ライフサイエンスコーパス: caspase 10

1 hat harbor independent missense mutations in Caspase 10.

2 prodeath role for both cleaved and uncleaved caspase-10.

3 f the initiator caspase, either caspase-8 or caspase-10.

4 se-8-deficient Jurkat cell express wild-type caspase-10.

5 s leads to the recruitment and activation of caspase-10.

6 onal in NB cells expressing caspase-8 and/or caspase-10.

7 complex (DISC) even in presence of abundant caspase-10.

8 down-regulation of caspase-7, caspase-8, and caspase-10.

9 pase-1, caspase-2, caspase-4, caspase-8, and caspase-10.

10 ase-3 with less efficiency than caspase-7 or caspase-10.

11 death is activation of the caspases through caspase-10.

12 apoptosis in target cells by first maturing caspase-10.

13 Furthermore, the drug induced activation of caspases-10, -8, -6, and -3, cleaved Bcl-2, Bid, poly(AD

14 f Hsp90 beta mediated by caspase-8-dependent caspase-10 activation promoted UVB-induced cell apoptosi

15 Caspase-10 activation, in turn, depended on caspase-8, w

16 Accordingly, caspase-10 activity also substantially increased in resp

17 er se, was insufficient to drive cell death, caspase-10 activity had little effect on cell viability,

18 We observed that inhibition of caspase-9 or caspase-10 activity, but not caspase-8, caused partial r

19 Furthermore, we determined that caspase-10, an initiator caspase in death receptor signa

20 BCG induced early activation of caspase 10 and 9, followed by caspase 3.

21 Caspase 10 and MRIT, two DEDs-containing homologs of Cas

22 The transcription factor IRF4 induces both caspase-10 and its associated protein cFLIPL in myeloma,

23 t negative forms of caspase-8, caspase-9, or caspase-10 and the caspase-8 inhibitor CrmA.

24 ath domain protein (FADD), the activation of caspases-10 and -8 as well as the downstream caspases, a

25 ceptors involves not only caspase-8 but also caspase-10, and both caspases may have equally important

26 quence of CLARP resemble those of caspase-8, caspase-10, and DCP2, a Drosophila melanogaster protein

27 Unlike caspase-8, caspase-10, and DCP2, however, two important residues pr

28 associated with the processing of caspase-8, caspase-10, and the proapoptotic Bid protein, resulting

29 profile, the downregulation of caspase-8 and caspase-10, and upregulation of oct3/4 and tgf-beta1, ma

30 erythematosus; 3) Type II, ALPS with mutant caspase 10; and 4) Type III, ALPS as yet without any def

31 FADD and caspase-8, but not caspase-10, are recruited to the receptor, and cells def

32 , CD95L and Apo2L/TRAIL recruited endogenous caspase-10 as well as caspase-8 to their DISC, where bot

33 d carcinoma cell lines tested, by activating caspase-10 at the receptor level and triggering a caspas

34 caspase-3, caspase-7, caspase-8, caspase-9, caspase-10, BID, and poly(ADP)ribose polymerase and by d

35 nor the dominant negative FADD, caspase 8 or caspase 10 blocked the ionizing radiation-induced apopto

36 nt apoptosis primarily through activation of caspase-10 but independently of death receptors.

37 the death receptor-associated caspase-8 and caspase-10 but not other caspases, and in vivo after sti

38 In contrast to the Fas signaling pathway, caspase-10, but not caspase-8 or the Fas-associated deat

39 Here we show that caspase-10 can function independently of caspase-8 in in

40 t apoptosis with TRAIL through activation of caspase-10, capase-8 (FLICE), caspase-3, and caspase-9.

41 GCDC promoted activation of caspase 10, caspase 3, and PARP; all were inhibited by G

42 uitment required the adaptor FADD/Mort1, and caspase-10 cleavage in vitro required DISC assembly, con

43 n turn, depended on caspase-8, which cleaved caspase-10 directly.

