenylacetylamide	0-17	TNF receptor superfamily member 10b	Homo sapiens	113-129
26349783-0	2015	Chaetocin induces endoplasmic reticulum stress response and leads to death receptor 5-dependent apoptosis in human non-small cell lung cancer cells.	chaetocin	0-9	TNF receptor superfamily member 10b	Homo sapiens	69-85
26349783-5	2015	We demonstrated here that chaetocin effectively suppressed the growth of multiple lung cancer cells through inducing apoptosis in a death receptor 5 (DR5)-dependent manner.	chaetocin	26-35	TNF receptor superfamily member 10b	Homo sapiens	150-153
26349783-10	2015	In summary, chaetocin pharmacologically inhibits the activity of SUV39H1 which provokes ER stress and results in up-regulation of ATF3 and CHOP, leading to DR5-dependent apoptosis eventually.	chaetocin	12-21	TNF receptor superfamily member 10b	Homo sapiens	156-159
26193760-4	2015	Compound 4b and the thiazole derivatives, 5b and 6b, increased the expression of tumor necrosis factor receptors TRAIL-R2 and TRAIL-R1, accompanied by down-modulation of pro-caspase 3 levels, and the augmentation of cleaved caspase 3.	Thiazoles	20-28	TNF receptor superfamily member 10b	Homo sapiens	113-121
26837170-12	2015	In conclusion, GA sensitizes HT-29 cells to TRAIL-induced apoptosis by promoting ROS-activated ERS pathways, up-regulating of DR4 and DR5, and inhibiting c-FLIP expression.	Gallium	15-17	TNF receptor superfamily member 10b	Homo sapiens	134-137
26491348-10	2015	The protein expressions of caspase-8, -3, and -9 were decreased in human anti-DR5 mAb-treated FLS in a dose-dependent manner through exposure to a caspase inhibitor, indicating that anti-DR5 mAb induction of apoptosis is through the caspase pathway.	CHEMBL1232769	94-97	TNF receptor superfamily member 10b	Homo sapiens	78-81
26491348-10	2015	The protein expressions of caspase-8, -3, and -9 were decreased in human anti-DR5 mAb-treated FLS in a dose-dependent manner through exposure to a caspase inhibitor, indicating that anti-DR5 mAb induction of apoptosis is through the caspase pathway.	CHEMBL1232769	94-97	TNF receptor superfamily member 10b	Homo sapiens	187-190
26304927-9	2015	Interestingly, alpha-mangostin, which is a xanthone derivative, canceled the resistance by increasing the expression level of DR5 through down-regulation of miR-133b and effectively induced the translocation of DR5 to the cancer cell surface membrane in TRAIL-resistant DLD-1 cells.	mangostin	15-30	TNF receptor superfamily member 10b	Homo sapiens	126-129
26304927-9	2015	Interestingly, alpha-mangostin, which is a xanthone derivative, canceled the resistance by increasing the expression level of DR5 through down-regulation of miR-133b and effectively induced the translocation of DR5 to the cancer cell surface membrane in TRAIL-resistant DLD-1 cells.	mangostin	15-30	TNF receptor superfamily member 10b	Homo sapiens	211-214
26304927-9	2015	Interestingly, alpha-mangostin, which is a xanthone derivative, canceled the resistance by increasing the expression level of DR5 through down-regulation of miR-133b and effectively induced the translocation of DR5 to the cancer cell surface membrane in TRAIL-resistant DLD-1 cells.	xanthone	43-51	TNF receptor superfamily member 10b	Homo sapiens	126-129
26547077-7	2015	Chemotherapeutic drugs such as doxorubicin, paclitaxel, and bortezomib augmented the effect of both TRAIL variants, and the enhancing effect was more pronounced for DR5-B.	Doxorubicin	31-42	TNF receptor superfamily member 10b	Homo sapiens	165-168
26295571-8	2015	Doxorubicin-resistant breast cancer cells (MCF-7/ADR) presented a higher expression of DR5 and were more sensitive to NK cells compared with doxorubicin-sensitive breast cancer cells (MCF-7).	Doxorubicin	0-11	TNF receptor superfamily member 10b	Homo sapiens	87-90
26136424-9	2015	Verticillin A also increased DR5 expression and overcame colon carcinoma resistance to DR5 agonist drozitumab-induced apoptosis.	verticillins	0-13	TNF receptor superfamily member 10b	Homo sapiens	29-32
26136424-9	2015	Verticillin A also increased DR5 expression and overcame colon carcinoma resistance to DR5 agonist drozitumab-induced apoptosis.	verticillins	0-13	TNF receptor superfamily member 10b	Homo sapiens	87-90
26124477-14	2015	CONCLUSION: Death-receptor-5 imaging with (111)In-CS-1008 reveals interpatient and intrapatient heterogeneity of uptake in tumor, is not dose dependent, and is predictive of clinical benefit in the treatment of patients who have mCRC.	Cesium	50-52	TNF receptor superfamily member 10b	Homo sapiens	12-28
26203587-16	2015	Taken together, these data suggest that TIIA enhances TRAIL-induced apoptosis by upregulating DR5 receptors through the ROS-JNK-CHOP signaling axis in human ovarian carcinoma cells.	ros	120-123	TNF receptor superfamily member 10b	Homo sapiens	94-97
26547077-7	2015	Chemotherapeutic drugs such as doxorubicin, paclitaxel, and bortezomib augmented the effect of both TRAIL variants, and the enhancing effect was more pronounced for DR5-B.	Paclitaxel	44-54	TNF receptor superfamily member 10b	Homo sapiens	165-168
26547077-7	2015	Chemotherapeutic drugs such as doxorubicin, paclitaxel, and bortezomib augmented the effect of both TRAIL variants, and the enhancing effect was more pronounced for DR5-B.	Bortezomib	60-70	TNF receptor superfamily member 10b	Homo sapiens	165-168
26044191-0	2015	NVP-BKM120 potentiates apoptosis in tumor necrosis factor-related apoptosis-inducing ligand-resistant glioma cell lines via upregulation of Noxa and death receptor 5.	NVP-BKM120	4-10	TNF receptor superfamily member 10b	Homo sapiens	149-165
26044191-8	2015	BKM120 upregulated cell surface expression of death receptor 5 (DR5), but did not increase levels of the other major TRAIL receptor, death receptor 4 (DR4).	NVP-BKM120	0-6	TNF receptor superfamily member 10b	Homo sapiens	46-62
26044191-8	2015	BKM120 upregulated cell surface expression of death receptor 5 (DR5), but did not increase levels of the other major TRAIL receptor, death receptor 4 (DR4).	NVP-BKM120	0-6	TNF receptor superfamily member 10b	Homo sapiens	64-67
25917567-0	2015	FLLL12 induces apoptosis in lung cancer cells through a p53/p73-independent but death receptor 5-dependent pathway.	flll12	0-6	TNF receptor superfamily member 10b	Homo sapiens	80-96
25930665-10	2015	DR4 or DR5 neutralizing antibodies abolished the effect of alpha-H on TRAIL-induced apoptosis, suggesting that sensitization was mediated through the death receptor pathway.	alpha-h	59-66	TNF receptor superfamily member 10b	Homo sapiens	7-10
26059173-6	2015	In an apoptosis array, betulin activated the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors TRAIL R1/DR4 and R2/DR5, and tumour necrosis factor receptor 1 (TNFR1), suggesting that betulin treatment leads to induction of apoptosis through both intrinsic and extrinsic apoptosis pathways in RCC4 cells.	betulin	23-30	TNF receptor superfamily member 10b	Homo sapiens	140-143
25917567-6	2015	Moreover, FLLL12 induced the expression of death receptor-5 (DR5).	flll12	10-16	TNF receptor superfamily member 10b	Homo sapiens	43-59
25917567-6	2015	Moreover, FLLL12 induced the expression of death receptor-5 (DR5).	flll12	10-16	TNF receptor superfamily member 10b	Homo sapiens	61-64
25917567-11	2015	Taken together, our results strongly suggest that FLLL12 induces apoptosis of lung cancer cell lines by posttranscriptional regulation of DR5 through activation of protein tyrosine phosphatase(s).	flll12	50-56	TNF receptor superfamily member 10b	Homo sapiens	138-141
25724522-2	2015	Because gene profiling studies have revealed that methionine depletion increases TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) mRNA, we postulated that methionine stress sensitizes breast cancer cells to proapoptotic TRAIL-R2 agonists.	Methionine	50-60	TNF receptor superfamily member 10b	Homo sapiens	81-129
26009898-0	2015	The novel proteasome inhibitor carfilzomib activates and enhances extrinsic apoptosis involving stabilization of death receptor 5.	carfilzomib	31-42	TNF receptor superfamily member 10b	Homo sapiens	113-129
26170696-0	2015	Gefitinib upregulates death receptor 5 expression to mediate rmhTRAIL-induced apoptosis in Gefitinib-sensitive NSCLC cell line.	Gefitinib	0-9	TNF receptor superfamily member 10b	Homo sapiens	22-38
26170696-0	2015	Gefitinib upregulates death receptor 5 expression to mediate rmhTRAIL-induced apoptosis in Gefitinib-sensitive NSCLC cell line.	Gefitinib	91-100	TNF receptor superfamily member 10b	Homo sapiens	22-38
26170696-4	2015	Therefore, we investigated the effects of the combination of drugs and the expression of the DR5 to analyze the growth of a gefitinib-responsive non-small cell lung cancer cell line PC9, which was treated with rmhTRAIL and gefitinib individually or in combination.	Gefitinib	124-133	TNF receptor superfamily member 10b	Homo sapiens	93-96
25724522-2	2015	Because gene profiling studies have revealed that methionine depletion increases TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) mRNA, we postulated that methionine stress sensitizes breast cancer cells to proapoptotic TRAIL-R2 agonists.	Methionine	50-60	TNF receptor superfamily member 10b	Homo sapiens	131-139
25724522-2	2015	Because gene profiling studies have revealed that methionine depletion increases TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) mRNA, we postulated that methionine stress sensitizes breast cancer cells to proapoptotic TRAIL-R2 agonists.	Methionine	50-60	TNF receptor superfamily member 10b	Homo sapiens	231-239
25724522-2	2015	Because gene profiling studies have revealed that methionine depletion increases TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) mRNA, we postulated that methionine stress sensitizes breast cancer cells to proapoptotic TRAIL-R2 agonists.	Methionine	166-176	TNF receptor superfamily member 10b	Homo sapiens	81-129
25724522-2	2015	Because gene profiling studies have revealed that methionine depletion increases TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) mRNA, we postulated that methionine stress sensitizes breast cancer cells to proapoptotic TRAIL-R2 agonists.	Methionine	166-176	TNF receptor superfamily member 10b	Homo sapiens	131-139
25724522-2	2015	Because gene profiling studies have revealed that methionine depletion increases TNF-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) mRNA, we postulated that methionine stress sensitizes breast cancer cells to proapoptotic TRAIL-R2 agonists.	Methionine	166-176	TNF receptor superfamily member 10b	Homo sapiens	231-239
25724522-7	2015	RESULTS: Methionine depletion sensitized TNBC cells to lexatumumab-induced caspase activation and apoptosis by increasing TRAIL-R2 mRNA and cell surface expression.	Methionine	9-19	TNF receptor superfamily member 10b	Homo sapiens	122-130
25724522-9	2015	Proteomics analyses revealed that MAGED2, which has been reported to reduce TRAIL-R2 expression, was suppressed by methionine stress.	Methionine	115-125	TNF receptor superfamily member 10b	Homo sapiens	76-84
25724522-12	2015	CONCLUSIONS: Methionine depletion exposes a targetable defect in TNBC cells by increasing TRAIL-R2 expression.	Methionine	13-23	TNF receptor superfamily member 10b	Homo sapiens	90-98
25955843-0	2015	Metformin Causes G1-Phase Arrest via Down-Regulation of MiR-221 and Enhances TRAIL Sensitivity through DR5 Up-Regulation in Pancreatic Cancer Cells.	Metformin	0-9	TNF receptor superfamily member 10b	Homo sapiens	103-106
25770930-4	2015	Combination of chrysin and cisplatin increased the phosphorylation and accumulation of p53 through activating ERK1/2 in Hep G2 cells, which led to the overexpression of the pro-apoptotic proteins Bax and DR5 and the inhibition of the anti-apoptotic protein Bcl-2.	chrysin	15-22	TNF receptor superfamily member 10b	Homo sapiens	204-207
25770930-4	2015	Combination of chrysin and cisplatin increased the phosphorylation and accumulation of p53 through activating ERK1/2 in Hep G2 cells, which led to the overexpression of the pro-apoptotic proteins Bax and DR5 and the inhibition of the anti-apoptotic protein Bcl-2.	Cisplatin	27-36	TNF receptor superfamily member 10b	Homo sapiens	204-207
25955843-9	2015	Metformin induced the expressions of death receptor 5 (DR5), a receptor for TRAIL, and Bim with a pro-apoptotic function in the downstream of TRAIL-DR5 pathway.	Metformin	0-9	TNF receptor superfamily member 10b	Homo sapiens	37-53
25955843-9	2015	Metformin induced the expressions of death receptor 5 (DR5), a receptor for TRAIL, and Bim with a pro-apoptotic function in the downstream of TRAIL-DR5 pathway.	Metformin	0-9	TNF receptor superfamily member 10b	Homo sapiens	55-58
25955843-9	2015	Metformin induced the expressions of death receptor 5 (DR5), a receptor for TRAIL, and Bim with a pro-apoptotic function in the downstream of TRAIL-DR5 pathway.	Metformin	0-9	TNF receptor superfamily member 10b	Homo sapiens	148-151
25991668-0	2015	Delphinidin sensitizes prostate cancer cells to TRAIL-induced apoptosis, by inducing DR5 and causing caspase-mediated HDAC3 cleavage.	delphinidin	0-11	TNF receptor superfamily member 10b	Homo sapiens	85-88
25721064-0	2015	Unexpected hepatotoxicity in a phase I study of TAS266, a novel tetravalent agonistic Nanobody  targeting the DR5 receptor.	tas266	48-54	TNF receptor superfamily member 10b	Homo sapiens	110-113
25721064-1	2015	PURPOSE: TAS266 is a novel agonistic tetravalent Nanobody( ) targeting the DR5 receptor.	tas266	9-15	TNF receptor superfamily member 10b	Homo sapiens	75-78
25991668-6	2015	TRAIL-induced apoptosis in prostate cancer cells pretreated with delphinidin was dependent on death receptor 5 (DR5) and downstream cleavage of histone deacetylase 3 (HDAC3).	delphinidin	65-76	TNF receptor superfamily member 10b	Homo sapiens	94-110
25991668-6	2015	TRAIL-induced apoptosis in prostate cancer cells pretreated with delphinidin was dependent on death receptor 5 (DR5) and downstream cleavage of histone deacetylase 3 (HDAC3).	delphinidin	65-76	TNF receptor superfamily member 10b	Homo sapiens	112-115
25991668-7	2015	In conclusion, delphinidin sensitizes prostate cancer cells to TRAIL-induced apoptosis by inducing DR5, thus causing caspase-mediated HDAC3 cleavage.	delphinidin	15-26	TNF receptor superfamily member 10b	Homo sapiens	99-102
25766325-0	2015	A benzimidazole derivative exhibiting antitumor activity blocks EGFR and HER2 activity and upregulates DR5 in breast cancer cells.	benzimidazole	2-15	TNF receptor superfamily member 10b	Homo sapiens	103-106
25932013-4	2015	We here show that selective activation of DR5 specifically induces calcium influx only in the primary cilia, whereas non-selective activation of dopamine receptor induces calcium fluxes in both cilioplasm and cytoplasm.	Calcium	67-74	TNF receptor superfamily member 10b	Homo sapiens	42-45
25932013-6	2015	Furthermore, calcium activation in the cilioplasm by DR5 increases length and mechanosensory function of primary cilia, leading to a greater response to fluid-shear stress.	Calcium	13-20	TNF receptor superfamily member 10b	Homo sapiens	53-56
25796504-8	2015	Together, we conclude that in TRAIL-treated MDR gastric carcinoma cells, cisplatin induces the death receptors DR4 and DR5 through the up-regulation of c-myc and strengthens the activation of caspases via promoting the release of cyt c.	Cisplatin	73-82	TNF receptor superfamily member 10b	Homo sapiens	119-122
25796504-0	2015	Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin.	Cisplatin	0-9	TNF receptor superfamily member 10b	Homo sapiens	132-135
25796504-0	2015	Cisplatin-mediated c-myc overexpression and cytochrome c (cyt c) release result in the up-regulation of the death receptors DR4 and DR5 and the activation of caspase 3 and caspase 9, likely responsible for the TRAIL-sensitizing effect of cisplatin.	Cisplatin	238-247	TNF receptor superfamily member 10b	Homo sapiens	132-135
25502339-0	2015	Parthenolide enhances sensitivity of colorectal cancer cells to TRAIL by inducing death receptor 5 and promotes TRAIL-induced apoptosis.	parthenolide	0-12	TNF receptor superfamily member 10b	Homo sapiens	82-98
25541375-7	2015	TaqMan low density array analysis of A549 cells also confirmed that the induction of apoptosis by the polysaccharide occurred through the TRAIL-DR4/DR5 pathways.	Polysaccharides	102-116	TNF receptor superfamily member 10b	Homo sapiens	148-151
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	Tretinoin	58-60	TNF receptor superfamily member 10b	Homo sapiens	121-130
25487639-0	2015	Thioether analogues of disulfide-bridged cyclic peptides targeting death receptor 5: conformational analysis, dimerisation and consequences for receptor activation.	Sulfides	0-9	TNF receptor superfamily member 10b	Homo sapiens	67-83
25487639-0	2015	Thioether analogues of disulfide-bridged cyclic peptides targeting death receptor 5: conformational analysis, dimerisation and consequences for receptor activation.	Disulfides	23-32	TNF receptor superfamily member 10b	Homo sapiens	67-83
25487639-2	2015	We report the effect of replacing the disulfide bridge with a lanthionine linkage in a 16-mer cyclic peptide that binds to death receptor 5 (DR5, TRAIL-R2).	Disulfides	38-47	TNF receptor superfamily member 10b	Homo sapiens	123-139
25487639-2	2015	We report the effect of replacing the disulfide bridge with a lanthionine linkage in a 16-mer cyclic peptide that binds to death receptor 5 (DR5, TRAIL-R2).	Disulfides	38-47	TNF receptor superfamily member 10b	Homo sapiens	141-144
25487639-2	2015	We report the effect of replacing the disulfide bridge with a lanthionine linkage in a 16-mer cyclic peptide that binds to death receptor 5 (DR5, TRAIL-R2).	Disulfides	38-47	TNF receptor superfamily member 10b	Homo sapiens	146-154
25487639-2	2015	We report the effect of replacing the disulfide bridge with a lanthionine linkage in a 16-mer cyclic peptide that binds to death receptor 5 (DR5, TRAIL-R2).	lanthionine	62-73	TNF receptor superfamily member 10b	Homo sapiens	123-139
25487639-2	2015	We report the effect of replacing the disulfide bridge with a lanthionine linkage in a 16-mer cyclic peptide that binds to death receptor 5 (DR5, TRAIL-R2).	lanthionine	62-73	TNF receptor superfamily member 10b	Homo sapiens	141-144
25487639-2	2015	We report the effect of replacing the disulfide bridge with a lanthionine linkage in a 16-mer cyclic peptide that binds to death receptor 5 (DR5, TRAIL-R2).	lanthionine	62-73	TNF receptor superfamily member 10b	Homo sapiens	146-154
25487639-3	2015	Upon covalent oligomerisation, the disulfide-bridged peptide has previously shown similar behaviour to that of TNF-related apoptosis inducing ligand (TRAIL), by selectively triggering the DR5 cell death pathway.	Disulfides	35-44	TNF receptor superfamily member 10b	Homo sapiens	188-191
25487639-6	2015	The same holds true for dimeric versions of these peptides: the thioether is able to induce DR5-mediated apoptosis of BJAB lymphoma and tumorigenic BJELR cells, albeit to a slightly lower extent compared to its disulfide homologue.	Sulfides	64-73	TNF receptor superfamily member 10b	Homo sapiens	92-95
25487639-6	2015	The same holds true for dimeric versions of these peptides: the thioether is able to induce DR5-mediated apoptosis of BJAB lymphoma and tumorigenic BJELR cells, albeit to a slightly lower extent compared to its disulfide homologue.	Disulfides	211-220	TNF receptor superfamily member 10b	Homo sapiens	92-95
25218028-2	2015	Celecoxib and its non-coxib analog, 2,5-dimethyl celecoxib, induced ULBP-1 and DR5 in both COX-2 negative HCT-15 cells and COX-2 positive HT-29 cells.	Celecoxib	0-9	TNF receptor superfamily member 10b	Homo sapiens	79-82
25218028-2	2015	Celecoxib and its non-coxib analog, 2,5-dimethyl celecoxib, induced ULBP-1 and DR5 in both COX-2 negative HCT-15 cells and COX-2 positive HT-29 cells.	2,5-dimethylcelecoxib	36-58	TNF receptor superfamily member 10b	Homo sapiens	79-82
25218028-4	2015	The inducibility of ULBP-1 and DR5 by celecoxib was not different between CD44- and CD44+ HCT-15 cells, and CD133- and CD133+ HT-29 cells.	Celecoxib	38-47	TNF receptor superfamily member 10b	Homo sapiens	31-34
25218028-6	2015	In addition, celecoxib induced CHOP, and thapsigargin, an inducer of ER (endoplasmic reticulum) stress, induced DR5 but not ULBP1 in HCT-15.	Thapsigargin	41-53	TNF receptor superfamily member 10b	Homo sapiens	112-115
25218028-7	2015	Taken together, these findings suggest that celecoxib induces the expression of ULBP-1 as well as DR5 in clonogenic colon cancer cells via COX-2 and ER stress-independent pathways, and increases their susceptibility to NK cells.	Celecoxib	44-53	TNF receptor superfamily member 10b	Homo sapiens	98-101
25593641-5	2015	Combined treatment with TSA and TRAIL significantly reduced the levels of the cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting enzyme (FLICE) inhibitory protein (c-FLIP), whereas those of death receptor (DR) 4, DR5, and FADD remained unchanged.	trichostatin A	24-27	TNF receptor superfamily member 10b	Homo sapiens	240-243
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	Tretinoin	58-60	TNF receptor superfamily member 10b	Homo sapiens	175-184
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	Tretinoin	58-60	TNF receptor superfamily member 10b	Homo sapiens	198-206
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	citral	350-356	TNF receptor superfamily member 10b	Homo sapiens	121-130
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	citral	350-356	TNF receptor superfamily member 10b	Homo sapiens	175-184
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	citral	350-356	TNF receptor superfamily member 10b	Homo sapiens	198-206
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	citral	358-385	TNF receptor superfamily member 10b	Homo sapiens	121-130
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	citral	358-385	TNF receptor superfamily member 10b	Homo sapiens	175-184
25208926-7	2015	Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal).	citral	358-385	TNF receptor superfamily member 10b	Homo sapiens	198-206
25344582-0	2015	Small molecule inhibitor YM155-mediated activation of death receptor 5 is crucial for chemotherapy-induced apoptosis in pancreatic carcinoma.	YM 155	25-30	TNF receptor superfamily member 10b	Homo sapiens	54-70
25333675-9	2015	Further investigation of the mechanism underlying these effects revealed that the evodiamine + TRAIL effect is associated with the increased expression of death receptor (DR)4, DR5, caspase-8 and cleaved caspase-3.	evodiamine	82-92	TNF receptor superfamily member 10b	Homo sapiens	177-180
26111475-10	2015	The ROS inhibitor NAC and silencing of DR5 by siRNA transfection inhibited the ability of combination to induce PARP cleavage and generate ROS.	Reactive Oxygen Species	139-142	TNF receptor superfamily member 10b	Homo sapiens	39-42
25344582-8	2015	We found that YM155 induced apoptosis by broad-spectrum inhibition of IAP family member proteins (e.g., CIAP1/2 and FLIP) and induced proapoptotic Bak protein upregulation and activation; the antitumor effect of YM155 treatment with either the DR5 agonist lexatumumab or gemcitabine on pancreatic cancer cells was synergistic.	YM 155	14-19	TNF receptor superfamily member 10b	Homo sapiens	244-247
25320841-3	2014	In this study, isoegomaketone (1) acted as a synergistic TRAIL sensitizer by mediating up-regulation of DR5 expression in primary prostate cancer RC-58T/h/SA#4 cells.	isoegomaketone	15-29	TNF receptor superfamily member 10b	Homo sapiens	104-107
25200008-4	2014	We describe the development of an optimized polymer-based nanotherapeutic incorporating both a functionalized polyethylene glycol (PEG) layer and targeting antibodies to limit premature phagocytic clearance whilst enabling targeting of DR5-expressing tumor cells.	Polymers	44-51	TNF receptor superfamily member 10b	Homo sapiens	236-239
25200008-5	2014	Using the HCT116 colorectal cancer model, we show that following binding to DR5, the nanoparticles activate caspase 8, enhancing the anti-tumor activity of the camptothecin payload both in vitro and in vivo.	Camptothecin	160-172	TNF receptor superfamily member 10b	Homo sapiens	76-79
25200008-6	2014	Importantly, the combination of nanoparticle-induced DR5 clustering with camptothecin delivery overcomes resistance to DR5-induced apoptosis caused by loss of BAX or overexpression of anti-apoptotic FLIP.	Camptothecin	73-85	TNF receptor superfamily member 10b	Homo sapiens	119-122
25506265-0	2014	Upregulation of death receptor 5 and activation of caspase 8/3 play a critical role in ergosterol peroxide induced apoptosis in DU 145 prostate cancer cells.	ergosterol-5,8-peroxide	87-106	TNF receptor superfamily member 10b	Homo sapiens	16-32
