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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
Show all 2 references for ABIN783699
CITA/NLRC5 and CIITA are transcriptional regulators that orchestrate the concerted expression of critical components in the MHC class I and class II pathways, respectively. [review]
NLRC5 expression was significantly associated with the activation of CD8 (show CD8A Antibodies)(+) cytotoxic T cells and patient survival in multiple cancer types. Thus, NLRC5 constitutes a novel prognostic biomarker and potential therapeutic target of cancers.
NLRC5 regulates TGFB1 (show TGFB1 Antibodies)-induced proliferation and activation of hepatic stellate cells during hepatic fibrosis.
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.
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.
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