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anti-Mouse (Murine) CARD9 Antikörper:
anti-Human CARD9 Antikörper:
anti-Rat (Rattus) CARD9 Antikörper:
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These results suggest that CARD9 may be involved in the wound-healing process through the regulation of macrophage-mediated inflammatory responses.
high fat diet (HFD) and zinc deficiency synergistically induce obesity-related cardiac hypertrophy (ORCH), by increasing oxidative stress-mediated activation of BCL10 (zeige BCL10 Antikörper)/CARD9/p38 MAPK (zeige MAPK14 Antikörper) signalling. Zinc supplement ameliorates ORCH through activation of metallothionein (zeige MT Antikörper) to repress oxidative stress-activated BCL10 (zeige BCL10 Antikörper) expression and p38 MAPK (zeige MAPK14 Antikörper) activation.
Our results reveal a molecular mechanism for CLR (zeige CALCR Antikörper)-mediated Card9 regulation that controls innate immunity to fungal infections
this report relates the potential of the Dectin-2 (zeige CLEC6A Antikörper)/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 (zeige IL1B Antikörper) within the damaged intestine and regulates the subsequent generation of IL-22 (zeige IL22 Antikörper) by group3 innate lymphoid cells, which promotes tumorigenesis via STAT3 (zeige STAT3 Antikörper) activation within the transformed epithelium
this study shows that oxidized low-density lipoprotein immune complex priming of the Nlrp3 (zeige NLRP3 Antikörper) inflammasome Is dependent on CARD9
results demonstrate that Dectin-1 (zeige CLEC7A Antikörper)-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 Antikörper) 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
CARD9 deficiency can present with a phenotype of spontaneous candidal endophthalmitis. We report 2 novel mutations in CARD9, both affecting splicing, expanding the range of morbid variants causing CARD9 deficiency, emphasising the importance of both genomic and cDNA sequencing for this condition.
Our results reveal a molecular mechanism for CLR (zeige DCLK3 Antikörper)-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 (zeige MRAP Antikörper)-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 Antikörper) 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 Antikörper)/ERK (zeige EPHB2 Antikörper)-mediated GM-CSF (zeige CSF2 Antikörper) response characterizes CARD9 deficiency in French-Canadians.
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