25506265-11	2014	CONCLUSION: Overall, our findings suggest that ergosterol peroxide induces apoptosis via activation of death receptor 5 and caspase 8/3 in DU 145 prostate cancer cells as a cancer chemopreventive agent or dietary factor.	ergosterol-5,8-peroxide	47-66	TNF receptor superfamily member 10b	Homo sapiens	103-119
25320841-7	2014	Furthermore, DR5 expression induced by 1 was mediated via a ROS-independent pathway that required CHOP and p53.	ros	60-63	TNF receptor superfamily member 10b	Homo sapiens	13-16
25320841-8	2014	Overall, these findings provide evidence that 1 potentiates TRAIL-mediated apoptosis through up-regulation of DR5 via a ROS-independent pathway.	ros	120-123	TNF receptor superfamily member 10b	Homo sapiens	110-113
25461556-0	2014	Camptothecin sensitizes human hepatoma Hep3B cells to TRAIL-mediated apoptosis via ROS-dependent death receptor 5 upregulation with the involvement of MAPKs.	Camptothecin	0-12	TNF receptor superfamily member 10b	Homo sapiens	97-113
25461556-6	2014	CPT-induced generation of reactive oxygen species (ROS) also preceded the upregulation of DR5 in response to TRAIL.	Reactive Oxygen Species	26-49	TNF receptor superfamily member 10b	Homo sapiens	90-93
25461556-6	2014	CPT-induced generation of reactive oxygen species (ROS) also preceded the upregulation of DR5 in response to TRAIL.	Reactive Oxygen Species	51-54	TNF receptor superfamily member 10b	Homo sapiens	90-93
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Reactive Oxygen Species	19-22	TNF receptor superfamily member 10b	Homo sapiens	26-29
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Acetylcysteine	100-119	TNF receptor superfamily member 10b	Homo sapiens	26-29
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Acetylcysteine	100-119	TNF receptor superfamily member 10b	Homo sapiens	204-207
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Glutathione	124-135	TNF receptor superfamily member 10b	Homo sapiens	26-29
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Glutathione	124-135	TNF receptor superfamily member 10b	Homo sapiens	204-207
24905183-4	2014	Moreover, honokiol elicited the extrinsic death receptor pathway of DR5 and caspase 8 and the intrinsic pathway of caspase 9.	honokiol	10-18	TNF receptor superfamily member 10b	Homo sapiens	68-71
25289891-7	2014	We tested synergistic apoptosis-inducing cotreatment strategies and determined that only the proteasome inhibitor bortezomib potently enhanced expression of the TRAIL receptors TRAIL-R1 and/or TRAIL-R2, the formation of the TRAIL death-inducing signaling complex, and activation of caspases; this treatment resulted in sensitization of all TRAIL-resistant meningioma samples to TRAIL-induced apoptosis.	Bortezomib	114-124	TNF receptor superfamily member 10b	Homo sapiens	193-201
25017974-4	2014	We found that CCT327 enhanced TRAIL-induced apoptosis through upregulation of death receptors DR4 and DR5.	CCT327	14-20	TNF receptor superfamily member 10b	Homo sapiens	102-105
25341043-6	2014	Bortezomib-mediated sensitisation to TRAIL was associated with enhanced activation of caspase-8, -9 and -3, elevated membrane expression levels of TRAIL-R2, cytochrome c release and G2/M arrest.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	147-155
24212133-5	2014	Immunohistochemical analysis for DR4 and DR5 was carried out on formalin-fixed paraffin-embedded sections of skin tissues using avidin-biotin peroxidase method.	Formaldehyde	64-72	TNF receptor superfamily member 10b	Homo sapiens	41-44
24970682-11	2014	Furthermore, upregulation of death receptor 5 by metformin-mediated Sirt1 downregulation enhanced the sensitivity of wild-type p53 cancer cells to TRAIL-induced apoptosis.	Metformin	49-58	TNF receptor superfamily member 10b	Homo sapiens	29-45
25321472-9	2014	In conclusion, our results suggest that Med sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the upregulation of DR5 through activation of the ROS-JNK-CHOP pathway.	ros	163-166	TNF receptor superfamily member 10b	Homo sapiens	133-136
25310712-0	2014	Combination of TRAIL with bortezomib shifted apoptotic signaling from DR4 to DR5 death receptor by selective internalization and degradation of DR4.	Bortezomib	26-36	TNF receptor superfamily member 10b	Homo sapiens	77-80
25310712-5	2014	The expression of death (DR4 and DR5) as well as decoy (DcR1 and DcR2) receptors was upregulated in the both cell lines either by TRAIL or by bortezomib.	Bortezomib	142-152	TNF receptor superfamily member 10b	Homo sapiens	33-36
25310712-7	2014	Interestingly DR5-B variant of TRAIL which do not bind with DR4 receptor also induced elimination of DR4 from cell surface in combination with bortezomib indicating the ligand-independent mechanism of the receptor internalization.	Bortezomib	143-153	TNF receptor superfamily member 10b	Homo sapiens	14-17
24930757-6	2014	Ilimaquinone also reduced the cell survival proteins Bcl2 and Bcl-xL, while strongly up-regulating death receptor (DR) 4 and DR5 expression.	ilimaquinone	0-12	TNF receptor superfamily member 10b	Homo sapiens	125-128
24930757-7	2014	Induction of DR4 and DR5 by ilimaquinone was mediated through up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP).	ilimaquinone	28-40	TNF receptor superfamily member 10b	Homo sapiens	21-24
24930757-9	2014	Finally, the generation of ROS was required for CHOP and DR5 up-regulation by ilimaquinone.	ros	27-30	TNF receptor superfamily member 10b	Homo sapiens	57-60
24930757-9	2014	Finally, the generation of ROS was required for CHOP and DR5 up-regulation by ilimaquinone.	ilimaquinone	78-90	TNF receptor superfamily member 10b	Homo sapiens	57-60
24930757-10	2014	These results demonstrate that ilimaquinone enhanced the sensitivity of human colon cancer cells to TRAIL-induced apoptosis through ROS-ERK/p38 MAPK-CHOP-mediated up-regulation of DR4 and DR5 expression, suggesting that ilimaquinone could be developed into an adjuvant chemotherapeutic drug.	ilimaquinone	31-43	TNF receptor superfamily member 10b	Homo sapiens	188-191
24930757-10	2014	These results demonstrate that ilimaquinone enhanced the sensitivity of human colon cancer cells to TRAIL-induced apoptosis through ROS-ERK/p38 MAPK-CHOP-mediated up-regulation of DR4 and DR5 expression, suggesting that ilimaquinone could be developed into an adjuvant chemotherapeutic drug.	ros	132-135	TNF receptor superfamily member 10b	Homo sapiens	188-191
24188478-0	2014	Cariporide sensitizes leukemic cells to tumor necrosis factor related apoptosis-inducing ligand by up-regulation of death receptor 5 via endoplasmic reticulum stress-CCAAT/enhancer binding protein homologous protein dependent mechanism.	cariporide	0-10	TNF receptor superfamily member 10b	Homo sapiens	116-132
24188478-4	2014	The present study showed that treatment with the NHE1 inhibitor cariporide led to ER stress-induced up-regulation of the death receptor 5 (DR5) which is mediated by CHOP at the transcriptional level.	cariporide	64-74	TNF receptor superfamily member 10b	Homo sapiens	121-137
24188478-4	2014	The present study showed that treatment with the NHE1 inhibitor cariporide led to ER stress-induced up-regulation of the death receptor 5 (DR5) which is mediated by CHOP at the transcriptional level.	cariporide	64-74	TNF receptor superfamily member 10b	Homo sapiens	139-142
25017974-8	2014	Moreover, CCT327-induced induction of DR5 and DR4 was mediated by reactive oxygen species (ROS), and N-acetylcysteine (NAC) blocked the induction of DRs by CCT327.	CCT327	10-16	TNF receptor superfamily member 10b	Homo sapiens	38-41
25017974-8	2014	Moreover, CCT327-induced induction of DR5 and DR4 was mediated by reactive oxygen species (ROS), and N-acetylcysteine (NAC) blocked the induction of DRs by CCT327.	Reactive Oxygen Species	66-89	TNF receptor superfamily member 10b	Homo sapiens	38-41
25017974-8	2014	Moreover, CCT327-induced induction of DR5 and DR4 was mediated by reactive oxygen species (ROS), and N-acetylcysteine (NAC) blocked the induction of DRs by CCT327.	Reactive Oxygen Species	91-94	TNF receptor superfamily member 10b	Homo sapiens	38-41
24789319-0	2014	Tumoricidal activity of combining the agonistic DR5 antibody D-6 with cisplatin in C30 cisplatin-resistant ovarian cancer in vitro and in vivo.	Cisplatin	87-96	TNF receptor superfamily member 10b	Homo sapiens	48-51
24939851-2	2014	In this report, we demonstrate that the stress response gene ATF3 is required for endoplasmic reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) in human p53-deficient colorectal cancer cells.	zerumbone	139-148	TNF receptor superfamily member 10b	Homo sapiens	120-123
24939851-2	2014	In this report, we demonstrate that the stress response gene ATF3 is required for endoplasmic reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) in human p53-deficient colorectal cancer cells.	Celecoxib	159-168	TNF receptor superfamily member 10b	Homo sapiens	120-123
24939851-2	2014	In this report, we demonstrate that the stress response gene ATF3 is required for endoplasmic reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) in human p53-deficient colorectal cancer cells.	Celecoxib	170-173	TNF receptor superfamily member 10b	Homo sapiens	120-123
24939851-6	2014	A reporter assay demonstrated that at least two ATF/cAMP response element motifs as well as C/EBP homologous protein motif at the proximal region of the human DR5 gene promoter were required for ZER-induced DR5 gene transcription.	Cyclic AMP	52-56	TNF receptor superfamily member 10b	Homo sapiens	207-210
24919794-0	2014	Quinazoline analog HMJ-30 inhibits angiogenesis: involvement of endothelial cell apoptosis through ROS-JNK-mediated death receptor 5 signaling.	Quinazolines	0-11	TNF receptor superfamily member 10b	Homo sapiens	116-132
24919794-0	2014	Quinazoline analog HMJ-30 inhibits angiogenesis: involvement of endothelial cell apoptosis through ROS-JNK-mediated death receptor 5 signaling.	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	19-25	TNF receptor superfamily member 10b	Homo sapiens	116-132
24919794-8	2014	We investigated the upstream of the death receptor pathway and further observed that the levels of death receptor 5 (DR5) and phosphorylated c-Jun N-terminal kinase (JNK) signals were upregulated in HUVECs following HMJ-30 challenge, which was confirmed by a JNK-specific inhibitor (SP600125).	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	216-222	TNF receptor superfamily member 10b	Homo sapiens	99-115
24919794-8	2014	We investigated the upstream of the death receptor pathway and further observed that the levels of death receptor 5 (DR5) and phosphorylated c-Jun N-terminal kinase (JNK) signals were upregulated in HUVECs following HMJ-30 challenge, which was confirmed by a JNK-specific inhibitor (SP600125).	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	216-222	TNF receptor superfamily member 10b	Homo sapiens	117-120
24919794-8	2014	We investigated the upstream of the death receptor pathway and further observed that the levels of death receptor 5 (DR5) and phosphorylated c-Jun N-terminal kinase (JNK) signals were upregulated in HUVECs following HMJ-30 challenge, which was confirmed by a JNK-specific inhibitor (SP600125).	pyrazolanthrone	283-291	TNF receptor superfamily member 10b	Homo sapiens	99-115
24919794-8	2014	We investigated the upstream of the death receptor pathway and further observed that the levels of death receptor 5 (DR5) and phosphorylated c-Jun N-terminal kinase (JNK) signals were upregulated in HUVECs following HMJ-30 challenge, which was confirmed by a JNK-specific inhibitor (SP600125).	pyrazolanthrone	283-291	TNF receptor superfamily member 10b	Homo sapiens	117-120
24919794-9	2014	Hence, HMJ-30-induced endothelial cell apoptosis involved the ROS/JNK-regulated DR5 pathway.	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	7-13	TNF receptor superfamily member 10b	Homo sapiens	80-83
24919794-9	2014	Hence, HMJ-30-induced endothelial cell apoptosis involved the ROS/JNK-regulated DR5 pathway.	Reactive Oxygen Species	62-65	TNF receptor superfamily member 10b	Homo sapiens	80-83
25015549-0	2014	Upregulation of microRNA135a-3p and death receptor 5 plays a critical role in Tanshinone I sensitized prostate cancer cells to TRAIL induced apoptosis.	tanshinone	78-88	TNF receptor superfamily member 10b	Homo sapiens	36-52
25015549-5	2014	RT-PCR and RT-qPCR analyses confirmed that co-treatment of Tanshinone I and TRAIL up-regulated DR5 and microRNA 135a-3p at mRNA level or activity of DR5 promoter and attenuated phosphorylation of extracellular signal regulated kinases in PC-3.	tanshinone	59-71	TNF receptor superfamily member 10b	Homo sapiens	95-98
25015549-5	2014	RT-PCR and RT-qPCR analyses confirmed that co-treatment of Tanshinone I and TRAIL up-regulated DR5 and microRNA 135a-3p at mRNA level or activity of DR5 promoter and attenuated phosphorylation of extracellular signal regulated kinases in PC-3.	tanshinone	59-71	TNF receptor superfamily member 10b	Homo sapiens	149-152
25015549-6	2014	Conversely, the silencing of DR5 blocked the increased cytotoxicity, sub G1 population and PARP cleavages induced by co-treatment of Tanshinone I and TRAIL.	tanshinone	133-145	TNF receptor superfamily member 10b	Homo sapiens	29-32
25015549-8	2014	Overall, our findings suggest that Tanshinone I enhances TRAIL mediated apoptosis via upregulation of miR135a-3p mediated DR5 in prostate cancer cells as a potent TRAIL sensitizer.	tanshinone	35-47	TNF receptor superfamily member 10b	Homo sapiens	122-125
25033286-6	2014	In the KatoIII cell line (TP53-null), DR5 silencing markedly attenuated tenovin-6-induced apoptosis, suggesting that the pivotal mechanism behind its antitumor effects is based on activation of the death receptor signal pathway.	tenovin-6	72-81	TNF receptor superfamily member 10b	Homo sapiens	38-41
24973666-6	2014	Cordycepin-induced cell death was also associated with induction of Fas and death receptor 5, activation of caspase-8, and truncation of Bid (tBid), suggesting that tBid might serve to connect activation of both the mitochondrial-mediated intrinsic and death receptor-mediated extrinsic apoptotic pathways.	cordycepin	0-10	TNF receptor superfamily member 10b	Homo sapiens	76-92
25102912-0	2014	Myeloid zinc finger 1 mediates sulindac sulfide-induced upregulation of death receptor 5 of human colon cancer cells.	sulindac sulfide	31-47	TNF receptor superfamily member 10b	Homo sapiens	72-88
25102912-2	2014	Sulindac sulfide had been shown to induce the expression of death receptor 5 (DR5), a receptor for TRAIL, and sensitize cancer cells to TRAIL-induced apoptosis; however, the molecular mechanism underlying the upregulation of DR5 has not yet been elucidated.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	60-76
25102912-2	2014	Sulindac sulfide had been shown to induce the expression of death receptor 5 (DR5), a receptor for TRAIL, and sensitize cancer cells to TRAIL-induced apoptosis; however, the molecular mechanism underlying the upregulation of DR5 has not yet been elucidated.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	78-81
25102912-2	2014	Sulindac sulfide had been shown to induce the expression of death receptor 5 (DR5), a receptor for TRAIL, and sensitize cancer cells to TRAIL-induced apoptosis; however, the molecular mechanism underlying the upregulation of DR5 has not yet been elucidated.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	225-228
25102912-3	2014	We demonstrate here that myeloid zinc finger 1 (MZF1) mediates the induction of DR5 by sulindac sulfide.	sulindac sulfide	87-103	TNF receptor superfamily member 10b	Homo sapiens	80-83
25102912-4	2014	Sulindac sulfide induced the expression of DR5 at the protein and mRNA levels in colon cancer SW480 cells.	sulindac sulfide	0-16	TNF receptor superfamily member 10b	Homo sapiens	43-46
25102912-5	2014	Furthermore, sulindac sulfide increased DR5 promoter activity.	sulindac sulfide	13-29	TNF receptor superfamily member 10b	Homo sapiens	40-43
25102912-6	2014	We showed that sulindac sulfide stimulated DR5 promoter activity via the -301 to -253 region.	sulindac sulfide	15-31	TNF receptor superfamily member 10b	Homo sapiens	43-46
25102912-8	2014	Site-directed mutations in the site abrogated the enhancement in DR5 promoter activity by sulindac sulfide.	sulindac sulfide	90-106	TNF receptor superfamily member 10b	Homo sapiens	65-68
25102912-9	2014	MZF1 directly bound to the putative MZF1-binding site of the DR5 promoter and the binding was increased by sulindac sulfide.	sulindac sulfide	107-123	TNF receptor superfamily member 10b	Homo sapiens	61-64
25102912-10	2014	The expression of MZF1 was also increased by sulindac sulfide, and MZF1 siRNA attenuated the upregulation of DR5 by sulindac sulfide.	sulindac sulfide	116-132	TNF receptor superfamily member 10b	Homo sapiens	109-112
25102912-11	2014	These results indicate that sulindac sulfide induces the expression of DR5 by up-regulating MZF1.	sulindac sulfide	28-44	TNF receptor superfamily member 10b	Homo sapiens	71-74
24710190-5	2014	Bufalin also promoted the clustering of death receptor 4 (DR4) and DR5 in aggregated lipid rafts.	bufalin	0-7	TNF receptor superfamily member 10b	Homo sapiens	67-70
24710190-6	2014	The cholesterol-sequestering agent methyl-beta-cyclodextrin reversed the DR4 and DR5 clustering and reduced bufalin+TRAIL-induced apoptosis.	Cholesterol	4-15	TNF receptor superfamily member 10b	Homo sapiens	81-84
24710190-6	2014	The cholesterol-sequestering agent methyl-beta-cyclodextrin reversed the DR4 and DR5 clustering and reduced bufalin+TRAIL-induced apoptosis.	methyl-beta-cyclodextrin	35-59	TNF receptor superfamily member 10b	Homo sapiens	81-84
24789319-1	2014	A previous study by our group reported that the agonistic DR5 antibody D-6 was capable of triggering apoptosis in A2780 cisplatin-sensitive ovarian cancer cells and that this marked effect was enhanced by cisplatin in vitro.	Cisplatin	120-129	TNF receptor superfamily member 10b	Homo sapiens	58-61
24789319-1	2014	A previous study by our group reported that the agonistic DR5 antibody D-6 was capable of triggering apoptosis in A2780 cisplatin-sensitive ovarian cancer cells and that this marked effect was enhanced by cisplatin in vitro.	Cisplatin	205-214	TNF receptor superfamily member 10b	Homo sapiens	58-61
25233628-5	2014	MTT assay showed that, rClone30- hDR5 in combination with TRAIL more efficiently inhibited the tumor growth of HepG2 cells compared to rClone30-hDR5 or TRAIL in vitro.	monooxyethylene trimethylolpropane tristearate	0-3	TNF receptor superfamily member 10b	Homo sapiens	33-37
25052611-8	2014	The expression of DR5 on the surface of KG-1a treated with resveratrol was (9.05 +- 3.57)%, significantly higher than (3.11 +- 0.54)% of untreated KG-1a (P&lt;0.05).	Resveratrol	59-70	TNF receptor superfamily member 10b	Homo sapiens	18-21
24662747-3	2014	Triptolide increases levels of death receptor DR5 and decreases the pro-survival FLICE-like inhibitory protein (c-FLIP), which contribute to the activation of caspase-8.	triptolide	0-10	TNF receptor superfamily member 10b	Homo sapiens	46-49
24882208-6	2014	E-cadherin bound specifically to ligated DR4/DR5, requiring extracellular cadherin domain 1 and calcium.	Calcium	96-103	TNF receptor superfamily member 10b	Homo sapiens	45-48
24104765-3	2014	Fluid-shear stress and dopamine receptor type-5 (DR5) agonist are among the few stimuli that require cilia for intracellular calcium signal transduction.	Calcium	125-132	TNF receptor superfamily member 10b	Homo sapiens	23-47
24104765-3	2014	Fluid-shear stress and dopamine receptor type-5 (DR5) agonist are among the few stimuli that require cilia for intracellular calcium signal transduction.	Calcium	125-132	TNF receptor superfamily member 10b	Homo sapiens	49-52
24104765-7	2014	While DR5-specific agonist induces calcium signaling mainly in the cilioplasm via ciliary CaV1.2, thrombin specifically induces cytosolic calcium signaling through the IP3 receptor.	Calcium	35-42	TNF receptor superfamily member 10b	Homo sapiens	6-9
24740347-5	2014	Treatment with low doses of salinomycin in combination with TRAIL augmented the activation of caspase-3 and increased TRAIL-R2 cell surface expression.	salinomycin	28-39	TNF receptor superfamily member 10b	Homo sapiens	118-126
24401154-7	2014	Moreover, OSU-A9 increased DR5 expression through a reactive oxygen species (ROS)-dependent mechanism.	Reactive Oxygen Species	52-75	TNF receptor superfamily member 10b	Homo sapiens	27-30
24401154-7	2014	Moreover, OSU-A9 increased DR5 expression through a reactive oxygen species (ROS)-dependent mechanism.	Reactive Oxygen Species	77-80	TNF receptor superfamily member 10b	Homo sapiens	27-30
24732433-4	2014	Through this route, WFA acted as an effective DR5 activator capable of potentiating the biologic effects of celecoxib, etoposide, and TRAIL.	withaferin A	20-23	TNF receptor superfamily member 10b	Homo sapiens	46-49
24732433-4	2014	Through this route, WFA acted as an effective DR5 activator capable of potentiating the biologic effects of celecoxib, etoposide, and TRAIL.	Celecoxib	108-117	TNF receptor superfamily member 10b	Homo sapiens	46-49
24732433-4	2014	Through this route, WFA acted as an effective DR5 activator capable of potentiating the biologic effects of celecoxib, etoposide, and TRAIL.	Etoposide	119-128	TNF receptor superfamily member 10b	Homo sapiens	46-49
24213373-0	2014	Indomethacin sensitizes TRAIL-resistant melanoma cells to TRAIL-induced apoptosis through ROS-mediated upregulation of death receptor 5 and downregulation of survivin.	Indomethacin	0-12	TNF receptor superfamily member 10b	Homo sapiens	119-135
24213373-0	2014	Indomethacin sensitizes TRAIL-resistant melanoma cells to TRAIL-induced apoptosis through ROS-mediated upregulation of death receptor 5 and downregulation of survivin.	Reactive Oxygen Species	90-93	TNF receptor superfamily member 10b	Homo sapiens	119-135
24213373-5	2014	Mechanistically, indomethacin induced cell surface expression of death receptor 5 (DR5) in melanoma cells and also in various types of cancer cells.	Indomethacin	17-29	TNF receptor superfamily member 10b	Homo sapiens	65-81
24213373-5	2014	Mechanistically, indomethacin induced cell surface expression of death receptor 5 (DR5) in melanoma cells and also in various types of cancer cells.	Indomethacin	17-29	TNF receptor superfamily member 10b	Homo sapiens	83-86
24213373-6	2014	DR5 knockdown abolished the enhancing effect of indomethacin on TRAIL responses.	Indomethacin	48-60	TNF receptor superfamily member 10b	Homo sapiens	0-3
24213373-7	2014	Induction of the DR5 by indomethacin was found to be p53 independent but dependent on the induction of CCAAT/enhancer-binding protein homologous protein (CHOP).	Indomethacin	24-36	TNF receptor superfamily member 10b	Homo sapiens	17-20
24213373-8	2014	Knockdown of CHOP abolished indomethacin-induced DR5 expression and the associated potentiation of TRAIL-mediated cell death.	Indomethacin	28-40	TNF receptor superfamily member 10b	Homo sapiens	49-52
24213373-9	2014	In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL.	Indomethacin	13-25	TNF receptor superfamily member 10b	Homo sapiens	109-112
24213373-9	2014	In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL.	Reactive Oxygen Species	34-57	TNF receptor superfamily member 10b	Homo sapiens	109-112
24213373-9	2014	In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL.	Reactive Oxygen Species	59-62	TNF receptor superfamily member 10b	Homo sapiens	109-112
24491546-6	2014	PEITC enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-induced-p53.	ros	153-156	TNF receptor superfamily member 10b	Homo sapiens	116-119
24612139-4	2014	The quercetin induced expression of death receptor DR5 but did not affect expression of DR4 in cancer cells.	Quercetin	4-13	TNF receptor superfamily member 10b	Homo sapiens	51-54
24612139-5	2014	The induction of DR5 was mediated through activation of JNK and through upregulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP); as silencing of these signaling molecules abrogated the effect of quercetin.	Quercetin	235-244	TNF receptor superfamily member 10b	Homo sapiens	17-20
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Reactive Oxygen Species	59-82	TNF receptor superfamily member 10b	Homo sapiens	16-19
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Reactive Oxygen Species	84-87	TNF receptor superfamily member 10b	Homo sapiens	16-19
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Reactive Oxygen Species	93-96	TNF receptor superfamily member 10b	Homo sapiens	16-19
