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 ll turnover such as TNFRSF10B, also known as death receptor 5, and immune cell attacking signals such

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

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

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

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

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

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

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

12 ancreatic cancers express elevated levels of Death Receptor 5 (DR5) and its downstream regulators/eff

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

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

15 We investigated death receptor 5 (DR5) as a CAR target based on its high

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

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

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

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

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

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

22 poptosis through intracellular activation of death receptor 5 (DR5) independent of its canonical extr

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

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

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

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

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

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

29 Death receptor 5 (DR5) mediates extrinsic apoptosis.

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

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

32 2ME2 treatment results in up-regulation of death receptor 5 (DR5) protein expression in vitro and i

33 Death Receptor 5 (DR5) targeted therapies offer signific

34 BET degradation transcriptionally activates Death Receptor 5 (DR5) to trigger immunogenic cell death

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

36 was designed to selectively bind and cluster death receptor 5 (DR5) upon engaging the tumor antigen M

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

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

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

40 on of p73, which transcriptionally activated death receptor 5 (DR5), a cytokine receptor and key comp

41 Furthermore, we identified death receptor 5 (DR5), a member of tumour necrosis fact

42 re, we report an unexpected finding that for death receptor 5 (DR5), a receptor in the tumor necrosis

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

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

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

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

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

48 We also discovered that death receptor 5 (DR5), TRAIL, and HS can form a ternary

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

50 jury-induced KIM1 binds to the ECD domain of death receptor 5 (DR5), which activates DR5 and the foll

51 Mechanistically, ASB3 interacted with death receptor 5 (DR5), which promoted ubiquitination an

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

53 mpared with free antibodies or Fc-fusions in death receptor 5 (DR5)-mediated apoptosis, angiopoietin-

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

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

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

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

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

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

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

61 TRAIL receptors: death receptor 4 (DR4) and death receptor 5 (DR5).

62 osis-inducing ligand (TRAIL) and its cognate death receptor 5 (DR5).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Assembling oligomers for Death Receptor 5 stimulation, we probed multivalency eff

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

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

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

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

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

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

87 e applied it to engineer an antibody against death receptor 5 with initial affinities in the subnanom

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