ArticleNucleic acids research2006
The molecular mechanism of DNA damage recognition by MutS homologs and its consequences for cell death response.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 73 citations in OpenAlex.
- Expression patterns of mismatch repair proteins in cervical cancer uncover independent prognostic value of MSH-2.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2024Article
- Exploring DNA Damage and Repair Mechanisms: A Review with Computational Insights.Biotech (Basel (Switzerland)) · 2024Review
- CircLIFR synergizes with MSH2 to attenuate chemoresistance via MutSα/ATM-p73 axis in bladder cancer.Molecular cancer · 2021Article
- Molecular Mechanisms of DNA Replication and Repair Machinery: Insights from Microscopic Simulations.Advanced theory and simulations · 2019Article
- All-atom molecular dynamics comparison of disease-associated zinc fingers.Journal of biomolecular structure & dynamics · 2018Article
- Visualizing correlated motion with HDBSCAN clustering.Protein science : a publication of the Protein Society · 2018Article
- Involvement of the DNA mismatch repair system in cisplatin sensitivity of testicular germ cell tumours.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- MutSFrontiers in physics · 2017Article
- Diffusion and Binding of Mismatch Repair Protein, MSH2, in Breast Cancer Cells at Different Stages of Neoplastic Transformation.PloS one · 2017Article
- Uncovering Large-Scale Conformational Change in Molecular Dynamics without Prior Knowledge.Journal of chemical theory and computation · 2016Article
- Long-Range Signaling in MutS and MSH Homologs via Switching of Dynamic Communication Pathways.PLoS computational biology · 2016Article
- Recapturing the Correlated Motions of Protein Using Coarse- Grained Models.Protein and peptide letters · 2015Article
- Non-specificity and synergy at the binding site of the carboplatin-induced DNA adduct via molecular dynamics simulations of the MutSα-DNA recognition complex.Journal of biomolecular structure & dynamics · 2014Article
- Genome-wide transcriptome and antioxidant analyses on gamma-irradiated phases of deinococcus radiodurans R1.PloS one · 2014Article
- Destabilization of the MutSα's protein-protein interface due to binding to the DNA adduct induced by anticancer agent carboplatin via molecular dynamics simulations.Journal of molecular modeling · 2013Article
- Sculpting of DNA at abasic sites by DNA glycosylase homolog mag2.Structure (London, England : 1993) · 2013Article
- Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment.Molecular cancer biology · 2013Article
- Article
- The molecular origin of the MMR-dependent apoptosis pathway from dynamics analysis of MutSα-DNA complexes.Journal of biomolecular structure & dynamics · 2012Article
- Insights into protein - DNA interactions, stability and allosteric communications: a computational study of mutSα-DNA recognition complexes.Journal of biomolecular structure & dynamics · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We determined the molecular mechanism of cell death response by MutS homologs in distinction to the repair event. Key protein-DNA contacts differ in the interaction of MutS homologs with cisplatinated versus mismatched DNA. Mutational analyses of protein-DNA contacts, which were predicted by molecular dynamics (MD) simulations, were performed. Mutations in suggested interaction sites can affect repair and cell death response independently, and to different extents. A glutamate residue is identified as the key contact with cisplatin-DNA. Mutation of the residue increases cisplatin resistance due to increased non-specific DNA binding. In contrast, the conserved phenylalanine that is instrumental and indispensable for mismatch recognition during repair is not required for cisplatin cytotoxicity. These differences in protein-DNA interactions are translated into localized conformational changes that affect nucleotide requirements and inter-subunit interactions. Specifically, the ability for ATP binding/hydrolysis has little consequence for the MMR-dependent damage response. As a consequence, intersubunit contacts are altered that most likely affect the interaction with downstream proteins. We here describe the interaction of MutS homologs with DNA damage, as it differs from the interaction with a mismatch, and its structural translation into all other functional regions of the protein as a mechanism to initiate cell death response and concomitantly inhibit repair.
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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.