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CARD11 (Caspase recruitment domain-containing protein 11) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Hepatocellular carcinoma, Skin cancer and 5 more.
Adapter protein that plays a key role in adaptive immune response by transducing the activation of NF-kappa-B downstream of T-cell receptor (TCR) and B-cell receptor (BCR) engagement. Transduces signals downstream TCR or BCR activation via the formation of a multiprotein complex together with BCL10 and MALT1 that induces NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways. Upon activation in response to TCR or BCR triggering, CARD11 homooligomerises to form a nucleating helical template that recruits BCL10 via CARD-CARD interaction, thereby promoting polymerisation of BCL10 and subsequent recruitment of MALT1: this leads to I-kappa-B kinase (IKK) phosphorylation and degradation, and release of NF-kappa-B proteins for nuclear translocation.
CIViC holds 2 clinical evidence items and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.68 (direct and indirect evidence; datatypes literature 0.84, animal model 0.54, genetic association 0.00, somatic mutation 0.87). IntOGen calls it a driver in 11 cohorts (9 activating, 2 loss-of-function), covering Burkitt Lymphoma, Colorectal Adenocarcinoma, Diffuse Large B-Cell Lymphoma, NOS, Hepatocellular Carcinoma, Malignant Lymphoma, Non-Hodgkin Lymphoma and others.
In plain words · CARD11 (Caspase recruitment domain-containing protein 11) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Hepatocellular carcinoma, Skin cancer and 5 more.
CARD11 (Caspase recruitment domain-containing protein 11) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Hepatocellular carcinoma, Skin cancer and 5 more.
Adapter protein that plays a key role in adaptive immune response by transducing the activation of NF-kappa-B downstream of T-cell receptor (TCR) and B-cell receptor (BCR) engagement.
No product in this corpus aims at CARD11 yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance) and a tumour suppressor (IntOGen finds it knocked out more often than chance), so the direction differs between cohorts but the alteration is somatic either way; what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA CARD11: RNA tissue enhanced (intestine 17 nTPM, lymphoid tissue 38 nTPM); no normal tissue stained high; highest cancer staining lymphoma (1 of 12 high). Distribution: 8 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Hepatocellular carcinoma, Skin cancer (all types), Colorectal cancer, Ovarian cancer, Leukaemia, Lung cancer (all types) and more); Open Targets associates it with 1 specific cancer type at or above 0.5 (diffuse large B-cell lymphoma). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt Q9BXL7; CIViC gene CARD11; IntOGen CARD11; Human Protein Atlas CARD11 tissue; Open Targets ENSG00000198286 associations
First described 2001. Earliest sequence paper UniProt cites for the protein: Bertin et al, J. Biol. Chem, 2001, "CARD11 and CARD14 are novel caspase recruitment domain (CARD)/membrane-associated guanylate kinase (MAGUK) family members that interact with Bcl10 and activate NF-kappaB". Source.
Sources: HGNC HGNC:16393 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q9BXL7 (protein name, function text, keywords and locations (REST API)); CIViC gene CARD11 (2 evidence items, 0 assertions, 1 variants; diseases: Diffuse Large B-cell Lymphoma, Mantle Cell Lymphoma (GraphQL API, CC0)); Open Targets ENSG00000198286 (association with cancer (MONDO_0004992) 0.68; per-cancer scores at or above 0.5: colorectal cancer 0.55, gastric cancer 0.51, melanoma 0.54, diffuse large B-cell lymphoma 0.63, non-Hodgkin lymphoma 0.70, skin cancer 0.58 (GraphQL API, CC0)); IntOGen CARD11 (driver in 11 cohorts (Act 9, LoF 2); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Adapter protein that plays a key role in adaptive immune response by transducing the activation of NF-kappa-B downstream of T-cell receptor (TCR) and B-cell receptor (BCR) engagement. Transduces signals downstream TCR or BCR activation via the formation of a multiprotein complex together with BCL10 and MALT1 that induces NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways. Upon activation in response to TCR or BCR triggering, CARD11 homooligomerises to form a nucleating helical template that recruits BCL10 via CARD-CARD interaction, thereby promoting polymerisation of BCL10 and subsequent recruitment of MALT1: this leads to I-kappa-B kinase (IKK) phosphorylation and degradation, and release of NF-kappa-B proteins for nuclear translocation. Its binding to DPP4 induces T-cell proliferation and NF-kappa-B activation in a T-cell receptor/CD3-dependent manner. Promotes linear ubiquitination of BCL10 by promoting the targeting of BCL10 to RNF31/HOIP. Stimulates the phosphorylation of BCL10. Location: Cytoplasm; Membrane raft (UniProt). Locus 7p22.2 (HGNC).
RNA: tissue enhanced (intestine 17 nTPM, lymphoid tissue 38 nTPM), detected in many normal tissues.
No normal tissue stained high; medium in Appendix, Lymph node, Spleen, Tonsil.
Medium only: cervical cancer, colorectal cancer, glioma, lung cancer.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
Query for this target: (TITLE:"CARD11" OR ABSTRACT:"CARD11" OR TITLE:"caspase recruitment domain family member 11" OR ABSTRACT:"caspase recruitment domain family member 11" OR TITLE:"Caspase recruitment domain-containing protein 11" OR ABSTRACT:"Caspase recruitment domain-containing protein 11" OR TITLE:"CARMA1" OR ABSTRACT:"CARMA1" OR TITLE:"BIMP3" OR ABSTRACT:"BIMP3") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about CARD11, not a curated reading list.
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, Leukaemia (all types), Skin cancer (all types).
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares Leukaemia (all types), Skin cancer (all types), Hepatocellular carcinoma, CIViC.
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, Leukaemia (all types), CIViC.
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, CIViC, IntOGen.
Shares Leukaemia (all types), Skin cancer (all types), CIViC, IntOGen.
Shares Inflammation & NF-κB, Leukaemia (all types), Skin cancer (all types), CIViC.