Ignet

Gene Information

Gene symbol: TNFRSF10B

Gene name: tumor necrosis factor receptor superfamily, member 10b

HGNC ID: 11905

Synonyms: DR5, KILLER, TRICK2A, TRAIL-R2, TRICKB, CD262

Related Genes

#	Gene Symbol	Number of hits
1	ATF3	1 hits
2	AXPC1	1 hits
3	BAK1	1 hits
4	BAX	1 hits
5	BBC3	1 hits
6	BCL2	1 hits
7	BCL2L1	1 hits
8	BCL2L11	1 hits
9	CAMK2G	1 hits
10	CASP8	1 hits
11	CFLAR	1 hits
12	CLU	1 hits
13	FADD	1 hits
14	FAS	1 hits
15	HDAC9	1 hits
16	IDDM2	1 hits
17	IGKV1-17	1 hits
18	INS	1 hits
19	LPL	1 hits
20	MCL1	1 hits
21	NDUFB4	1 hits
22	NFKB1	1 hits
23	NOS2A	1 hits
24	PEA15	1 hits
25	PMAIP1	1 hits
26	RIPK1	1 hits
27	THM	1 hits
28	TNF	1 hits
29	TNFRSF10A	1 hits
30	TNFRSF10C	1 hits
31	TNFRSF10D	1 hits
32	TNFRSF21	1 hits
33	TNFRSF25	1 hits
34	TNFSF10	1 hits
35	TOR1B	1 hits
36	TP53	1 hits

Related Sentences

#	PMID	Sentence
1	2075785	The purpose of our study was to evaluate what kind of relationships exist between HLA antigens and insulin-dependent diabetes mellitus (IDDM), in 20 families and in 40 single patients coming from and living in North Eastern Italy.
2	2075785	We also noticed a negative association between IDDM and DR5 rather than DR2 and DR7.
3	2451692	HLA-DR (DR3, DR4, and DR5) and HLA-DQ (DQw2/DQw3) Ag can restrict these T cell responses to human insulin epitopes.
4	2648900	[HLA, A, B, C, DR, C4, Bf in insulin-dependent diabetics in the Tunisian population].
5	2648900	The frequency of HLA-A-B and DR antigens as well as the Bf and C4 allotypes have been investigated in insulinodependant diabetes mellitus (IDDM) and compared to that of healthy controls in Tunisian population.
6	2648900	An increase of A30, DR3, DR4, BfF1, C4AQ0 and C4BQ0 and decrease of B40, DR2, DR5 and DR6 were found in diabetes when compared to the value observation controls.
7	2648900	The strongest association was noticed with HLA, DR3 and DR4.
8	2714046	The frequency of HLA A, B, and DR antigens as well as the Bf and C4 allotypes have been investigated in insulin-dependent diabetes mellitus (IDDM) and compared to that of healthy controls in the Tunisian population.
9	2714046	An increase of A30, DR3, DR4, BfF1, C4Ao, and C4Bo and decrease of B40, DR2, DR5, and DR6 were found in diabetics when compared to the value observed in controls.
10	2714046	The strongest association was noticed with HLA DR3 and DR4.
11	2714046	Heterozygotes DR3 DR4 were very frequent in diabetics: 24.2 per cent versus 3.6 per cent in controls (relative risk 7.72).
12	2979618	DR3 and DR4 have been the most positive and DR2 the most negative.
13	2979618	In 952 Caucasian proband patients reported here, only 57 or 6% had no DR3 or DR4 alleles.
14	2979618	When these 57 patients were compared to 249 Caucasian controls similarly lacking DR3 and DR4 antigens, there were excesses of DR1 (P = 0.13) and DRW8 (P = 0.01) and deficiencies of DR2 (P = 0.03) and DR5 (P = 0.03) in the patient group.
15	2979618	Only four DR-homozygous patients involving alleles other than DR3 and DR4 were found by genotyping, and all were DR1 homozygotes.
16	2979618	We conclude that DR1 is an additional risk DR allele for IDD to that of DR3 and DR4, and DR5 an additional protective DR allele to that of DR2.
17	2999795	This restriction fragment pattern was found for several haplotypes associated with the DQw3 specificity, including some haplotypes positive for the HLA-DR specificities DR4, DR5, DRw8, and DRw12.
