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NFKB2 (Nuclear factor NF-kappa-B p100 subunit) is a protein that switches other genes on and off. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Mesothelioma, Colorectal cancer, Skin cancer and 3 more.
NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity.
Open Targets scores its association with cancer at 0.64 (direct and indirect evidence; datatypes literature 0.97, animal model 0.52, genetic association 0.19, somatic mutation 0.97). IntOGen calls it a driver in 2 cohorts (1 activating, 1 loss-of-function), covering Diffuse Large B-Cell Lymphoma, NOS, Pleural Mesothelioma.
In plain words · NFKB2 (Nuclear factor NF-kappa-B p100 subunit) is a protein that switches other genes on and off. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Mesothelioma, Colorectal cancer, Skin cancer and 3 more.
NFKB2 (Nuclear factor NF-kappa-B p100 subunit) is a protein that switches other genes on and off. The public catalogues list it as an oncogene driver, a tumour suppressor and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Mesothelioma, Colorectal cancer, Skin cancer and 3 more.
NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis.
No product in this corpus aims at NFKB2 yet. Transcription factors have no pocket to plug, so drugs either degrade them or block the partner protein they need to dock on DNA.
First described 1991. Earliest sequence paper UniProt cites for the protein: Schmid R.M. et al, Nature, 1991, "Cloning of an NF-kappa B subunit which stimulates HIV transcription in synergy with p65". Source.
Sources: HGNC HGNC:7795 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q00653 (protein name, function text, keywords and locations (REST API)); Open Targets ENSG00000077150 (association with cancer (MONDO_0004992) 0.64; per-cancer scores at or above 0.5: colorectal cancer 0.54, melanoma 0.52, skin cancer 0.53 (GraphQL API, CC0)); IntOGen NFKB2 (driver in 2 cohorts (Act 1, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalisation as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. Location: Nucleus; Cytoplasm (UniProt). Locus 10q24.32 (HGNC).
Query for this target: (TITLE:"NFKB2" OR ABSTRACT:"NFKB2" OR TITLE:"nuclear factor kappa B subunit 2" OR ABSTRACT:"nuclear factor kappa B subunit 2" OR TITLE:"Nuclear factor NF-kappa-B p100 subunit" OR ABSTRACT:"Nuclear factor NF-kappa-B p100 subunit" OR TITLE:"LYT-10" OR ABSTRACT:"LYT-10" OR TITLE:"p52" OR ABSTRACT:"p52" OR TITLE:"p105" OR ABSTRACT:"p105") 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 NFKB2, not a curated reading list.
Shares Pleural mesothelioma, Mesothelioma, Skin cancer (all types), IntOGen.
Shares Pleural mesothelioma, Mesothelioma, Skin cancer (all types), IntOGen.
Shares Pleural mesothelioma, Mesothelioma, Skin cancer (all types), IntOGen.
Shares Pleural mesothelioma, Mesothelioma, IntOGen, Melanoma.
Shares Pleural mesothelioma, Mesothelioma, IntOGen, Colorectal cancer.
Shares Pleural mesothelioma, Mesothelioma, IntOGen.
Shares Pleural mesothelioma, Mesothelioma, IntOGen.
Shares Pleural mesothelioma, Mesothelioma, IntOGen.