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Caspase recruitment domain family, member 9

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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PrP, Dectin-1, Syk, BCL10, CAN
Papers on CARD9
Successful Granulocyte Colony Stimulating Factor Treatment of Relapsing Candida albicans Meningoencephalitis Caused by CARD9 Deficiency.
Grimbacher et al., London, United Kingdom. In Pediatr Infect Dis J, Jan 2016
UNASSIGNED: Caspase-associated recruitment domain-9 (CARD9) deficiency is an autosomal-recessive primary immunodeficiency with genetic defects in Th17 immunity marked by susceptibility to recurrent and invasive Candida infections.
CARD9-Dependent Neutrophil Recruitment Protects against Fungal Invasion of the Central Nervous System.
Lionakis et al., Chapel Hill, United States. In Plos Pathog, Dec 2015
Humans deficient in the C-type lectin pathway adaptor protein CARD9 develop spontaneous fungal disease that targets the central nervous system (CNS).
Genetic errors of the human caspase recruitment domain-B-cell lymphoma 10-mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (CBM) complex: Molecular, immunologic, and clinical heterogeneity.
Puel et al., Madrid, Spain. In J Allergy Clin Immunol, Nov 2015
Three members of the caspase recruitment domain (CARD) family of adaptors (CARD9, CARD10, and CARD11) are known to form heterotrimers with B-cell lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue lymphoma-translocation gene 1 (MALT1).
Ubiquitin Ligase TRIM62 Regulates CARD9-Mediated Anti-fungal Immunity and Intestinal Inflammation.
Xavier et al., Boston, United States. In Immunity, Nov 2015
CARD9 is a central component of anti-fungal innate immune signaling via C-type lectin receptors, and several immune-related disorders are associated with CARD9 alterations.
Loss of CARD9-mediated innate activation attenuates severe influenza pneumonia without compromising host viral immunity.
Hara et al., Saga, Japan. In Sci Rep, 2014
In this study, we focused on CARD9, a signaling adaptor known to regulate innate immune activation through multiple innate sensor proteins, and investigated its role in anti-IFV defense and lung pathogenesis in a mouse model recapitulating severe influenza pneumonia with ARDS.
Genetic association between CARD9 variants and inflammatory bowel disease was not replicated in a Chinese Han population.
Zhong et al., Shanghai, China. In Int J Clin Exp Pathol, 2014
OBJECTIVE: In order to investigate whether CARD9 gene is associated with IBD in Chinese Han population, we replicated 2 SNPs of CARD9 which have been reported to be significantly associated with IBD.
AAL exacerbates pro-inflammatory response in macrophages by regulating Mincle/Syk/Card9 signaling along with the Nlrp3 inflammasome assembly.
Wang et al., Wuhan, China. In Am J Transl Res, 2014
Mechanistic studies revealed that AAL likely targets macrophages through receptor Mincle to activate Syk/Card9 signaling, which then couples to the Nlrp3 inflammasome assembly.
Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens.
Gharavi et al., New York City, United States. In Nat Genet, 2014
We identified six new genome-wide significant associations, four in ITGAM-ITGAX, VAV3 and CARD9 and two new independent signals at HLA-DQB1 and DEFA.
Rad50-CARD9 interactions link cytosolic DNA sensing to IL-1β production.
Ruland et al., München, Germany. In Nat Immunol, 2014
Here we report a direct cytosolic interaction between the DNA-damage sensor Rad50 and the innate immune system adaptor CARD9.
Innate immune activity conditions the effect of regulatory variants upon monocyte gene expression.
Knight et al., Oxford, United Kingdom. In Science, 2014
Induced eQTL are significantly enriched for genome-wide association study loci, identifying context-specific associations to putative causal genes including CARD9, ATM, and IRF8.
[Up-to-date findings in the host defence mechanism to cryptococcus infection].
Kawakami et al., In Nihon Ishinkin Gakkai Zasshi, 2013
Recently, we found that caspase recruitment domain family member (CARD9), an adaptor protein in a signal transduction triggered by C-type lectin receptors, plays a key role in the early production of IFN-γ at the site of infection by recruiting NK cells and CD4(+) and CD8(+) memory-phenotype T cells.
Do genetic mutations and genotypes contribute to onychomycosis?
Brintnell et al., Toronto, Canada. In Dermatology, 2013
RESULTS: There are mutations in the innate immune receptors Dectin-1 and its adaptor protein CARD9 which result in familial mucocutaneous infections.
Primary immunodeficiencies underlying fungal infections.
Puel et al., New York City, United States. In Curr Opin Pediatr, 2013
Inborn errors of interleukin-17 immunity have recently been shown to underlie chronic mucocutaneous candidiasis (CMC), while inborn errors of caspase recruitment domain-containing protein 9 (CARD9) immunity underlie deep dermatophytosis and invasive candidiasis.
Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy and other primary immunodeficiency diseases help to resolve the nature of protective immunity against chronic mucocutaneous candidiasis.
Peterson et al., Tartu, Estonia. In Curr Opin Pediatr, 2013
Mutations in CARD9, STAT3, IL17RA, IL17F, STAT1, and IL12RB and polymorphisms in Dectin 1 and interleukin-22 (IL-22) encoding genes have been shown to impair the development or function of Th17 cells and are associated with susceptibility to candidiasis.
Deep dermatophytosis and inherited CARD9 deficiency.
Puel et al., Aş Şanamayn, Syria. In N Engl J Med, 2013
Because CARD9 (caspase recruitment domain-containing protein 9) deficiency has been reported in an Iranian family with invasive fungal infections, we also sequenced CARD9 in the patients.
The autophagy regulator Rubicon is a feedback inhibitor of CARD9-mediated host innate immunity.
Jung et al., Los Angeles, United States. In Cell Host Microbe, 2012
Rubicon as a specific feedback inhibitor of CARD9-mediated pattern recognition receptor-signal transduction, preventing unbalanced proinflammatory responses.
Experimental cerebral malaria develops independently of caspase recruitment domain-containing protein 9 signaling.
Matuschewski et al., London, United Kingdom. In Infect Immun, 2012
The authors conclude that experimental cerebral malaria develops independently of the CARD9 signaling pathway.
Syk kinase-coupled C-type lectin receptors engage protein kinase C-σ to elicit Card9 adaptor-mediated innate immunity.
Ruland et al., München, Germany. In Immunity, 2012
PKCdelta is an essential link between Syk activation and Card9 signaling for CLR-mediated innate immunity and host protection
Human coronavirus-induced neuronal programmed cell death is cyclophilin d dependent and potentially caspase dispensable.
Talbot et al., Québec, Canada. In J Virol, 2012
Human coronavirus-induced neuronal programmed cell death required cyclophilin d but not caspase 3 caspase 9 activities.
Variation in genes of β-glucan recognition pathway and susceptibility to opportunistic infections in HIV-positive patients.
Netea et al., Nijmegen, Netherlands. In Immunol Invest, 2010
variation in CARD9 genes was not associated with susceptibility to opportunistic fungal or bacterial infections in HIV-positive patients.
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