Use your antibodies-online credentials, if available.
results suggest that CARD9 knockout protects the heart from ischemia/reperfusion (I/R) injury, possibly through reduction of neutrophil infiltration and attenuation of CARD9-associated acute inflammatory signaling.
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/CARD9/p38 MAPK signalling. Zinc supplement ameliorates ORCH through activation of metallothionein to repress oxidative stress-activated BCL10 expression and p38 MAPK activation.
Our results reveal a molecular mechanism for CLR-mediated Card9 regulation that controls innate immunity to fungal infections
this report relates the potential of the Dectin-2/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 within the damaged intestine and regulates the subsequent generation of IL-22 by group3 innate lymphoid cells, which promotes tumorigenesis via STAT3 activation within the transformed epithelium
this study shows that oxidized low-density lipoprotein immune complex priming of the Nlrp3 inflammasome Is dependent on CARD9
results demonstrate that Dectin-1-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 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-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 Activation and the Syk/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.
Ubiquitination of CARD9 by TRIM62 regulates CARD9-mediated anti-fungal immunity.
CARD9-dependent production of TNF-alpha enhances the candidacidal capacity of neutrophils, limiting fungal disease during disseminated C. tropicalis infection.
Results indicating that CARD9 is a regulator of metastasis-associated macrophages will lead to new insights into evolution of the microenvironments supporting tumor metastasis.
Rapid CD4+ T-cell responses to bacterial flagellin require dendritic cell expression of Syk and CARD9.
CARD9 regulates H-Ras activation by linking Ras-GRF1 to H-Ras, which mediates Dectin-1-induced extracellular signal-regulated protein kinase (ERK) activation and proinflammatory responses when stimulated by their ligands.
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.
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 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/ERK-mediated GM-CSF response characterizes CARD9 deficiency in French-Canadians.
homozygous mutation results in deep dermatophytosis due to impaired neutrophil fungal killing
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.
These results indicate that CARD9 is indispensable for Phialophora verrucosa killing by polymorphonuclear neutrophils.
Data indicate that MINCLE receptor is able to mediate the response to trehalose-6,6-dimycolate (TDM) dependent on SYK kinase and CARD9 protein.
MyD88 and CARD9 act in two discrete phases and in two cellular compartments to direct chemokine- and neutrophil-dependent host defense.
In a patient with CARD9 deficiency, clinical remission with adjunctive GM-CSF therapy suggested that a CARD9/GM-CSF axis contributes to susceptibility to candidiasis.
Invasive infections of the CNS or digestive tract caused by Candida species in previously healthy children and adults might be caused by inherited CARD9 deficiency.
These are the first 2 patients with inherited CARD9 deficiency.
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