ライフサイエンスコーパス: caspase 12

1 trigger apoptosis through the ER-associated caspase 12.

2 ts possible earlier cleavage of caspase-3 by caspase-12.

3 the Mn(II)-induced apoptosis is mediated by caspase-12.

4 pase localized in the ER, to generate active caspase-12.

5 an earlier activation of Abeta(1-42)-induced caspase-12.

6 the activation of cJun N-terminal kinase and caspase-12.

7 n of African descendents express full-length caspase-12.

8 human caspase-4 is the counterpart of murine caspase-12.

9 a production to the same extent as wild-type caspase-12.

10 hRPE cells express a high level of caspase-12S.

11 was also observed during disease, including caspase-12, -9, and -3 cleavage.

12 ucose-regulated protein-78 and activation of caspase-12, a cysteine proteinase in the ER, mediating c

13 estinal epithelial cells because of elevated caspase 12 activation during an enhanced unfolded protei

14 ng unfolded protein response, which mediates caspase-12 activation and apoptosis.

15 y induce apoptosis through calpain- mediated caspase-12 activation and Bcl-xL inactivation.

16 rsodeoxycholic acid (TUDCA) in inhibition of caspase-12 activation and its effect on calcium homeosta

17 by increasing Ca(2+) content into ER, delays caspase-12 activation and thus neuronal death.

18 hat parkin reduces proteasome impairment and caspase-12 activation induced by an expanded polyglutami

19 hondrial pathway, or MAGE-3, an inhibitor of caspase-12 activation, did not delay apoptosis induction

20 alcium-mediated apoptotic pathway as well as caspase-12 activation.

21 induce apoptosis through caspase-7-mediated caspase-12 activation.

22 content triggered ER stress, as revealed by caspase-12 activation.

23 es endoplasmic reticulum (ER) stress-induced caspase-12 activation.

24 by endoplasmic reticulum (ER) stress-induced caspase-12 activation.

25 calcium efflux, induction of Bip/GRP78, and caspase-12 activation; and subsequently inhibited activa

26 kCh-induced caspase-8 activity but increased caspase-12 activities, suggesting that caspase-8 and cas

27 Caspase-12 activity was detected by Western blotting.

28 Caspase-12 activity was increased after 7kCh treatment c

29 doplasmic reticulum (ER) stress and elevated caspase-12 activity.

30 so prevented the activation of caspase-9 and caspase-12, along with the cleavage of Bid to tBid, all

31 The dearth of potential substrates for caspase-12 also was confirmed by whole-cell diagonal-gel

32 Caspase 12, an endoplasmic reticulum (ER)-specific caspa

33 g transcription factor 6 (ATF6) or activated caspase 12 and calbindin.

34 We report here that both caspase-12 and caspase-3 are activated in INS-1 cells fo

35 These data suggest that caspase-12 and caspase-4 are not required for the induct

36 e cysteine protease calpains and cleavage of caspase-12 and caspase-7 were found in the channel-defic

37 Caspase-7 associates with caspase-12 and cleaves the prodomain to generate active

38 vation of m-calpain, which in turn activates caspase-12 and degrades Bcl-xL.

39 e mitochondrial pathway or the activation of caspase-12 and ER stress.

40 s supported by the presence of ERS-activated caspase-12 and the accumulation of ER-associated polyubi

41 pathway, including its downstream effectors caspase-12 and the transcription factor C/EBP homologous

42 d endoplasmic reticulum (ER) stress (cleaved caspase-12) and, though less active, NF-kappaB subunits

43 optotic Bcl-2 protein, induced expression of caspase 12, and a decrease in intracellular glutathione

44 and DNA damage-inducible gene 153 (GADD153), caspase 12, and transcription factor sterol response ele

45 doplasmic reticulum calcium stores, activate caspase-12, and increase apoptosis in macrophages.

46 We detected complexes between BiP, caspase-12, and the BH3-only protein BiK that may contri

47 ptors via the up-regulation of caspase-3 and caspase-12, and the release of AIF1 from the mitochondri

48 ent-binding protein-1, and proapoptotic gene caspase-12; and decreasing global DNA methylation.

49 LC-PK1 cells that were transfected with anti-caspase 12 antibody significantly attenuated cisplatin-i

50 hat pretreatment of NIH3T3 cells with either caspase-12 antisense RNA or dsRNA corresponding to the f

51 This molecular role for caspase-12 appears to be akin to the role of cFLIP in re

52 R stress-induced activation of JNK/c-Jun and caspase 12 are reduced by Herp, whereas induction of maj

53 icular, caspase-1, caspase-4, caspase-5, and caspase-12 are activated during innate immune responses

54 Mice that are deficient in caspase-12 are resistant to ER stress-induced apoptosis,

55 whereas the expressions of CHOP and cleaved caspase-12 as well as the number of apoptotic neurons we

56 ced cell death showed specific activation of caspase 12, as well as of caspases 8, 9, 7, and 3, and c

57 iated by C/EBP homologous protein (CHOP) and caspase-12, as their activation is intact in p53(-/-) ME

58 Mechanistically, caspase-12 associated with caspase-1 and inhibited its a

59 tion due to enhanced expression of activated caspase 12 at 20 weeks.

