ArticleMolecular & cellular proteomics : MCP2016
Proteomic Analysis Reveals a Novel Mutator S (MutS) Partner Involved in Mismatch Repair Pathway.
Article in Molecular & cellular proteomics : MCP, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Integrating proteomics and bioinformatics for the identification of breast cancer biomarkers interacting with telomeric G-quadruplex.Cancer cell international · 2025Article
- Proteomic analysis of ferroptosis pathways reveals a role of CEPT1 in suppressing ferroptosis.Protein & cell · 2024Article
- Integrative bioinformatics analysis of WDHD1: a potential biomarker for pan-cancer prognosis, diagnosis, and immunotherapy.World journal of surgical oncology · 2023Article
- WD Repeat and HMG Box DNA Binding Protein 1: An Oncoprotein at the Hub of Tumorigenesis and a Novel Therapeutic Target.International journal of molecular sciences · 2023Review
- WDHD1 is over-expressed in nasopharyngeal carcinoma and may control the expression of ITGAV.FEBS open bio · 2023Article
- SLX4 dampens MutSα-dependent mismatch repair.Nucleic acids research · 2022Article
- Rad5 and Its Human Homologs, HLTF and SHPRH, Are Novel Interactors of Mismatch Repair.Frontiers in cell and developmental biology · 2022Article
- The Involvement of WDHD1 in the Occurrence of Esophageal Cancer as a Downstream Target of PI3K/AKT Pathway.Journal of oncology · 2022Review
- Damage-Net: A program for DNA repair meta-analysis identifies a network of novel repair genes that facilitate cancer evolution.DNA repair · 2021Article
- Mass spectrometry-based protein‒protein interaction techniques and their applications in studies of DNA damage repair.Journal of Zhejiang University. Science. B · 2021Review
- AMPK Interactome Reveals New Function in Non-homologous End Joining DNA Repair.Molecular & cellular proteomics : MCP · 2020Article
- SMARCAD1-mediated recruitment of the DNA mismatch repair protein MutLα to MutSα on damaged chromatin induces apoptosis in human cells.The Journal of biological chemistry · 2020Article
- The Mechanism of Chromatin Remodeler SMARCAD1/Fun30 in Response to DNA Damage.Frontiers in cell and developmental biology · 2020Review
- SLX4IP acts with SLX4 and XPF-ERCC1 to promote interstrand crosslink repair.Nucleic acids research · 2019Article
- Article
- Global phosphoproteomic analysis reveals ARMC10 as an AMPK substrate that regulates mitochondrial dynamics.Nature communications · 2019Article
- Nucleosome Remodeling by Fun30Frontiers in molecular biosciences · 2019Review
- Replisome Dynamics and Their Functional Relevance upon DNA Damage through the PCNA Interactome.Cell reports · 2018Article
- Identification of Exo1-Msh2 interaction motifs in DNA mismatch repair and new Msh2-binding partners.Nature structural & molecular biology · 2018Article
- Nucleosomes around a mismatched base pair are excluded via an Msh2-dependent reaction with the aid of SNF2 family ATPase Smarcad1.Genes & development · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The mismatch repair (MMR) family is a highly conserved group of proteins that function in correcting base-base and insertion-deletion mismatches generated during DNA replication. Disruption of this process results in characteristic microsatellite instability (MSI), repair defects, and susceptibility to cancer. However, a significant fraction of MSI-positive cancers express MMR genes at normal levels and do not carry detectable mutation in known MMR genes, suggesting that additional factors and/or mechanisms may exist to explain these MSI phenotypes in patients. To systematically investigate the MMR pathway, we conducted a proteomic analysis and identified MMR-associated protein complexes using tandem-affinity purification coupled with mass spectrometry (TAP-MS) method. The mass spectrometry data have been deposited to the ProteomeXchange with identifier PXD003014 and DOI 10.6019/PXD003014. We identified 230 high-confidence candidate interaction proteins (HCIPs). We subsequently focused on MSH2, an essential component of the MMR pathway and uncovered a novel MSH2-binding partner, WDHD1. We further demonstrated that WDHD1 forms a stable complex with MSH2 and MSH3 or MSH6,i.e.the MutS complexes. The specific MSH2/WDHD1 interaction is mediated by the second lever domain of MSH2 and Ala(1123)site of WDHD1. Moreover, we showed that, just like MSH2-deficient cells, depletion of WDHD1 also led to 6-thioguanine (6-TG) resistance, indicating that WDHD1 likely contributes to the MMR pathway. Taken together, our study uncovers new components involved in the MMR pathway, which provides candidate genes that may be responsible for the development of MSI-positive cancers.
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