18	3059902	Type III groups together 10 autoimmune diseases (autoimmune thyroid disease, myasthenia and/or thymoma, Sjögren's syndrome, pernicious anaemia, idiopathic thrombocytopaenic purpura, Addison's disease, insulin-dependent diabetes, vitiligo, autoimmune haemolytic anaemia, systemic lupus erythematosus) for which a genetic predisposition (phenotype HLA B8 and/or DR3 or DR5) seems to be an important factor.
19	3160593	Her HLA type was A3, A9, B8, B15, DR3, DR5.
20	3545954	The Type 1 diabetic patients showed a typical HLA pattern, with increased frequencies of B15, DR3, DR4, B8/B15 and DR3/DR4 and decreased frequencies of B7 and DR2.
21	3545954	The Type 2 diabetic patients could be distinguished from blood donors by increased frequencies of Cw4, DR4, DR5 and DR3/DR4, and from Type 1 diabetic patients by increased frequencies of B7, DR2, DR5 and decreased frequency of A9, Bw22 and DR4.
22	3545954	Age at onset and body mass index were unrelated to HLA antigens, but the Type 2 diabetic patients with HLA-Cw4, DR5 and DR6 showed a strong family history for Type 2 diabetes.
23	3545954	Type 2 diabetic patients with HLA-B8, DR4, B8/B15 and DR3/DR4 showed significantly lower C-peptide concentrations (p less than 0.05) than patients without these HLA antigens.
24	3545954	Twelve patients who were positive for both DR3 and DR4 and 23 patients who were DR3/DR4 negative were followed with repeated C-peptide determinations during a period of three years.
25	3545954	The C-peptide concentrations of the DR3/DR4 positive patients decreased during this period, whereas there was no change in C-peptide levels in the DR3/DR4 negative patients.
26	3545954	The Type 1 diabetic patients showed a typical HLA pattern, with increased frequencies of B15, DR3, DR4, B8/B15 and DR3/DR4 and decreased frequencies of B7 and DR2.
27	3545954	The Type 2 diabetic patients could be distinguished from blood donors by increased frequencies of Cw4, DR4, DR5 and DR3/DR4, and from Type 1 diabetic patients by increased frequencies of B7, DR2, DR5 and decreased frequency of A9, Bw22 and DR4.
28	3545954	Age at onset and body mass index were unrelated to HLA antigens, but the Type 2 diabetic patients with HLA-Cw4, DR5 and DR6 showed a strong family history for Type 2 diabetes.
29	3545954	Type 2 diabetic patients with HLA-B8, DR4, B8/B15 and DR3/DR4 showed significantly lower C-peptide concentrations (p less than 0.05) than patients without these HLA antigens.
30	3545954	Twelve patients who were positive for both DR3 and DR4 and 23 patients who were DR3/DR4 negative were followed with repeated C-peptide determinations during a period of three years.
31	3545954	The C-peptide concentrations of the DR3/DR4 positive patients decreased during this period, whereas there was no change in C-peptide levels in the DR3/DR4 negative patients.
32	6602084	The results show that the most common coeliac phenotypes are DR3/DR7, DR7/DR5, DR3/other DR, and DR3/DR3.
33	7660388	Fifty-seven Thai IDDM patients were studied for HLA class I by LCT and HLA class II by LCT and PCR-RFLP.
34	7660388	In contrast, DQA10101, DRB30301, DR5 and DQ1 were significantly decreased with R.R. = 0.2, 0.2, 0.3 and 0.5 and Pc < 0.01, 0.05, 0.01 and 0.05, respectively.
35	7660388	However, DR3/DR4 genotype was increased only in female patients with a family history of DM and early onset.
36	7835212	Fifty juvenile insulin dependent diabetes mellitus (JIDDM) patients of Tamil Nadu (South India) were typed for HLA-A, -B, -C, -DR, and -DQ, ESD, GLOI, C3 and HP polymorphisms.
37	7835212	The frequencies of B8, DR3, DR4, DR53 and DQ2 antigens of the HLA system were significantly higher in the patients than in controls (relative risk, RR = 4.81; 5.14; 3.98; 3.36 and 2.53, respectively).
