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NLRC5 encodes a member of the caspase recruitment domain-containing NLR family.
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Human Polyclonal NLRC5 Primary Antibody for EIA, IF - ABIN783699
Benko, Magalhaes, Philpott, Girardin: NLRC5 limits the activation of inflammatory pathways. in Journal of immunology (Baltimore, Md. : 1950) 2010
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In a transformed cell line, NLRC5 plays a significant role in IL-6 (show IL6 Antibodies) and IL-1Beta (show IL1B Antibodies) secretion.
NLRC5 function is shaped by reversible ubiquitination, which modulates the NF-kappaB (show NFKB1 Antibodies) activation switch
RSV infection of lung epithelial cells induces expression of RIG-I, NLRC5, and subsequent upregulation of HLA-A, HLA-B and HLA-C.
a novel role for NLRC5 in RIG-I-mediated antiviral host responses against influenza virus infection, distinguished from the role of NLRC5 in MHC class I gene regulation.
This study presents a detailed functional study of the domains of NLRC5 revealing that the N-terminal domain of human NLRC5 has intrinsic transcriptional activity.
Unusual structural features revealed by the solution NMR structure of the NLRC5 caspase (show CASP3 Antibodies) recruitment domain.
A model for full-length human NLRC5 was prepared and, besides the closed conformation of monomeric NLRC5, a heptameric platform was also modeled for the opened conformational NLRC5 monomers.
rhinovirus ion channel protein (show TRPC3 Antibodies) 2B triggers NLRP3 (show NLRP3 Antibodies) and NLRC5 inflammasome activation and IL-1beta (show IL1B Antibodies) secretion in bronchial cells
Expression of NLRC5 positively correlates with histocompatibility class I expression in human tissues.
NLRC5 can cooperate with X1 box-binding transcription factor RFX (show RFX1 Antibodies) and X2 box-binding transcription factor ATF1 (show AFT1 Antibodies) in activation of histocompatibility class I promoter region.
NLRC5 is differentially expressed in hepatic tissues and hepatic stellate cells during hepatic fibrosis and its reversal
NLRC5 expression in T cells is required to protect them from NK-cell-mediated elimination upon inflammation.
NLRC5 and CIITA (show CIITA Antibodies) thus emerge as paradigms for a novel class of transcriptional regulators dedicated for transactivating extremely few, phylogenetically related genes.
Data conclude that Nlrc5 is important in the regulation of MHC-I expression by reducing H3K27me3 on MHC-I promoter and joins CIITA as an NLR subfamily that controls MHC gene transcription.
NLRC5 is required for both constitutive and inducible histocompatibility class I gene expression and host defense.
NLRC5 ablation reduces MHC class I expression, and enhances IKK (show CHUK Antibodies) and IRF3 (show IRF3 Antibodies) phosphorylation in response to TLR stimulation or viral infection.
NLRC5-deficient mice showed a profound defect in the expression of MHC class I genes and a concomitant failure to activate L. monocytogenes-specific CD8 (show CD8A Antibodies)(+) T cell responses, including activation, proliferation and cytotoxicity.
NLRC5 overexpression promotes interleukin (IL)-1beta (show IL1B Antibodies) production via caspase-1 (show CASP1 Antibodies) and is dispensable for cytokine induction in virus and bacterial infections under physiologic conditions.
NLRC5 expression is critical for lipopolysaccharide-induced interleukin (IL)-10 (show IL10 Antibodies) production in RAW264.7 macrophages.
This gene encodes a member of the caspase recruitment domain-containing NLR family. This gene plays a role in cytokine response and antiviral immunity through its inhibition of NF-kappa-B activation and negative regulation of type I interferon signaling pathways.
NLR family, CARD domain containing 5
, protein NLRC5
, NOD-like receptor C5
, caterpiller protein 16.1
, nucleotide-binding oligomerization domain protein 4
, nucleotide-binding oligomerization domain, leucine rich repeat and CARD domain containing 5
, nucleotide-binding oligomerization domains 27