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 an apoptotic cascade by the co-activation of Caspase 12 and Cleaved Caspase 3 transducers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Although caspase-12 could mediate autoproteolytic maturation of i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 Caspase-12 has been shown to negatively modulate inflamm

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 12 activities, suggesting that caspase-8 and caspase-12 pathways are independent of each other.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 ting Chop in within embryonic precursors and Caspase 12 within placental precursors.