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investigated the function of Card9-mediated innate immunity in inflammation-associated colon carcinogenesis; report that Card9-signaling drives the production of IL-1beta (zeige IL1B Proteine) within the damaged intestine and regulates the subsequent generation of IL-22 (zeige IL22 Proteine) by group3 innate lymphoid cells, which promotes tumorigenesis via STAT3 (zeige STAT3 Proteine) activation within the transformed epithelium
this study shows that oxidized low-density lipoprotein immune complex priming of the Nlrp3 (zeige NLRP3 Proteine) inflammasome Is dependent on CARD9
results demonstrate that Dectin-1 (zeige CLEC7A Proteine)-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 (zeige INS Proteine) 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 (zeige SYK Proteine)-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.
Mincle (zeige CLEC4E Proteine) Activation and the Syk (zeige SYK Proteine)/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye
CARD9 reduces viability specifically in males and promotes tumorigenesis specifically in the large intestines of these male mice.
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 (zeige MAP3K14 Proteine) 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 (zeige RASGRF1 Proteine)/ERK (zeige EPHB2 Proteine)-mediated GM-CSF (zeige CSF2 Proteine) response characterizes CARD9 deficiency in French-Canadians.
our data highlight the critical role of CARD9-dependent neutrophil trafficking into the central nervous system
A CARD9 variant (protective against inflammatory bowel disease)is C-terminally truncated and acts in a dominant-negative manner for CARD9-mediated cytokine production. K125 is the CARD9 ubiquitinated residue. Ubiquitination is needed for CARD9 activity.
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