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Quercetin	130-139	TNF receptor superfamily member 10b	Homo sapiens	16-19
24612139-7	2014	Furthermore, quercetin enhances TRAIL mediated inhibition of tumor growth of human SKOV-3 xenograft was associated with induction of apoptosis, activation of caspase-3, CHOP and DR5.	Quercetin	13-22	TNF receptor superfamily member 10b	Homo sapiens	178-181
24612139-8	2014	Overall, our data suggest that quercetin enhances apoptotic death of ovarian cancer cells to TRAIL through upregulation of CHOP-induced DR5 expression following ROS mediated endoplasmic reticulum-stress.	Quercetin	31-40	TNF receptor superfamily member 10b	Homo sapiens	136-139
24740347-6	2014	TRAIL-R2 upmodulation was required for mediating the stimulatory effect of salinomycin on TRAIL-mediated apoptosis, since it was abrogated by siRNA-mediated TRAIL-R2 knockdown.	salinomycin	75-86	TNF receptor superfamily member 10b	Homo sapiens	0-8
24740347-6	2014	TRAIL-R2 upmodulation was required for mediating the stimulatory effect of salinomycin on TRAIL-mediated apoptosis, since it was abrogated by siRNA-mediated TRAIL-R2 knockdown.	salinomycin	75-86	TNF receptor superfamily member 10b	Homo sapiens	157-165
24535016-10	2014	Combined treatment of ZD55-TRAIL and MG132 (a proteasome inhibitor) robustly increased the expression of death receptor 5 (DR5), which enhanced the apoptosis response without significant toxicity to normal liver cells.	zd55	22-26	TNF receptor superfamily member 10b	Homo sapiens	105-121
24639349-8	2014	CTL resistance was due to DR5 downregulation and an inverted ratio of pro- to antiapoptotic molecules, both of which were reversed by the histone deacetylase inhibitor suberoylanilide hydroxanic acid.	suberoylanilide hydroxanic acid	168-199	TNF receptor superfamily member 10b	Homo sapiens	26-29
24535016-10	2014	Combined treatment of ZD55-TRAIL and MG132 (a proteasome inhibitor) robustly increased the expression of death receptor 5 (DR5), which enhanced the apoptosis response without significant toxicity to normal liver cells.	zd55	22-26	TNF receptor superfamily member 10b	Homo sapiens	123-126
24535016-10	2014	Combined treatment of ZD55-TRAIL and MG132 (a proteasome inhibitor) robustly increased the expression of death receptor 5 (DR5), which enhanced the apoptosis response without significant toxicity to normal liver cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	TNF receptor superfamily member 10b	Homo sapiens	105-121
24535016-10	2014	Combined treatment of ZD55-TRAIL and MG132 (a proteasome inhibitor) robustly increased the expression of death receptor 5 (DR5), which enhanced the apoptosis response without significant toxicity to normal liver cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	TNF receptor superfamily member 10b	Homo sapiens	123-126
24616705-5	2014	To determine the roles of DR5 and sensory cilia, we used dopamine to non-selectively and fenoldopam to selectively activate ciliary DR5.	Fenoldopam	89-99	TNF receptor superfamily member 10b	Homo sapiens	132-135
24286513-7	2014	The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin.	Acetylcarnitine	4-22	TNF receptor superfamily member 10b	Homo sapiens	110-119
24286513-7	2014	The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin.	Cisplatin	23-32	TNF receptor superfamily member 10b	Homo sapiens	110-119
24286513-7	2014	The acetyl-L-carnitine-cisplatin combination caused reduced expression of genes Casp8, Fas, Casp1, Tnfrsf11b, Tnfrsf10b induced by cisplatin.	Cisplatin	131-140	TNF receptor superfamily member 10b	Homo sapiens	110-119
24276615-2	2014	In the present study, we showed that co-treatment with troglitazone (TGZ), a synthetic ligand of peroxisome proliferator-activated receptor gamma (PPARgamma), and TRAIL synergistically induced apoptosis through DR5 upregulation in human colon cancer DLD-1 cells.	Troglitazone	55-67	TNF receptor superfamily member 10b	Homo sapiens	211-214
24276615-2	2014	In the present study, we showed that co-treatment with troglitazone (TGZ), a synthetic ligand of peroxisome proliferator-activated receptor gamma (PPARgamma), and TRAIL synergistically induced apoptosis through DR5 upregulation in human colon cancer DLD-1 cells.	Troglitazone	69-72	TNF receptor superfamily member 10b	Homo sapiens	211-214
24045365-0	2014	Digitoxin sensitizes glioma cells to TRAIL-mediated apoptosis by upregulation of death receptor 5 and downregulation of survivin.	Digitoxin	0-9	TNF receptor superfamily member 10b	Homo sapiens	81-97
24270523-7	2014	Co-treatment with MESC and an ERK inhibitor (PD98059) significantly increased the expression of DR5 to induce apoptosis in MC-3 cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	45-52	TNF receptor superfamily member 10b	Homo sapiens	96-99
24270523-7	2014	Co-treatment with MESC and an ERK inhibitor (PD98059) significantly increased the expression of DR5 to induce apoptosis in MC-3 cells.	mc-3	123-127	TNF receptor superfamily member 10b	Homo sapiens	96-99
24387758-0	2014	Parthenolide induces apoptosis via TNFRSF10B and PMAIP1 pathways in human lung cancer cells.	parthenolide	0-12	TNF receptor superfamily member 10b	Homo sapiens	35-44
24387758-13	2014	CONCLUSION: We showed that parthenolide not only triggered extrinsic apoptosis by up-regulating TNFRSF10B and down-regulating CFLAR, but also induced intrinsic apoptosis through increasing the expression of PMAIP1 and decreasing the level of MCL1 in NSCLC cells.	parthenolide	27-39	TNF receptor superfamily member 10b	Homo sapiens	96-105
24270523-0	2014	Extracellular signal-regulated kinase inhibition is required for methanol extract of Smilax china L.-induced apoptosis through death receptor 5 in human oral mucoepidermoid carcinoma cells.	Methanol	65-73	TNF receptor superfamily member 10b	Homo sapiens	127-143
24436439-8	2014	We demonstrated that TMZ effectively increased the sensitivity to TRAIL-induced apoptosis via extracellular signal-regulated kinase-mediated upregulation of the death receptor 5 and downregulation of antiapoptotic proteins, such as X-linked inhibitor of apoptosis protein and cellular FLICE-inhibitory protein.	Temozolomide	21-24	TNF receptor superfamily member 10b	Homo sapiens	161-177
24045365-7	2014	We demonstrate that inactivation of survivin and death receptor 5 expression by DT is sufficient to restore TRAIL sensitivity in resistant glioma cells.	Digitoxin	80-82	TNF receptor superfamily member 10b	Homo sapiens	49-65
24734951-5	2014	Increasing expressions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor 5 (DR5) were found in 2"-hydroxyflavanone-treated cells.	2'-hydroxyflavanone	131-150	TNF receptor superfamily member 10b	Homo sapiens	94-110
25292102-6	2014	In addition, inhibition of IDO activity by the IDO inhibitor 1-MT or tryptophan significantly reduced IFN-gamma-induced apoptosis and death receptor 5 (DR5) expression, which suggests that IDO enzymatic activity plays an important role in the anti-NSCLC cancer effect of IFN-gamma.	Tryptophan	69-79	TNF receptor superfamily member 10b	Homo sapiens	134-150
25292102-6	2014	In addition, inhibition of IDO activity by the IDO inhibitor 1-MT or tryptophan significantly reduced IFN-gamma-induced apoptosis and death receptor 5 (DR5) expression, which suggests that IDO enzymatic activity plays an important role in the anti-NSCLC cancer effect of IFN-gamma.	Tryptophan	69-79	TNF receptor superfamily member 10b	Homo sapiens	152-155
24734951-5	2014	Increasing expressions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor 5 (DR5) were found in 2"-hydroxyflavanone-treated cells.	2'-hydroxyflavanone	131-150	TNF receptor superfamily member 10b	Homo sapiens	112-115
24287697-0	2013	Identification of DR5 as a critical, NF-kappaB-regulated mediator of Smac-induced apoptosis.	smac	69-73	TNF receptor superfamily member 10b	Homo sapiens	18-21
24008361-2	2013	We have previously observed that the saturated free fatty acids (FFAs) induce hepatocyte apoptosis in part via a death receptor 5 (DR5)-mediated signaling pathway.	saturated free fatty acids	37-63	TNF receptor superfamily member 10b	Homo sapiens	131-134
24136147-9	2013	Addition of the chemotherapeutic drug cisplatin to the combination further increased p53 and DR5 levels and rhTRAIL- and D269H/E195R-induced apoptosis.	Cisplatin	38-47	TNF receptor superfamily member 10b	Homo sapiens	93-96
24136147-12	2013	Addition of DNA-damaging agents such as cisplatin further enhances DR5-mediated apoptosis.	Cisplatin	40-49	TNF receptor superfamily member 10b	Homo sapiens	67-70
24008361-2	2013	We have previously observed that the saturated free fatty acids (FFAs) induce hepatocyte apoptosis in part via a death receptor 5 (DR5)-mediated signaling pathway.	saturated free fatty acids	37-63	TNF receptor superfamily member 10b	Homo sapiens	113-129
24002210-5	2013	As detected by western blot analysis and real-time RT-PCR, ibuprofen upregulated the expression of death receptor 5 (DR5), a TRAIL receptor.	Ibuprofen	59-68	TNF receptor superfamily member 10b	Homo sapiens	99-115
24045184-7	2013	(111)In-labeled CS-1008 was specifically taken up in mice bearing COLO 205 and WiDr tumors with prolonged tumor retention (26.25 +- 2.85%ID/g vs. 12.20 +- 2.24 at 168 hours post injection; n = 5, SD), and uptake correlated both with DR5 expression on tumor cells and antitumor activity.	Cesium	16-18	TNF receptor superfamily member 10b	Homo sapiens	233-236
23846485-6	2013	Curcumin-induced production of reactive oxygen species did not affect total expression of DR5 but it enhanced mobilization of DR5 to the plasma membrane.	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	126-129
23846485-6	2013	Curcumin-induced production of reactive oxygen species did not affect total expression of DR5 but it enhanced mobilization of DR5 to the plasma membrane.	Reactive Oxygen Species	31-54	TNF receptor superfamily member 10b	Homo sapiens	126-129
24078627-4	2013	The limonoid induced expression of death receptor (DR) 5 and DR4 but did not affect expression of decoy receptors in cancer cells.	Limonins	4-12	TNF receptor superfamily member 10b	Homo sapiens	35-56
24078627-7	2013	The CHOP binding site on the DR5 gene was required for induction of DR5 by azadirone.	azadirone	75-84	TNF receptor superfamily member 10b	Homo sapiens	29-32
24078627-7	2013	The CHOP binding site on the DR5 gene was required for induction of DR5 by azadirone.	azadirone	75-84	TNF receptor superfamily member 10b	Homo sapiens	68-71
24078627-12	2013	Overall, this study indicates that azadirone can sensitize cancer cells to TRAIL through ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins, and up-regulation of proapoptotic proteins.	azadirone	35-44	TNF receptor superfamily member 10b	Homo sapiens	128-131
24078627-12	2013	Overall, this study indicates that azadirone can sensitize cancer cells to TRAIL through ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins, and up-regulation of proapoptotic proteins.	Reactive Oxygen Species	89-92	TNF receptor superfamily member 10b	Homo sapiens	128-131
24002210-5	2013	As detected by western blot analysis and real-time RT-PCR, ibuprofen upregulated the expression of death receptor 5 (DR5), a TRAIL receptor.	Ibuprofen	59-68	TNF receptor superfamily member 10b	Homo sapiens	117-120
24002210-6	2013	TRAIL-induced apoptosis enhanced by ibuprofen was effectively decreased by a caspase inhibitor and dominant-negative DR5.	Ibuprofen	36-45	TNF receptor superfamily member 10b	Homo sapiens	117-120
23732517-5	2013	Knockdown of DR5 and DR4 significantly (&gt;85%) reduced the sensitizing effect of the AR inhibitor fidarestat on TRAIL-induced apoptosis.	fidarestat	100-110	TNF receptor superfamily member 10b	Homo sapiens	13-16
23700228-8	2013	Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis.	Reactive Oxygen Species	71-94	TNF receptor superfamily member 10b	Homo sapiens	28-31
24002210-0	2013	Ibuprofen enhances TRAIL-induced apoptosis through DR5 upregulation.	Ibuprofen	0-9	TNF receptor superfamily member 10b	Homo sapiens	51-54
23700228-8	2013	Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis.	Reactive Oxygen Species	96-99	TNF receptor superfamily member 10b	Homo sapiens	28-31
23700228-8	2013	Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis.	Acetylcysteine	105-121	TNF receptor superfamily member 10b	Homo sapiens	28-31
23700228-8	2013	Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis.	Acetylcysteine	105-121	TNF receptor superfamily member 10b	Homo sapiens	147-150
23857473-4	2013	Moreover, TRAIL receptors, such as DR4 and DR5 were significantly upregulated by CAPE treatment, and both DR4/Fc and DR5/Fc chimera markedly abrogated apoptosis induced by CAPE and TRAIL, demonstrating the critical role of these death receptors in combination-induced apoptosis.	caffeic acid phenethyl ester	81-85	TNF receptor superfamily member 10b	Homo sapiens	43-46
23857473-8	2013	In contrast, JNK-specific inhibition, by SP600125, triggered upregulation of DR4 and DR5, and sensitized SK-Hep1 cells to TRAIL, indicating that the CAPE-induced suppression of JNK may contribute to the sensitizing effect of CAPE through the upregulation of death receptors.	caffeic acid phenethyl ester	149-153	TNF receptor superfamily member 10b	Homo sapiens	85-88
23504627-5	2013	The central role of the TRAIL signaling pathway was further supported by an increased expression of TRAIL-R2 on DOX-treated tumor cells and by downregulation of cellular FLICE inhibitory protein, the inhibitors of death receptor-mediated apoptosis.	Doxorubicin	112-115	TNF receptor superfamily member 10b	Homo sapiens	100-108
23857473-4	2013	Moreover, TRAIL receptors, such as DR4 and DR5 were significantly upregulated by CAPE treatment, and both DR4/Fc and DR5/Fc chimera markedly abrogated apoptosis induced by CAPE and TRAIL, demonstrating the critical role of these death receptors in combination-induced apoptosis.	caffeic acid phenethyl ester	172-176	TNF receptor superfamily member 10b	Homo sapiens	43-46
23857473-4	2013	Moreover, TRAIL receptors, such as DR4 and DR5 were significantly upregulated by CAPE treatment, and both DR4/Fc and DR5/Fc chimera markedly abrogated apoptosis induced by CAPE and TRAIL, demonstrating the critical role of these death receptors in combination-induced apoptosis.	caffeic acid phenethyl ester	172-176	TNF receptor superfamily member 10b	Homo sapiens	117-120
23912708-8	2013	Pretreatment with cisplatin significantly enhanced the expression of DR5.	Cisplatin	18-27	TNF receptor superfamily member 10b	Homo sapiens	69-72
23754197-4	2013	We demonstrated that Asp induced cell death through the activation of TRAIL DR4/DR5 death receptors leading to the activation of caspase-8 and caspase-3 and to cell apoptosis.	Aspartic Acid	21-24	TNF receptor superfamily member 10b	Homo sapiens	80-83
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	polyether antibiotics	21-42	TNF receptor superfamily member 10b	Homo sapiens	187-190
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	salinomycin	52-63	TNF receptor superfamily member 10b	Homo sapiens	187-190
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	Nigericin	65-74	TNF receptor superfamily member 10b	Homo sapiens	187-190
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	narasin	76-83	TNF receptor superfamily member 10b	Homo sapiens	187-190
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	Lasalocid	88-99	TNF receptor superfamily member 10b	Homo sapiens	187-190
23994633-6	2013	The results indicated that combination of MG132 and TRAIL had the effect of up-regulating expression of DR5, caspase-3, caspase-8 and p27(kip1), down-regulating expression of MMP-9 and inducing apoptosis as well as suppressing the ability of invasion of OS732 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	TNF receptor superfamily member 10b	Homo sapiens	104-107
23554101-0	2013	The chalcone 2"-hydroxy-4",5"-dimethoxychalcone activates death receptor 5 pathway and leads to apoptosis in human nonsmall cell lung cancer cells.	Chalcone	4-12	TNF receptor superfamily member 10b	Homo sapiens	58-74
23605004-0	2013	Induction of death receptor 5 expression in tumor vasculature by perifosine restores the vascular disruption activity of TRAIL-expressing CD34(+) cells.	perifosine	65-75	TNF receptor superfamily member 10b	Homo sapiens	13-29
23428290-0	2013	Carbenoxolone enhances TRAIL-induced apoptosis through the upregulation of death receptor 5 and inhibition of gap junction intercellular communication in human glioma.	Carbenoxolone	0-13	TNF receptor superfamily member 10b	Homo sapiens	75-91
23428290-7	2013	CBX enhanced TRAIL-induced apoptosis through upregulation of death receptor 5, blockade of GJ intercellular communication, and downregulation of connexin 43.	Carbenoxolone	0-3	TNF receptor superfamily member 10b	Homo sapiens	61-77
23435998-0	2013	Upregulation of DR5 receptor by the diaminothiazole DAT1 [4-amino-5-benzoyl-2-(4-methoxy phenyl amino) thiazole] triggers an independent extrinsic pathway of apoptosis in colon cancer cells with compromised pro and antiapoptotic proteins.	Thiazole-2,4-diamine	36-51	TNF receptor superfamily member 10b	Homo sapiens	16-19
23435998-0	2013	Upregulation of DR5 receptor by the diaminothiazole DAT1 [4-amino-5-benzoyl-2-(4-methoxy phenyl amino) thiazole] triggers an independent extrinsic pathway of apoptosis in colon cancer cells with compromised pro and antiapoptotic proteins.	4-amino-5-benzoyl-2-(4-methoxyphenylamino)thiazole	58-111	TNF receptor superfamily member 10b	Homo sapiens	16-19
23620163-6	2013	Notably, while SAHA induced upregulation of death receptor 4 (DR4) and DR5, HHT upregulated tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression in a dose-dependent manner.	Vorinostat	15-19	TNF receptor superfamily member 10b	Homo sapiens	71-74
23554101-0	2013	The chalcone 2"-hydroxy-4",5"-dimethoxychalcone activates death receptor 5 pathway and leads to apoptosis in human nonsmall cell lung cancer cells.	2'-hydroxy-4',5'-dimethoxychalcone	13-47	TNF receptor superfamily member 10b	Homo sapiens	58-74
23554101-6	2013	In conclusion, HDMC induces apoptosis in human nonsmall cell lung cancer cells via activation of DR5 signaling pathway, and ROS-mediated ATF4-CHOP axis is involved in the process.	2'-hydroxy-4',5'-dimethoxychalcone	15-19	TNF receptor superfamily member 10b	Homo sapiens	97-100
23499682-6	2013	Indeed, treatment with 2-DG resulted in upregulation of TRAIL receptor 2 (TRAIL-R2), downregulation of cIAP1 and XIAP, and reduction in RIP1.	Deoxyglucose	23-27	TNF receptor superfamily member 10b	Homo sapiens	56-72
23523585-7	2013	HMJ-38-influenced HUVECs were performed by determining the oxidative stress (ROS production) and ATM/p53-modulated Fas and DR4/DR5 signals that were examined by flow cytometry, Western blotting, siRNA and real-time RT-PCR analyses, respectively.	2-(3'-methoxyphenyl)-6-pyrrolidinyl-4-quinazolinone	0-6	TNF receptor superfamily member 10b	Homo sapiens	127-130
23696862-6	2013	Additionally, DTCD stimulated extracellular signal-regulated kinase (ERK) activation, while the ERK inhibitor PD98059 blocked DTCD-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	dtcd	126-130	TNF receptor superfamily member 10b	Homo sapiens	139-142
23696862-6	2013	Additionally, DTCD stimulated extracellular signal-regulated kinase (ERK) activation, while the ERK inhibitor PD98059 blocked DTCD-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	dtcd	126-130	TNF receptor superfamily member 10b	Homo sapiens	191-194
23608376-0	2013	Casticin induces caspase-mediated apoptosis via activation of mitochondrial pathway and upregulation of DR5 in human lung cancer cells.	casticin	0-8	TNF receptor superfamily member 10b	Homo sapiens	104-107
23608376-1	2013	OBJECTIVE: To assess if casticin induces caspase-mediated apoptosis via activation of mitochondrial pathway and upregulation of DR5 in human lung cancer cells.	casticin	24-32	TNF receptor superfamily member 10b	Homo sapiens	128-131
23608376-12	2013	In H157 cell line, casticin increased expression of DR5 at protein levels but not affect the expression of DR4.	casticin	19-27	TNF receptor superfamily member 10b	Homo sapiens	52-55
23608376-13	2013	The pretreatment with DR5/Fc chimera protein effectively attenuated casticin-induced apoptosis in H157 cells.	casticin	68-76	TNF receptor superfamily member 10b	Homo sapiens	22-25
23608376-15	2013	CONCLUSIONS: Our results demonstrate that casticin induces caspase-mediated apoptosis via activation of mitochondrial pathway and upregulation of DR5 in human lung cancer cells.	casticin	42-50	TNF receptor superfamily member 10b	Homo sapiens	146-149
23696862-4	2013	In vitro, DTCD enhanced TRAIL-induced cytotoxicity in human ovarian cancer cells through up-regulation of DR5.	dtcd	10-14	TNF receptor superfamily member 10b	Homo sapiens	106-109
23696862-5	2013	Luciferase analysis and CHIP assays showed that DTCD increased DR5 promoter activity via Sp1 activation.	dtcd	48-52	TNF receptor superfamily member 10b	Homo sapiens	63-66
23696862-6	2013	Additionally, DTCD stimulated extracellular signal-regulated kinase (ERK) activation, while the ERK inhibitor PD98059 blocked DTCD-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	110-117	TNF receptor superfamily member 10b	Homo sapiens	139-142
23696862-6	2013	Additionally, DTCD stimulated extracellular signal-regulated kinase (ERK) activation, while the ERK inhibitor PD98059 blocked DTCD-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	110-117	TNF receptor superfamily member 10b	Homo sapiens	191-194
23396090-10	2013	In contrast, liposomal CDDP induced expression of genes from DNA damage pathways and several genes of the extrinsic pathway of apoptosis (TNFRSF10B-DR5, CD70-TNFSF7).	Cisplatin	23-27	TNF receptor superfamily member 10b	Homo sapiens	138-151
23499682-6	2013	Indeed, treatment with 2-DG resulted in upregulation of TRAIL receptor 2 (TRAIL-R2), downregulation of cIAP1 and XIAP, and reduction in RIP1.	Deoxyglucose	23-27	TNF receptor superfamily member 10b	Homo sapiens	74-82
23001792-5	2013	This increased apoptosis in human colon cancer cells after RA or DZNep treatment was associated with a ~2.5-fold increase in TNFRSF10B (DR5) transcript levels and a 42% reduction in the H3K27me3 epigenetic mark at the TNFRSF10B promoter after DZNep addition.	3-deazaneplanocin	65-70	TNF receptor superfamily member 10b	Homo sapiens	125-134
23564786-0	2013	Salinomycin induces apoptosis via death receptor-5 up-regulation in cisplatin-resistant ovarian cancer cells.	salinomycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	34-50
23564786-0	2013	Salinomycin induces apoptosis via death receptor-5 up-regulation in cisplatin-resistant ovarian cancer cells.	Cisplatin	68-77	TNF receptor superfamily member 10b	Homo sapiens	34-50
23564786-9	2013	Salinomycin increased the expression of death receptor-5 (DR5), caspase-8 and Fas-associated protein with death domain (FADD).	salinomycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	40-56
23564786-9	2013	Salinomycin increased the expression of death receptor-5 (DR5), caspase-8 and Fas-associated protein with death domain (FADD).	salinomycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	58-61
23564786-12	2013	CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent.	salinomycin	141-152	TNF receptor superfamily member 10b	Homo sapiens	96-99
23564786-12	2013	CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent.	Cisplatin	161-170	TNF receptor superfamily member 10b	Homo sapiens	96-99
23564786-12	2013	CONCLUSION: These findings provide important insights regarding the activation of caspase-8 and DR5, to our knowledge, for the first time in salinomycin-treated cisplatin-resistant ovarian cancer and demonstrate that salinomycin could be a prominent anticancer agent.	salinomycin	217-228	TNF receptor superfamily member 10b	Homo sapiens	96-99
23378009-4	2013	We observed that LiCl significantly enhanced A549 cells apoptosis through up-regulation of death receptors DR4 and DR5 and activation of caspase cascades.	Lithium Chloride	17-21	TNF receptor superfamily member 10b	Homo sapiens	115-118
23001792-5	2013	This increased apoptosis in human colon cancer cells after RA or DZNep treatment was associated with a ~2.5-fold increase in TNFRSF10B (DR5) transcript levels and a 42% reduction in the H3K27me3 epigenetic mark at the TNFRSF10B promoter after DZNep addition.	3-deazaneplanocin	65-70	TNF receptor superfamily member 10b	Homo sapiens	136-139