38	7835212	However HLA-DR2, -DR5 and -DQ1, observed less frequently in the patient group, appear to play a role of protection against the disease (RR = 0.32; 0.30 and 0.20 respectively).
39	11004907	We studied the grade of associated organ-specific autoimmunity and the pattern of prevalence of TPO and PCA by age, gender, duration, age at onset of diabetes, and HLA DR haplotype in 783 type 1 diabetic patients, consisting of 286 children and 497 adults (M/F: 389/394), with a mean diabetes duration of 11.8 +/- 10.1 years.
40	11004907	We observed an association between HLA DR5 and PCA (p = 0.0012).
41	11221847	Induction and intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediated apotosis in human malignant glioma cells.
42	11221847	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) preferentially triggers apoptosis in tumor cells versus normal cells, thus providing a therapeutic potential.
43	11221847	TRAIL-induced cell death was characterized by activation of caspase-8 and -3, poly(ADP-ribose) polymerase cleavage, and DNA fragmentation.
44	11221847	Decoy receptor (DcR1 and DcR2) expression was limited in the glioma cell lines and did not correlate with TRAIL sensitivity.
45	11221847	Both sensitive and resistant cell lines expressed TRAIL death receptor (DR5), adapter protein Fas-associated death domain (FADD), and caspase-8; but resistant cell lines expressed 2-fold higher levels of the apoptosis inhibitor phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes-15 kDa (PED/PEA-15).
46	11221847	In contrast, cellular FADD-like IL-1beta-converting enzyme-like inhibitory protein (cFLIP) expression was similar in sensitive and resistant cells.
47	11221847	Inhibition of protein kinase C (PKC) activity restored TRAIL sensitivity in resistant cells, suggesting that PED/ PEA-15 function might be dependent on PKC-mediated phosphorylation.
48	11221847	This caspase-8-induced apoptotic cascade is regulated by intracellular PED/PEA-15, but not by cFLIP or decoy receptors.
49	12706864	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to exert potent cytotoxic activity against many tumor cells but not normal cells.
50	12706864	We found that most TRAIL-resistant and -partial resistant clones expressed low levels of DR5, whereas most TRAIL-sensitive clones expressed high levels of Death Receptor (DR5).
51	12706864	However, there were clones with a range of different TRAIL-sensitivities that had similar levels of DR5 expression.
52	12706864	The expression levels of DR4 and the decoy receptors, DcR1 and DcR2, did not correlate with TRAIL sensitivities.
53	12706864	We also compared the subgroups in terms of the expression of Fas-associated death domain protein (FADD), the levels of activation of Receptor Interacting Protein (RIP) and caspases, and cleavage of Poly (ADP-Ribose)Polymerase (PARP).
54	12706864	After treatment with TRAIL, both TRAIL-sensitive and partial resistant clones showed high levels of activation of caspase-3, caspase-8, RIP and PARP.
55	12706864	Relative basal level and induced level of Phosphoprotein over Expressed in Diabetes/Phosphoprotein Enriched in Astrocytes (PED/PEA-15) after TRAIL treatment were compared in the clones.
56	12706864	TRAIL did not change the PED/PEA-15 level in the clones.
57	12706864	In addition, transduction and expression of the dominant negative form of the I-kBalpha gene did not change TRAIL-sensitivities.
58	12706864	Our results showed that the expression levels of DR5, the activation levels of caspase-8, -3 and RIP were critical factors in determining TRAIL-sensitivities in Jurkat cells.
59	12706864	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to exert potent cytotoxic activity against many tumor cells but not normal cells.
60	12706864	We found that most TRAIL-resistant and -partial resistant clones expressed low levels of DR5, whereas most TRAIL-sensitive clones expressed high levels of Death Receptor (DR5).
61	12706864	However, there were clones with a range of different TRAIL-sensitivities that had similar levels of DR5 expression.
62	12706864	The expression levels of DR4 and the decoy receptors, DcR1 and DcR2, did not correlate with TRAIL sensitivities.
63	12706864	We also compared the subgroups in terms of the expression of Fas-associated death domain protein (FADD), the levels of activation of Receptor Interacting Protein (RIP) and caspases, and cleavage of Poly (ADP-Ribose)Polymerase (PARP).
64	12706864	After treatment with TRAIL, both TRAIL-sensitive and partial resistant clones showed high levels of activation of caspase-3, caspase-8, RIP and PARP.
