ArticleOncogene2003
Interactions of the DNA mismatch repair proteins MLH1 and MSH2 with c-MYC and MAX.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Association between MutL homolog 1 polymorphisms and the risk of colorectal cancer: a meta-analysis.Journal of cancer research and clinical oncology · 2015Pooled it
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- Endometrial cancer: from clinical reality to molecular treatment.Discover oncology · 2025Review
- DNA mismatch repair defect and intratumor heterogeneous deficiency differently impact immune responses in diffuse large B-cell lymphoma.Oncoimmunology · 2024Article
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- A study of deregulated MMR pathways and anticancer potential of curcuma derivatives using computational approach.Scientific reports · 2021Article
- Diffusion and Binding of Mismatch Repair Protein, MSH2, in Breast Cancer Cells at Different Stages of Neoplastic Transformation.PloS one · 2017Article
- Candidate colorectal cancer predisposing gene variants in Chinese early-onset and familial cases.World journal of gastroenterology · 2015Article
- Reduced migration of MLH1 deficient colon cancer cells depends on SPTAN1.Molecular cancer · 2014Article
- Mutation and association analyses of the candidate genes ESR1, ESR2, MAX, PCNA, and KAT2A in patients with unexplained MSH2-deficient tumors.Familial cancer · 2012Article
- C-terminal fluorescent labeling impairs functionality of DNA mismatch repair proteins.PloS one · 2012Article
- Assessing pathogenicity of MLH1 variants by co-expression of human MLH1 and PMS2 genes in yeast.BMC cancer · 2009Article
- Finding common protein interaction patterns across organisms.Evolutionary bioinformatics online · 2007Article
- The molecular mechanism of DNA damage recognition by MutS homologs and its consequences for cell death response.Nucleic acids research · 2006Article
- c-Myc induces chromosomal rearrangements through telomere and chromosome remodeling in the interphase nucleus.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MSH2 and MLH1 have a central role in correcting mismatches in DNA occurring during DNA replication and have been implicated in the engagement of apoptosis induced by a number of cytotoxic anticancer agents. The function of MLH1 is not clearly defined, although it is required for mismatch repair (MMR) and engagement of apoptosis after certain types of DNA damage. In order to identify other partners of MLH1 that may be involved in signalling MMR or apoptosis, we used human MLH1 in yeast two-hybrid screens of normal human breast and ovarian cDNA libraries. As well as known partners of MLH1 such as PMS1, MLH3 and MBD4, we identified the carboxy terminus of the human c-MYC proto-oncogene as an interacting sequence. We demonstrate, both in vitro by yeast two-hybrid and GST-fusion pull-down experiments, as well as in vivo by coimmunoprecipitation from human tumour cell extracts, that MLH1 interacts with the c-MYC protein. We further demonstrate that the heterodimeric partner of c-MYC, MAX, interacts with a different MMR protein, MSH2, both in vitro and in vivo. Using an inducible c-MYC-ER fusion gene, we show that elevated c-MYC expression leads to an increased HGPRT mutation rate of Rat1 cells and an increase in the number of frameshift mutants at the HGPRT locus. The effect on HGPRT mutation rate is small (2-3-fold), but is consistent with deregulated c-MYC expression partially inhibiting MMR activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.