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anti-Mouse (Murine) CARD9 Anticorps:
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Our results reveal a molecular mechanism for CLR (Montrer CALCR Anticorps)-mediated Card9 regulation that controls innate immunity to fungal infections
this report relates the potential of the Dectin-2 (Montrer CLEC6A Anticorps)/Card9-coupled pathway in ocular autoimmunity. Not only does it contribute to understanding of how innate immune receptors orchestrate T cell-mediated autoimmunity, it also reveals a previously unappreciated ability of fungal-derived signals to promote autoimmunity.
investigated the function of Card9-mediated innate immunity in inflammation-associated colon carcinogenesis; report that Card9-signaling drives the production of IL-1beta (Montrer IL1B Anticorps) within the damaged intestine and regulates the subsequent generation of IL-22 (Montrer IL22 Anticorps) by group3 innate lymphoid cells, which promotes tumorigenesis via STAT3 (Montrer STAT3 Anticorps) activation within the transformed epithelium
this study shows that oxidized low-density lipoprotein immune complex priming of the Nlrp3 (Montrer NLRP3 Anticorps) inflammasome Is dependent on CARD9
results demonstrate that Dectin-1 (Montrer CLEC7A Anticorps)-triggered Card9 signaling but not inflammasome activation can potently cross-prime Ag-specific cytotoxic T-cells, suggesting that this pathway would be a candidate for immunotherapy and vaccine development
CARD9 promotes recovery from colitis by promoting interleukin (IL)-22 production, and Card9(-/-) mice are more susceptible to colitis. The microbiota from Card9(-/-) mice fails to metabolize tryptophan into metabolites that act as aryl hydrocarbon receptor (AHR) ligands.
The findings suggest that CARD9 mediates the innate immune and Th17-mediated adaptive immune responses against dematiaceous fungal infections at the early stage of infection.
CARD9 knockout alleviated HFD-induced insulin (Montrer INS Anticorps) resistance and glucose intolerance, prevented myocardial dysfunction with preserved cardiac fractional shortening and cardiomyocyte contractile properties. CARD9 knockout also significantly decreased the number of infiltrated macrophages in the heart with reduced myocardium-, plasma-, and macrophage-derived cytokines
a possible role for the Syk (Montrer SYK Anticorps)-CARD9 pathway in DCs in excessive inflammation of IFV-infected lungs.
CARD9 mediates necrotic smooth muscle cell-induced inflammation in macrophages contributing to neointima formation of vein grafts.
Our results reveal a molecular mechanism for CLR (Montrer DCLK3 Anticorps)-mediated Card9 regulation that controls innate immunity to fungal infections
The IBD risk allele at CARD9 rs10781499 is associated with reduced aryl hydrocarbon activation by microbiota-derived metabolites extracted from fecal samples of IBD patients.
Card9 in severe acute pancreatitis patients was overexpressed, suggesting the close correlation with the outcome and severity of pancreatic injury in patients.
CARD9 allele C (p = 0.012) and genotype CC (p = 0.012) were significant protective factors against ankylosing spondylitis only in HLA-B27-negative patients.
The findings linked, for the first time, mutations leading to CARD9 deficiencies with susceptibility to opportunistic filamentous fungi.
Chronic and invasive fungal infections have been described in a Turkish consanguineous family with CARD9 deficiency.
We observed no significant association between the investigated CARD9 SNPs and the susceptibility of either Crohn's disease or ulcerative colitis
This study identified two novel independent loci (MAP3K14 (Montrer MAP3K14 Anticorps) and CARD9) strongly associated with joint damage in Mexican Americans and European Americans and a few shared loci showing suggestive evidence for association.
Impaired RASGRF1 (Montrer RASGRF1 Anticorps)/ERK (Montrer EPHB2 Anticorps)-mediated GM-CSF (Montrer CSF2 Anticorps) response characterizes CARD9 deficiency in French-Canadians.
our data highlight the critical role of CARD9-dependent neutrophil trafficking into the central nervous system
The protein encoded by this gene is a member of the CARD protein family, which is defined by the presence of a characteristic caspase-associated recruitment domain (CARD). CARD is a protein interaction domain known to participate in activation or suppression of CARD containing members of the caspase family, and thus plays an important regulatory role in cell apoptosis. This protein was identified by its selective association with the CARD domain of BCL10, a postive regulator of apoptosis and NF-kappaB activation, and is thought to function as a molecular scaffold for the assembly of a BCL10 signaling complex that activates NF-kappaB. Several alternatively spliced transcript variants have been observed, but their full-length nature is not clearly defined.
caspase recruitment domain-containing protein 9
, Caspase recruitment domain-containing protein 9
, caspase recruitment domain family, member 9
, caspase recruitment domain protein 9
, caspase recruitment domain-containing protein 9-like