65	12706864	Relative basal level and induced level of Phosphoprotein over Expressed in Diabetes/Phosphoprotein Enriched in Astrocytes (PED/PEA-15) after TRAIL treatment were compared in the clones.
66	12706864	TRAIL did not change the PED/PEA-15 level in the clones.
67	12706864	In addition, transduction and expression of the dominant negative form of the I-kBalpha gene did not change TRAIL-sensitivities.
68	12706864	Our results showed that the expression levels of DR5, the activation levels of caspase-8, -3 and RIP were critical factors in determining TRAIL-sensitivities in Jurkat cells.
69	12706864	Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to exert potent cytotoxic activity against many tumor cells but not normal cells.
70	12706864	We found that most TRAIL-resistant and -partial resistant clones expressed low levels of DR5, whereas most TRAIL-sensitive clones expressed high levels of Death Receptor (DR5).
71	12706864	However, there were clones with a range of different TRAIL-sensitivities that had similar levels of DR5 expression.
72	12706864	The expression levels of DR4 and the decoy receptors, DcR1 and DcR2, did not correlate with TRAIL sensitivities.
73	12706864	We also compared the subgroups in terms of the expression of Fas-associated death domain protein (FADD), the levels of activation of Receptor Interacting Protein (RIP) and caspases, and cleavage of Poly (ADP-Ribose)Polymerase (PARP).
74	12706864	After treatment with TRAIL, both TRAIL-sensitive and partial resistant clones showed high levels of activation of caspase-3, caspase-8, RIP and PARP.
75	12706864	Relative basal level and induced level of Phosphoprotein over Expressed in Diabetes/Phosphoprotein Enriched in Astrocytes (PED/PEA-15) after TRAIL treatment were compared in the clones.
76	12706864	TRAIL did not change the PED/PEA-15 level in the clones.
77	12706864	In addition, transduction and expression of the dominant negative form of the I-kBalpha gene did not change TRAIL-sensitivities.
78	12706864	Our results showed that the expression levels of DR5, the activation levels of caspase-8, -3 and RIP were critical factors in determining TRAIL-sensitivities in Jurkat cells.
79	15718275	Immunohistochemistry displayed a greater amount of TNF-related apoptosis-inducing ligand (TRAIL) and KILLER, a key murine ligand and receptor involved in the extrinsic pathway, expressed in cumulus cells from hyperglycemic mice compared with controls, suggesting that this apoptotic pathway may be up-regulated under diabetic stress.
80	16554480	Human astrocytes are resistant to Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.
81	16554480	Here, we report that calcium/calmodulin-dependent protein kinase II (CaMKII) is constitutively activated in human astrocytes and protects the cells from apoptotic stimulation by Fas agonist.
82	16554480	Once stimulated, Fas recruits Fas-associated death domain and caspase-8 for the assembly of the death-inducing signaling complex (DISC); however, caspase-8 cleavage is inhibited in the DISC.
83	16554480	Inhibition of CaMKII kinase activity inhibits the expression of phosphoprotein enriched astrocytes-15 kDa/phosphoprotein enriched in diabetes (PEA-15/PED) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP), thus releasing their inhibition of caspase-8 cleavage.
84	16554480	Inhibition of PEA-15/PED or c-FLIP by small interfering RNA sensitizes human astrocytes to Fas-induced apoptosis.
85	16554480	In contrast, inhibition of CaMKII, PEA-15, or c-FLIP does not affect the sensitivity of human astrocytes to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
86	16554480	TRAIL death receptors (DR4, DR5) are weakly expressed at mRNA, protein, and cell surface levels and thus fail to mediate the assembly of the DISC in human astrocytes.
87	16554480	Overexpression of DR5 restores TRAIL signaling pathways and sensitizes the human astrocytes to TRAIL-induced apoptosis if CaMKII kinase activity or expression of PEA-15 and c-FLIP is inhibited; the results suggest that CaMKII-mediated pathways prevent TRAIL-induced apoptosis in human astrocytes under conditions in which TRAIL death receptors are upregulated.
88	16554480	This study has therefore identified the molecular mechanisms that protect normal human astrocytes from apoptosis induced by Fas ligand and TRAIL.
89	16554480	Human astrocytes are resistant to Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis.
