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1 cular glue between danger-signal sensors and 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 omprises a sensor, an adaptor, and a zymogen procaspase-1.
9  is the activation of the initiator caspase, procaspase-1.
10 ion of a multiprotein complex that activates procaspase-1.
11 IL18) or close to genes that are involved in procaspase-1 activation (NLRC4 and CARD16, CARD17, and C
12 ily receptors), and TNF in the regulation of procaspase-1 activation, cytokine production, and contro
13                                              Procaspase-1 also contains an NH2-terminal CARD domain,
14 e autocatalytic processing and activation of procaspase-1 and caspase-1-dependent apoptosis in transf
15 t Ipaf is a specific and direct activator of procaspase-1 and could be involved in activation of casp
16 tion-defective NLRC4 S533A failed to recruit procaspase-1 and did not assemble inflammasome specks du
17 osolic pattern recognition receptors recruit procaspase-1 and procaspase-8 via the adaptor protein AS
18 ain, with procaspase-1 induced activation of procaspase-1 and processing of pro-interleukin-1beta in
19  danger signals, triggering self-cleavage of procaspase-1 and production of the proinflammatory cytok
20                                Maturation of procaspase-1 and release of the mature enzyme subunits t
21 ardiak/Rip2/Rick-mediated oligomerization of procaspase-1 and suppresses activation this protease, as
22 ypically a Nod-like receptor), the precursor procaspase-1 and the adaptor ASC.
23   We show here that ASC binds by its CARD to procaspase-1 and to adapter proteins involved in caspase
24 not C/EBPbeta-Ala(217), were associated with procaspases 1 and 8 in vivo and in vitro and inhibited t
25 nd cellular stress signals via activation of procaspases-1 and -8.
26 RP3 inflammasome components (NLRP3, ASC, and procaspase-1) and pro-IL-1beta in ARPE-19 cells.
27        In a transfection model, such variant procaspase-1 binds receptor interacting protein kinase 2
28                       In conclusion, variant procaspase-1 binds RIP2 and thereby activates NF-kappaB.
29 s corroborated by molecular docking with the procaspase-1 CARD domain.
30                       Finally, C1q decreased procaspase-1 cleavage and caspase-1-dependent cleavage o
31 ntaining protein 3 (NLRP3) inflammasome with procaspase-1 cleavage into active caspase-1.
32 ssed mouse hearts with a 30-fold increase in procaspase-1 content, unprocessed procaspase-1 was well
33 ither WT or enzymatically inactive (p.C284A) procaspase-1 fusion reporter proteins.
34 schemia and suggest that conditions in which procaspase-1 in the heart is increased may predispose to
35  not its isolated CARD or PYRIN domain, with procaspase-1 induced activation of procaspase-1 and proc
36                  Moreover, ASC also recruits procaspase-1 into ASC-formed cytosolic specks, separatin
37                     In post-ischemic hearts, procaspase-1 overexpression was associated with striking
38                         NLRC5, together with procaspase 1, pro-IL-1beta, and the inflammasome adaptor
39         Tissue culture studies revealed that procaspase-1 processing/activation is stimulated by hypo
40 large oligomeric filaments, which facilitate procaspase-1 recruitment.
41 ereby activates NF-kappaB, whereas wild-type procaspase-1 reduces intracellular RIP2 levels by enzyma
42 h a caspase recruitment domain) and effector procaspase-1, resulting in active caspase-1 formation wh
43 eck-like protein containing a CARD (ASC) and procaspase-1 that plays a pivotal role in various neurod
44 tly and specifically with the CARD domain of procaspase-1 through CARD-CARD interaction.
45 omplexes, which facilitate the maturation of procaspase 1 to caspase 1, leading to IL-1beta and IL-18
46  CD44 ECD-shedding reduced the conversion of procaspase-1 to active caspase-1, caspase-1 activity and
47 me in the nuclei and interacted with ASC and procaspase-1 to form a functional inflammasome.
48 via a homotypic PYD interaction and recruits procaspase-1 via a homotypic caspase recruitment domain
49             ASC interacted specifically with procaspase-1 via CARD-CARD interactions and induced its
50  expression of pro-IL-1beta, NLRP3, ASC, and procaspase-1 was not affected in Pml(-/-) macrophages.
51 ncrease in procaspase-1 content, unprocessed procaspase-1 was well tolerated, without detectable path
52 uences of increased myocardial expression of procaspase-1 were examined on the normal and ischemicall
53  bridging NLRP proteins, such as NLRP3, with procaspase-1 within the inflammasome complex, which subs
54 esented here is the crystal structure of the procaspase-1 zymogen without its caspase recruitment dom