23001792-5	2013	This increased apoptosis in human colon cancer cells after RA or DZNep treatment was associated with a ~2.5-fold increase in TNFRSF10B (DR5) transcript levels and a 42% reduction in the H3K27me3 epigenetic mark at the TNFRSF10B promoter after DZNep addition.	3-deazaneplanocin	65-70	TNF receptor superfamily member 10b	Homo sapiens	218-227
23644112-4	2013	KB cells treated with 5 mmol/L 2-DG with or without TRAIL for 0, 6, 16, or 24 h were examined with Western blotting for protein expressions of death receptor 5 (DR5) and caspase-3.	Deoxyglucose	31-35	TNF receptor superfamily member 10b	Homo sapiens	143-159
23644112-4	2013	KB cells treated with 5 mmol/L 2-DG with or without TRAIL for 0, 6, 16, or 24 h were examined with Western blotting for protein expressions of death receptor 5 (DR5) and caspase-3.	Deoxyglucose	31-35	TNF receptor superfamily member 10b	Homo sapiens	161-164
23644112-7	2013	2-DG treatment markedly up-regulated DR5 and caspase-3 expression and enhanced the inhibitory effect of TRAIL on cell colony formation.	Deoxyglucose	0-4	TNF receptor superfamily member 10b	Homo sapiens	37-40
23644112-8	2013	CONCLUSION: 2-DG sensitizes oral cancer cells to TRAIL- induced apoptosis by up-regulating DR5 and caspase-3 expressions.	Deoxyglucose	12-16	TNF receptor superfamily member 10b	Homo sapiens	91-94
22665066-4	2013	Second-generation tyrosine kinase inhibitors (dasatinib and nilotinib) and short hairpin RNA against bcr-abl also downregulated DR4 and DR5 expression in Ph(+) leukemia cells, and transfection of bcr-abl into a Ph(-) leukemia cell line induced DR4 and DR5 expression, which was abrogated by imatinib treatment.	Dasatinib	46-55	TNF receptor superfamily member 10b	Homo sapiens	136-139
21803611-10	2013	The isoflavone sensitized the TRAIL-resistant LNCaP cells through the inhibition of transcription factor NF-kappaB(p65) activity, increased the expression of the death receptor TRAIL-R2 (DR5), and disrupted mitochondrial membrane potential (DeltaPsim).	Isoflavones	4-14	TNF receptor superfamily member 10b	Homo sapiens	177-185
21803611-10	2013	The isoflavone sensitized the TRAIL-resistant LNCaP cells through the inhibition of transcription factor NF-kappaB(p65) activity, increased the expression of the death receptor TRAIL-R2 (DR5), and disrupted mitochondrial membrane potential (DeltaPsim).	Isoflavones	4-14	TNF receptor superfamily member 10b	Homo sapiens	187-190
22665066-3	2013	Here we demonstrate that imatinib specifically downregulated DR4 and DR5 expression in cell lines and clinical samples of Ph(+) leukemia.	Imatinib Mesylate	25-33	TNF receptor superfamily member 10b	Homo sapiens	69-72
22665066-4	2013	Second-generation tyrosine kinase inhibitors (dasatinib and nilotinib) and short hairpin RNA against bcr-abl also downregulated DR4 and DR5 expression in Ph(+) leukemia cells, and transfection of bcr-abl into a Ph(-) leukemia cell line induced DR4 and DR5 expression, which was abrogated by imatinib treatment.	nilotinib	60-69	TNF receptor superfamily member 10b	Homo sapiens	136-139
23082969-0	2013	(E)-2,4-bis(p-hydroxyphenyl)-2-butenal has an antiproliferative effect on NSCLC cells induced by p38 MAPK-mediated suppression of NF-kappaB and up-regulation of TNFRSF10B (DR5).	SCHEMBL6784264	0-38	TNF receptor superfamily member 10b	Homo sapiens	161-170
23352978-7	2013	Both I3C and EGCG significantly increased caspase-3 activity, DNA fragmentation percentage, DR4 and DR5 protein expression as well as decreased Bcl-2 protein expression when compared to control groups.	epigallocatechin gallate	13-17	TNF receptor superfamily member 10b	Homo sapiens	100-103
23082969-0	2013	(E)-2,4-bis(p-hydroxyphenyl)-2-butenal has an antiproliferative effect on NSCLC cells induced by p38 MAPK-mediated suppression of NF-kappaB and up-regulation of TNFRSF10B (DR5).	SCHEMBL6784264	0-38	TNF receptor superfamily member 10b	Homo sapiens	172-175
23082969-9	2013	Even though all the MAPKs were activated, only pretreatment with a p38 MAPK inhibitor reversed (E)-2,4-bis(p-hydroxyphenyl)-2-butenal-induced cell growth inhibition, increase in cleaved caspase-3, -9 and TNFRSF10B expression, and NF-kappaB inactivation.	SCHEMBL6784264	95-133	TNF receptor superfamily member 10b	Homo sapiens	204-213
23082969-8	2013	Of the death receptors activated, only TNFRSF10B knock down with siRNA reversed the effect of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal.	SCHEMBL6784264	94-132	TNF receptor superfamily member 10b	Homo sapiens	39-48
23082969-10	2013	CONCLUSIONS AND IMPLICATIONS: (E)-2,4-bis(p-hydroxyphenyl)-2-butenal induces apoptosis in NSCLC cells by p38 MAPK-mediated suppression of NF-kappaB and activation of TNFRSF10B, which then activates the caspase-3 and caspase-9 pathways.	SCHEMBL6784264	30-68	TNF receptor superfamily member 10b	Homo sapiens	166-175
22978563-0	2013	Sorafenib and its derivative SC-49 sensitize hepatocellular carcinoma cells to CS-1008, a humanized anti-TNFRSF10B (DR5) antibody.	Sorafenib	0-9	TNF receptor superfamily member 10b	Homo sapiens	105-114
23291741-10	2013	The expression levels of DR5 and p-AKT proteins were increased             and decreased, respectively, as a result of the effects of sphingoid bases from             sea cucumber.	sphingoid bases	134-149	TNF receptor superfamily member 10b	Homo sapiens	25-28
23291741-11	2013	The results indicate that sphingoid bases from sea cucumber induce             apoptosis in HepG2 cells through upregulation of DR5, Bax, GADD45 and PPARgamma and             downregulation of p-AKT.	sphingoid bases	26-41	TNF receptor superfamily member 10b	Homo sapiens	128-131
23261452-0	2013	Lipoxygenase inhibitor MK886 potentiates TRAIL-induced apoptosis through CHOP- and p38 MAPK-mediated up-regulation of death receptor 5 in malignant glioma.	MK-886	23-28	TNF receptor superfamily member 10b	Homo sapiens	118-134
23261452-5	2013	We found that MK886 sensitized glioma cells to TRAIL-induced apoptosis by upregulating the death receptor 5 (DR5) and that specific knockdown of DR5 attenuated cell death.	MK-886	14-19	TNF receptor superfamily member 10b	Homo sapiens	91-107
23261452-5	2013	We found that MK886 sensitized glioma cells to TRAIL-induced apoptosis by upregulating the death receptor 5 (DR5) and that specific knockdown of DR5 attenuated cell death.	MK-886	14-19	TNF receptor superfamily member 10b	Homo sapiens	109-112
23261452-6	2013	The mechanisms underlying this sensitization involved activation of the MK886-induced p38 mitogen-activated protein kinase (MAPK) pathway and subsequent DR5 overexpression.	MK-886	72-77	TNF receptor superfamily member 10b	Homo sapiens	153-156
23261452-8	2013	Taken together, our findings indicate that the increased expression of DR5 in a p38 MAPK-dependent manner plays an important role in the sensitization of MK886 to TRAIL-induced apoptosis.	MK-886	154-159	TNF receptor superfamily member 10b	Homo sapiens	71-74
23291741-0	2013	Sphingoid bases from sea cucumber induce apoptosis in human hepatoma             HepG2 cells through p-AKT and DR5.	Sphingosine	0-9	TNF receptor superfamily member 10b	Homo sapiens	111-114
23429289-6	2013	Consequently, when we generated MSCs that secreted TRAIL-R2-specific variants of soluble TRAIL (sTRAIL), we found that such engineered MSCs, labeled MSC.sTRAIL(DR5), had enhanced antitumor activity in combination with 5-FU when compared with MSC.sTRAIL.	Fluorouracil	218-222	TNF receptor superfamily member 10b	Homo sapiens	51-59
23429289-6	2013	Consequently, when we generated MSCs that secreted TRAIL-R2-specific variants of soluble TRAIL (sTRAIL), we found that such engineered MSCs, labeled MSC.sTRAIL(DR5), had enhanced antitumor activity in combination with 5-FU when compared with MSC.sTRAIL.	Fluorouracil	218-222	TNF receptor superfamily member 10b	Homo sapiens	160-163
22978563-0	2013	Sorafenib and its derivative SC-49 sensitize hepatocellular carcinoma cells to CS-1008, a humanized anti-TNFRSF10B (DR5) antibody.	Sorafenib	0-9	TNF receptor superfamily member 10b	Homo sapiens	116-119
22978563-2	2013	Here, we report that sorafenib and SC-49 sensitize HCC cells to CS-1008, a novel anti-human death receptor 5 (TNFRSF10B) antibody.	Sorafenib	21-30	TNF receptor superfamily member 10b	Homo sapiens	92-108
22978563-2	2013	Here, we report that sorafenib and SC-49 sensitize HCC cells to CS-1008, a novel anti-human death receptor 5 (TNFRSF10B) antibody.	Sorafenib	21-30	TNF receptor superfamily member 10b	Homo sapiens	110-119
23258590-9	2013	Further studies showed that nystatin partially prevented lipid raft aggregation and DR4 and DR5 clustering and reduced apoptosis in H460 cells again.	Nystatin	28-36	TNF receptor superfamily member 10b	Homo sapiens	92-95
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	43-71	TNF receptor superfamily member 10b	Homo sapiens	116-119
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	43-71	TNF receptor superfamily member 10b	Homo sapiens	182-185
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	73-77	TNF receptor superfamily member 10b	Homo sapiens	116-119
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	73-77	TNF receptor superfamily member 10b	Homo sapiens	182-185
22960596-0	2013	Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway.	Simvastatin	0-11	TNF receptor superfamily member 10b	Homo sapiens	119-122
22960596-0	2013	Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway.	Mevalonic Acid	26-36	TNF receptor superfamily member 10b	Homo sapiens	119-122
22960596-1	2013	Simvastatin (SVA) was shown to up-regulate expression of death receptor-5 (DR5), CCAAT/enhancer binding protein homologous protein (CHOP) and phosphorylated c-Jun N-terminal kinase (pJNK) in human breast cancer cell lines.	Simvastatin	0-11	TNF receptor superfamily member 10b	Homo sapiens	57-73
22960596-1	2013	Simvastatin (SVA) was shown to up-regulate expression of death receptor-5 (DR5), CCAAT/enhancer binding protein homologous protein (CHOP) and phosphorylated c-Jun N-terminal kinase (pJNK) in human breast cancer cell lines.	Simvastatin	0-11	TNF receptor superfamily member 10b	Homo sapiens	75-78
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	Mevalonic Acid	29-39	TNF receptor superfamily member 10b	Homo sapiens	116-119
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	Mevalonic Acid	29-39	TNF receptor superfamily member 10b	Homo sapiens	182-185
23348585-0	2013	Salirasib sensitizes hepatocarcinoma cells to TRAIL-induced apoptosis through DR5 and survivin-dependent mechanisms.	farnesylthiosalicylic acid	0-9	TNF receptor superfamily member 10b	Homo sapiens	78-81
23135489-0	2013	Casticin, a flavonoid, potentiates TRAIL-induced apoptosis through modulation             of anti-apoptotic proteins and death receptor 5 in colon cancer cells.	casticin	0-8	TNF receptor superfamily member 10b	Homo sapiens	121-137
23135489-3	2013	Casticin downregulated             cell survival proteins including Bcl-xL, Bcl-2, survivin, XIAP and cFLIP, and             induced death receptor 5 (DR5), but had no effect on DR4 and decoy receptors (DcR1             or DcR2).	casticin	0-8	TNF receptor superfamily member 10b	Homo sapiens	133-149
23135489-3	2013	Casticin downregulated             cell survival proteins including Bcl-xL, Bcl-2, survivin, XIAP and cFLIP, and             induced death receptor 5 (DR5), but had no effect on DR4 and decoy receptors (DcR1             or DcR2).	casticin	0-8	TNF receptor superfamily member 10b	Homo sapiens	151-154
23135489-4	2013	Deletion of DR5 by siRNA significantly reduced the apoptosis induced             by TRAIL and casticin.	casticin	94-102	TNF receptor superfamily member 10b	Homo sapiens	12-15
23135489-6	2013	Collectively, the present study showed             that casticin potentiates TRAIL-induced apoptosis through downregulation of cell             survival proteins and induction of DR5 mediated by ROS.	casticin	56-64	TNF receptor superfamily member 10b	Homo sapiens	179-182
23135489-6	2013	Collectively, the present study showed             that casticin potentiates TRAIL-induced apoptosis through downregulation of cell             survival proteins and induction of DR5 mediated by ROS.	Reactive Oxygen Species	195-198	TNF receptor superfamily member 10b	Homo sapiens	179-182
23335397-0	2013	Oligomycin A enhances apoptotic effect of TRAIL through CHOP-mediated death receptor 5 expression.	oligomycin A	0-12	TNF receptor superfamily member 10b	Homo sapiens	70-86
23335397-6	2013	Collectively, our data suggest that OMA enhances apoptotic death of cervical cancer cells to TRAIL through upregulation of CHOP-mediated DR5 expression following ER-stress.	oligomycin A	36-39	TNF receptor superfamily member 10b	Homo sapiens	137-140
22982206-0	2013	Verrucarin A sensitizes TRAIL-induced apoptosis via the upregulation of DR5 in an eIF2alpha/CHOP-dependent manner.	muconomycin A	0-12	TNF receptor superfamily member 10b	Homo sapiens	72-75
22982206-5	2013	We first found that VA induces a major molecule of ER stress, CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 induction and subsequently increases TRAIL-induced cleavage of caspases and PARP in TRAIL-resistant Hep3B cells.	muconomycin A	20-22	TNF receptor superfamily member 10b	Homo sapiens	129-132
22982206-10	2013	Therefore, VA-induced eIF2alpha phosphorylation seemed to be important for CHOP and DR5 upregulation and TRAIL-induced apoptosis.	muconomycin A	11-13	TNF receptor superfamily member 10b	Homo sapiens	84-87
22982206-12	2013	We concluded that VA triggers TRAIL-induced apoptosis by eIF2alpha/CHOP-dependent DR5 induction via ROS generation.	Reactive Oxygen Species	100-103	TNF receptor superfamily member 10b	Homo sapiens	82-85
23348585-9	2013	Furthermore, TRAIL-induced apoptosis in HCC cells pretreated with salirasib was dependent on activation of death receptor (DR) 5.	farnesylthiosalicylic acid	66-75	TNF receptor superfamily member 10b	Homo sapiens	107-128
23348585-10	2013	In conclusion, salirasib sensitizes hepatocarcinoma cells to TRAIL-induced apoptosis by a mechanism involving the DR5 receptor and survivin inhibition.	farnesylthiosalicylic acid	15-24	TNF receptor superfamily member 10b	Homo sapiens	114-117
24289635-7	2013	The general caspase inhibitor Z-VAD- FMK could inhibit the embelin-enhanced sensitivity of A549 cells to TRAILR2 mAb (75.97+-3.17%)(P&lt;0.05).	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	30-40	TNF receptor superfamily member 10b	Homo sapiens	105-112
24324958-6	2013	Our results showed that there were significant synergistic effects of low dose 5-Fu and TRAIL on TRAIL-resistant AGS cells, and this effect was supposed to be mediated by decreasing DcR2 expression and increasing DR5 expression.	Fluorouracil	79-83	TNF receptor superfamily member 10b	Homo sapiens	213-216
23065795-3	2012	siRNA knockdown of JNK, CHOP, or DR5 shows that gammaT-induced apoptosis is JNK/CHOP/DR5 signaling dependent, which is similar to gammaT3-mediated apoptotic signaling.	gamma-Tocopherol	48-54	TNF receptor superfamily member 10b	Homo sapiens	33-36
24377552-7	2013	Expression of DR4 and DR5 on the cell surfaces, and the apoptosis rate were increased after treatment by ATO alone or combined with bortezomib.	Arsenic Trioxide	105-108	TNF receptor superfamily member 10b	Homo sapiens	22-25
24377552-7	2013	Expression of DR4 and DR5 on the cell surfaces, and the apoptosis rate were increased after treatment by ATO alone or combined with bortezomib.	Bortezomib	132-142	TNF receptor superfamily member 10b	Homo sapiens	22-25
23255955-9	2013	In addition, PA increased the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling-related death receptor 5 (DR5), mediating caspase-8-involved extrinsic pathway.	pomolic acid	13-15	TNF receptor superfamily member 10b	Homo sapiens	145-161
23255955-9	2013	In addition, PA increased the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis signaling-related death receptor 5 (DR5), mediating caspase-8-involved extrinsic pathway.	pomolic acid	13-15	TNF receptor superfamily member 10b	Homo sapiens	163-166
23431365-3	2013	We and others have shown that several anticancer agents and flavonoids overcome resistance to Apo2L/TRAIL by upregulating death receptor 5 (DR5) in malignant tumor cells.	Flavonoids	60-70	TNF receptor superfamily member 10b	Homo sapiens	122-138
23431365-3	2013	We and others have shown that several anticancer agents and flavonoids overcome resistance to Apo2L/TRAIL by upregulating death receptor 5 (DR5) in malignant tumor cells.	Flavonoids	60-70	TNF receptor superfamily member 10b	Homo sapiens	140-143
23431365-5	2013	Here we show that the dietary flavonoid apigenin binds and inhibits adenine nucleotide translocase-2 (ANT2), resulting in enhancement of Apo2L/TRAIL-induced apoptosis by upregulation of DR5.	Flavonoids	30-39	TNF receptor superfamily member 10b	Homo sapiens	186-189
22923501-8	2012	The free radical scavenger Mn(III)tetrakis(4-benzoic acid)porphyrin chloride blocked ROS generation, DR5 up-regulation, caspase-8 activation, DNA damage, and apoptosis, which indicates a primary role for oxidative injury in lethality.	mn(iii)tetrakis(4-benzoic acid)porphyrin chloride	27-76	TNF receptor superfamily member 10b	Homo sapiens	101-104
23224239-9	2013	Inhibition of ERK1/2 by U0126 significantly decreased the apigenin/TRAIL-induced DR5 expression and apoptosis.	U 0126	24-29	TNF receptor superfamily member 10b	Homo sapiens	81-84
23536831-7	2013	Casticin dramatically upregulated DR5 receptor expression but had no effects on DR4 or decoy receptors.	casticin	0-8	TNF receptor superfamily member 10b	Homo sapiens	34-37
23536831-8	2013	Deletion of DR5 by siRNA significantly reduced the apoptosis induced by the co-application of TRAIL and casticin.	casticin	104-112	TNF receptor superfamily member 10b	Homo sapiens	12-15
23536831-9	2013	Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production.	casticin	172-180	TNF receptor superfamily member 10b	Homo sapiens	189-192
23536831-9	2013	Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production.	Reactive Oxygen Species	232-235	TNF receptor superfamily member 10b	Homo sapiens	189-192
23536831-11	2013	In addition, casticin also induced the expressions of DR5 protein in other gastric cancer cells (SGC-7901 and MGC-803).	casticin	13-21	TNF receptor superfamily member 10b	Homo sapiens	54-57
23536831-12	2013	CONCLUSION/SIGNIFICANCE: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway.	casticin	25-33	TNF receptor superfamily member 10b	Homo sapiens	144-147
23536831-12	2013	CONCLUSION/SIGNIFICANCE: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway.	Reactive Oxygen Species	181-184	TNF receptor superfamily member 10b	Homo sapiens	144-147
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	pyrazolanthrone	62-70	TNF receptor superfamily member 10b	Homo sapiens	194-197
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Reactive Oxygen Species	79-102	TNF receptor superfamily member 10b	Homo sapiens	194-197
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Reactive Oxygen Species	104-107	TNF receptor superfamily member 10b	Homo sapiens	194-197
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Acetylcysteine	119-135	TNF receptor superfamily member 10b	Homo sapiens	194-197
23065795-3	2012	siRNA knockdown of JNK, CHOP, or DR5 shows that gammaT-induced apoptosis is JNK/CHOP/DR5 signaling dependent, which is similar to gammaT3-mediated apoptotic signaling.	gamma-Tocopherol	48-54	TNF receptor superfamily member 10b	Homo sapiens	85-88
23065795-5	2012	Inhibition of de novo ceramide synthesis using chemical inhibitors blocked the ability of gammaT and gammaT3 to induce apoptosis as detected by Annexin V-FITC/PI assay and to activate JNK/CHOP/DR5 pro-apoptotic signaling thereby demonstrating the involvement of de novo ceramide synthesis in gammaT- and gammaT3-induced apoptosis.	Ceramides	22-30	TNF receptor superfamily member 10b	Homo sapiens	193-196
23065795-6	2012	CONCLUSION: Taken together, data show that both gammaT and gammaT3 induce apoptosis via de novo ceramide synthesis dependent activation of JNK/CHOP/DR5 pro-apoptotic signaling.	Ceramides	96-104	TNF receptor superfamily member 10b	Homo sapiens	148-151
23203129-11	2012	Chalcones enhance TRAIL-induced apoptosis in HeLa cells through increased expression of  TRAIL-R2.	Chalcones	0-9	TNF receptor superfamily member 10b	Homo sapiens	89-97
23203129-0	2012	Targeting death receptor TRAIL-R2 by chalcones for TRAIL-induced apoptosis in cancer cells.	Chalcones	37-46	TNF receptor superfamily member 10b	Homo sapiens	25-33
22922338-5	2012	Capsazepine induced death receptors (DRs) DR5 and DR4, but not decoy receptors, at the transcriptional level and in a non-cell-type-specific manner.	capsazepine	0-11	TNF receptor superfamily member 10b	Homo sapiens	42-45
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	24-47	TNF receptor superfamily member 10b	Homo sapiens	215-218
22922338-8	2012	Capsazepine"s effects appeared to be mediated via JNK, as shown by capsazepine"s ability to induce JNK and by the suppression of both CHOP and DR5 activation by inhibition of JNK.	capsazepine	0-11	TNF receptor superfamily member 10b	Homo sapiens	143-146
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	49-52	TNF receptor superfamily member 10b	Homo sapiens	215-218
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	capsazepine	77-88	TNF receptor superfamily member 10b	Homo sapiens	215-218
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	TNF receptor superfamily member 10b	Homo sapiens	215-218
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Glutathione	164-175	TNF receptor superfamily member 10b	Homo sapiens	215-218
22354145-0	2012	AW00179 potentiates TRAIL-mediated death of human lung cancer H1299 cells through ROS-JNK-c-Jun-mediated up-regulation of DR5 and down-regulation of anti-apoptotic molecules.	Reactive Oxygen Species	82-85	TNF receptor superfamily member 10b	Homo sapiens	122-125
22922573-9	2012	The synergistic apoptotic effect of CPT-11 and TRAIL was proposed to be mediated by upregulating DR5 mRNA expression and increasing expression of Bax and caspase-9 proteins.	Irinotecan	36-42	TNF receptor superfamily member 10b	Homo sapiens	97-100
23063980-3	2012	Ayanin diacetate-induced cell death was found to be associated with: (i) loss of inner mitochondrial membrane potential, (ii) the release of cytochrome c, (iii) the activation of multiple caspases, (iv) cleavage of poly(ADP-ribose) polymerase and (v) the up-regulation of death receptors for TRAIL, DR4 and DR5.	ayanin diacetate	0-16	TNF receptor superfamily member 10b	Homo sapiens	307-310
22354145-7	2012	In conclusion, AW00179 has the potential to sensitize H1299 cells to TRAIL-mediated apoptosis through two distinct mechanisms: ROS-JNK-c-Jun-mediated up-regulation of DR5, and down-regulation of anti-apoptotic molecules.	Reactive Oxygen Species	127-130	TNF receptor superfamily member 10b	Homo sapiens	167-170
22784708-5	2012	Methylglyoxal suppressed the expression of antiapoptotic factors, X-linked inhibitor of apoptosis protein (XIAP), survivin, cIAP1, Bcl-2, and Bcl-xL, without affecting TRAIL receptors, DR4 and DR5.	Pyruvaldehyde	0-13	TNF receptor superfamily member 10b	Homo sapiens	193-196
22842544-0	2012	Antimycin A sensitizes cells to TRAIL-induced apoptosis through upregulation of DR5 and downregulation of c-FLIP and Bcl-2.	Antimycin A	0-11	TNF receptor superfamily member 10b	Homo sapiens	80-83
22735465-14	2012	Artepillin C increased the expression of TRAIL-R2 and decreased             the activity of NF-kappaB.	artepillin C	0-12	TNF receptor superfamily member 10b	Homo sapiens	41-49
22848091-2	2012	Our previous work has shown that PS-341 induces death receptor 5 (DR5)-dependent apoptosis and enhances the TNF-related apoptosis-inducing ligand-induced apoptosis in human non-small cell lung cancer cells.	Bortezomib	33-39	TNF receptor superfamily member 10b	Homo sapiens	48-64
22848091-2	2012	Our previous work has shown that PS-341 induces death receptor 5 (DR5)-dependent apoptosis and enhances the TNF-related apoptosis-inducing ligand-induced apoptosis in human non-small cell lung cancer cells.	Bortezomib	33-39	TNF receptor superfamily member 10b	Homo sapiens	66-69
22848091-4	2012	In the present study, we reveal that PKCdelta and RSK2 mediate PS-341-induced DR5 upregulation, involving coactivation of endoplasmic reticulum (ER) stress.	Bortezomib	63-69	TNF receptor superfamily member 10b	Homo sapiens	78-81
22848091-10	2012	In addition, we discovered that the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and RSK2 were elevated after PS-341 treatment and inhibition of their phosphorylation using MAP-ERK kinase 1/2 inhibitor decreased the DR5 level, indicating that ERK/RSK2 signaling is involved in DR5 upregulation.	Bortezomib	132-138	TNF receptor superfamily member 10b	Homo sapiens	238-241