90	16554480	Here, we report that calcium/calmodulin-dependent protein kinase II (CaMKII) is constitutively activated in human astrocytes and protects the cells from apoptotic stimulation by Fas agonist.
91	16554480	Once stimulated, Fas recruits Fas-associated death domain and caspase-8 for the assembly of the death-inducing signaling complex (DISC); however, caspase-8 cleavage is inhibited in the DISC.
92	16554480	Inhibition of CaMKII kinase activity inhibits the expression of phosphoprotein enriched astrocytes-15 kDa/phosphoprotein enriched in diabetes (PEA-15/PED) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP), thus releasing their inhibition of caspase-8 cleavage.
93	16554480	Inhibition of PEA-15/PED or c-FLIP by small interfering RNA sensitizes human astrocytes to Fas-induced apoptosis.
94	16554480	In contrast, inhibition of CaMKII, PEA-15, or c-FLIP does not affect the sensitivity of human astrocytes to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
95	16554480	TRAIL death receptors (DR4, DR5) are weakly expressed at mRNA, protein, and cell surface levels and thus fail to mediate the assembly of the DISC in human astrocytes.
96	16554480	Overexpression of DR5 restores TRAIL signaling pathways and sensitizes the human astrocytes to TRAIL-induced apoptosis if CaMKII kinase activity or expression of PEA-15 and c-FLIP is inhibited; the results suggest that CaMKII-mediated pathways prevent TRAIL-induced apoptosis in human astrocytes under conditions in which TRAIL death receptors are upregulated.
97	16554480	This study has therefore identified the molecular mechanisms that protect normal human astrocytes from apoptosis induced by Fas ligand and TRAIL.
98	17569614	Resveratrol induces apoptosis by up-regulating the expression of Bax, Bak, PUMA, Noxa, Bim, p53, TRAIL, TRAIL-R1/DR4 and TRAIL-R2/DR5 and simultaneously down-regulating the expression of Bcl-2, Bcl-XL, Mcl-1 and survivin.
99	17569614	Resveratrol causes growth arrest at G1 and G1/S phases of cell cycle by inducing the expression of CDK inhibitors p21/WAF1/CIP1 and p27/KIP1.
100	19432816	DR5-mediated DISC controls caspase-8 cleavage and initiation of apoptosis in human glioblastomas.
101	19432816	TRAIL has four membrane-anchored receptors, death receptor 4/5 (DR4/5) and decoy receptor 1/2 (DcR1/2).
102	19432816	Of these receptors, only DR5 was expressed consistently in glioblastoma cell lines and tumour tissues, ruling out the role of DcR1/2 in TRAIL resistance.
103	19432816	Upon TRAIL binding, DR5 was homotrimerized and recruited Fas-associated death domain (FADD) and caspase-8 for the assembly of death-inducing signalling complex (DISC) in the lipid rafts of the plasma membrane.
104	19432816	In the DISC, caspase-8 was cleaved and initiated apoptosis by cleaving downstream caspases in TRAIL-sensitive glioblastoma cells.
105	19432816	In TRAIL-resistant cells, however, DR5-mediated DISC was modified by receptor-interacting protein (RIP), cellular FADD-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) and phosphoprotein enriched in diabetes or in astrocyte-15 (PED/PEA-15).
106	19432816	This DISC modification occurred in the non-raft fractions of the plasma membrane and resulted in the inhibition of caspase-8 cleavage and activation of nuclear factor-kappaB (NF-kappaB).
107	19432816	Treatment of resistant cells with parthenolide, an inhibitor of inhibitor of kappaB (I-kappaB), eliminated TRAIL-induced NF-kappaB activity but not TRAIL resistance.
108	19432816	In contrast, however, targeting of RIP, c-FLIP or PED/PEA-15 with small interfering RNA (siRNA) led to the redistribution of the DISC from non-rafts to lipid rafts and eliminated the inhibition of caspase-8 cleavage and thereby TRAIL resistance.
109	19432816	Taken together, this study indicates that the DISC modification by RIP, c-FLIP and PED/PEA-15 is the most upstream event in TRAIL resistance in glioblastomas.
110	19432816	DR5-mediated DISC controls caspase-8 cleavage and initiation of apoptosis in human glioblastomas.
