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DTX1 (E3 ubiquitin-protein ligase DTX1) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Diffuse large B-cell lymphoma and Chronic lymphocytic leukaemia.
E3 ubiquitin-protein ligase that mediates ubiquitination and proteasomal degradation of MEKK1, thereby modulating signalling pathways involved in cell fate determination. Regulates the Notch signalling pathway, acting predominantly as a positive regulator but functioning as a context-dependent negative regulator in specific developmental or cellular settings. Mediates the antineural activity of Notch signalling, likely by inhibiting transcriptional activation mediated by MATCH1.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. IntOGen calls it a driver in 1 cohort (0 activating, 1 loss-of-function), covering Chronic Lymphocytic Leukaemia/Small Lymphocytic Lymphoma.
In plain words · DTX1 (E3 ubiquitin-protein ligase DTX1) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Diffuse large B-cell lymphoma and Chronic lymphocytic leukaemia.
DTX1 (E3 ubiquitin-protein ligase DTX1) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Diffuse large B-cell lymphoma and Chronic lymphocytic leukaemia.
E3 ubiquitin-protein ligase that mediates ubiquitination and proteasomal degradation of MEKK1, thereby modulating signalling pathways involved in cell fate determination.
No product in this corpus aims at DTX1 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 a tumour suppressor (IntOGen finds it knocked out more often than chance); 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 DTX1: RNA tissue enhanced (adipose tissue 9 nTPM, lymphoid tissue 12 nTPM); no normal tissue stained high; highest cancer staining head and neck cancer (1 of 4 high). Distribution: 2 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Leukaemia); Open Targets associates it with 0 specific cancer types at or above 0.5. (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt Q86Y01; CIViC gene DTX1; IntOGen DTX1; Human Protein Atlas DTX1 tissue; Open Targets ENSG00000135144 associations
First described 1998. Earliest sequence paper UniProt cites for the protein: Matsuno et al, Nat. Genet, 1998, "Human deltex is a conserved regulator of Notch signalling". Source.
Sources: HGNC HGNC:3060 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q86Y01 (protein name, function text, keywords and locations (REST API)); CIViC gene DTX1 (1 evidence items, 0 assertions, 1 variants; diseases: Diffuse Large B-cell Lymphoma (GraphQL API, CC0)); IntOGen DTX1 (driver in 1 cohort (Act 0, LoF 1); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
E3 ubiquitin-protein ligase that mediates ubiquitination and proteasomal degradation of MEKK1, thereby modulating signalling pathways involved in cell fate determination. Regulates the Notch signalling pathway, acting predominantly as a positive regulator but functioning as a context-dependent negative regulator in specific developmental or cellular settings. Mediates the antineural activity of Notch signalling, likely by inhibiting transcriptional activation mediated by MATCH1. Negatively regulates Notch signalling by controlling the activity of PIP4K2C, a lipid kinase that promotes recycling of Notch receptors from RAB4A-positive endosomes to the cell surface. Participates in several developmental and immune processes, including neurogenesis, lymphogenesis, and myogenesis. Influences lymphocyte differentiation by promoting B-cell development at the expense of T-cell development, suggesting functional antagonism of NOTCH1 in this context. Location: Cytoplasm; Nucleus; Endosome (UniProt). Locus 12q24.13 (HGNC).
RNA: tissue enhanced (adipose tissue 9 nTPM, lymphoid tissue 12 nTPM), detected in many normal tissues.
No normal tissue stained high; medium in Appendix, Bronchus, Caudate, Cerebellum, Cerebral cortex, Colon and more.
RNA cancer enhanced: Glioblastoma Multiforme 8 pTPM.
Medium only: carcinoid, cervical cancer, colorectal cancer, endometrial 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:"DTX1" OR ABSTRACT:"DTX1" OR TITLE:"deltex E3 ubiquitin ligase 1" OR ABSTRACT:"deltex E3 ubiquitin ligase 1" OR TITLE:"E3 ubiquitin-protein ligase DTX1" OR ABSTRACT:"E3 ubiquitin-protein ligase DTX1" OR TITLE:"hDx-1" OR ABSTRACT:"hDx-1" OR TITLE:"RNF140" OR ABSTRACT:"RNF140") 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 DTX1, not a curated reading list.