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抗Human NLRC4 抗体:
抗Mouse (Murine) NLRC4 抗体:
抗Rat (Rattus) NLRC4 抗体:
Human Polyclonal NLRC4 Primary Antibody for IHC, ELISA - ABIN1002684
Larisch, Yi, Lotan, Kerner, Eimerl, Tony Parks, Gottfried, Birkey Reffey, de Caestecker, Danielpour, Book-Melamed, Timberg, Duckett, Lechleider, Steller, Orly, Kim, Roberts: A novel mitochondrial septin-like protein, ARTS, mediates apoptosis dependent on its P-loop motif. in Nature cell biology 2001
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Human Polyclonal NLRC4 Primary Antibody for ICC, ELISA - ABIN1002685
Poyet, Srinivasula, Tnani, Razmara, Fernandes-Alnemri, Alnemri: Identification of Ipaf, a human caspase-1-activating protein related to Apaf-1. in The Journal of biological chemistry 2001
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Human Polyclonal NLRC4 Primary Antibody for IHC (fro), IHC (p) - ABIN252142
Akhter, Caution, Abu Khweek, Tazi, Abdulrahman, Abdelaziz, Voss, Doseff, Hassan, Azad, Schlesinger, Wewers, Gavrilin, Amer: Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization. in Immunity 2012
Human Polyclonal NLRC4 Primary Antibody for WB - ABIN153028
Cividini, Tozzi, Galli, Pesi, Camici, Dumontet, Jordheim, Allegrini: Cytosolic 5'-nucleotidase II interacts with the leucin rich repeat of NLR family member Ipaf. in PLoS ONE 2015
Guinea Pig Polyclonal NLRC4 Primary Antibody for IHC, WB - ABIN2792097
Clark, Gurney, Abaya, Baker, Baldwin, Brush, Chen, Chow, Chui, Crowley, Currell, Deuel, Dowd, Eaton, Foster, Grimaldi, Gu, Hass, Heldens, Huang, Kim, Klimowski, Jin, Johnson, Lee, Lewis, Liao, Mark et al.: The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment. ... in Genome research 2003
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The authors describe a novel mutation in NLRC4 in a large pedigree causing an NLRC4-associated, partially anakinra-responsive AID, dominated by cutaneous erythematous nodes and urticarial rash, arthralgias, and late-onset enterocolitis.
Results found that NLRC4 expression increased in for promoting DN progression and demonstrate NLRC4-driven IL-1beta (显示 IL1B 抗体) production as critical for the progression of DN.
Ubiquitin-tagged NLRC4 could induce cell death and activate caspase-8 (显示 CASP8 抗体) independent of Ser (显示 SIGLEC1 抗体)(533) phosphorylation. Our
LPS (显示 IRF6 抗体) activates the MAPK (显示 MAPK1 抗体) pathway in macrophages, thus resulting in the upregulation of NLRC4; however, NLRC4 inhibits IL1beta (显示 IL1B 抗体) and IL18 (显示 IL18 抗体) production, contributing to the anti-inflammatory response.
High expression of NLRP3 (显示 NLRP3 抗体), NLRC4, and CASP1 (显示 CASP1 抗体) in background non-tumorous liver is significantly correlated with poor prognosis of patients after resection of hepatocellular carcinoma.
association of IL-18 (显示 IL18 抗体) levels with a single nucleotide polymorphism in the untranslated exon 2 of the inflammasome component NLRC4
While both contributing to pathogen clearance, NLRP3 (显示 NLRP3 抗体) more than NLRC4 contributes to deleterious inflammatory responses in cystic fibrosis (显示 S100A8 抗体) and correlates with defective NLRC4-dependent IL-1Ra (显示 IL1RN 抗体) production.
analysis of a subset of inflammasome receptors including NLRP3 (显示 NLRP3 抗体), NLRC4 and AIM2 (显示 AIM2 抗体) that triggers formation of the micrometer-sized spherical supramolecular complex called the ASC (显示 PYCARD 抗体) speck
Thus, pathogenic inflammasome activity during Candida infection is negatively regulated by the IL-22 (显示 IL22 抗体)/NLRC4/IL-1Ra (显示 IL1RN 抗体) axis.
cN-II (显示 NT5C2 抗体) co-immunoprecipitated both with wild type Ipaf and its LRR domain after transfection with corresponding expression vectors, but not with Ipaf lacking the LRR domain.
data provide evidence that the NLRC4 inflammasome contributes to resistance through regulation of caspase-1 (显示 CASP1 抗体), IL-1beta (显示 IL1B 抗体) and IL-18 (显示 IL18 抗体) in a CD11blowLy6Glow population of cells
NLRC4 expression controls melanoma tumor growth.
The interplay between NLRP3 (显示 NLRP3 抗体) and NLRC4 reveals an unexpected overlap between what had been considered distinct inflammasome scaffolds.
The activation of NLRC4 by flagellin (显示 FliC 抗体) downregulated the flagellin (显示 FliC 抗体)-induced and TLR5 (显示 TLR5 抗体)-mediated immune responses against flagellin (显示 FliC 抗体).
TLR5 (显示 TLR5 抗体) but not NLRC4 is required for S. pneumoniae FliC (显示 FliC 抗体)-induced protection.
Data indicate that NLRC4 activation in Intestinal epithelial cells (IECs) leads to cell expulsion and IL-18 (显示 IL18 抗体) release, and implicate Caspase-8 (显示 CASP8 抗体) in NLRC4 inflammasome responses in vivo by generation of doubly deficient in Caspase-1 (显示 CASP1 抗体) and Caspase-8 (显示 CASP8 抗体).
The tick protein sialostatin L2 binds to annexin A2 (显示 ANXA2 抗体) and inhibits NLRC4-mediated inflammasome activation.
LPS (显示 TLR4 抗体) activates the MAPK (显示 MAPK1 抗体) pathway in macrophages, thus resulting in the upregulation of NLRC4; however, NLRC4 inhibits IL1beta (显示 IL1B 抗体) and IL18 (显示 IL18 抗体) production, contributing to the anti-inflammatory response.
These data reveal mild constitutive activation of the Nlrc4 inflammasome as the results of two SNPs, which leads to the stimulation of hepatocyte proliferation. The increased liver regeneration induces rapid liver mass recovery after hepatectomy and may prevent the development of hepatotoxin-induced liver fibrosis.
In C. elegans, Ced4 binds and activates Ced3, an apoptotic initiator caspase, via caspase-associated recruitment domains (CARDs). Human Ced4 homologs include APAF1 (MIM 602233), NOD1/CARD4 (MIM 605980), and NOD2/CARD15 (MIM 605956). These proteins have at least 1 N-terminal CARD domain followed by a centrally located nucleotide-binding domain (NBD or NACHT) and a C-terminal regulatory domain, found only in mammals, that contains either WD40 repeats or leucine-rich repeats (LRRs). CARD12 is a member of the Ced4 family and can induce apoptosis.
caspase recruitment domain protein 12
, NLR family CARD domain-containing protein 4
, ice protease-activating factor
, NLR family, CARD domain containing 4
, CARD, LRR, and NACHT-containing protein
, ICE-protease activating factor
, NOD-like receptor C4
, caspase recruitment domain family, member 12
, caspase recruitment domain-containing protein 12
, nucleotide-binding oligomerization domain, leucine rich repeat and CARD domain containing 4