ArticleMolecular cancer2013
MutS homologue hMSH4: interaction with eIF3f and a role in NHEJ-mediated DSB repair.
Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Epigenetic inactivation of DNA repair genes as promising prognostic and predictive biomarkers in urothelial bladder carcinoma patients.Molecular genetics and genomics : MGG · 2022Article
- Article
- BCAS2, a protein enriched in advanced prostate cancer, interacts with NBS1 to enhance DNA double-strand break repair.British journal of cancer · 2020Article
- Article
- DNA Mismatch Repair Gene Variants in Sporadic Solid Cancers.International journal of molecular sciences · 2020Review
- Complete response to anti-PD-L1 antibody in a metastatic bladder cancer associated with novel MSH4 mutation and microsatellite instability.Journal for immunotherapy of cancer · 2020Article
- High-Throughput Analysis of DNA Break-Induced Chromosome Rearrangements by Amplicon Sequencing.Methods in enzymology · 2018Article
- Systematic Identification of Determinants for Single-Strand Annealing-Mediated Deletion Formation inG3 (Bethesda, Md.) · 2017Article
- The eukaryotic translation initiation factor 3f (eIF3f) interacts physically with the alpha 1B-adrenergic receptor and stimulates adrenoceptor activity.BMC biochemistry · 2015Article
- VBP1 facilitates proteasome and autophagy-mediated degradation of MutS homologue hMSH4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- DNA damage induced MutS homologue hMSH4 acetylation.International journal of molecular sciences · 2013Article
- MutS homologue hMSH5: recombinational DSB repair and non-synonymous polymorphic variants.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDNA mismatch repair proteins participate in diverse cellular functions including DNA damage response and repair. As a member of this protein family, the molecular mechanisms of hMSH4 in mitotic cells are poorly defined. It is known that hMSH4 is promiscuous, and among various interactions the hMSH4-hMSH5 interaction is involved in recognizing DNA intermediate structures arising from homologous recombination (HR).
resultsWe identified a new hMSH4 interacting protein eIF3f--a protein that functions not only in translation but also in the regulation of apoptosis and tumorigenesis in humans. Our studies have demonstrated that hMSH4-eIF3f interaction is mediated through the N-terminal regions of both proteins. The interaction with eIF3f fosters hMSH4 protein stabilization, which in turn sustains γ-H2AX foci and compromises cell survival in response to ionizing radiation (IR)-induced DNA damage. These effects can be, at least partially, attributed to the down-regulation of NHEJ activity by hMSH4. Furthermore, the interplay between hMSH4 and eIF3f inhibits IR-induced AKT activation, and hMSH4 promotes eIF3f-mediated bypass of S phase arrest, and ultimately enhancing an early G2/M arrest in response to IR treatment.
conclusionOur current study has revealed a role for hMSH4 in the maintenance of genomic stability by suppressing NHEJ-mediated DSB repair.
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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 Socratic graph.