111	19432816	TRAIL has four membrane-anchored receptors, death receptor 4/5 (DR4/5) and decoy receptor 1/2 (DcR1/2).
112	19432816	Of these receptors, only DR5 was expressed consistently in glioblastoma cell lines and tumour tissues, ruling out the role of DcR1/2 in TRAIL resistance.
113	19432816	Upon TRAIL binding, DR5 was homotrimerized and recruited Fas-associated death domain (FADD) and caspase-8 for the assembly of death-inducing signalling complex (DISC) in the lipid rafts of the plasma membrane.
114	19432816	In the DISC, caspase-8 was cleaved and initiated apoptosis by cleaving downstream caspases in TRAIL-sensitive glioblastoma cells.
115	19432816	In TRAIL-resistant cells, however, DR5-mediated DISC was modified by receptor-interacting protein (RIP), cellular FADD-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) and phosphoprotein enriched in diabetes or in astrocyte-15 (PED/PEA-15).
116	19432816	This DISC modification occurred in the non-raft fractions of the plasma membrane and resulted in the inhibition of caspase-8 cleavage and activation of nuclear factor-kappaB (NF-kappaB).
117	19432816	Treatment of resistant cells with parthenolide, an inhibitor of inhibitor of kappaB (I-kappaB), eliminated TRAIL-induced NF-kappaB activity but not TRAIL resistance.
118	19432816	In contrast, however, targeting of RIP, c-FLIP or PED/PEA-15 with small interfering RNA (siRNA) led to the redistribution of the DISC from non-rafts to lipid rafts and eliminated the inhibition of caspase-8 cleavage and thereby TRAIL resistance.
119	19432816	Taken together, this study indicates that the DISC modification by RIP, c-FLIP and PED/PEA-15 is the most upstream event in TRAIL resistance in glioblastomas.
120	19432816	DR5-mediated DISC controls caspase-8 cleavage and initiation of apoptosis in human glioblastomas.
121	19432816	TRAIL has four membrane-anchored receptors, death receptor 4/5 (DR4/5) and decoy receptor 1/2 (DcR1/2).
122	19432816	Of these receptors, only DR5 was expressed consistently in glioblastoma cell lines and tumour tissues, ruling out the role of DcR1/2 in TRAIL resistance.
123	19432816	Upon TRAIL binding, DR5 was homotrimerized and recruited Fas-associated death domain (FADD) and caspase-8 for the assembly of death-inducing signalling complex (DISC) in the lipid rafts of the plasma membrane.
124	19432816	In the DISC, caspase-8 was cleaved and initiated apoptosis by cleaving downstream caspases in TRAIL-sensitive glioblastoma cells.
125	19432816	In TRAIL-resistant cells, however, DR5-mediated DISC was modified by receptor-interacting protein (RIP), cellular FADD-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) and phosphoprotein enriched in diabetes or in astrocyte-15 (PED/PEA-15).
126	19432816	This DISC modification occurred in the non-raft fractions of the plasma membrane and resulted in the inhibition of caspase-8 cleavage and activation of nuclear factor-kappaB (NF-kappaB).
127	19432816	Treatment of resistant cells with parthenolide, an inhibitor of inhibitor of kappaB (I-kappaB), eliminated TRAIL-induced NF-kappaB activity but not TRAIL resistance.
128	19432816	In contrast, however, targeting of RIP, c-FLIP or PED/PEA-15 with small interfering RNA (siRNA) led to the redistribution of the DISC from non-rafts to lipid rafts and eliminated the inhibition of caspase-8 cleavage and thereby TRAIL resistance.
129	19432816	Taken together, this study indicates that the DISC modification by RIP, c-FLIP and PED/PEA-15 is the most upstream event in TRAIL resistance in glioblastomas.
130	19432816	DR5-mediated DISC controls caspase-8 cleavage and initiation of apoptosis in human glioblastomas.
131	19432816	TRAIL has four membrane-anchored receptors, death receptor 4/5 (DR4/5) and decoy receptor 1/2 (DcR1/2).
132	19432816	Of these receptors, only DR5 was expressed consistently in glioblastoma cell lines and tumour tissues, ruling out the role of DcR1/2 in TRAIL resistance.