22848091-10	2012	In addition, we discovered that the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 and RSK2 were elevated after PS-341 treatment and inhibition of their phosphorylation using MAP-ERK kinase 1/2 inhibitor decreased the DR5 level, indicating that ERK/RSK2 signaling is involved in DR5 upregulation.	Bortezomib	132-138	TNF receptor superfamily member 10b	Homo sapiens	299-302
22848091-13	2012	Collectively, we show that PS-341 induces PKCdelta-dependent DR5 expression through activation of ERK/RSK2 and ER stress signaling pathway.	Bortezomib	27-33	TNF receptor superfamily member 10b	Homo sapiens	61-64
22359244-6	2012	Expression of TRAIL-mediated apoptosis signaling-related death receptor DR5 was increased in 3-O-acetyloleanolic acid-treated HCT-116 cells.	oleanolic acid 3-acetate	93-117	TNF receptor superfamily member 10b	Homo sapiens	72-75
22359244-8	2012	The results indicate that 3-O-acetyloleanolic acid induces apoptosis in HCT-116 cells mediated by an extrinsic apoptosis signaling cascade via up-regulation of DR5.	oleanolic acid 3-acetate	26-50	TNF receptor superfamily member 10b	Homo sapiens	160-163
22962275-4	2012	MK886 effectively increased the sensitivity to TRAIL-induced apoptosis via upregulation of the death receptor 5 and downregulation of the antiapoptotic protein survivin in human glioma cell lines and in primary glioma cells.	MK-886	0-5	TNF receptor superfamily member 10b	Homo sapiens	95-111
22824956-7	2012	In addition, U0126 reduced UDCA-triggered             TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2/DR5) expression.	U 0126	13-18	TNF receptor superfamily member 10b	Homo sapiens	54-102
22824956-7	2012	In addition, U0126 reduced UDCA-triggered             TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2/DR5) expression.	U 0126	13-18	TNF receptor superfamily member 10b	Homo sapiens	104-112
22824956-7	2012	In addition, U0126 reduced UDCA-triggered             TNF-related apoptosis-inducing ligand receptor 2 (TRAIL-R2/DR5) expression.	U 0126	13-18	TNF receptor superfamily member 10b	Homo sapiens	113-116
22936321-0	2012	Induction of apoptosis in human Hep3B hepatoma cells by norcantharidin through a p53 independent pathway via TRAIL/DR5 signal transduction.	norcantharidin	56-70	TNF receptor superfamily member 10b	Homo sapiens	115-118
22815059-5	2012	The anthracycline anticancer drug epirubicin (EPB) synergizes the cytotoxicity of HMCAZ5 in cancer cells by upregulating DR5 expression on the cell surfaces, enhancing p53 expression, Bid cleavage, and JNK phosphorylation and downregulating c-FLIP expression and Akt phosphorylation.	Anthracyclines	4-17	TNF receptor superfamily member 10b	Homo sapiens	121-124
22555452-6	2012	Up-regulation of death receptor 4 (DR4) and DR5 by silibinin was shown by RT-PCR and by flow cytometry.	Silybin	51-60	TNF receptor superfamily member 10b	Homo sapiens	44-47
22815059-5	2012	The anthracycline anticancer drug epirubicin (EPB) synergizes the cytotoxicity of HMCAZ5 in cancer cells by upregulating DR5 expression on the cell surfaces, enhancing p53 expression, Bid cleavage, and JNK phosphorylation and downregulating c-FLIP expression and Akt phosphorylation.	Epirubicin	34-44	TNF receptor superfamily member 10b	Homo sapiens	121-124
22707197-0	2012	Triptolide sensitizes TRAIL-induced apoptosis in prostate cancer cells via p53-mediated DR5 up-regulation.	triptolide	0-10	TNF receptor superfamily member 10b	Homo sapiens	88-91
22707197-3	2012	In this study, we found that Triptolide, a Chinese medicine, significantly sensitizes prostate cancer cells to TRAIL-mediated cellular apoptosis by up-regulating DR5 expression.	triptolide	29-39	TNF receptor superfamily member 10b	Homo sapiens	162-165
22707197-4	2012	Triptolide treatment can suppress Akt/Hdm2 signaling pathway, and lead to p53 accumulation, thereby up-regulating DR5 expression.	triptolide	0-10	TNF receptor superfamily member 10b	Homo sapiens	114-117
22483777-5	2012	Knockdown of SIRT1 or treatment with amurensin G, a potent new SIRT1 inhibitor, up-regulated the levels of DR5 and c-Myc and down-regulated the level of c-FLIP(L/S).	amurensin G	37-48	TNF receptor superfamily member 10b	Homo sapiens	107-110
22555452-7	2012	Human recombinant DR5/Fc chimera protein that has a dominant-negative effect by competing with the endogenous receptors abrogated cell death induced by silibinin and TRAIL, demonstrating the activation of the death receptor pathway.	Silybin	152-161	TNF receptor superfamily member 10b	Homo sapiens	18-21
22562097-8	2012	Our results showed that DR5 monoclonal antibody (D-6) was able to induce the apoptosis and increase the cell growth inhibition rates of ovarian cancer cells in a dose-dependent manner, and the effect was enhanced by cisplatin.	Cisplatin	216-225	TNF receptor superfamily member 10b	Homo sapiens	24-27
22562097-10	2012	The combination treatment of the DR5 monoclonal antibody (D-6) with cisplatin may be a promising treatment for ovarian cancer.	Cisplatin	68-77	TNF receptor superfamily member 10b	Homo sapiens	33-36
21801305-0	2012	Salermide up-regulates death receptor 5 expression through the ATF4-ATF3-CHOP axis and leads to apoptosis in human cancer cells.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	0-9	TNF receptor superfamily member 10b	Homo sapiens	23-39
22447040-7	2012	Transfection studies were used to determine the involvement of DR4, DR5 and Cbl-b in the synergistic effect of bufalin and TRAIL.	bufalin	111-118	TNF receptor superfamily member 10b	Homo sapiens	68-71
22447040-11	2012	Blocking the up-regulation of DR4 and DR5 by siRNA rendered cells less sensitive to apoptosis induced by the combination of bufalin and TRAIL.	bufalin	124-131	TNF receptor superfamily member 10b	Homo sapiens	38-41
22447040-15	2012	Bufalin-induced down-regulation of Cbl-b contributed to the up-regulation of DR4 and DR5, which might be partially mediated by the activation of ERK, JNK and p38 MAPK.	bufalin	0-7	TNF receptor superfamily member 10b	Homo sapiens	85-88
22788777-6	2012	Based on distance geometry method and intermolecular hydrogen bonding analysis, the key functional domain in DR5 was predicted and the DR5 mutants were designed.	Hydrogen	53-61	TNF receptor superfamily member 10b	Homo sapiens	109-112
22788777-6	2012	Based on distance geometry method and intermolecular hydrogen bonding analysis, the key functional domain in DR5 was predicted and the DR5 mutants were designed.	Hydrogen	53-61	TNF receptor superfamily member 10b	Homo sapiens	135-138
21801305-11	2012	This suggests that DR5 is modulated by the ATF4-ATF3-CHOP axis in NSCLC after Sirt1/2 inhibition or salermide treatment.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	100-109	TNF receptor superfamily member 10b	Homo sapiens	19-22
21801305-4	2012	In this study, we show that salermide up-regulates the expression of death receptor 5 (DR5) in human non-small cell lung cancer (NSCLC) cells.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	28-37	TNF receptor superfamily member 10b	Homo sapiens	69-85
21801305-4	2012	In this study, we show that salermide up-regulates the expression of death receptor 5 (DR5) in human non-small cell lung cancer (NSCLC) cells.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	28-37	TNF receptor superfamily member 10b	Homo sapiens	87-90
21801305-6	2012	Increasing DR5 protein expression correlates with salermide-induced apoptosis in human NSCLC cells.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	50-59	TNF receptor superfamily member 10b	Homo sapiens	11-14
21801305-7	2012	We discovered that IRE-1alpha, Bip, activating transcription factor 3 (ATF4), activating transcription factor 3 (ATF3) and C/EBP homologous protein (CHOP) are induced by salermide, which suggests that DR5-dependent apoptosis is induced by endoplasmic reticulum stress.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	170-179	TNF receptor superfamily member 10b	Homo sapiens	201-204
23124518-2	2012	We provide evidence that pretreatment with etoposide significantly enhanced TRAIL-mediated apoptosis via up-regulation of DR5 (death receptor 5 or TRAIL-R2) expression in the caspase 8 expressing neuroblastoma cell line, SK-N-MC.	Etoposide	43-52	TNF receptor superfamily member 10b	Homo sapiens	122-125
22309674-0	2012	beta-Phenethyl isothiocyanate induces death receptor 5 to induce apoptosis in human oral cancer cells via p38.	phenethyl isothiocyanate	0-29	TNF receptor superfamily member 10b	Homo sapiens	38-54
22309674-8	2012	This result was confirmed by blockage of PEITC-induced cleavages of Poly(ADP-ribose) Polymerase, caspase-3, caspase-8, and DR5 by p38 MAPK inhibitor, SB203580.	phenethyl isothiocyanate	41-46	TNF receptor superfamily member 10b	Homo sapiens	123-126
22309674-8	2012	This result was confirmed by blockage of PEITC-induced cleavages of Poly(ADP-ribose) Polymerase, caspase-3, caspase-8, and DR5 by p38 MAPK inhibitor, SB203580.	SB 203580	150-158	TNF receptor superfamily member 10b	Homo sapiens	123-126
23124518-4	2012	Although TRAIL-R2 expression increased in IMR-32 cells in response to etoposide treatment, cell death was not increased by concurrent treatment with TRAIL compared with etoposide alone, because the cells lacked caspase 8 expression.	Etoposide	70-79	TNF receptor superfamily member 10b	Homo sapiens	9-17
23124518-2	2012	We provide evidence that pretreatment with etoposide significantly enhanced TRAIL-mediated apoptosis via up-regulation of DR5 (death receptor 5 or TRAIL-R2) expression in the caspase 8 expressing neuroblastoma cell line, SK-N-MC.	Etoposide	43-52	TNF receptor superfamily member 10b	Homo sapiens	127-143
23124518-7	2012	These results indicate that the etoposide-mediated sensitization of neuroblastoma cells to TRAIL is associated with an increase in TRAIL-R2 expression and requires caspase 8 expression.	Etoposide	32-41	TNF receptor superfamily member 10b	Homo sapiens	131-139
23124518-2	2012	We provide evidence that pretreatment with etoposide significantly enhanced TRAIL-mediated apoptosis via up-regulation of DR5 (death receptor 5 or TRAIL-R2) expression in the caspase 8 expressing neuroblastoma cell line, SK-N-MC.	Etoposide	43-52	TNF receptor superfamily member 10b	Homo sapiens	147-155
22367066-3	2012	Exposure to MEMC was found to result in growth inhibition by the induction             of caspase-dependent apoptosis in NCI-H460 cells, which correlated with upregulated             expression of death receptor (DR)4, DR5 and FasL, downregulation of anti-apoptotic             Bcl-2 and Bcl-xL expression, cleavage of Bid, and loss of mitochondrial membrane             potential.	Mercury, chloro(2-methoxyethyl)-	12-16	TNF receptor superfamily member 10b	Homo sapiens	219-222
22681760-9	2012	Snake venom toxin also induced JNK phosphorylation and ROS generation, however, pretreatment of JNK inhibitor and ROS scavenger reversed the inhibitory effect of snake venom toxin on cancer cell proliferation, and reduced the snake venom toxin-induced upregulation of DR4 and DR5 expression.	Reactive Oxygen Species	114-117	TNF receptor superfamily member 10b	Homo sapiens	276-279
22681760-10	2012	CONCLUSIONS: Our results indicated that snake venom toxin could inhibit human colon cancer cell growth, and these effects may be related to ROS and JNK mediated activation of death receptor (DR4 and DR5) signals.	Reactive Oxygen Species	140-143	TNF receptor superfamily member 10b	Homo sapiens	199-202
22522053-6	2012	Curcumin induced upregulation of Fas, FasL, and DR5 expression in chondrosarcoma cells.	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	48-51
22522053-7	2012	Transfection of cells with Fas, FasL, or DR5 siRNA reduced curcumin-induced cell death.	Curcumin	59-67	TNF receptor superfamily member 10b	Homo sapiens	41-44
22522053-8	2012	In addition, p53 involved in curcumin-mediated Fas, FasL, and DR5 expression and cell apoptosis in chondrosarcoma cells.	Curcumin	29-37	TNF receptor superfamily member 10b	Homo sapiens	62-65
22395735-8	2012	In view of the finding             that DR5 silencing abrogated the combination-stimulated apoptosis, we propose             that apoptotic synergy induced by sulindac sulfide plus DHA is mediated via DR5.	Docosahexaenoic Acids	181-184	TNF receptor superfamily member 10b	Homo sapiens	201-204
22472572-0	2012	Inostamycin enhanced TRAIL-induced apoptosis through DR5 upregulation on the cell surface.	inostamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	53-56
22472572-6	2012	Inostamycin upregulated DR5, and a knockdown of DR5 suppressed the apoptosis that was synergistically induced by co-treatment with inostamycin and TRAIL.	inostamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	24-27
22472572-6	2012	Inostamycin upregulated DR5, and a knockdown of DR5 suppressed the apoptosis that was synergistically induced by co-treatment with inostamycin and TRAIL.	inostamycin	131-142	TNF receptor superfamily member 10b	Homo sapiens	48-51
22472572-7	2012	Moreover, inostamycin increased the expression of DR5 on the cell surface.	inostamycin	10-21	TNF receptor superfamily member 10b	Homo sapiens	50-53
22472572-8	2012	Therefore, inostamycin-increased cell surface expression of DR5 may have contributed to the enhancement of TRAIL-induced apoptosis.	inostamycin	11-22	TNF receptor superfamily member 10b	Homo sapiens	60-63
22395735-8	2012	In view of the finding             that DR5 silencing abrogated the combination-stimulated apoptosis, we propose             that apoptotic synergy induced by sulindac sulfide plus DHA is mediated via DR5.	sulindac sulfide	159-175	TNF receptor superfamily member 10b	Homo sapiens	40-43
22131069-8	2012	Epirubicin treatment up-regulated death receptor 4 (DR-4) and DR-5 expression and down-regulated FLIP expression, thereby enhancing the activation of procaspase 3, procaspase 8, and procaspase 9.	Epirubicin	0-10	TNF receptor superfamily member 10b	Homo sapiens	62-66
22395735-8	2012	In view of the finding             that DR5 silencing abrogated the combination-stimulated apoptosis, we propose             that apoptotic synergy induced by sulindac sulfide plus DHA is mediated via DR5.	sulindac sulfide	159-175	TNF receptor superfamily member 10b	Homo sapiens	201-204
22395735-8	2012	In view of the finding             that DR5 silencing abrogated the combination-stimulated apoptosis, we propose             that apoptotic synergy induced by sulindac sulfide plus DHA is mediated via DR5.	Docosahexaenoic Acids	181-184	TNF receptor superfamily member 10b	Homo sapiens	40-43
22707267-3	2012	METHODS AND RESULTS: DHA induces apoptosis as detected by Annexin V-FITC/PI assay as well as induces cleavage of caspase-8 and -9, endoplasmic reticulum stress (ERS), and elevated levels of death receptor-5 (DR5) protein expression as detected by western blot assays.	Docosahexaenoic Acids	21-24	TNF receptor superfamily member 10b	Homo sapiens	190-206
22707267-3	2012	METHODS AND RESULTS: DHA induces apoptosis as detected by Annexin V-FITC/PI assay as well as induces cleavage of caspase-8 and -9, endoplasmic reticulum stress (ERS), and elevated levels of death receptor-5 (DR5) protein expression as detected by western blot assays.	Docosahexaenoic Acids	21-24	TNF receptor superfamily member 10b	Homo sapiens	208-211
22707267-4	2012	Chemical inhibitors of caspase-8 and -9 and small interfering RNAs (siRNAs) show DHA to induce ERS/CHOP/DR5-mediated caspase-8 and -9 dependent apoptosis.	Docosahexaenoic Acids	81-84	TNF receptor superfamily member 10b	Homo sapiens	104-107
22707267-7	2012	CONCLUSION: Data, for the first time, demonstrate that DHA induces apoptosis in TNBC cells via activation of ERS/CHOP/DR5-mediated caspase-8 and -9 dependent pro-apoptotic events, and that different forms of vitamin E exhibit distinct effects on DHA-induced apoptosis; namely, inhibition by alphaT and enhancement by gammaT3.	Docosahexaenoic Acids	55-58	TNF receptor superfamily member 10b	Homo sapiens	118-121
22400995-0	2012	Isoobtusilactone A sensitizes human hepatoma Hep G2 cells to TRAIL-induced apoptosis via ROS and CHOP-mediated up-regulation of DR5.	isoobtusilactone A	0-18	TNF receptor superfamily member 10b	Homo sapiens	128-131
21927023-4	2012	In this report, we demonstrate that ATF3 is required for efficient DR5 induction upon DNA damage by camptothecin (CPT) in colorectal cancer cells.	Camptothecin	100-112	TNF receptor superfamily member 10b	Homo sapiens	67-70
21927023-4	2012	In this report, we demonstrate that ATF3 is required for efficient DR5 induction upon DNA damage by camptothecin (CPT) in colorectal cancer cells.	Camptothecin	114-117	TNF receptor superfamily member 10b	Homo sapiens	67-70
22328338-8	2012	Moreover,             orlistat induced reactive oxygen species (ROS), and a ROS scavenger diminished             the sensitivity to TRAIL through the suppression of CHOP and DR5 expression in             both cell lines.	Reactive Oxygen Species	76-79	TNF receptor superfamily member 10b	Homo sapiens	174-177
22328338-9	2012	These results suggest that there are two pathways of upregulation             of DR5 by orlistat, which are the ROS-CHOP pathway and the ROS-direct pathway.	Reactive Oxygen Species	112-115	TNF receptor superfamily member 10b	Homo sapiens	81-84
22328338-9	2012	These results suggest that there are two pathways of upregulation             of DR5 by orlistat, which are the ROS-CHOP pathway and the ROS-direct pathway.	Reactive Oxygen Species	137-140	TNF receptor superfamily member 10b	Homo sapiens	81-84
22400995-8	2012	DR5 expression after IOA treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation.	Reactive Oxygen Species	78-101	TNF receptor superfamily member 10b	Homo sapiens	0-3
22400995-8	2012	DR5 expression after IOA treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation.	Reactive Oxygen Species	103-106	TNF receptor superfamily member 10b	Homo sapiens	0-3
22200406-0	2012	Capsaicin sensitizes TRAIL-induced apoptosis through Sp1-mediated DR5 up-regulation: involvement of Ca(2+) influx.	Capsaicin	0-9	TNF receptor superfamily member 10b	Homo sapiens	66-69
22244504-6	2012	Furthermore, epirubicin therapy significantly improved recurrence-free rate for the patients with DR4-high (P = .006) or DR5-high (P = .042) tumor.	Epirubicin	13-23	TNF receptor superfamily member 10b	Homo sapiens	121-124
22244504-8	2012	In addition, patients with high expression of both DR4 and DR5 might benefit from epirubicin therapy.	Epirubicin	82-92	TNF receptor superfamily member 10b	Homo sapiens	59-62
22008998-11	2012	Taken together, RU486 enhances TRAIL-mediated apoptosis through down-regulation of Bcl-2 and c-FLIP(L) as well as CHOP-mediated DR5 up-regulation.	Mifepristone	16-21	TNF receptor superfamily member 10b	Homo sapiens	128-131
22205156-6	2012	Epirubicin and pirarubicin significantly increased the TRAIL-R2 expression at both the mRNA and the protein levels.	Epirubicin	0-10	TNF receptor superfamily member 10b	Homo sapiens	55-63
22205156-6	2012	Epirubicin and pirarubicin significantly increased the TRAIL-R2 expression at both the mRNA and the protein levels.	pirarubicin	15-26	TNF receptor superfamily member 10b	Homo sapiens	55-63
22205156-11	2012	The present study demonstrates that anthracylines sensitize RCC cells to lexatumumab-mediated apoptosis by inducing TRAIL-R2 expression, and the utility of PCR array to elucidate the mechanism of synergistic apoptosis.	anthracylines	36-49	TNF receptor superfamily member 10b	Homo sapiens	116-124
22230479-0	2012	Dovitinib sensitizes hepatocellular carcinoma cells to TRAIL and tigatuzumab, a novel anti-DR5 antibody, through SHP-1-dependent inhibition of STAT3.	4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one	0-9	TNF receptor superfamily member 10b	Homo sapiens	91-94
22008998-5	2012	We found that up-regulation of death receptor 5 (DR5; receptor for TRAIL ligand), and down-regulation of Bcl-2 and c-FLIP (caspase regulator) contributes to RU-486 induced TRAIL sensitization.	Mifepristone	157-163	TNF receptor superfamily member 10b	Homo sapiens	31-47
22008998-5	2012	We found that up-regulation of death receptor 5 (DR5; receptor for TRAIL ligand), and down-regulation of Bcl-2 and c-FLIP (caspase regulator) contributes to RU-486 induced TRAIL sensitization.	Mifepristone	157-163	TNF receptor superfamily member 10b	Homo sapiens	49-52
22008998-6	2012	Down-regulation of DR5 by siRNA also blocked RU486 induced TRAIL sensitization.	Mifepristone	45-50	TNF receptor superfamily member 10b	Homo sapiens	19-22
22200406-4	2012	In addition, we found that capsaicin induces the cell surface expression of TRAIL receptor DR5, but not DR4 through the activation Sp1 on its promoter region.	Capsaicin	27-36	TNF receptor superfamily member 10b	Homo sapiens	91-94
22200406-5	2012	Furthermore, we investigated that capsaicin-induced DR5 expression and apoptosis are inhibited by calcium chelator or inhibitors for calmodulin-dependent protein kinase.	Capsaicin	34-43	TNF receptor superfamily member 10b	Homo sapiens	52-55
22200406-6	2012	Taken together, our data suggest that capsaicin sensitizes TRAIL-mediated HCC cell apoptosis by DR5 up-regulation via calcium influx-dependent Sp1 activation.	Capsaicin	38-47	TNF receptor superfamily member 10b	Homo sapiens	96-99
22077238-0	2012	Aclarubicin enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis through death receptor 5 upregulation.	Aclarubicin	0-11	TNF receptor superfamily member 10b	Homo sapiens	103-119
22077238-6	2012	In contrast, another anthracycline, doxorubicin (DOX), only slightly sensitized Jurkat cells and A549 cells to TRAIL-induced apoptosis, with weaker enhancement of death receptor 5 (DR5) expression than ACR.	Doxorubicin	36-47	TNF receptor superfamily member 10b	Homo sapiens	163-179
22077238-6	2012	In contrast, another anthracycline, doxorubicin (DOX), only slightly sensitized Jurkat cells and A549 cells to TRAIL-induced apoptosis, with weaker enhancement of death receptor 5 (DR5) expression than ACR.	Doxorubicin	36-47	TNF receptor superfamily member 10b	Homo sapiens	181-184
22077238-6	2012	In contrast, another anthracycline, doxorubicin (DOX), only slightly sensitized Jurkat cells and A549 cells to TRAIL-induced apoptosis, with weaker enhancement of death receptor 5 (DR5) expression than ACR.	Doxorubicin	49-52	TNF receptor superfamily member 10b	Homo sapiens	163-179
21660448-0	2012	5, 7-Dimethoxyflavone sensitizes TRAIL-induced apoptosis through DR5 upregulation in hepatocellular carcinoma cells.	5,7-dimethoxyflavone	0-21	TNF receptor superfamily member 10b	Homo sapiens	65-68
22158615-2	2012	Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells.	Superoxides	211-227	TNF receptor superfamily member 10b	Homo sapiens	46-49
22158615-2	2012	Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells.	Superoxides	211-227	TNF receptor superfamily member 10b	Homo sapiens	101-104
22158615-2	2012	Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells.	Reactive Oxygen Species	271-294	TNF receptor superfamily member 10b	Homo sapiens	46-49
22158615-2	2012	Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells.	Reactive Oxygen Species	271-294	TNF receptor superfamily member 10b	Homo sapiens	101-104
22158615-2	2012	Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells.	Reactive Oxygen Species	296-299	TNF receptor superfamily member 10b	Homo sapiens	46-49
22158615-2	2012	Here we report that stimulation of DR4 and/or DR5 by the agonistic protein KD548-Fc, an Fc-fused DR4/DR5 dual-specific Kringle domain variant, activates plasma membrane-associated Nox1 NADPH oxidase to generate superoxide anion and subsequently accumulates intracellular reactive oxygen species (ROS), leading to sustained c-Jun N-terminal kinase activation and eventual apoptotic cell death in human HeLa and Jurkat tumor cells.	Reactive Oxygen Species	296-299	TNF receptor superfamily member 10b	Homo sapiens	101-104
22158615-7	2012	Our results suggest that DR4 and DR5 have a capability to activate Nox1 by recruiting RFK, resulting in ROS-mediated apoptotic cell death in tumor cells.	Reactive Oxygen Species	104-107	TNF receptor superfamily member 10b	Homo sapiens	33-36
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-34	TNF receptor superfamily member 10b	Homo sapiens	79-82
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	36-39	TNF receptor superfamily member 10b	Homo sapiens	79-82
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Dimethylformamide	51-54	TNF receptor superfamily member 10b	Homo sapiens	79-82
