DTX1
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.
Overview
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.
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
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.
- 1 · What it is
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.
- 2 · What goes wrong in cancer
E3 ubiquitin-protein ligase that mediates ubiquitination and proteasomal degradation of MEKK1, thereby modulating signalling pathways involved in cell fate determination.
- 3 · How drugs use it
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).
External identifiers
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)
Biology
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).
- Diffuse large B-cell lymphoma: CIViC evidence names this disease
- Chronic lymphocytic leukaemia: IntOGen driver in 1 cohort (CLLSLL)
Notes
top- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: IntOGen calls it a loss-of-function (LoF) driver in 1 cohort; CIViC holds 1 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
Latest papers
topQuery 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.