60 In intact cells, caspase-12 autoproteolysis occurred in the inhibitory co

61 is-related proteins, including CHOP/GADD153, caspase-12, Bcl-2 and nuclear factor (NF)-kappaB.

62 ugh the majority of people lack a functional caspase-12 because of a T(125) single nucleotide polymor

63 Western blot analysis (caspase-3, caspase-8, caspase-12, Bid, NF-kappaB, cFlip, XIAP), staining for M

64 not significantly altered in the absence of caspase-12, but muscle fibre degeneration found in the m

65 with (1) activation of caspase-8, caspase-9, caspase-12, caspase-3, and poly(ADP) ribose polymerase;

66 P94; and (b) the apoptotic molecules such as caspase-12, caspase-7, and CAAT/enhancer binding protein

67 late phospho-PERK, phospho-eIF2alpha, GRP94, caspase-12, caspase-7, and CHOP/GADD153 was significantl

68 In wild-type cells, this is associated with caspase 12 cleavage that is abolished in bax-/-bak-/- ce

69 progressive depletion of ER Ca2+ and induces caspase 12 cleavage.

70 c reticulum stress can lead to activation of caspase 12; compared to the results seen with mock and w

71 Although caspase-12 could mediate autoproteolytic maturation of i

72 Caspase-12 dampened the production of the pro-inflammato

73 In mice, caspase-12 deficiency confers resistance to sepsis and i

74 Furthermore, we show that caspase-12-deficient cortical neurons are defective in a

75 e pathway mediated the metabolic syndrome of caspase-12-deficient mice as ablation of Nlrp3 reversed

76 After challenge with West Nile virus (WNV), caspase-12-deficient mice had greater mortality, higher

77 dvantage was conferred by the ability of the caspase-12-deficient mice to clear bacterial infection m

78 was crucial in mediating survival of septic caspase-12-deficient mice, because administration of neu

79 rSV5VDeltaC-induced apoptosis can occur in a caspase 12-dependent manner.

80 me c release and activation of caspase-9 and caspase-12, depends on activation of caspase-8, which in

81 mmediate activation of proteases calpain and caspase-12, events consistent with drug-induced ER stres

82 Taken together, these studies establish that caspase-12 expression in murine megakaryocytes is regula

83 diated proapoptotic signaling, reduced renal caspase-12 expression, and a 50% reduction in renal casp

84 lcium from their ER nor did they translocate caspase-12 from the ER to the cytoplasm.

85 nd sequenced the 5'-flanking region of mouse caspase-12 gene by a PCR-mediated chromosome-walking tec

86 However, the human caspase-12 gene contains several mutations, which make i

87 rgin were even more potent enhancers of hRPE caspase-12S gene expression.

88 Caspase-12 has been shown to negatively modulate inflamm

89 her expression of CHOP, enhanced cleavage of caspase-12, higher caspase-3 activity, and increased pho

90 The direct role of caspase 12 in any model of renal injury has not previous

91 f procaspase 11, and decreased processing of caspase 12 in caspase 3(-/-)/caspase 7(-/-) cells.

92 The finding of increased activated caspase 12 in the dendrites supports an increased tenden

93 We now report an important role for caspase-12 in controlling viral infection via the patter

94 ivate specific signaling pathways, including caspase-12 in mouse, caspase-4 in human, NFkappaB, and B

95 s as an effective technique for knocking out caspase-12 in NIH3T3 cells without causing apoptosis.

96 y, we investigated a role for caspase-11 and caspase-12 in obesity and insulin resistance.

97 that caspase-12S is the predominant form of caspase-12 in the examined hRPE cells of this study, wit

98 marrow chimeras determined that deletion of caspase-12 in the radio-resistant compartment was respon

99 Loss of caspase-12 in two independently generated mouse strains

100 ge-inducible protein 153 (CHOP/GADD153), and caspase-12 indicative of an ER stress response were amon

101 Caspase-12 is a dominant-negative regulator of caspase-1

102 like cFLIP/Usurpin, we demonstrate here that caspase-12 is catalytically competent.