44 We also found that the expression of caspase-10 elicits a simultaneous activation of the MAP

45 CASPASE-10 expression was found to be potently induced b

46 ro dimerization assays strongly suggest that caspase-10 follows the proximity-induced dimerization mo

47 we discovered that all myeloma lines require caspase-10 for survival irrespective of their genetic ab

48 O(3) on histone H3 phosphoacetylation at the CASPASE-10 gene may play an important role in the induct

49 Although earlier evidence implicated caspase-10 in apoptosis signaling by CD95L and Apo2L/TRA

50 esults indicate that the expression of human caspase-10 in S. cerevisiae activates an intracellular d

51 The heterologous expression of human caspase-10 in Saccharomyces cerevisiae induces a lethal

52 ted protein kinases and apical caspase-9 and caspase-10 in the GC-induced apoptosis of pre-B lymphocy

53 ses and pathways that are responsible of the caspase-10-induced cell death we have designed a loss-of

54 hibited taxol-induced apoptosis, whereas the caspase-10 inhibitor totally abrogated this process.

55 Caspase-10 inhibits autophagy by cleaving the BCL2-inter

56 However, under circumstances where caspase-10 is absent or dysfunctional, GrB can act throu

57 aturation of caspase-7 does not occur unless caspase-10 is present.

58 In this study we concentrate on caspase-10, its mechanism of activation, and the role of

59 nhances histone H3 phosphoacetylation at the CASPASE-10 locus.

60 JNK activation blocks apoptosis mediated by caspase-10, Mach-related inducer of toxicity/cFLIP, and

61 for TRAIL-induced apoptosis and suggest that caspase-10 may play a minor role, if any, in TRAIL-induc

62 at the death proteases caspase 8 (FLICE) and caspase 10 (Mch4/FLICE2) are recruited to the CD-95 and

63 optosis, failure to express caspase-8 and/or caspase-10 might be an important mechanism of resistance

64 Surprisingly, caspase-8 and caspase-10 mRNA expression was detected in only 5 of 18

65 A role for caspase-10, previously implicated in the autoimmune lymp

66 esting a possible selective pressure against caspase-10 production in cancer cells.

67 ; however, immunoblot analysis revealed that caspase-10 protein expression was more frequently absent

68 ssociated death domain (FADD), caspase-8 and caspase-10 proteins into a death-inducing signalling com

69 However, both caspase 8 and caspase 10 recruitment and processing within the TRAIL d

70 Caspase-10 recruitment required the adaptor FADD/Mort1,

71 rs, but the role of its structural relative, caspase-10, remains controversial.

72 We characterized a series of caspase-10-specific antibodies and found that certain co

73 ire a basal level of autophagy for survival, caspase-10 tempers this response to avoid cell death.

74 ant negative versions of FADD, caspase 8 and caspase 10, that block the apoptotic axis of TNFR1 at di

75 r signaling with activation of caspase-8 and caspase-10 to be responsible for apoptosis induction.

76 death domain (FADD) protein to caspase-8 and caspase-10 to mediate formation of the death-inducing si

77 h receptor ligands recruit caspase-8 but not caspase-10 to their death-inducing signaling complex (DI

78 l kinases and phosphatases are essential for caspase-10 toxicity.

79 und that Hsp90 beta was cleaved by activated caspase-10 under UVB irradiation.

80 terozygous mutations in CD95, CD95 ligand or caspase-10 underlie most cases of autoimmune lymphoproli

81 DNA fragmentation factor-45 (DFF45), but not caspase-10, upon TRAIL treatment in sensitive MM cells,

82 nal inactivation of the closely related gene caspase 10 was present in many cell lines.

83 sion alone induced active caspases, of which caspase-10 was the most active.

84 dary complex containing FADD, caspase 8, and caspase 10, which results in caspase activation.

85 UVB irradiation contributed to activation of caspase-10, which cleaved Hsp90 beta at D278, P293, and

86 A selective inhibitor of caspase-10, Z-AEVD-FMK, effectively blocked caspase-3 ac