Loading
NFKBIE (NF-kappa-B inhibitor epsilon) is a gene whose normal job is to hold cell growth in check. 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, Leukaemia, Skin cancer and 5 more.
Sequesters NF-kappa-B transcription factor complexes in the cytoplasm, thereby inhibiting their activity. Sequestered complexes include NFKB1-RELA (p50-p65) and NFKB1-REL (p50-c-Rel) complexes. Limits B-cell activation in response to pathogens, and also plays an important role in B-cell development.
CIViC holds 2 clinical evidence items and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.62 (direct and indirect evidence; datatypes literature 0.72, genetic association 0.00, somatic mutation 0.81). IntOGen calls it a driver in 7 cohorts (3 activating, 4 loss-of-function), covering Chronic Lymphocytic Leukaemia/Small Lymphocytic Lymphoma, Diffuse Large B-Cell Lymphoma, NOS, Lung Adenocarcinoma, Malignant Lymphoma, Non-Hodgkin Lymphoma.
In plain words · NFKBIE (NF-kappa-B inhibitor epsilon) is a gene whose normal job is to hold cell growth in check. 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, Leukaemia, Skin cancer and 5 more.
NFKBIE (NF-kappa-B inhibitor epsilon) is a gene whose normal job is to hold cell growth in check. 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, Leukaemia, Skin cancer and 5 more.
Sequesters NF-kappa-B transcription factor complexes in the cytoplasm, thereby inhibiting their activity. Sequestered complexes include NFKB1-RELA (p50-p65) and NFKB1-REL (p50-c-Rel) complexes.
No product in this corpus aims at NFKBIE yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
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 NFKBIE: RNA tissue enhanced (lymphoid tissue 34 nTPM); high antibody staining in 10 normal tissues; highest cancer staining endometrial cancer (4 of 11 high). Distribution: 4 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Leukaemia, Skin cancer (all types), Lung cancer (all types)); Open Targets associates it with 1 specific cancer type at or above 0.5 (B-cell chronic lymphocytic leukemia). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt O00221; CIViC gene NFKBIE; IntOGen NFKBIE; Human Protein Atlas NFKBIE tissue; Open Targets ENSG00000146232 associations
First described 1997. Earliest sequence paper UniProt cites for the protein: Whiteside S.T. et al, EMBO J, 1997, "IkappaB epsilon, a novel member of the IkappaB family, controls RelA and cRel NF-kappaB activity". Source.
Sources: HGNC HGNC:7799 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt O00221 (protein name, function text, keywords and locations (REST API)); CIViC gene NFKBIE (2 evidence items, 0 assertions, 1 variants; diseases: Mantle Cell Lymphoma, Diffuse Large B-cell Lymphoma (GraphQL API, CC0)); Open Targets ENSG00000146232 (association with cancer (MONDO_0004992) 0.62; per-cancer scores at or above 0.5: melanoma 0.55, acute lymphoblastic leukaemia 0.54, diffuse large B-cell lymphoma 0.53, non-Hodgkin lymphoma 0.68, skin cancer 0.56, leukaemia 0.62 (GraphQL API, CC0)); IntOGen NFKBIE (driver in 7 cohorts (Act 3, LoF 4); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Sequesters NF-kappa-B transcription factor complexes in the cytoplasm, thereby inhibiting their activity. Sequestered complexes include NFKB1-RELA (p50-p65) and NFKB1-REL (p50-c-Rel) complexes. Limits B-cell activation in response to pathogens, and also plays an important role in B-cell development. Location: Cytoplasm (UniProt). Locus 6p21.1 (HGNC).
RNA: tissue enhanced (lymphoid tissue 34 nTPM), detected in all normal tissues.
Medium: Adrenal gland, Appendix, Breast, Caudate, Cerebellum, Cerebral cortex, Cervix, Colon.
Medium only: carcinoid, colorectal cancer, head and neck cancer, 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:"NFKBIE" OR ABSTRACT:"NFKBIE" OR TITLE:"NFKB inhibitor epsilon" OR ABSTRACT:"NFKB inhibitor epsilon" OR TITLE:"NF-kappa-B inhibitor epsilon" OR ABSTRACT:"NF-kappa-B inhibitor epsilon") 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 NFKBIE, not a curated reading list.
Shares Leukaemia (all types), Chronic lymphocytic leukaemia, Skin cancer (all types), CIViC.
Shares Leukaemia (all types), Chronic lymphocytic leukaemia, Skin cancer (all types), IntOGen.
Shares Leukaemia (all types), Mantle cell lymphoma, Chronic lymphocytic leukaemia, Skin cancer (all types).
Shares Leukaemia (all types), Skin cancer (all types), CIViC, IntOGen.
Shares Leukaemia (all types), Skin cancer (all types), CIViC, IntOGen.
Shares Leukaemia (all types), Skin cancer (all types), CIViC, IntOGen.
Shares Leukaemia (all types), Skin cancer (all types), CIViC, IntOGen.
Shares Leukaemia (all types), Skin cancer (all types), IntOGen, Melanoma.