103 We propose that the proteolytic activity of caspase-12 is confined to its own proenzyme and that aut

104 Moreover, although caspase-12 is highly expressed in mature megakaryocytes,

105 The activation of caspase-12 is involved in endoplasmic reticulum-mediated

106 Here we show that caspase-12 is localized to the ER and activated by ER st

107 Caspase-12 is the most down-regulated gene we identified

108 To investigate how caspase-12 is transcriptionally and translationally regu

109 RT-PCR results showed that caspase-12S is the predominant form of caspase-12 in the

110 BiP and CHOP and the activation of JNK2 and caspase-12 leads to neuronal apoptosis in the mouse mode

111 NA or dsRNA corresponding to the full-length caspase-12 led to a dramatic decrease in caspase-3-like

112 RNA interference to knock down caspase-12 levels or salubrinal (an ER stress inhibitor)

113 Caspase-12, like most other members of the caspase famil

114 The activation of caspase-12-like activity was Ca(2+)-dependent, and inhib

115 Thus, caspase-12 mediates an ER-specific apoptosis pathway and

116 tivation was determined using platelets from caspase-12(-/-) mice.

117 PS and coculture with monocytes reduced hRPE caspase-12S mRNA expression within 6 hours.

118 and the cytokine IL-10 for 6 hours increased caspase-12S mRNA expression.

119 r this effect, as the catalytically inactive caspase-12 mutant Cys299Ala also inhibited caspase-1 and

120 oral limitation of the inhibitory effects of caspase-12 on proinflammatory cytokine maturation.

121 Last, analysis of Grp78 expression and Caspase 12 or 4 activation indicated that hyperthermia i

122 cess that does not require the expression of caspase-12 or caspase-4 but can be inhibited by overexpr

123 ethylcoumarin, in the presence or absence of caspase-12 or caspase-4 expression, whereas Bcl-x(L) or

124 agents in the presence or absence of murine caspase-12 or human caspase-4 expression and in cells th

125 ly or indirectly, by NF-E2, and suggest that caspase-12 participates in the development of fully func

126 and the endoplasmic reticulum stress-induced caspase-12 pathway but not the mitochondrial caspase-9 p

127 12 activities, suggesting that caspase-8 and caspase-12 pathways are independent of each other.

128 s the caspase-3 along with the caspase-8 and caspase-12 pathways.

129 Despite wild-type levels of alphaIIbbeta3, caspase-12(-/-) platelets exhibit reduced fibrinogen bin

130 Taken together, these data indicate that caspase 12 plays a pivotal role in cisplatin-induced apo

131 and mouse embryonic fibroblasts showed that caspase-12 positively modulated the production of type I

132 We found that deleting caspase-12 preserved mdx muscle function, resulting in a

133 rtment, suggesting a potential mechanism for caspase 12 processing and its role as an amplifier in th

134 Autolytic cleavage within the caspase-12 proenzyme was mapped to a single site at the

135 -A or thapsigargin induces the expression of caspase-12 protein and also leads to translocation of cy

136 show that in mice, gene-targeted deletion of caspase-12 renders animals resistant to peritonitis and

137 and cleaves the prodomain to generate active caspase-12, resulting in increased cell death.

138 In this regard, caspase-12 seems to be the cFLIP counterpart for regulat

139 tein (CHOP) expression and the activation of caspase 12, suggesting that ER stress contributes to cel

140 ing protein-homologous protein and activated caspase-12, suggesting that young animals possess an eff

141 The regulated expression of caspase-12S suggests that this caspase recruitment domai

142 We then crossed mdx mice with mice null for caspase-12, the murine equivalent of human caspase-4, wh

143 mdx muscles was normalized in the absence of caspase-12; this was found to be due to decreased fibre

144 anslocation of apoptosis-inducing factor and caspase 12 to the nucleus.

145 sigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress,

146 wed an increase in activities of calpain and caspase-12, upregulation of Bax:Bcl-2 ratio, release of

147 Furthermore, caspase-12 was cleaved in Mn(II)-treated cells, suggesti

148 To examine these catalytic properties, rat caspase-12 was cloned, and the recombinant enzyme was us

149 Expression of caspase-12 was linked to decreased systemic and adipose

150 Notably, the protease function of caspase-12 was not necessary for this effect, as the cat

151 ays, Fas activations, 8-OHdG expression, and caspase-12 were demonstrated in type 1 diabetic BB/Wor r

152 e pro-apoptotic proteins of CHOP/GADD153 and caspase-12 were dramatically decreased, while the anti-a

153 es of caspase-3/7, caspase-8, caspase-9, and caspase-12 were measured by a fluorescence image scanner

154 rkers (BiP, pIRE1alpha, sXBP1, CHOP, cleaved caspase-12) were increased in septic WT mice, but not in

155 ded protein response (UPR) markers, CHOP and Caspase 12, were also increased in the MECD mice.

156 nitiator caspases, caspase-8, caspase-9, and caspase-12, were activated during infection with the rM5

157 ATAD(319), and this motif was recognized by caspase-12 when incorporated into synthetic fluorogenic

158 ced apoptosis and activate the ER-associated caspase-12, which is required specifically for nuclear a

159 The specific activity of caspase-12 with these substates was several orders of ma