ライフサイエンスコーパス: pro-caspase 3

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1 factant protein-B, type III procollagen, and pro-caspase 3.

2 oliferating cell nuclear antigen (PCNA), and pro-caspase-3.

3 was followed by an accelerated activation of pro-caspase-3.

4 the K8/18 intermediate filament network and pro-caspase-3.

5 ntly induce apoptosis by directly processing pro-caspase-3.

6 apoptotic activity of pro-caspase-1 but not pro-caspase-3.

7 ase activities and proteolytic processing of pro-caspase-3.

8 P2 can prevent the proteolytic processing of pro-caspases -3, -6 and -7 by blocking the cytochrome c-

9 prevented Bid cleavage and the activation of pro-caspases-3/7 in cultures treated with TNFalpha + CHX

10 tosis and inhibits proteolytic processing of pro-caspases-3, -8, and -9 and poly(ADP-ribose) polymera

11 In contrast, the kinetics/magnitude of pro-caspase-3 activation in the two cell lines were iden

12 In addition to an RGD motif, pro-caspase-3 also contains a potential RGD-binding moti

13 oblotting analysis confirmed the cleavage of pro-caspase 3 and 9, and of specific caspase substrates.

14 nces in the subcellular localization of both pro-caspase-3 and ICAD between the analyzed cell lines.

15 ivation, alphaB-crystallin selectively binds pro-caspase-3 and its cleavage intermediates in vitro an

16 showed further that caspase-2 interacts with pro-caspase-3 and that p38 MAPK reduced this interaction

17 DEDD coimmunoprecipitated with both K18 and pro-caspase-3, and kinetic analyses placed apoptotic DED

18 Further, pro-caspase-3 at 32 kDa was proteolyzed to a fragment at

19 iggering conformational changes that promote pro-caspase-3 autoprocessing and activation.

20 te the apoptotic process in cells expressing pro-caspase 3 but that cytochrome c release is not suffi

21 cells with an expression plasmid coding for pro-caspase 3, but not other pro-caspases, restores cyto

22 ties, and analyses of Bid, procaspase-9, and pro-caspase-3 cleavage.

23 D-3/caspase-3-related caspases revealed that pro-caspases-3 (CPP32) and -7 (Mch-3alpha) were rapidly

24 Because overexpressed pro-caspase-3 did not undergo autocatalytic activation i

25 In MCF7-Fas cells that are deficient for pro-caspase-3, even high amounts of caspase-8 produced a

26 caspase-8-induced proteolytic activation of pro-caspase-3; however, they subsequently inhibited acti

27 and rate of caspase-8 induced activation of pro-caspase-3 in cytosolic extracts was the same as in a

28 orrelated with the appearance of cleavage of pro-caspase-3 into its 20-kDa active form.

29 we overexpressed the proapoptotic molecules pro-caspase-3, pro-caspase-7, and Bax to induce therapeu

30 to STS-triggered apoptosis, as determined by pro-caspase-3 processing, cytochrome c efflux and DNA fr

31 scence, which correlated with an increase in pro-caspase-3 processing.

32 merase, as well as proteolytic processing of pro-caspase 3 to active subunits.

33 ATP treatment resulted in the processing of pro-caspase 3 to its active form and cleavage of the nuc

34 Substantial proteolytic activation of pro-caspase 3 was relatively delayed.

35 Intact pro-caspase-3 was in fact cleaved by activated calpain d

36 s-8 and -10 directly process the executioner pro-caspase-3 with activation rates (kcat/Km) of 8.7 x 1

37 he initiator caspase-8 can directly activate pro-caspase-3 without the requirement for an accelerator

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