anti-CARD9 (CARD9) Antikörper

Mouse (Murine) Caspase Recruitment Domain Family, Member 9 (CARD9) Interaktionspartner

1. 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.

2. Our results reveal a molecular mechanism for CLR (zeige CALCR Antikörper)-mediated Card9 regulation that controls innate immunity to fungal infections

3. 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.

4. 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

5. this study shows that oxidized low-density lipoprotein immune complex priming of the Nlrp3 (zeige NLRP3 Antikörper) inflammasome Is dependent on CARD9

6. 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

7. 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.

8. 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.

9. 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

10. a possible role for the Syk (zeige SYK Antikörper)-CARD9 pathway in DCs in excessive inflammation of IFV-infected lungs.

Human Caspase Recruitment Domain Family, Member 9 (CARD9) Interaktionspartner

1. Our results reveal a molecular mechanism for CLR (zeige DCLK3 Antikörper)-mediated Card9 regulation that controls innate immunity to fungal infections

2. 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.

3. Card9 in severe acute pancreatitis patients was overexpressed, suggesting the close correlation with the outcome and severity of pancreatic injury in patients.

4. 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.

5. The findings linked, for the first time, mutations leading to CARD9 deficiencies with susceptibility to opportunistic filamentous fungi.

6. Chronic and invasive fungal infections have been described in a Turkish consanguineous family with CARD9 deficiency.

7. We observed no significant association between the investigated CARD9 SNPs and the susceptibility of either Crohn's disease or ulcerative colitis

8. 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.

9. Impaired RASGRF1 (zeige RASGRF1 Antikörper)/ERK (zeige EPHB2 Antikörper)-mediated GM-CSF (zeige CSF2 Antikörper) response characterizes CARD9 deficiency in French-Canadians.

10. our data highlight the critical role of CARD9-dependent neutrophil trafficking into the central nervous system