ArticleOncogene2004
Mlh1 mediates tissue-specific regulation of mitotic recombination.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
The trial behind it
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
11 citing papers in PubMed, 24 citations in OpenAlex.
- Human MLH1 suppresses the insertion of telomeric sequences at intra-chromosomal sites in telomerase-expressing cells.Nucleic acids research · 2017Article
- MutS homologue hMSH4: interaction with eIF3f and a role in NHEJ-mediated DSB repair.Molecular cancer · 2013Article
- CCR2-dependent recruitment of macrophages by tumor-educated mesenchymal stromal cells promotes tumor development and is mimicked by TNFα.Cell stem cell · 2012Article
- Assessment of anti-recombination and double-strand break-induced gene conversion in human cells by a chromosomal reporter.The Journal of biological chemistry · 2012Article
- Prdx1 deficiency in mice promotes tissue specific loss of heterozygosity mediated by deficiency in DNA repair and increased oxidative stress.Mutation research · 2012Article
- Embryonic lethality after combined inactivation of Fancd2 and Mlh1 in mice.Cancer research · 2009Article
- Mutagenesis in vivo in T cells of p21-deficient mice.Mutation research · 2009Article
- Human MutL-complexes monitor homologous recombination independently of mismatch repair.DNA repair · 2009Article
- Role of the mismatch repair gene, Msh6, in suppressing genome instability and radiation-induced mutations.Mutation research · 2008Article
- The spectra of large second-step mutations are similar for two different mouse autosomes.Mutation research · 2008Article
- The frequency and structure of recombinant products is determined by the cellular level of MutL.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Mitotic recombination (MR) between chromosome homologs in somatic cells is a major pathway to the loss of heterozygosity (LOH), which may cause cancer if tumor suppressor genes are involved. MR can be suppressed by DNA sequence heterology (homeology) in hybrid mice from matings between species or between subspecies. We now report that MR is relatively suppressed in F1 hybrids between inbred strains C57BL/6 and 129S2. The frequency of MR in fibroblasts is lower in F1 hybrid mice than in either of the two parental strains. However, MR in T cells is not affected by strain background. Thus, relatively small genetic differences are capable of restricting MR in a tissue-specific manner. Using Mlh1-deficient mice, we tested the role of mismatch repair in MR in two isogenic cell types. In fibroblasts of C57BL/6 x 129S2 F1 mice, the suppression of MR is alleviated in the absence of MLH1. In contrast, MR is not affected by Mlh1 status in T cells. The frequency of point mutations at the reporter gene loci Aprt and Hprt, on the other hand, is significantly increased in both T cells and fibroblasts of Mlh1(-/-) mice. Thus, different cell types respond differently to MLH1 deficiency, and the contribution of MR to tumorigenesis may be tissue-dependent in the absence of mismatch 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 OpenQuestion graph.