MSH3
MSH3 (DNA mismatch repair protein Msh3) is a gene. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Endometrial cancer and Colorectal cancer.
Overview
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerises with MSH2 to form MutS beta which binds to DNA mismatches thereby initiating DNA repair. When bound, the MutS beta heterodimer bends the DNA helix and shields approximately 20 base pairs.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant, naming 7-Ethyl-10-Hydroxycamptothecin and Oxaliplatin. Open Targets scores its association with cancer at 0.71 (direct and indirect evidence; datatypes genetic literature 0.49, affected pathway 0.61, literature 0.93, genetic association 0.92, somatic mutation 0.58, animal model 0.45).
- Target · the protein and the cell it sits on
- Drug · antibody, small molecule, cell or radioligand
- Effect · signal, damage or kill
In plain words · MSH3 (DNA mismatch repair protein Msh3) is a gene. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Endometrial cancer and Colorectal cancer.
- 1 · What it is
MSH3 (DNA mismatch repair protein Msh3) is a gene. The public catalogues list it as a drug target, a biomarker and a DNA repair gene, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Endometrial cancer and Colorectal cancer.
- 2 · What goes wrong in cancer
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerises with MSH2 to form MutS beta which binds to DNA mismatches thereby initiating DNA repair.
- 3 · How drugs use it
No product in this corpus aims at MSH3 yet. Drugs bind the molecule precisely: to switch it off, flag the cell for the immune system, or deliver a payload.
External identifiers
Sources: HGNC HGNC:7326 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P20585 (protein name, function text, keywords and locations (REST API)); CIViC gene MSH3 (1 evidence items, 0 assertions, 1 variants; diseases: Colon Carcinoma (GraphQL API, CC0)); Open Targets ENSG00000113318 (association with cancer (MONDO_0004992) 0.71; per-cancer scores at or above 0.5: endometrial cancer 0.69 (GraphQL API, CC0))
Biology
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerises with MSH2 to form MutS beta which binds to DNA mismatches thereby initiating DNA repair. When bound, the MutS beta heterodimer bends the DNA helix and shields approximately 20 base pairs. MutS beta recognises large insertion-deletion loops (IDL) up to 13 nucleotides long. After mismatch binding, forms a ternary complex with the MutL alpha heterodimer, which is thought to be responsible for directing the downstream MMR events, including strand discrimination, excision, and resynthesis. Locus 5q14.1 (HGNC).
- Endometrial cancer: Open Targets association 0.69 with endometrial cancer (MONDO_0011962)
- Colorectal cancer: CIViC evidence names this disease
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: CIViC lists 2 therapies; CIViC holds 1 clinical evidence items on its variants; UniProt keyword "DNA repair". 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:"MSH3" OR ABSTRACT:"MSH3" OR TITLE:"mutS homolog 3" OR ABSTRACT:"mutS homolog 3" OR TITLE:"DNA mismatch repair protein Msh3" OR ABSTRACT:"DNA mismatch repair protein Msh3" OR TITLE:"MRP1" OR ABSTRACT:"MRP1") 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 MSH3, not a curated reading list.