21660448-8	2012	RESULTS: Our results demonstrated subtoxic concentrations of DMF sensitize HCC cells to TRAIL-induced apoptosis and induce the death receptor 5 (DR5) expression level, accompanying the generation of reactive oxygen species (ROS) and the upregulation of CHOP, GPR78, and ATF4 protein expression.	Dimethylformamide	61-64	TNF receptor superfamily member 10b	Homo sapiens	127-143
21660448-10	2012	Furthermore, DMF-mediated sensitization of HCC cells to TRAIL was reduced by administration of a blocking antibody or small interfering RNAs for DR5, salubrinal, an inhibitor of ER stress, and the small interfering RNAs for CHOP.	Dimethylformamide	13-16	TNF receptor superfamily member 10b	Homo sapiens	145-148
21660448-12	2012	CONCLUSION: The present study demonstrates that DMF selectively enhances TRAIL-induced apoptosis by ROS-stimulated ER-stress triggering CHOP-mediated DR5 upregulation in HCC.	Dimethylformamide	48-51	TNF receptor superfamily member 10b	Homo sapiens	150-153
21660448-8	2012	RESULTS: Our results demonstrated subtoxic concentrations of DMF sensitize HCC cells to TRAIL-induced apoptosis and induce the death receptor 5 (DR5) expression level, accompanying the generation of reactive oxygen species (ROS) and the upregulation of CHOP, GPR78, and ATF4 protein expression.	Dimethylformamide	61-64	TNF receptor superfamily member 10b	Homo sapiens	145-148
21660448-12	2012	CONCLUSION: The present study demonstrates that DMF selectively enhances TRAIL-induced apoptosis by ROS-stimulated ER-stress triggering CHOP-mediated DR5 upregulation in HCC.	Reactive Oxygen Species	100-103	TNF receptor superfamily member 10b	Homo sapiens	150-153
21887462-5	2012	Cotreatment of bufotalin with TRAIL resulted in the             downregulation of anti-apoptotic proteins, including Bcl-XL, Mcl-1, survivin and             XIAP, and the up-regulation of MAPKs and TRAIL receptor DR5.	bufotalin	15-24	TNF receptor superfamily member 10b	Homo sapiens	213-216
22666346-9	2012	CONCLUSIONS/SIGNIFICANCE: These results suggest that DHA enhances Apo2L/TRAIL-mediated apoptosis in human pancreatic cancer cells through reactive oxygen species-mediated up-regulation of DR5.	Reactive Oxygen Species	138-161	TNF receptor superfamily member 10b	Homo sapiens	188-191
21978492-6	2011	PHA665752 treatment also caused increased expression of DR5 via generation of reactive oxygen species, and combination treatment with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and PHA665752 induced significant apoptosis.	Reactive Oxygen Species	78-101	TNF receptor superfamily member 10b	Homo sapiens	56-59
22666346-0	2012	Dihydroartemisinin enhances Apo2L/TRAIL-mediated apoptosis in pancreatic cancer cells via ROS-mediated up-regulation of death receptor 5.	artenimol	0-18	TNF receptor superfamily member 10b	Homo sapiens	120-136
22666346-0	2012	Dihydroartemisinin enhances Apo2L/TRAIL-mediated apoptosis in pancreatic cancer cells via ROS-mediated up-regulation of death receptor 5.	Reactive Oxygen Species	90-93	TNF receptor superfamily member 10b	Homo sapiens	120-136
22666346-6	2012	The effect of DHA was mediated through the generation of reactive oxygen species, the induction of death receptor 5 (DR5) and the modulation of apoptosis-related proteins.	artenimol	14-17	TNF receptor superfamily member 10b	Homo sapiens	99-115
22666346-6	2012	The effect of DHA was mediated through the generation of reactive oxygen species, the induction of death receptor 5 (DR5) and the modulation of apoptosis-related proteins.	artenimol	14-17	TNF receptor superfamily member 10b	Homo sapiens	117-120
22666346-8	2012	In addition, knockdown of DR5 by small interfering RNA also significantly reduced the amount of apoptosis induced by DHA and Apo2L/TRAIL.	artenimol	117-120	TNF receptor superfamily member 10b	Homo sapiens	26-29
22666346-9	2012	CONCLUSIONS/SIGNIFICANCE: These results suggest that DHA enhances Apo2L/TRAIL-mediated apoptosis in human pancreatic cancer cells through reactive oxygen species-mediated up-regulation of DR5.	artenimol	53-56	TNF receptor superfamily member 10b	Homo sapiens	188-191
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	TNF receptor superfamily member 10b	Homo sapiens	55-58
21903093-0	2011	Guggulsterone sensitizes hepatoma cells to TRAIL-induced apoptosis through the induction of CHOP-dependent DR5: involvement of ROS-dependent ER-stress.	pregna-4,17-diene-3,16-dione	0-13	TNF receptor superfamily member 10b	Homo sapiens	107-110
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Acetylcysteine	18-37	TNF receptor superfamily member 10b	Homo sapiens	100-103
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Glutathione	42-53	TNF receptor superfamily member 10b	Homo sapiens	100-103
22019170-12	2011	CONCLUSIONS: Data suggest that paclitaxel induces nuclear translocation and activation of PKC-delta, which in turn causes Golgi-Cdk1 activation, leading to Golgi associated DR5 up-regulation, and caspase-8 and 3 activation.	Paclitaxel	31-41	TNF receptor superfamily member 10b	Homo sapiens	173-176
21769428-7	2011	It suggested that the TRAIL-induced redistribution of DR4 and DR5 in lipid rafts contributed to the sensitivity to TRAIL in TRAIL-sensitive NSCLC H460 cell line, which was also confirmed by intervention tests of the cholesterol-sequestering agent nystatin.	Cholesterol	216-227	TNF receptor superfamily member 10b	Homo sapiens	62-65
21769428-7	2011	It suggested that the TRAIL-induced redistribution of DR4 and DR5 in lipid rafts contributed to the sensitivity to TRAIL in TRAIL-sensitive NSCLC H460 cell line, which was also confirmed by intervention tests of the cholesterol-sequestering agent nystatin.	Nystatin	247-255	TNF receptor superfamily member 10b	Homo sapiens	62-65
22019170-7	2011	Data revealed that paclitaxel induced an increase of Cdk1 activity and DR5 expression on the Golgi complex that was associated with increased cleavage of caspase-8, a DR5 downstream factor, and caspase-3 into catalytically active fragments.	Paclitaxel	19-29	TNF receptor superfamily member 10b	Homo sapiens	71-74
22019170-7	2011	Data revealed that paclitaxel induced an increase of Cdk1 activity and DR5 expression on the Golgi complex that was associated with increased cleavage of caspase-8, a DR5 downstream factor, and caspase-3 into catalytically active fragments.	Paclitaxel	19-29	TNF receptor superfamily member 10b	Homo sapiens	167-170
21941003-5	2011	The toxic saturated free fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor clustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.	saturated	10-19	TNF receptor superfamily member 10b	Homo sapiens	69-72
21941003-5	2011	The toxic saturated free fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor clustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.	saturated	10-19	TNF receptor superfamily member 10b	Homo sapiens	142-145
21941003-5	2011	The toxic saturated free fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor clustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.	free fatty acid palmitate	20-45	TNF receptor superfamily member 10b	Homo sapiens	69-72
21875750-6	2011	We also demonstrate that DR5-targeted nanoparticles encapsulating the cytotoxic drug camptothecin are effectively targeted to the tumour cells, thereby producing enhanced cytotoxic effects through simultaneous drug delivery and apoptosis induction.	Camptothecin	85-97	TNF receptor superfamily member 10b	Homo sapiens	25-28
21941003-5	2011	The toxic saturated free fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor clustering with subsequent recruitment of the initiator caspase-8, and ultimately cellular demise.	free fatty acid palmitate	20-45	TNF receptor superfamily member 10b	Homo sapiens	142-145
21941003-8	2011	Likewise, knockdown of DR5 or caspase-8 expression by shRNA technology attenuated palmitate-induced Bax activation and apoptosis in Huh-7 cells, without altering induction of ER stress markers.	Palmitates	82-91	TNF receptor superfamily member 10b	Homo sapiens	23-26
21726997-0	2011	Death receptor 5 and cellular FLICE-inhibitory protein regulate pemetrexed-induced apoptosis in human lung cancer cells.	Pemetrexed	64-74	TNF receptor superfamily member 10b	Homo sapiens	0-16
21726997-5	2011	We showed that pemetrexed induced apoptosis via up-regulation of Death Receptor 5 (DR5), an important death receptor for tumour necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL).	Pemetrexed	15-25	TNF receptor superfamily member 10b	Homo sapiens	65-81
21726997-5	2011	We showed that pemetrexed induced apoptosis via up-regulation of Death Receptor 5 (DR5), an important death receptor for tumour necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL).	Pemetrexed	15-25	TNF receptor superfamily member 10b	Homo sapiens	83-86
21726997-7	2011	Modulating DR5 induction by small interfering RNA abrogated the ability of pemetrexed to induce apoptosis.	Pemetrexed	75-85	TNF receptor superfamily member 10b	Homo sapiens	11-14
21726997-8	2011	In addition, silencing of C/EBP homologous protein (CHOP) expression reduced DR5 expression, demonstrating that the transcriptional factor CHOP has a pivotal role on DR5 up-regulation following pemetrexed treatment.	Pemetrexed	194-204	TNF receptor superfamily member 10b	Homo sapiens	77-80
21726997-8	2011	In addition, silencing of C/EBP homologous protein (CHOP) expression reduced DR5 expression, demonstrating that the transcriptional factor CHOP has a pivotal role on DR5 up-regulation following pemetrexed treatment.	Pemetrexed	194-204	TNF receptor superfamily member 10b	Homo sapiens	166-169
21757445-2	2011	We have identified lanatoside C as a sensitizer of GBM cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death partly by upregulation of the death receptor 5.	lanatoside C	19-31	TNF receptor superfamily member 10b	Homo sapiens	177-193
21854768-0	2011	Acrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.	Acrolein	0-8	TNF receptor superfamily member 10b	Homo sapiens	111-127
21854768-0	2011	Acrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.	Acrolein	0-8	TNF receptor superfamily member 10b	Homo sapiens	129-132
21854768-0	2011	Acrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.	ros	81-84	TNF receptor superfamily member 10b	Homo sapiens	111-127
21854768-0	2011	Acrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.	ros	81-84	TNF receptor superfamily member 10b	Homo sapiens	129-132
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	49-65	TNF receptor superfamily member 10b	Homo sapiens	101-104
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	67-70	TNF receptor superfamily member 10b	Homo sapiens	101-104
21854768-9	2011	Taken together, our results demonstrated that acrolein enhances TRAIL-induced apoptosis in Caki cells through down-regulation of Bcl-2 and ROS dependent up-regulation of DR5.	Acrolein	46-54	TNF receptor superfamily member 10b	Homo sapiens	170-173
21965726-7	2011	However, PA also increases surface expression of death receptors 4 and 5 (DR4 and DR5, respectively).	Paclitaxel	9-11	TNF receptor superfamily member 10b	Homo sapiens	82-85
21779837-5	2011	Silibinin enhanced the expression (protein and mRNA) of TNF-related apoptosis-inducing ligand (TRAIL) death receptors (DR4/DR5) at the cell surface in SW480 cells, and induced their expression in TRAIL-resistant SW620 cells normally not expressing DR4/DR5.	Silybin	0-9	TNF receptor superfamily member 10b	Homo sapiens	123-126
22090786-0	2011	Casticin-induced apoptosis involves death receptor 5 upregulation in hepatocellular carcinoma cells.	casticin	0-8	TNF receptor superfamily member 10b	Homo sapiens	36-52
22090786-15	2011	In the HCC cells treated with casticin for 24 h, DR5 protein level was increased.	casticin	30-38	TNF receptor superfamily member 10b	Homo sapiens	49-52
22090786-16	2011	The expression of DR5 protein induced by casticin was inhibited by NAC.	casticin	41-49	TNF receptor superfamily member 10b	Homo sapiens	18-21
22090786-17	2011	Pretreatment with DR5/Fc chimera protein, a blocking antibody, effectively attenuated the induction of apoptosis by casticin.	casticin	116-124	TNF receptor superfamily member 10b	Homo sapiens	18-21
22090786-18	2011	CONCLUSION: Casticin-induced apoptosis of HCC cells is involved in GSH depletion and DR5 upregulation.	casticin	12-20	TNF receptor superfamily member 10b	Homo sapiens	85-88
21751122-8	2011	Etoposide and doxorubicin induced DR5 but not DR4 in NB cell lines.	Etoposide	0-9	TNF receptor superfamily member 10b	Homo sapiens	34-37
21751122-8	2011	Etoposide and doxorubicin induced DR5 but not DR4 in NB cell lines.	Doxorubicin	14-25	TNF receptor superfamily member 10b	Homo sapiens	34-37
21722984-3	2011	This study focused on the interaction of cisplatin/radiation with the anti-human DR5 monoclonal antibody TRA-8 in SCLC cells.	Cisplatin	41-50	TNF receptor superfamily member 10b	Homo sapiens	81-84
21877938-0	2011	Cisplatin restores TRAIL apoptotic pathway in glioblastoma-derived stem cells through up-regulation of DR5 and down-regulation of c-FLIP.	Cisplatin	0-9	TNF receptor superfamily member 10b	Homo sapiens	103-106
21877938-3	2011	However, treatment with cisplatin leads to the upregulation of DR5 and downregulation of c-FLIP and restores TRAIL apoptotic pathway in the neurospheres.	Cisplatin	24-33	TNF receptor superfamily member 10b	Homo sapiens	63-66
21325634-9	2011	Fourth, curcumin upregulated death receptors, DR4 and DR5.	Curcumin	8-16	TNF receptor superfamily member 10b	Homo sapiens	54-57
21597379-7	2011	In addition, C-DIMs inhibited cell proliferation and induced PARP cleavage through death receptor 5 and CHOP in HEp-2 and HN22 cells.	c-dims	13-19	TNF receptor superfamily member 10b	Homo sapiens	83-99
21697087-0	2011	Modulation of CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 expression by nelfinavir sensitizes glioblastoma multiforme cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Nelfinavir	99-109	TNF receptor superfamily member 10b	Homo sapiens	81-84
21697087-5	2011	We found that Nelfinavir treatment led to ER stress-induced up-regulation of the DR5 receptor.	Nelfinavir	14-24	TNF receptor superfamily member 10b	Homo sapiens	81-84
21697087-10	2011	We provide evidence that Nelfinavir-induced ER stress modulates DR5 expression in human glioblastoma multiforme cells and can enhance TRAIL efficacy.	Nelfinavir	25-35	TNF receptor superfamily member 10b	Homo sapiens	64-67
21697087-9	2011	Combining Nelfinavir with TRAIL led to a significantly enhanced level of apoptosis that was abrogated by siRNA silencing of DR5.	Nelfinavir	10-20	TNF receptor superfamily member 10b	Homo sapiens	124-127
21354251-9	2011	Bupropion also induced the mRNA expression of the death receptors DR4 (TRAILR1) and DR5 (TRAILR2).	Bupropion	0-9	TNF receptor superfamily member 10b	Homo sapiens	84-87
21702500-9	2011	PD98059 increased the expression of DR4 and DR5, activated caspase-3, and cleaved PARP.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	TNF receptor superfamily member 10b	Homo sapiens	44-47
21601561-7	2011	We further found that Redd1-induced mTOR down-regulation and ATF4/CHOP-induced expression of the TRAIL receptor DR5 associated with sorafenib treatment helped sensitize cells to TRAIL-induced apoptosis.	Sorafenib	132-141	TNF receptor superfamily member 10b	Homo sapiens	112-115
21822052-0	2011	Mcl-1 and YY1 inhibition and induction of DR5 by the BH3-mimetic Obatoclax (GX15-070) contribute in the sensitization of B-NHL cells to TRAIL apoptosis.	BH 3	53-56	TNF receptor superfamily member 10b	Homo sapiens	42-45
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	33-43	TNF receptor superfamily member 10b	Homo sapiens	110-113
21725212-5	2011	Co-treatment of these cells with quinacrine and TRAIL induces overwhelming cell death within 3-4 h. Levels of DR5, a pro-apoptotic death receptor of TRAIL, are increased upon treatment with quinacrine, while levels of Mcl-1, an anti-apoptotic member of the Bcl-2 family, are decreased.	Quinacrine	190-200	TNF receptor superfamily member 10b	Homo sapiens	110-113
21565489-0	2011	Seleno-cyclodextrin sensitises human breast cancer cells to TRAIL-induced apoptosis through DR5 induction and NF-kappaB suppression.	seleno-cyclodextrin	0-19	TNF receptor superfamily member 10b	Homo sapiens	92-95
21801359-9	2011	In addition, we found that treatment of A549 cells with AFMC significantly induced the expression of death receptor 5 (DR5).	afmc	56-60	TNF receptor superfamily member 10b	Homo sapiens	101-117
21801359-9	2011	In addition, we found that treatment of A549 cells with AFMC significantly induced the expression of death receptor 5 (DR5).	afmc	56-60	TNF receptor superfamily member 10b	Homo sapiens	119-122
21801359-10	2011	AFMC-mediated sensitization of A549 cells to TRAIL was efficiently reduced by administration of a blocking antibody or small interfering RNAs against DR5.	afmc	0-4	TNF receptor superfamily member 10b	Homo sapiens	150-153
21801359-11	2011	AFMC also caused increase of the Sub-G1 cells by TRAIL treatment and increased the expression levels of DR5 in other NSCLC H460 and H157 cell lines.	afmc	0-4	TNF receptor superfamily member 10b	Homo sapiens	104-107
21801359-12	2011	In contrast, AFMC-mediated induction of DR5 expression was not observed in human embryo lung WI-38 cells, and AFMC did not sensitize WI-38 cells to TRAIL-induced apoptosis.	afmc	13-17	TNF receptor superfamily member 10b	Homo sapiens	40-43
21801359-13	2011	CONCLUSIONS: AFMC synergistically enhances TRAIL-mediated apoptosis in NSCLC cells through up-regulating DR5 expression.	afmc	13-17	TNF receptor superfamily member 10b	Homo sapiens	105-108
21354251-9	2011	Bupropion also induced the mRNA expression of the death receptors DR4 (TRAILR1) and DR5 (TRAILR2).	Bupropion	0-9	TNF receptor superfamily member 10b	Homo sapiens	89-96
21653830-6	2011	Lapatinib up-regulated the proapoptotic TRAIL death receptors DR4 and DR5, leading to more efficient induction of apoptosis in the presence of TRAIL receptor agonists.	Lapatinib	0-9	TNF receptor superfamily member 10b	Homo sapiens	70-73
21519792-1	2011	We previously reported that the chemopreventive agent lupulone induces apoptosis through activation of the extrinsic pathway via TRAIL DR4/DR5 death receptors overcoming SW620 cell resistance to TRAIL.	lupulon	54-62	TNF receptor superfamily member 10b	Homo sapiens	139-142
21519792-6	2011	In contrast to JNK and ERK inhibition, the specific inactivation of p38 inhibited the lupulone-triggered up-regulation of p53 and TRAIL-death receptor DR4/DR5 expression, and prevented DNA fragmentation.	lupulon	86-94	TNF receptor superfamily member 10b	Homo sapiens	155-158
21653830-8	2011	The off-target induction of DR5 by lapatinib resulted from activation of the c-Jun amino-terminal kinase (JNK)/c-Jun signaling axis.	Lapatinib	35-44	TNF receptor superfamily member 10b	Homo sapiens	28-31
21811429-0	2011	Up-regulation of the DR5 expression by proteasome inhibitor MG132 augments TRAIL-induced apoptosis in soft tissue sarcoma cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	TNF receptor superfamily member 10b	Homo sapiens	21-24
21362627-0	2011	Lipid raft-dependent death receptor 5 (DR5) expression and activation are critical for ursodeoxycholic acid-induced apoptosis in gastric cancer cells.	Ursodeoxycholic Acid	87-107	TNF receptor superfamily member 10b	Homo sapiens	21-37
21571804-2	2011	The purpose of this study was to characterize (64)Cu-labeled conatumumab as a PET tracer for imaging DR5 in tumors.	Copper	50-52	TNF receptor superfamily member 10b	Homo sapiens	101-104
21362627-0	2011	Lipid raft-dependent death receptor 5 (DR5) expression and activation are critical for ursodeoxycholic acid-induced apoptosis in gastric cancer cells.	Ursodeoxycholic Acid	87-107	TNF receptor superfamily member 10b	Homo sapiens	39-42
21362627-7	2011	In addition, reactive oxygen species (ROS) and protein kinase C (PKC) delta appeared to be implicated in UDCA-induced raft-dependent DR5 expression.	Reactive Oxygen Species	13-36	TNF receptor superfamily member 10b	Homo sapiens	133-136
21362627-7	2011	In addition, reactive oxygen species (ROS) and protein kinase C (PKC) delta appeared to be implicated in UDCA-induced raft-dependent DR5 expression.	Reactive Oxygen Species	38-41	TNF receptor superfamily member 10b	Homo sapiens	133-136
21362627-8	2011	Our results indicate that UDCA-induced apoptosis is mediated by DR5 expression, which is regulated by the raft formation/ROS production/PKCdelta activation pathway and DR5 localization into lipid rafts in gastric cancer cells.	Reactive Oxygen Species	121-124	TNF receptor superfamily member 10b	Homo sapiens	64-67
21393428-2	2011	Here, we report that bortezomib sensitizes these TRAIL-resistant cells, including Huh-7, Hep3B, and Sk-Hep1, to CS-1008, a humanized agonistic antihuman death receptor 5 antibody.	Bortezomib	21-31	TNF receptor superfamily member 10b	Homo sapiens	153-169
21539448-4	2011	The apoptotic effects of mDRA-6 on Jurkat cells, which express DR5 on the cell surface, were detected by flow cytometry and western blot after exposure to different doses of mDRA-6 and at fixed doses of mDRA-6 at different times.	mdra-6	25-31	TNF receptor superfamily member 10b	Homo sapiens	63-66
21468584-6	2011	Epirubicin significantly promoted lipid raft DR4 and DR5 aggregation, as well as the localization of DR4 and DR5 in the lipid rafts.	Epirubicin	0-10	TNF receptor superfamily member 10b	Homo sapiens	53-56
21468584-6	2011	Epirubicin significantly promoted lipid raft DR4 and DR5 aggregation, as well as the localization of DR4 and DR5 in the lipid rafts.	Epirubicin	0-10	TNF receptor superfamily member 10b	Homo sapiens	109-112
21468584-8	2011	Pretreatment with 50 microg/ml nystatin, a cholesterol-sequestering agent, partially prevented epirubicin-induced lipid raft aggregation and DR4 and DR5 clustering.	Nystatin	31-39	TNF receptor superfamily member 10b	Homo sapiens	149-152
21468584-8	2011	Pretreatment with 50 microg/ml nystatin, a cholesterol-sequestering agent, partially prevented epirubicin-induced lipid raft aggregation and DR4 and DR5 clustering.	Epirubicin	95-105	TNF receptor superfamily member 10b	Homo sapiens	149-152
21483669-3	2011	Furthermore, recombinant soluble TRAIL and an agonistic anti-DR5 antibody, AD5-10, treatment stimulates reactive oxygen species (ROS) generation and JNK phosphorylation.	Reactive Oxygen Species	104-127	TNF receptor superfamily member 10b	Homo sapiens	61-64
21483669-3	2011	Furthermore, recombinant soluble TRAIL and an agonistic anti-DR5 antibody, AD5-10, treatment stimulates reactive oxygen species (ROS) generation and JNK phosphorylation.	Reactive Oxygen Species	129-132	TNF receptor superfamily member 10b	Homo sapiens	61-64
21168266-6	2011	Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported.	celastrol	0-9	TNF receptor superfamily member 10b	Homo sapiens	159-162
21393428-0	2011	Bortezomib sensitizes HCC cells to CS-1008, an antihuman death receptor 5 antibody, through the inhibition of CIP2A.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	57-73
20619923-6	2011	Bortezomib treatment activated endoplasmic reticulum (ER) stress-mediated apoptosis, as demonstrated by the induction of GADD153, an ER stress-inducible transcription factor, and of the death receptor DR5, in EGFR inhibitor-resistant cells, but not in parental cells.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	201-204
21167276-0	2011	Piceatannol enhances TRAIL-induced apoptosis in human leukemia THP-1 cells through Sp1- and ERK-dependent DR5 up-regulation.	3,3',4,5'-tetrahydroxystilbene	0-11	TNF receptor superfamily member 10b	Homo sapiens	106-109
21167276-8	2011	In conclusion, our results suggest that PIC sensitizes TRAIL-induced-apoptosis via Sp1- and ERK-dependent DR5 up-regulation.	3,3',4,5'-tetrahydroxystilbene	40-43	TNF receptor superfamily member 10b	Homo sapiens	106-109
21297379-0	2011	Bisphosphonate enhances TRAIL sensitivity to human osteosarcoma cells via death receptor 5 upregulation.	Diphosphonates	0-14	TNF receptor superfamily member 10b	Homo sapiens	74-90
21297379-6	2011	Bisphosphonates significantly induced mRNA and protein expression of the TRAIL receptor, DR5.	Diphosphonates	0-15	TNF receptor superfamily member 10b	Homo sapiens	89-92
21206980-7	2011	MG132 enhanced the expression of the TRAIL receptors DR4 and DR5, and neutralization of DR5 receptors showed a marked reduction of TRAIL-mediated apoptosis, whereas that of DR4 was a partial reduction.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	TNF receptor superfamily member 10b	Homo sapiens	61-64
21292685-0	2011	Amiodarone sensitizes human glioma cells but not astrocytes to TRAIL-induced apoptosis via CHOP-mediated DR5 upregulation.	Amiodarone	0-10	TNF receptor superfamily member 10b	Homo sapiens	105-108