133	19432816	Upon TRAIL binding, DR5 was homotrimerized and recruited Fas-associated death domain (FADD) and caspase-8 for the assembly of death-inducing signalling complex (DISC) in the lipid rafts of the plasma membrane.
134	19432816	In the DISC, caspase-8 was cleaved and initiated apoptosis by cleaving downstream caspases in TRAIL-sensitive glioblastoma cells.
135	19432816	In TRAIL-resistant cells, however, DR5-mediated DISC was modified by receptor-interacting protein (RIP), cellular FADD-like interleukin-1beta-converting enzyme inhibitory protein (c-FLIP) and phosphoprotein enriched in diabetes or in astrocyte-15 (PED/PEA-15).
136	19432816	This DISC modification occurred in the non-raft fractions of the plasma membrane and resulted in the inhibition of caspase-8 cleavage and activation of nuclear factor-kappaB (NF-kappaB).
137	19432816	Treatment of resistant cells with parthenolide, an inhibitor of inhibitor of kappaB (I-kappaB), eliminated TRAIL-induced NF-kappaB activity but not TRAIL resistance.
138	19432816	In contrast, however, targeting of RIP, c-FLIP or PED/PEA-15 with small interfering RNA (siRNA) led to the redistribution of the DISC from non-rafts to lipid rafts and eliminated the inhibition of caspase-8 cleavage and thereby TRAIL resistance.
139	19432816	Taken together, this study indicates that the DISC modification by RIP, c-FLIP and PED/PEA-15 is the most upstream event in TRAIL resistance in glioblastomas.
140	20410100	Genetic variation in APOJ, LPL, and TNFRSF10B affects plasma fatty acid distribution in Alaskan Eskimos.
141	20451496	TRAIL upregulates decoy receptor 1 and mediates resistance to apoptosis in insulin-secreting INS-1 cells.
142	20451496	TRAIL/Apo2L (tumor necrosis factor-related apoptosis-inducing ligand) is a multifunctional protein regulating the homeostasis of the immune system, infection, autoimmune diseases, and apoptosis.
143	20451496	A previous study found that TRAIL did not have significant cytotoxic effects on the insulin-secreting pancreatic beta cell line, INS-1.
144	20451496	TRAIL treatment showed NF-kappaB translocation to the nucleus in TRAIL-resistant INS-1 cells, and TRAIL-induced NF-kappaB activation was preceded by IkappaBalpha degradation.
145	20451496	A pharmacological inhibitor of NF-kappaB, Bay 11-7082, blocked TRAIL-induced NF-kappaB translocation to the nucleus and IkappaBalpha degradation.
146	20451496	Four related receptors bind TRAIL: two death receptors (DR4 and DR5) that promote apoptosis, and two decoy receptors (DcR1 and DcR2) that act as dominant-negative inhibitors of TRAIL-mediated apoptosis.
147	20451496	In the present study, TRAIL treatment in INS-1 cells upregulated DcR1 and downregulated DR5 without altering the expression of DcR2 and DR4.
148	20451496	The resistance to apoptosis in INS-1 cells might therefore, be a consequence of DcR1 upregulation and DR5 downregulation, and the transcription factor, NF-kappaB, could regulate the sensitivity of cells to TRAIL by controlling the ratio of decoy to death receptors.
149	20451496	Thus, TRAIL may play an important role in the survival of pancreatic beta cells by regulating receptor expression in an NF-kappaB-dependent manner.
150	20451496	TRAIL upregulates decoy receptor 1 and mediates resistance to apoptosis in insulin-secreting INS-1 cells.
151	20451496	TRAIL/Apo2L (tumor necrosis factor-related apoptosis-inducing ligand) is a multifunctional protein regulating the homeostasis of the immune system, infection, autoimmune diseases, and apoptosis.
152	20451496	A previous study found that TRAIL did not have significant cytotoxic effects on the insulin-secreting pancreatic beta cell line, INS-1.
153	20451496	TRAIL treatment showed NF-kappaB translocation to the nucleus in TRAIL-resistant INS-1 cells, and TRAIL-induced NF-kappaB activation was preceded by IkappaBalpha degradation.
154	20451496	A pharmacological inhibitor of NF-kappaB, Bay 11-7082, blocked TRAIL-induced NF-kappaB translocation to the nucleus and IkappaBalpha degradation.
