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NLRC5 encodes a member of the caspase recruitment domain-containing NLR family. Additionally we are shipping NLRC5 Antibodies (14) and many more products for this protein.
NLRC5 regulates TGFB1 (show TGFB1 ELISA Kits)-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 ELISA Kits) and IL-1Beta (show IL1B ELISA Kits) secretion.
NLRC5 function is shaped by reversible ubiquitination, which modulates the NF-kappaB (show NFKB1 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) 2B triggers NLRP3 (show NLRP3 ELISA Kits) and NLRC5 inflammasome activation and IL-1beta (show IL1B ELISA Kits) secretion in bronchial cells
Expression of NLRC5 positively correlates with histocompatibility class I expression in human tissues.
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 ELISA Kits) 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 ELISA Kits) and IRF3 (show IRF3 ELISA Kits) 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 ELISA Kits)(+) T cell responses, including activation, proliferation and cytotoxicity.
NLRC5 overexpression promotes interleukin (IL)-1beta (show IL1B ELISA Kits) production via caspase-1 (show CASP1 ELISA Kits) 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