21292685-5	2011	Suppression of DR5 expression by small interfering (si) RNAs almost completely blocked amiodarone/TRAIL-induced apoptosis in U251MG glioma cells, demonstrating that DR5 is critical to this cell death.	Amiodarone	87-97	TNF receptor superfamily member 10b	Homo sapiens	15-18
21292685-5	2011	Suppression of DR5 expression by small interfering (si) RNAs almost completely blocked amiodarone/TRAIL-induced apoptosis in U251MG glioma cells, demonstrating that DR5 is critical to this cell death.	Amiodarone	87-97	TNF receptor superfamily member 10b	Homo sapiens	165-168
21292685-6	2011	siRNA-mediated CHOP suppression reduced amiodarone-induced DR5 upregulation and attenuated the cell death induced by amiodarone plus TRAIL.	Amiodarone	40-50	TNF receptor superfamily member 10b	Homo sapiens	59-62
21292685-7	2011	In addition, omitting Ca(2+) from the external medium using ethylene glycol tetraacetic acid markedly inhibited this cell death, reducing the protein levels of CHOP and DR5.	Egtazic Acid	60-92	TNF receptor superfamily member 10b	Homo sapiens	169-172
21292685-8	2011	These results suggest that amiodarone-induced influx of Ca(2+) plays an important role in sensitizing U251MG cells to TRAIL-mediated apoptosis through CHOP-mediated DR5 upregulation.	Amiodarone	27-37	TNF receptor superfamily member 10b	Homo sapiens	165-168
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	Bepridil	31-39	TNF receptor superfamily member 10b	Homo sapiens	214-217
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	cifenline	44-55	TNF receptor superfamily member 10b	Homo sapiens	214-217
21282356-5	2011	Curcumin-mediated ER stress via inhibiting the activity of SERCA2 caused increasing expressions of CHOP and its transcription target death receptor 5 (TRAIL-R2), leading to a caspase-3 and caspase-8 cascade-dependent apoptosis in SW872 cells in vitro and in vivo.	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	133-149
21282356-5	2011	Curcumin-mediated ER stress via inhibiting the activity of SERCA2 caused increasing expressions of CHOP and its transcription target death receptor 5 (TRAIL-R2), leading to a caspase-3 and caspase-8 cascade-dependent apoptosis in SW872 cells in vitro and in vivo.	Curcumin	0-8	TNF receptor superfamily member 10b	Homo sapiens	151-159
21206980-9	2011	Therefore, MG132 provides partial regulation of TRAIL-mediated apoptosis in OSCC cells via modulation of DR5, c-FLIP, cIAP-1, XIAP and survivin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	11-16	TNF receptor superfamily member 10b	Homo sapiens	105-108
21156789-9	2011	Induction of DRs was independent of p53 because UA induced DR4 and DR5 in HCT116 p53(-/-) cells.	ursolic acid	48-50	TNF receptor superfamily member 10b	Homo sapiens	67-70
21270522-6	2011	In addition, differently from saquinavir, Saq-NO restored TRAIL sensitivity that was correlated with increased expression of DR5 independent from ROS/RNS production and YY1 repression.	saquinavir-NO	42-48	TNF receptor superfamily member 10b	Homo sapiens	125-128
21195543-5	2011	Mechanisms underlying this sensitization mainly involved diosgenin-induced p38 MAPK pathway activation and subsequent DR5 overexpression.	Diosgenin	57-66	TNF receptor superfamily member 10b	Homo sapiens	118-121
21081474-0	2011	2-Tellurium-bridged beta-cyclodextrin, a thioredoxin reductase inhibitor, sensitizes human breast cancer cells to TRAIL-induced apoptosis through DR5 induction and NF-kappaB suppression.	2-tellurium	0-11	TNF receptor superfamily member 10b	Homo sapiens	146-149
21081474-0	2011	2-Tellurium-bridged beta-cyclodextrin, a thioredoxin reductase inhibitor, sensitizes human breast cancer cells to TRAIL-induced apoptosis through DR5 induction and NF-kappaB suppression.	betadex	20-37	TNF receptor superfamily member 10b	Homo sapiens	146-149
21081474-6	2011	From a mechanistic standpoint, we showed that 2-TeCD treatment of breast cancer cells significantly upregulated the messenger RNA and protein levels of TRAIL receptor, death receptor (DR) 5, in a transcription factor Sp1-dependent manner.	2-tecd	46-52	TNF receptor superfamily member 10b	Homo sapiens	168-189
21270522-7	2011	NF-kappaB activation may be responsible of the Saq-NO induced DR5 expression.	saquinavir-NO	47-53	TNF receptor superfamily member 10b	Homo sapiens	62-65
21152876-0	2011	Cisplatin sensitizes human hepatocellular carcinoma cells, but not hepatocytes and mesenchymal stem cells, to TRAIL within a therapeutic window partially depending on the upregulation of DR5.	Cisplatin	0-9	TNF receptor superfamily member 10b	Homo sapiens	187-190
20669244-0	2011	Naringenin up-regulates the expression of death receptor 5 and enhances TRAIL-induced apoptosis in human lung cancer A549 cells.	naringenin	0-10	TNF receptor superfamily member 10b	Homo sapiens	42-58
20669244-9	2011	We could show that following exposure to naringenin, DR5 proteins were up-regulated and knockdown of DR5 expression by siRNA attenuated naringenin plus TRAIL-induced apoptosis.	naringenin	41-51	TNF receptor superfamily member 10b	Homo sapiens	53-56
20669244-9	2011	We could show that following exposure to naringenin, DR5 proteins were up-regulated and knockdown of DR5 expression by siRNA attenuated naringenin plus TRAIL-induced apoptosis.	naringenin	41-51	TNF receptor superfamily member 10b	Homo sapiens	101-104
20669244-9	2011	We could show that following exposure to naringenin, DR5 proteins were up-regulated and knockdown of DR5 expression by siRNA attenuated naringenin plus TRAIL-induced apoptosis.	naringenin	136-146	TNF receptor superfamily member 10b	Homo sapiens	101-104
21152878-0	2011	Death receptor 5-mediated TNFR family signaling pathways modulate gamma-humulene-induced apoptosis in human colorectal cancer HT29 cells.	gamma-Humulene	66-80	TNF receptor superfamily member 10b	Homo sapiens	0-16
21152878-6	2011	gamma-Humulene stimulated the death receptor 5 (DR5), DR4, Fas-associated protein with death domain (FADD), the cleavage of caspase-8 and cleavage caspase-3, but reduced the protein levels of cellular Fas-associated death-domain-like IL-1ss-converting enzyme inhibitory protein (c-FLIP) by Western blot analysis.	gamma-Humulene	0-14	TNF receptor superfamily member 10b	Homo sapiens	30-46
21152878-6	2011	gamma-Humulene stimulated the death receptor 5 (DR5), DR4, Fas-associated protein with death domain (FADD), the cleavage of caspase-8 and cleavage caspase-3, but reduced the protein levels of cellular Fas-associated death-domain-like IL-1ss-converting enzyme inhibitory protein (c-FLIP) by Western blot analysis.	gamma-Humulene	0-14	TNF receptor superfamily member 10b	Homo sapiens	48-51
21152878-7	2011	Consequently, gamma-humulene-triggered cell death was significantly attenuated by DR5 siRNA and the caspase-8 inhibitor.	gamma-Humulene	14-28	TNF receptor superfamily member 10b	Homo sapiens	82-85
21152878-8	2011	Based on our results, we suggest that gamma-humulene induced apoptotic cell death in HT29 cells through a DR5-mediated caspase-8 and -3-dependent signaling pathway.	gamma-Humulene	38-52	TNF receptor superfamily member 10b	Homo sapiens	106-109
21935477-10	2011	Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8.	Imatinib Mesylate	41-49	TNF receptor superfamily member 10b	Homo sapiens	131-134
21272366-13	2011	Surprisingly, MG-132 but not IFN-gamma could also increase DR5-mediated apoptosis in SW948-TR.	Magnesium	14-16	TNF receptor superfamily member 10b	Homo sapiens	59-62
21078664-4	2011	This limonoid also enhanced expression of death receptors (DRs) DR5 and DR4 in cancer cells.	Limonins	5-13	TNF receptor superfamily member 10b	Homo sapiens	64-67
20951126-0	2011	Activation of p38 MAPK by damnacanthal mediates apoptosis in SKHep 1 cells through the DR5/TRAIL and TNFR1/TNF-alpha and p53 pathways.	damnacanthal	26-38	TNF receptor superfamily member 10b	Homo sapiens	87-90
20951126-4	2011	This is first demonstration that damnacanthal-mediated apoptosis involves the sustained activation of the p38 MAPK pathway, leading to the transcription of the death receptor family genes encoding DR5/TRAIL and TNF-R1/TNF-alpha genes as well as the p53-regulated Bax gene.	damnacanthal	33-45	TNF receptor superfamily member 10b	Homo sapiens	197-200
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	35-44	TNF receptor superfamily member 10b	Homo sapiens	252-268
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	Doxorubicin	50-54	TNF receptor superfamily member 10b	Homo sapiens	252-268
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	Cisplatin	58-62	TNF receptor superfamily member 10b	Homo sapiens	252-268
21037225-5	2011	Both platinum complexes increased DR5 surface expression in colon cancer cells.	Platinum	5-13	TNF receptor superfamily member 10b	Homo sapiens	34-37
21037225-6	2011	Small interfering RNA-mediated DR5 silencing rescued cells from sensitizing effects of platinum drugs on TRAIL-induced caspase-8 activation and apoptosis, showing the functional importance of DR5 in the effects observed.	Platinum	87-95	TNF receptor superfamily member 10b	Homo sapiens	31-34
21037225-6	2011	Small interfering RNA-mediated DR5 silencing rescued cells from sensitizing effects of platinum drugs on TRAIL-induced caspase-8 activation and apoptosis, showing the functional importance of DR5 in the effects observed.	Platinum	87-95	TNF receptor superfamily member 10b	Homo sapiens	192-195
21037225-7	2011	In addition, both cisplatin and LA-12 triggered the relocalization of DR4 and DR5 receptors to lipid rafts and accelerated internalization of TRAIL, which may also affect TRAIL signaling.	Cisplatin	18-27	TNF receptor superfamily member 10b	Homo sapiens	78-81
21037225-7	2011	In addition, both cisplatin and LA-12 triggered the relocalization of DR4 and DR5 receptors to lipid rafts and accelerated internalization of TRAIL, which may also affect TRAIL signaling.	UNII-37WM0V5E17	32-37	TNF receptor superfamily member 10b	Homo sapiens	78-81
21037225-8	2011	Collectively, modulations of the initial steps of the extrinsic apoptotic pathway at the level of DR5 and plasma membrane are important for sensitization of colon and prostate cancer cells to TRAIL-induced apoptosis mediated by LA-12 and cisplatin.	UNII-37WM0V5E17	228-233	TNF receptor superfamily member 10b	Homo sapiens	98-101
21037225-8	2011	Collectively, modulations of the initial steps of the extrinsic apoptotic pathway at the level of DR5 and plasma membrane are important for sensitization of colon and prostate cancer cells to TRAIL-induced apoptosis mediated by LA-12 and cisplatin.	Cisplatin	238-247	TNF receptor superfamily member 10b	Homo sapiens	98-101
21976975-0	2011	Anti-DR5 monoclonal antibody-mediated DTIC-loaded nanoparticles combining chemotherapy and immunotherapy for malignant melanoma: target formulation development and in vitro anticancer activity.	Dacarbazine	38-42	TNF receptor superfamily member 10b	Homo sapiens	5-8
21976975-4	2011	METHODS: The chemotherapeutic drug, dacarbazine (DTIC), that induces apoptosis through the intrinsic pathway which typically responds to severe DNA damage, was used as a model drug to prepare DTIC-loaded polylactic acid (PLA) nanoparticles (DTIC-NPs), which were covalently conjugated to a highly specific targeting functional TRAIL-receptor 2 (DR5) monoclonal antibody (mAb) that can contribute directly to cancer cell apoptosis or growth inhibition through the extrinsic pathway.	Dacarbazine	36-47	TNF receptor superfamily member 10b	Homo sapiens	345-348
21976975-4	2011	METHODS: The chemotherapeutic drug, dacarbazine (DTIC), that induces apoptosis through the intrinsic pathway which typically responds to severe DNA damage, was used as a model drug to prepare DTIC-loaded polylactic acid (PLA) nanoparticles (DTIC-NPs), which were covalently conjugated to a highly specific targeting functional TRAIL-receptor 2 (DR5) monoclonal antibody (mAb) that can contribute directly to cancer cell apoptosis or growth inhibition through the extrinsic pathway.	Dacarbazine	49-53	TNF receptor superfamily member 10b	Homo sapiens	345-348
21976975-4	2011	METHODS: The chemotherapeutic drug, dacarbazine (DTIC), that induces apoptosis through the intrinsic pathway which typically responds to severe DNA damage, was used as a model drug to prepare DTIC-loaded polylactic acid (PLA) nanoparticles (DTIC-NPs), which were covalently conjugated to a highly specific targeting functional TRAIL-receptor 2 (DR5) monoclonal antibody (mAb) that can contribute directly to cancer cell apoptosis or growth inhibition through the extrinsic pathway.	Dacarbazine	192-196	TNF receptor superfamily member 10b	Homo sapiens	345-348
21976975-4	2011	METHODS: The chemotherapeutic drug, dacarbazine (DTIC), that induces apoptosis through the intrinsic pathway which typically responds to severe DNA damage, was used as a model drug to prepare DTIC-loaded polylactic acid (PLA) nanoparticles (DTIC-NPs), which were covalently conjugated to a highly specific targeting functional TRAIL-receptor 2 (DR5) monoclonal antibody (mAb) that can contribute directly to cancer cell apoptosis or growth inhibition through the extrinsic pathway.	poly(lactide)	204-219	TNF receptor superfamily member 10b	Homo sapiens	345-348
21976975-4	2011	METHODS: The chemotherapeutic drug, dacarbazine (DTIC), that induces apoptosis through the intrinsic pathway which typically responds to severe DNA damage, was used as a model drug to prepare DTIC-loaded polylactic acid (PLA) nanoparticles (DTIC-NPs), which were covalently conjugated to a highly specific targeting functional TRAIL-receptor 2 (DR5) monoclonal antibody (mAb) that can contribute directly to cancer cell apoptosis or growth inhibition through the extrinsic pathway.	Dacarbazine	192-196	TNF receptor superfamily member 10b	Homo sapiens	345-348
22087285-8	2011	Furthermore, Bcl-2 was down-regulated whereas TRAIL-R1/DR4 and TRAIL-R2/DR5 expression was increased following the treatment of CSCs with GDC-0449.	HhAntag691	138-146	TNF receptor superfamily member 10b	Homo sapiens	63-71
22087285-8	2011	Furthermore, Bcl-2 was down-regulated whereas TRAIL-R1/DR4 and TRAIL-R2/DR5 expression was increased following the treatment of CSCs with GDC-0449.	HhAntag691	138-146	TNF receptor superfamily member 10b	Homo sapiens	72-75
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Resveratrol	180-191	TNF receptor superfamily member 10b	Homo sapiens	240-243
21931821-5	2011	CONCLUSION/SIGNIFICANCE: Altogether, these data suggest that Resveratrol acts as a suppressor of AKT/PKB pathway leading to apoptosis via generation of ROS and at the same time primes DLBCL cells via up-regulation of DR5 to TRAIL-mediated apoptosis.	Resveratrol	61-72	TNF receptor superfamily member 10b	Homo sapiens	217-220
21127198-7	2011	DBA also induced both death receptor (DR)-5 and DR4.	dibenzylidene acetone	0-3	TNF receptor superfamily member 10b	Homo sapiens	22-43
21127198-8	2011	Knockdown of DR5 and DR4 by small interfering RNA (SiRNA) reduced the sensitizing effect of DBA on TRAIL-induced apoptosis.	dibenzylidene acetone	92-95	TNF receptor superfamily member 10b	Homo sapiens	13-16
21127198-10	2011	Knockdown of CHOP by siRNA decreased the induction of DBA-induced DR5 expression and apoptosis.	dibenzylidene acetone	54-57	TNF receptor superfamily member 10b	Homo sapiens	66-69
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	dibenzylidene acetone	17-20	TNF receptor superfamily member 10b	Homo sapiens	42-45
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	Reactive Oxygen Species	89-112	TNF receptor superfamily member 10b	Homo sapiens	42-45
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	Reactive Oxygen Species	114-117	TNF receptor superfamily member 10b	Homo sapiens	42-45
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	Acetylcysteine	123-139	TNF receptor superfamily member 10b	Homo sapiens	42-45
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	dibenzylidene acetone	226-229	TNF receptor superfamily member 10b	Homo sapiens	42-45
21078664-11	2011	Overall, our results indicate that nimbolide can sensitize colon cancer cells to TRAIL-induced apoptosis through three distinct mechanisms: reactive oxygen species- and ERK-mediated up-regulation of DR5 and DR4, down-regulation of cell survival proteins, and up-regulation of p53 and Bax.	nimbolide	35-44	TNF receptor superfamily member 10b	Homo sapiens	199-202
21078664-11	2011	Overall, our results indicate that nimbolide can sensitize colon cancer cells to TRAIL-induced apoptosis through three distinct mechanisms: reactive oxygen species- and ERK-mediated up-regulation of DR5 and DR4, down-regulation of cell survival proteins, and up-regulation of p53 and Bax.	Reactive Oxygen Species	140-163	TNF receptor superfamily member 10b	Homo sapiens	199-202
20951126-8	2011	TRAIL- and TNF-alpha-mediated damnacanthal-induced apoptosis could be suppressed by treatment with caspase inhibitors as well as soluble death receptors Fc:DR5 and Fc:TNF-R1 chimera.	damnacanthal	30-42	TNF receptor superfamily member 10b	Homo sapiens	156-159
22115051-8	2011	alpha-TEA disrupted cholesterol-rich microdomains, acted cooperatively with TAM to reduce prosurvival mediators, and induced DR5-mediated mitochondria-dependent apoptosis via an endoplasmic reticulum stress-triggered pro-death pJNK/CHOP/DR5 amplification loop.	alpha-TEA	0-9	TNF receptor superfamily member 10b	Homo sapiens	125-128
22115051-8	2011	alpha-TEA disrupted cholesterol-rich microdomains, acted cooperatively with TAM to reduce prosurvival mediators, and induced DR5-mediated mitochondria-dependent apoptosis via an endoplasmic reticulum stress-triggered pro-death pJNK/CHOP/DR5 amplification loop.	alpha-TEA	0-9	TNF receptor superfamily member 10b	Homo sapiens	237-240
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Resveratrol	16-27	TNF receptor superfamily member 10b	Homo sapiens	100-103
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Resveratrol	16-27	TNF receptor superfamily member 10b	Homo sapiens	240-243
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Resveratrol	16-27	TNF receptor superfamily member 10b	Homo sapiens	240-243
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Reactive Oxygen Species	70-73	TNF receptor superfamily member 10b	Homo sapiens	100-103
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Resveratrol	180-191	TNF receptor superfamily member 10b	Homo sapiens	100-103
21931821-4	2011	Simultaneously, Resveratrol treatment of DLBCL cell lines also caused ROS dependent upregulation of DR5; and interestingly, co-treatment of DLBCL with sub-toxic doses of TRAIL and Resveratrol synergistically induced apoptosis via utilizing DR5, on the other hand, gene silencing of DR5 abolished this effect.	Resveratrol	180-191	TNF receptor superfamily member 10b	Homo sapiens	240-243
21172010-6	2010	Perifosine increased phosphorylated c-Jun NH2-terminal kinase (JNK) and c-Jun levels, which were paralleled with DR4 and DR5 induction.	perifosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	121-124
21044953-3	2010	The current study has revealed a novel ERK/ribosomal S6 kinase (RSK)-dependent mechanism that regulates DR5 expression primarily using celecoxib as a DR5 inducer.	Celecoxib	135-144	TNF receptor superfamily member 10b	Homo sapiens	104-107
21044953-3	2010	The current study has revealed a novel ERK/ribosomal S6 kinase (RSK)-dependent mechanism that regulates DR5 expression primarily using celecoxib as a DR5 inducer.	Celecoxib	135-144	TNF receptor superfamily member 10b	Homo sapiens	150-153
21044953-4	2010	Both C/EBP homologous protein (CHOP) and Elk1 are required for celecoxib-induced DR5 expression based on promoter deletion and mutation analysis and siRNA-mediated gene silencing results.	Celecoxib	63-72	TNF receptor superfamily member 10b	Homo sapiens	81-84
21044953-7	2010	Inhibition of either ERK signaling with a MEK inhibitor or ERK1/2 siRNA, or RSK2 signaling with an RSK2 inhibitor or RSK2 siRNA abrogated DR5 up-regulation by celecoxib as well as other agents.	Celecoxib	159-168	TNF receptor superfamily member 10b	Homo sapiens	138-141
21044953-10	2010	Additionally, celecoxib increased CHOP promoter activity in an ATF4-dependent manner, and siRNA-mediated blockade of ATF4 abrogated both CHOP induction and DR5 up-regulation, indicating that ATF4 is involved in celecoxib-induced CHOP and DR5 expression.	Celecoxib	211-220	TNF receptor superfamily member 10b	Homo sapiens	156-159
21044953-10	2010	Additionally, celecoxib increased CHOP promoter activity in an ATF4-dependent manner, and siRNA-mediated blockade of ATF4 abrogated both CHOP induction and DR5 up-regulation, indicating that ATF4 is involved in celecoxib-induced CHOP and DR5 expression.	Celecoxib	211-220	TNF receptor superfamily member 10b	Homo sapiens	238-241
21044953-11	2010	Collectively, we conclude that small molecules such as celecoxib induce DR5 expression through activating ERK/RSK signaling and subsequent Elk1 activation and ATF4-dependent CHOP induction.	Celecoxib	55-64	TNF receptor superfamily member 10b	Homo sapiens	72-75
21172010-0	2010	c-Jun NH2-terminal kinase-dependent upregulation of DR5 mediates cooperative induction of apoptosis by perifosine and TRAIL.	perifosine	103-113	TNF receptor superfamily member 10b	Homo sapiens	52-55
21172010-4	2010	Interestingly, perifosine primarily increased cell surface levels of DR5 although it elevated the expression of both DR4 and DR5.	perifosine	15-25	TNF receptor superfamily member 10b	Homo sapiens	69-72
21172010-4	2010	Interestingly, perifosine primarily increased cell surface levels of DR5 although it elevated the expression of both DR4 and DR5.	perifosine	15-25	TNF receptor superfamily member 10b	Homo sapiens	125-128
21172010-7	2010	However, only DR5 upregulaiton induced by perifosine could be abrogated by both the JNK inhibitor SP600125 and JNK siRNA.	perifosine	42-52	TNF receptor superfamily member 10b	Homo sapiens	14-17
21172010-5	2010	Blockade of DR5, but not DR4 upregulation, via small interfering RNA (siRNA) inhibited perifosine/TRAIL-induced apoptosis.	perifosine	87-97	TNF receptor superfamily member 10b	Homo sapiens	12-15
21172010-7	2010	However, only DR5 upregulaiton induced by perifosine could be abrogated by both the JNK inhibitor SP600125 and JNK siRNA.	pyrazolanthrone	98-106	TNF receptor superfamily member 10b	Homo sapiens	14-17
21172010-8	2010	The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5.	Acetylcysteine	18-34	TNF receptor superfamily member 10b	Homo sapiens	139-142
21172010-8	2010	The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5.	Glutathione	39-50	TNF receptor superfamily member 10b	Homo sapiens	139-142
21172010-8	2010	The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5.	perifosine	90-100	TNF receptor superfamily member 10b	Homo sapiens	139-142
21172010-10	2010	CONCLUSIONS: DR5 induction plays a critical role in mediating perifosine/TRAIL-induced apoptosis.	perifosine	62-72	TNF receptor superfamily member 10b	Homo sapiens	13-16
21172010-11	2010	Perifosine induces DR5 expression through a JNK-dependent mechanism independent of reactive oxygen species.	perifosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	19-22
21067180-2	2010	TCN induced cancer cell death treatment by triggering mitochondrial and death receptor 5 (DR5) apoptotic pathways.	tricetin	0-3	TNF receptor superfamily member 10b	Homo sapiens	72-88
21179458-15	2010	Inhibition of FOXO transcription factors by shRNA blocked resveratrol-induced upregulation of Bim, TRAIL, DR4, DR5, p27/KIP1 and apoptosis, and inhibition of cyclin D1 by resveratrol.	Resveratrol	58-69	TNF receptor superfamily member 10b	Homo sapiens	111-114
21067180-2	2010	TCN induced cancer cell death treatment by triggering mitochondrial and death receptor 5 (DR5) apoptotic pathways.	tricetin	0-3	TNF receptor superfamily member 10b	Homo sapiens	90-93
21067180-4	2010	Both of the antioxidants vitamin C and catalase significantly decreased apoptosis by inhibiting the phosphorylation of JNK and subsequently triggering DR5 cell death pathways.	Ascorbic Acid	25-34	TNF receptor superfamily member 10b	Homo sapiens	151-154
20804743-7	2010	Moreover, combined silencing of DR4 and DR5 by small interfering RNA abrogates the ability of PTX to induce TRAIL-mediated apoptosis.	Pentoxifylline	94-97	TNF receptor superfamily member 10b	Homo sapiens	40-43
21159614-0	2010	Contrasting effects of nutlin-3 on TRAIL- and docetaxel-induced apoptosis due to upregulation of TRAIL-R2 and Mcl-1 in human melanoma cells.	Docetaxel	46-55	TNF receptor superfamily member 10b	Homo sapiens	97-105