155	20451496	Four related receptors bind TRAIL: two death receptors (DR4 and DR5) that promote apoptosis, and two decoy receptors (DcR1 and DcR2) that act as dominant-negative inhibitors of TRAIL-mediated apoptosis.
156	20451496	In the present study, TRAIL treatment in INS-1 cells upregulated DcR1 and downregulated DR5 without altering the expression of DcR2 and DR4.
157	20451496	The resistance to apoptosis in INS-1 cells might therefore, be a consequence of DcR1 upregulation and DR5 downregulation, and the transcription factor, NF-kappaB, could regulate the sensitivity of cells to TRAIL by controlling the ratio of decoy to death receptors.
158	20451496	Thus, TRAIL may play an important role in the survival of pancreatic beta cells by regulating receptor expression in an NF-kappaB-dependent manner.
159	20451496	TRAIL upregulates decoy receptor 1 and mediates resistance to apoptosis in insulin-secreting INS-1 cells.
160	20451496	TRAIL/Apo2L (tumor necrosis factor-related apoptosis-inducing ligand) is a multifunctional protein regulating the homeostasis of the immune system, infection, autoimmune diseases, and apoptosis.
161	20451496	A previous study found that TRAIL did not have significant cytotoxic effects on the insulin-secreting pancreatic beta cell line, INS-1.
162	20451496	TRAIL treatment showed NF-kappaB translocation to the nucleus in TRAIL-resistant INS-1 cells, and TRAIL-induced NF-kappaB activation was preceded by IkappaBalpha degradation.
163	20451496	A pharmacological inhibitor of NF-kappaB, Bay 11-7082, blocked TRAIL-induced NF-kappaB translocation to the nucleus and IkappaBalpha degradation.
164	20451496	Four related receptors bind TRAIL: two death receptors (DR4 and DR5) that promote apoptosis, and two decoy receptors (DcR1 and DcR2) that act as dominant-negative inhibitors of TRAIL-mediated apoptosis.
165	20451496	In the present study, TRAIL treatment in INS-1 cells upregulated DcR1 and downregulated DR5 without altering the expression of DcR2 and DR4.
166	20451496	The resistance to apoptosis in INS-1 cells might therefore, be a consequence of DcR1 upregulation and DR5 downregulation, and the transcription factor, NF-kappaB, could regulate the sensitivity of cells to TRAIL by controlling the ratio of decoy to death receptors.
167	20451496	Thus, TRAIL may play an important role in the survival of pancreatic beta cells by regulating receptor expression in an NF-kappaB-dependent manner.
168	20696468	The immunohistochemical study revealed increased immunostaining of TRAIL and DR5 in osteoblastic cells of the diaphysis (pre-metaphysis) and epiphysis treated with STZ and L-NAME, related to activation of osteoblastic apoptotic death, while the group receiving L-arginine was comparable to the control group and the higher indications of iNOS activity that may reflect its induction by L-arginine administration.
169	22020928	To further increase the collaborative effect, the histone deacetylase (HDAC) inhibitor valproic acid (VPA), a known potentiator for PPARγ function, was added to the combinatorial treatment, robustly inducing apoptosis mediated by highly expressed death receptors, including Fas/CD95 and DR5.
170	22046379	Systems analysis of ATF3 in stress response and cancer reveals opposing effects on pro-apoptotic genes in p53 pathway.
171	22046379	Further analysis of effects of ATF3 knockdown on these targets revealed that stress-induced ATF3 regulates genes in metabolic pathways, cell cycle, apoptosis, cell adhesion, and signalling including insulin, p53, Wnt, and VEGF pathways.
172	22046379	Cancer-associated ATF3 is involved in regulation of distinct sets of genes in processes such as calcium signalling, Wnt, p53 and diabetes pathways.
173	22046379	Notably, stress-induced ATF3 binds to 40% of p53 targets and activates pro-apoptotic genes such as TNFRSF10B/DR5 and BBC3/PUMA.
174	22046379	Cancer-associated ATF3, by contrast, represses these pro-apoptotic genes in addition to CDKN1A/p21.
175	22046379	Taken together, our data reveal an extensive network of stress-inducible transcription factors and demonstrate that ATF3 has opposing, cell context-dependent effects on p53 target genes in DNA damage response and cancer development.