ArticlePLoS genetics2009
Altered hematopoiesis in mice lacking DNA polymerase mu is due to inefficient double-strand break repair.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Exploring the Origin and Physiological Significance of DNA Double Strand Breaks in the Developing Neuroretina.International journal of molecular sciences · 2022Review
- DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Genes lost during the transition from land to water in cetaceans highlight genomic changes associated with aquatic adaptations.Science advances · 2019Article
- Ribonucleotide incorporation enables repair of chromosome breaks by nonhomologous end joining.Science (New York, N.Y.) · 2018Article
- Vitamin transporters in mice brain with aging.Journal of anatomy · 2018Article
- Mutational signatures of non-homologous and polymerase theta-mediated end-joining in embryonic stem cells.The EMBO journal · 2017Article
- Increased neuronal death and disturbed axonal growth in the Polμ-deficient mouse embryonic retina.Scientific reports · 2016Article
- Gadd45b deficiency promotes premature senescence and skin aging.Oncotarget · 2016Article
- Essential role for polymerase specialization in cellular nonhomologous end joining.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Nonhomologous end joining: a good solution for bad ends.DNA repair · 2014Review
- Sustained active site rigidity during synthesis by human DNA polymerase μ.Nature structural & molecular biology · 2014Article
- Article
- Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?Experimental hematology · 2013Review
- A human iPSC model of Ligase IV deficiency reveals an important role for NHEJ-mediated-DSB repair in the survival and genomic stability of induced pluripotent stem cells and emerging haematopoietic progenitors.Cell death and differentiation · 2013Article
- Biological and therapeutic relevance of nonreplicative DNA polymerases to cancer.Antioxidants & redox signaling · 2013Review
- Cell autonomous and nonautonomous mechanisms drive hematopoietic stem/progenitor cell loss in the absence of DNA repair.Stem cells (Dayton, Ohio) · 2013Article
- DNA expansions generated by human Polμ on iterative sequences.Nucleic acids research · 2013Article
- Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ.PloS one · 2013Article
- Polymerases in nonhomologous end joining: building a bridge over broken chromosomes.Antioxidants & redox signaling · 2011Review
- Choosing the right path: does DNA-PK help make the decision?Mutation research · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polymerase micro (Polmicro) is an error-prone, DNA-directed DNA polymerase that participates in non-homologous end-joining (NHEJ) repair. In vivo, Polmicro deficiency results in impaired Vkappa-Jkappa recombination and altered somatic hypermutation and centroblast development. In Polmicro(-/-) mice, hematopoietic development was defective in several peripheral and bone marrow (BM) cell populations, with about a 40% decrease in BM cell number that affected several hematopoietic lineages. Hematopoietic progenitors were reduced both in number and in expansion potential. The observed phenotype correlates with a reduced efficiency in DNA double-strand break (DSB) repair in hematopoietic tissue. Whole-body gamma-irradiation revealed that Polmicro also plays a role in DSB repair in non-hematopoietic tissues. Our results show that Polmicro function is required for physiological hematopoietic development with an important role in maintaining early progenitor cell homeostasis and genetic stability in hematopoietic and non-hematopoietic tissues.
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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.