20804743-6	2010	PTX induces the expression of death receptors DR4 and DR5 on cell surface of both the cell types where c-Jun NH2-terminal kinase (JNK) pathway plays an important role.	Pentoxifylline	0-3	TNF receptor superfamily member 10b	Homo sapiens	54-57
20832390-6	2010	Knocking down DR5 using siRNA completely attenuated Chl-induced caspase-8 cleavage but partially inhibited apoptosis.	Chlorogenic Acid	52-55	TNF receptor superfamily member 10b	Homo sapiens	14-17
20832390-7	2010	Antioxidant NAC attenuated Chl-induced oxidative stress-mediated inhibition of Bcr-Abl phosphorylation, DR5 upregulation, caspase activation and CML cell death.	Chlorogenic Acid	27-30	TNF receptor superfamily member 10b	Homo sapiens	104-107
20623264-8	2010	The enhancement of Ad-TRAIL by cisplatin was due to the up-regulation of DR5 but not DR4 expression, and followed by the down-regulation of survivin and activation of Caspase 3.	Cisplatin	31-40	TNF receptor superfamily member 10b	Homo sapiens	73-76
20605676-2	2010	Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization.	celastrol	33-42	TNF receptor superfamily member 10b	Homo sapiens	86-89
20605676-2	2010	Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization.	celastrol	33-42	TNF receptor superfamily member 10b	Homo sapiens	191-194
20605676-5	2010	Taken together, the present study demonstrates that the enhanced mRNA and protein expression of DR4 and DR5 play prominent roles in the sensitization of celastrol to TRAIL/Apo-2L-induced apoptosis, in a p38 MAPK-independent manner.	celastrol	153-162	TNF receptor superfamily member 10b	Homo sapiens	104-107
20605676-2	2010	Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization.	celastrol	282-291	TNF receptor superfamily member 10b	Homo sapiens	86-89
20837473-11	2010	Overall, our results show that gossypol enhances TRAIL-induced apoptosis through the down-regulation of cell survival proteins and the up-regulation of TRAIL death receptors through the ROS-ERK-CHOP-DR5 pathway.	Reactive Oxygen Species	186-189	TNF receptor superfamily member 10b	Homo sapiens	199-202
20580868-4	2010	Sensitizing doses of vorinostat, valproic acid, sodium butyrate and MS-275 regulated the expression of TRAIL-R2, c-FLIP and Apaf-1 in leukemic cells while TSA modulated only the expression of Apaf-1.	Vorinostat	21-31	TNF receptor superfamily member 10b	Homo sapiens	103-111
20837473-6	2010	Gossypol-induced receptor induction was not cell type-specific, as DR5 induction was observed in other cell types.	Gossypol	0-8	TNF receptor superfamily member 10b	Homo sapiens	67-70
20837473-7	2010	Deletion of DR5 by siRNA significantly reduced the apoptosis induced by TRAIL and gossypol.	Gossypol	82-90	TNF receptor superfamily member 10b	Homo sapiens	12-15
20837473-8	2010	Gossypol induction of the death receptor required the induction of CHOP, and thus, gene silencing of CHOP abolished gossypol-induced DR5 expression and associated potentiation of apoptosis.	Gossypol	116-124	TNF receptor superfamily member 10b	Homo sapiens	133-136
20837473-9	2010	ERK1/2 (but not p38 MAPK or JNK) activation was also required for gossypol-induced TRAIL receptor induction; gene silencing of ERK abolished both DR5 induction and potentiation of apoptosis by TRAIL.	Gossypol	66-74	TNF receptor superfamily member 10b	Homo sapiens	146-149
20837473-11	2010	Overall, our results show that gossypol enhances TRAIL-induced apoptosis through the down-regulation of cell survival proteins and the up-regulation of TRAIL death receptors through the ROS-ERK-CHOP-DR5 pathway.	Gossypol	31-39	TNF receptor superfamily member 10b	Homo sapiens	199-202
20580868-4	2010	Sensitizing doses of vorinostat, valproic acid, sodium butyrate and MS-275 regulated the expression of TRAIL-R2, c-FLIP and Apaf-1 in leukemic cells while TSA modulated only the expression of Apaf-1.	Valproic Acid	33-46	TNF receptor superfamily member 10b	Homo sapiens	103-111
20580868-4	2010	Sensitizing doses of vorinostat, valproic acid, sodium butyrate and MS-275 regulated the expression of TRAIL-R2, c-FLIP and Apaf-1 in leukemic cells while TSA modulated only the expression of Apaf-1.	Butyric Acid	48-63	TNF receptor superfamily member 10b	Homo sapiens	103-111
20851102-6	2010	Mechanistically, 2DG and GD enhanced surface levels for both death receptors (DR4 and DR5); which was accompanied by reductions in levels of Mcl-1, Bcl-2 and survivin.	Deoxyglucose	17-20	TNF receptor superfamily member 10b	Homo sapiens	86-89
20886583-0	2010	alpha-TEA induces apoptosis of human breast cancer cells via activation of TRAIL/DR5 death receptor pathway.	alpha-TEA	0-9	TNF receptor superfamily member 10b	Homo sapiens	81-84
20886583-2	2010	alpha-TEA induces increased levels of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor-5 (DR5) and decreased levels of antiapoptotic factor, cellular FLICE-like inhibitory protein (c-FLIP L).	alpha-TEA	0-9	TNF receptor superfamily member 10b	Homo sapiens	106-122
20886583-2	2010	alpha-TEA induces increased levels of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor-5 (DR5) and decreased levels of antiapoptotic factor, cellular FLICE-like inhibitory protein (c-FLIP L).	alpha-TEA	0-9	TNF receptor superfamily member 10b	Homo sapiens	124-127
20886583-3	2010	DR5/TRAIL induced apoptosis involves downregulation of c-FLIP (L), caspase-8 activation, activated proapoptotic mediators tBid and Bax, mitochondrial permeability transition, and activation of caspase-9.	tBID	122-126	TNF receptor superfamily member 10b	Homo sapiens	0-3
20886583-4	2010	siRNA knockdown of either DR5 or TRAIL blocks the ability of alpha-TEA to enhance DR5 protein levels, downregulate c-FLIP(L) protein levels and induce apoptosis.	alpha-TEA	61-70	TNF receptor superfamily member 10b	Homo sapiens	26-29
20886583-4	2010	siRNA knockdown of either DR5 or TRAIL blocks the ability of alpha-TEA to enhance DR5 protein levels, downregulate c-FLIP(L) protein levels and induce apoptosis.	alpha-TEA	61-70	TNF receptor superfamily member 10b	Homo sapiens	82-85
20886583-5	2010	Combination of alpha-TEA + TRAIL acts cooperatively to induce apoptosis, and increase DR5 and decrease c-FLIP (L) protein levels.	alpha-tea +	15-26	TNF receptor superfamily member 10b	Homo sapiens	86-89
20886583-7	2010	Taken together, these studies show that alpha-TEA induces TRAIL/DR5 mitochondria-dependent apoptosis in human breast cancer cells, and that TRAIL/DR5-dependent increases in DR5 and decreases in c-FLIP expression are triggered by TRAIL or alpha-TEA treatments.	alpha-TEA	40-49	TNF receptor superfamily member 10b	Homo sapiens	64-67
20886583-7	2010	Taken together, these studies show that alpha-TEA induces TRAIL/DR5 mitochondria-dependent apoptosis in human breast cancer cells, and that TRAIL/DR5-dependent increases in DR5 and decreases in c-FLIP expression are triggered by TRAIL or alpha-TEA treatments.	alpha-TEA	40-49	TNF receptor superfamily member 10b	Homo sapiens	146-149
20886583-7	2010	Taken together, these studies show that alpha-TEA induces TRAIL/DR5 mitochondria-dependent apoptosis in human breast cancer cells, and that TRAIL/DR5-dependent increases in DR5 and decreases in c-FLIP expression are triggered by TRAIL or alpha-TEA treatments.	alpha-TEA	40-49	TNF receptor superfamily member 10b	Homo sapiens	146-149
20851102-7	2010	Mannose pre-treatment reduced enhanced killing by combination treatments, accompanied by reduced DR5 levels.	Mannose	0-7	TNF receptor superfamily member 10b	Homo sapiens	97-100
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	1-(3',4',5'-trimethoxyphenyl)-3-(3'',4''-dimethoxy-2'-hydroxyphenyl)propane	0-2	TNF receptor superfamily member 10b	Homo sapiens	365-368
20974006-2	2010	alpha-TEA induces apoptosis via activation of extrinsic death receptors Fas (CD95) and DR5, JNK/p73/Noxa pathways, and suppression of anti-apoptotic mediators Akt, ERK, c-FLIP and survivin in breast, ovarian and prostate cancer cells.	alpha-TEA	0-9	TNF receptor superfamily member 10b	Homo sapiens	87-90
20974006-3	2010	RESULTS: In this study, we demonstrate that alpha-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells.	alpha-TEA	44-53	TNF receptor superfamily member 10b	Homo sapiens	151-154
20974006-3	2010	RESULTS: In this study, we demonstrate that alpha-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells.	Ceramides	104-112	TNF receptor superfamily member 10b	Homo sapiens	151-154
20974006-5	2010	Functional knockdown of ASMase with either the chemical inhibitor, desipramine, or siRNA markedly reduces alpha-TEA-induced cell surface membrane accumulation of ceramide and its co-localization with Fas, DR5, and FADD, cleavage of caspases-8 and -9 and apoptosis, suggesting an early and critical role for ASMase in alpha-TEA-induced apoptosis.	alpha-TEA	106-115	TNF receptor superfamily member 10b	Homo sapiens	205-208
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	1-(3',4',5'-trimethoxyphenyl)-3-(3'',4''-dimethoxy-2'-hydroxyphenyl)propane	131-133	TNF receptor superfamily member 10b	Homo sapiens	365-368
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	TNF receptor superfamily member 10b	Homo sapiens	365-368
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	TNF receptor superfamily member 10b	Homo sapiens	365-368
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	1-(3',4',5'-trimethoxyphenyl)-3-(3'',4''-dimethoxy-2'-hydroxyphenyl)propane	131-133	TNF receptor superfamily member 10b	Homo sapiens	365-368
21713362-2	2010	Previously, apple procyanidins (Pcy) have been shown to upregulate the expression of TRAIL-DR4/-DR5 and thereby overcoming the resistance of human colon cancer-derived metastatic SW620 cells to TRAIL.	Proanthocyanidins	32-35	TNF receptor superfamily member 10b	Homo sapiens	96-99
20410100-7	2010	We genotyped single nucleotide polymorphisms (SNPs) in candidate genes in 8p12-p21 and found a significant association between fatty acids and SNPs in apolipoprotein J (APOJ), lipoprotein lipase (LPL), macrophage scavenger receptor 1 (MSR1), and tumor necrosis factor receptor superfamily member 10b (TNFRSF10B).	Fatty Acids	127-138	TNF receptor superfamily member 10b	Homo sapiens	246-299
20354842-7	2010	Interestingly, inhibition of PKC by Goe6983 enabled DR5 to trigger apoptotic signaling in response to TRAIL and also strongly enhanced lexatumumab-mediated cell death.	goe6983	36-43	TNF receptor superfamily member 10b	Homo sapiens	52-55
21713362-2	2010	Previously, apple procyanidins (Pcy) have been shown to upregulate the expression of TRAIL-DR4/-DR5 and thereby overcoming the resistance of human colon cancer-derived metastatic SW620 cells to TRAIL.	Proanthocyanidins	18-30	TNF receptor superfamily member 10b	Homo sapiens	96-99
20660600-0	2010	A combination of DR5 agonistic monoclonal antibody with gemcitabine targets pancreatic cancer stem cells and results in long-term disease control in human pancreatic cancer model.	gemcitabine	56-67	TNF receptor superfamily member 10b	Homo sapiens	17-20
20686688-0	2010	Role of endoplasmic reticulum stress in alpha-TEA mediated TRAIL/DR5 death receptor dependent apoptosis.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	40-49	TNF receptor superfamily member 10b	Homo sapiens	65-68
20686688-5	2010	CONCLUSION: Taken together, ER stress plays an important role in alpha-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/caspase-8 signaling.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	65-74	TNF receptor superfamily member 10b	Homo sapiens	106-109
20686688-5	2010	CONCLUSION: Taken together, ER stress plays an important role in alpha-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/caspase-8 signaling.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	65-74	TNF receptor superfamily member 10b	Homo sapiens	232-235
20410100-0	2010	Genetic variation in APOJ, LPL, and TNFRSF10B affects plasma fatty acid distribution in Alaskan Eskimos.	Fatty Acids	61-71	TNF receptor superfamily member 10b	Homo sapiens	36-45
20410100-7	2010	We genotyped single nucleotide polymorphisms (SNPs) in candidate genes in 8p12-p21 and found a significant association between fatty acids and SNPs in apolipoprotein J (APOJ), lipoprotein lipase (LPL), macrophage scavenger receptor 1 (MSR1), and tumor necrosis factor receptor superfamily member 10b (TNFRSF10B).	Fatty Acids	127-138	TNF receptor superfamily member 10b	Homo sapiens	301-310
20410100-8	2010	A Bayesian quantitative trait nucleotide analysis based on a measured genotype model showed that SNPs in LPL, TNFRSF10B, and APOJ had strong statistical evidence of a functional effect (posterior probability &gt; or =75%) on plasma fatty acid distribution.	Fatty Acids	232-242	TNF receptor superfamily member 10b	Homo sapiens	110-119
19538462-3	2010	While nickel treatment increased surface expression of the apoptosis-inducing TRAIL receptors TRAIL-R1 and TRAIL-R2, it also up-regulated the apoptosis-deficient TRAIL-R4, suggesting that modulation of TRAIL receptor expression alone is unlikely to fully account for the dramatic sensitization effect of nickel.	Nickel	6-12	TNF receptor superfamily member 10b	Homo sapiens	107-115
19538480-6	2010	Gene reporter assays confirmed that the RA-induced t-PA gene expression occurred through interactions of retinoid receptors (RARs and RXRs) with a DR5 response element located at -7 kb from the transcription site.	Tretinoin	40-42	TNF receptor superfamily member 10b	Homo sapiens	147-150
19538480-8	2010	Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment.	Tretinoin	69-71	TNF receptor superfamily member 10b	Homo sapiens	145-148
19538480-8	2010	Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment.	Tretinoin	69-71	TNF receptor superfamily member 10b	Homo sapiens	224-227
19538480-8	2010	Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment.	Tretinoin	119-121	TNF receptor superfamily member 10b	Homo sapiens	145-148
19538480-8	2010	Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment.	Tretinoin	119-121	TNF receptor superfamily member 10b	Homo sapiens	224-227
20515942-0	2010	Butein sensitizes human hepatoma cells to TRAIL-induced apoptosis via extracellular signal-regulated kinase/Sp1-dependent DR5 upregulation and NF-kappaB inactivation.	butein	0-6	TNF receptor superfamily member 10b	Homo sapiens	122-125
20515942-4	2010	In this study, we determined that butein enhances TRAIL-induced apoptosis in hepatoma cells through upregulation of DR5.	butein	34-40	TNF receptor superfamily member 10b	Homo sapiens	116-119
20515942-6	2010	Electrophoretic mobility shift assays and chromatin immunoprecipitation studies were used to analyze the elevation of Sp1 binding to DR5 promoter sites by butein.	butein	155-161	TNF receptor superfamily member 10b	Homo sapiens	133-136
20515942-8	2010	Furthermore, pretreatment of the blocking chimeric antibody and small interfering RNA for DR5 significantly suppressed TRAIL-mediated apoptosis by butein in Hep3B cells.	butein	147-153	TNF receptor superfamily member 10b	Homo sapiens	90-93
20515942-9	2010	Butein also stimulated extracellular signal-regulated kinase (ERK) activation, and the ERK inhibitor PD98059 blocked butein-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	101-108	TNF receptor superfamily member 10b	Homo sapiens	132-135
20515942-9	2010	Butein also stimulated extracellular signal-regulated kinase (ERK) activation, and the ERK inhibitor PD98059 blocked butein-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	101-108	TNF receptor superfamily member 10b	Homo sapiens	184-187
20515942-9	2010	Butein also stimulated extracellular signal-regulated kinase (ERK) activation, and the ERK inhibitor PD98059 blocked butein-induced DR5 expression and suppressed binding of Sp1 to the DR5 promoter.	butein	117-123	TNF receptor superfamily member 10b	Homo sapiens	132-135
20224297-3	2010	Our data indicate that DHA suppresses the PI3-K/Akt and ERK cell survival pathways and triggers the induction of death receptor DR5 and activation of extrinsic and intrinsic cell death signaling.	artenimol	23-26	TNF receptor superfamily member 10b	Homo sapiens	128-131
20224297-4	2010	DHA-mediated DR5 induction appears to occur via increased transcriptional activity of DR5 promoter.	artenimol	0-3	TNF receptor superfamily member 10b	Homo sapiens	13-16
20224297-4	2010	DHA-mediated DR5 induction appears to occur via increased transcriptional activity of DR5 promoter.	artenimol	0-3	TNF receptor superfamily member 10b	Homo sapiens	86-89
20356045-0	2010	6-dehydrogingerdione sensitizes human hepatoblastoma Hep G2 cells to TRAIL-induced apoptosis via reactive oxygen species-mediated increase of DR5.	6-dehydrogingerdione	0-20	TNF receptor superfamily member 10b	Homo sapiens	142-145
19900759-2	2010	In the gene expression assay using a DNA microalley, adenosine upregulated mRNAs for tumor necrosis factor (TNF), TNF receptor 1-associated death domain protein (TRADD), TNF related apoptosis-inducing ligand receptor 2 (TRAIL-R2), TRADD/receptor-interacting protein kinase 1 (RIPK1), Fas-associated death domain protein (FADD), and caspase-9, involving activation of caspase-8 and -9 followed by the effector caspase-3.	Adenosine	53-62	TNF receptor superfamily member 10b	Homo sapiens	170-218
19900759-2	2010	In the gene expression assay using a DNA microalley, adenosine upregulated mRNAs for tumor necrosis factor (TNF), TNF receptor 1-associated death domain protein (TRADD), TNF related apoptosis-inducing ligand receptor 2 (TRAIL-R2), TRADD/receptor-interacting protein kinase 1 (RIPK1), Fas-associated death domain protein (FADD), and caspase-9, involving activation of caspase-8 and -9 followed by the effector caspase-3.	Adenosine	53-62	TNF receptor superfamily member 10b	Homo sapiens	220-228
20356045-9	2010	Taken together, these data suggested that in addition to the mitochondrial- and Fas receptor-mediated apoptotic pathways involved, ROS-dependent and p53-regulated DR5 expression was also demonstrated to play a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by 6-DG in Hep G2 cells.	Reactive Oxygen Species	131-134	TNF receptor superfamily member 10b	Homo sapiens	163-166
20356045-0	2010	6-dehydrogingerdione sensitizes human hepatoblastoma Hep G2 cells to TRAIL-induced apoptosis via reactive oxygen species-mediated increase of DR5.	Reactive Oxygen Species	97-120	TNF receptor superfamily member 10b	Homo sapiens	142-145
20356045-9	2010	Taken together, these data suggested that in addition to the mitochondrial- and Fas receptor-mediated apoptotic pathways involved, ROS-dependent and p53-regulated DR5 expression was also demonstrated to play a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by 6-DG in Hep G2 cells.	6-dehydrogingerdione	295-299	TNF receptor superfamily member 10b	Homo sapiens	163-166
20356045-5	2010	Abrogation of p53 expression by p53 small interfering RNA significantly attenuated 6-DG-induced DR5 expression, thus rendering these cells resistant to TRAIL-induced apoptosis.	6-dehydrogingerdione	83-87	TNF receptor superfamily member 10b	Homo sapiens	96-99
20356045-6	2010	DR5 expression after 6-DG treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation.	6-dehydrogingerdione	21-25	TNF receptor superfamily member 10b	Homo sapiens	0-3
20356045-6	2010	DR5 expression after 6-DG treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation.	Reactive Oxygen Species	79-102	TNF receptor superfamily member 10b	Homo sapiens	0-3
20356045-6	2010	DR5 expression after 6-DG treatment was accompanied by provoking intracellular reactive oxygen species (ROS) generation.	Reactive Oxygen Species	104-107	TNF receptor superfamily member 10b	Homo sapiens	0-3
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	Acetylcysteine	18-37	TNF receptor superfamily member 10b	Homo sapiens	68-71
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	Acetylcysteine	39-42	TNF receptor superfamily member 10b	Homo sapiens	68-71
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	6-dehydrogingerdione	55-59	TNF receptor superfamily member 10b	Homo sapiens	68-71
20356045-8	2010	In contrast to Hep G2 cells, DR5 up-regulation and sensitization to TRAIL-induced apoptosis instigated by 6-DG were not observed in normal MDCK cells.	6-dehydrogingerdione	106-110	TNF receptor superfamily member 10b	Homo sapiens	29-32
19965642-7	2010	In CLL patients receiving lenalidomide, similar evidence of CD154 activation is observed including BID, DR5, and p73 induction and also development of anti-ROR1 tumor-directed antibodies.	Lenalidomide	26-38	TNF receptor superfamily member 10b	Homo sapiens	104-107
20154087-8	2010	We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL.	Reactive Oxygen Species	83-86	TNF receptor superfamily member 10b	Homo sapiens	152-155
20154087-8	2010	We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL.	celastrol	111-120	TNF receptor superfamily member 10b	Homo sapiens	152-155
20154087-4	2010	In addition, we found that celastrol induced the cell surface expression of both the TRAIL receptors DR4 and DR5.	celastrol	27-36	TNF receptor superfamily member 10b	Homo sapiens	109-112
20154087-7	2010	Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis.	triterpenoid TP-222	39-51	TNF receptor superfamily member 10b	Homo sapiens	233-236
20371719-5	2010	The combination of AD5-10 with carboplatin exerts a more than additive effect in vitro, which may at least partially be explained by the fact that carboplatin triggers DR5 expression on ovarian cancer cells.	ad5-10	19-25	TNF receptor superfamily member 10b	Homo sapiens	168-171
20156289-4	2010	To identify peptides that specifically interact with DR5, a disulfide-constrained phage display peptide library was screened for binders towards this receptor.	Disulfides	60-69	TNF receptor superfamily member 10b	Homo sapiens	53-56
20354117-0	2010	beta-Ionone enhances TRAIL-induced apoptosis in hepatocellular carcinoma cells through Sp1-dependent upregulation of DR5 and downregulation of NF-kappaB activity.	beta-ionone	0-11	TNF receptor superfamily member 10b	Homo sapiens	117-120
20371719-5	2010	The combination of AD5-10 with carboplatin exerts a more than additive effect in vitro, which may at least partially be explained by the fact that carboplatin triggers DR5 expression on ovarian cancer cells.	Carboplatin	31-42	TNF receptor superfamily member 10b	Homo sapiens	168-171
20371719-5	2010	The combination of AD5-10 with carboplatin exerts a more than additive effect in vitro, which may at least partially be explained by the fact that carboplatin triggers DR5 expression on ovarian cancer cells.	Carboplatin	147-158	TNF receptor superfamily member 10b	Homo sapiens	168-171
20096292-0	2010	Quercetin enhances TRAIL-induced apoptosis in prostate cancer cells via increased protein stability of death receptor 5.	Quercetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	103-119
19922463-10	2010	Bortezomib also increased DR4 and DR5 expression in the presence of stroma.	Bortezomib	0-10	TNF receptor superfamily member 10b	Homo sapiens	34-37
20106985-4	2010	The cysteine-rich domains of DR5 have a conservative role in tumor necrosis factor-related apoptosis-inducing ligand-DR5-mediated apoptosis, and the pre-ligand assembly domain within the N1-cap contributes to the ligand-independent formation of receptor complexes.	Cysteine	4-12	TNF receptor superfamily member 10b	Homo sapiens	29-32
20106985-4	2010	The cysteine-rich domains of DR5 have a conservative role in tumor necrosis factor-related apoptosis-inducing ligand-DR5-mediated apoptosis, and the pre-ligand assembly domain within the N1-cap contributes to the ligand-independent formation of receptor complexes.	Cysteine	4-12	TNF receptor superfamily member 10b	Homo sapiens	117-120
20106985-9	2010	Moreover, permutation analysis showed that Leu(6) was pivotal for the interaction of DR5 and the agonistic antibody.	Leucine	43-46	TNF receptor superfamily member 10b	Homo sapiens	85-88
20096292-1	2010	AIMS: Quercetin has been shown to enhance tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis of prostate cancer cells via mechanisms that include upregulation of death receptor (DR) 5, a protein reported to play an important role in sensitizing cancer cells to apoptosis.	Quercetin	6-15	TNF receptor superfamily member 10b	Homo sapiens	193-214
20096292-2	2010	We aimed to determine the specific mechanisms underlying quercetin-induced DR5 expression.	Quercetin	57-66	TNF receptor superfamily member 10b	Homo sapiens	75-78
20096292-8	2010	Quercetin dose-dependently increased DR5 levels in prostate cancer cells, which was mediated by increased transcription and protein stability, but not mRNA stability.	Quercetin	0-9	TNF receptor superfamily member 10b	Homo sapiens	37-40