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1 omprises a sensor, an adaptor, and a zymogen procaspase-1.
2 ciency selectively reduced the processing of procaspase-1.
3 n containing CARD), and the effector protein procaspase-1.
4 NLRP3 promotes clustering and activation of procaspase-1.
5 cells were found to express NLRP3, ASC, and procaspase-1.
6 ic speck-containing protein with a card) and procaspase-1.
7 , a response that requires the activation of procaspase-1.
8 is the activation of the initiator caspase, procaspase-1.
9 ion of a multiprotein complex that activates procaspase-1.
10 IL18) or close to genes that are involved in procaspase-1 activation (NLRC4 and CARD16, CARD17, and C
11 ily receptors), and TNF in the regulation of procaspase-1 activation, cytokine production, and contro
13 e autocatalytic processing and activation of procaspase-1 and caspase-1-dependent apoptosis in transf
14 t Ipaf is a specific and direct activator of procaspase-1 and could be involved in activation of casp
15 tion-defective NLRC4 S533A failed to recruit procaspase-1 and did not assemble inflammasome specks du
16 osolic pattern recognition receptors recruit procaspase-1 and procaspase-8 via the adaptor protein AS
17 ain, with procaspase-1 induced activation of procaspase-1 and processing of pro-interleukin-1beta in
18 danger signals, triggering self-cleavage of procaspase-1 and production of the proinflammatory cytok
20 ardiak/Rip2/Rick-mediated oligomerization of procaspase-1 and suppresses activation this protease, as
22 We show here that ASC binds by its CARD to procaspase-1 and to adapter proteins involved in caspase
23 not C/EBPbeta-Ala(217), were associated with procaspases 1 and 8 in vivo and in vitro and inhibited t
29 ssed mouse hearts with a 30-fold increase in procaspase-1 content, unprocessed procaspase-1 was well
31 schemia and suggest that conditions in which procaspase-1 in the heart is increased may predispose to
32 not its isolated CARD or PYRIN domain, with procaspase-1 induced activation of procaspase-1 and proc
38 ereby activates NF-kappaB, whereas wild-type procaspase-1 reduces intracellular RIP2 levels by enzyma
39 h a caspase recruitment domain) and effector procaspase-1, resulting in active caspase-1 formation wh
41 omplexes, which facilitate the maturation of procaspase 1 to caspase 1, leading to IL-1beta and IL-18
43 via a homotypic PYD interaction and recruits procaspase-1 via a homotypic caspase recruitment domain
45 expression of pro-IL-1beta, NLRP3, ASC, and procaspase-1 was not affected in Pml(-/-) macrophages.
46 ncrease in procaspase-1 content, unprocessed procaspase-1 was well tolerated, without detectable path
47 uences of increased myocardial expression of procaspase-1 were examined on the normal and ischemicall
48 bridging NLRP proteins, such as NLRP3, with procaspase-1 within the inflammasome complex, which subs
49 esented here is the crystal structure of the procaspase-1 zymogen without its caspase recruitment dom
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