ライフサイエンスコーパス: death receptor 5

1 apoptotic pathway, primarily by induction of death receptor 5 and down-regulation of c-FLIP.

2 ome inhibition-induced alterations in TRAIL, death receptor 5, and Bim could not be implicated in the

3 Abs target the cell surface receptors HER2, death receptor 5, and CD20, and are more efficacious tha

4 of the TNF-related apoptosis-inducing ligand death receptor 5, and potentiation of death receptor 5-i

5 Early therapeutic efficacy of anti-death receptor 5 antibody (TRA-8) combined with gemcitab

6 that activation of the apoptosis-initiating Death Receptor 5, as well as other structurally homologo

7 is factor-related apoptosis-inducing ligand, death receptor 5, decoy receptor 2, FLICE-like inhibitor

8 gest that Bax is not absolutely required for death receptor 5-dependent apoptotic signals and MG132 b

9 in combination with Fas ligand (FasL) or the death receptor 5 (DR5) agonist antibody synergistically

10 d a novel COX-2 inhibitor ON09310 upregulate death receptor 5 (DR5) and cooperate with tumor necrosis

11 IDs, sulindac sulfide and SC-'236 engage the death receptor 5 (DR5) and mitochondrial pathways to med

12 gulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the

13 The receptor designated death receptor 5 (DR5) contained a cytoplasmic death dom

14 xtracellular domain (ECD) of long isoform of death receptor 5 (DR5) could block endogenous receptor a

15 c-Jun NH(2)-terminal kinase (JNK)-dependent death receptor 5 (DR5) expression and augments death rec

16 TRAIL to induce apoptosis, and up-regulated death receptor 5 (DR5) expression in human non-small cel

17 Moreover, no significant increase in death receptor 5 (DR5) expression was seen in CD4(+) T c

18 t study investigates the expression of TRAIL death receptor 5 (DR5) in the peripheral-blood mononucle

19 Death receptor 5 (DR5) is a cell surface pro-apoptotic d

20 Death receptor 5 (DR5) is a death domain-containing tran

21 Death receptor 5 (DR5) is a pro-apoptotic protein involv

22 Death receptor 5 (DR5) is an apoptosis-inducing member o

23 or-related apoptosis-inducing ligand (TRAIL) death receptor 5 (DR5) is significantly elevated in pati

24 studying the modulatory effects of b-AP15 on death receptor 5 (DR5) levels and DR5 activation-induced

25 The fatty acid palmitate can activate death receptor 5 (DR5) on hepatocytes, leading to their

26 ed expression of the death receptors Fas and death receptor 5 (DR5) on thymic stromal cells (especial

27 2ME2 treatment results in up-regulation of death receptor 5 (DR5) protein expression in vitro and i

28 These interactions were associated with death receptor 5 (DR5) up-regulation and caspase-8 activ

29 in vivo and correlate with up-regulation of death receptor 5 (DR5) via an unknown mechanism.

30 ults in activation of the FAS and TNFRSF10B (death receptor 5 (DR5)) promoters, increased Fas and DR5

31 Death receptor 5 (DR5), a cell surface pro-apoptotic pro

32 tein (CHOP), which leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3,

33 ibodies to apoptosis-inducing TNFRs, such as death receptor 5 (DR5), although displaying impressive a

34 that R115777 up-regulated the expression of death receptor 5 (DR5), an important death receptor for

35 s-inducing ligand (TRAIL) with its receptor, death receptor 5 (DR5), leading to induction of apoptosi

36 cognate receptors death receptor 4 (DR4) and death receptor 5 (DR5), preferentially in malignant cell

37 hibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increas

38 meostasis are coupled with activation of the death receptor 5 (DR5)-dependent apoptotic pathway in hu

39 ell-autonomous, UPR-controlled activation of death receptor 5 (DR5).

40 athways in upregulating transcription of the death receptor 5 (DR5).

41 us protein (CHOP), Bcl-2 family members, and death receptor 5 (DR5).

42 Het-induced apoptosis involving induction of death receptor 5 (DR5).

43 genes, including death receptor 4 (DR4) and death receptor 5 (DR5).

44 ducing pathways and death receptors, such as death receptor 5 (DR5).

45 CE inhibitory protein (FLIP) but not that of death receptor 5 (DR5).

46 Bile acids up-regulate death receptor 5 (DR5)/TRAIL-receptor 2 (TRAIL-R2) expre

47 ssion of death receptor 4 (DR4, TRAILR1) and death receptor 5 (DR5, TRAILR2) occur following exposure

48 l antibody that binds to and activates human death receptor 5 (DR5; also known as TRAIL receptor 2).

49 Activation of death receptor-5 (DR5) leads to the formation of death i

50 poptosis of liver cancer cell lines requires death receptor-5 (DR5)-dependent permeabilization of lys

51 duction of apoptosis and is hence designated death receptor-5 (DR5).

52 by expression of a dominant negative mutant death receptor 5 (DR5Delta) or by Bcl-2.

53 on induced GADD153-mediated up-regulation of death receptor 5 expression and subsequent activation of

54 some inhibitor MG132 upregulates Apo2L/TRAIL death receptor 5 expression in both Bax-proficient and -

55 evious work has shown that celecoxib induces death receptor 5 expression, resulting in induction of a

56 ligand death receptor 5, and potentiation of death receptor 5-induced apoptosis in vitro and in vivo.

57 l tumor necrosis factor receptors, including Death Receptor 5, involves a scissorlike opening of the

58 ion of p53 target genes such as p21(WAF1) or death receptor 5 (KILLER/DR5) of TNF-related apoptosis-i

59 revealed that up-regulation of cell surface death receptor 5 levels by treatment with 7-ethyl-10-hyd

60 steriosis, and blocking TRAIL with a soluble death receptor 5 markedly ameliorated the disease.

61 sion of TRAIL receptors death receptor 4 and death receptor 5, purified TRAIL could not induce progra

62 sing the TRAIL protein and a TRAIL receptor (death receptor 5) revealed that both the dimer and the t

63 eath receptor 4) and TRAIL-R2 (also known as death receptor 5), that are members of the TNF receptor

64 , the first direct biophysical evidence that Death Receptor 5 TM-dimers open in response to ligand bi

65 Although both TRAIL and its death receptor 5 were constitutively expressed in the li

66 containing receptor for TRAIL (designated as death receptor-5), which preferentially engaged a FLICE

67 s such as Fas ligand, its receptor (Fas) and death receptor 5, which are regulated by IRF-1.

68 AIL) and its receptors, death receptor 4 and death receptor 5, which were up-regulated in HCV infecti

69 d that both the dimer and the trimer bind to death receptor 5 with similar affinity.