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Nijmegen breakage syndrome disease protein and MRE11 at PML nuclear bodies and meiotic telomeres.

Authors: D B, Lombard; L, Guarente;

Nijmegen breakage syndrome disease protein and MRE11 at PML nuclear bodies and meiotic telomeres.

Abstract

Nijmegen breakage syndrome is a disease characterized by immunodeficiency, genomic instability, and cancer susceptibility. The gene product defective in Nijmegen breakage syndrome, p95, associates with two other proteins, MRE11 and RAD50. Here we demonstrate that in the absence of DNA damage, a portion of p95 and MRE11 is concentrated in PML nuclear bodies (NBs); MRE11 localization to the NBs is p95-dependent. In mammalian meiocytes, these proteins are specifically found at the telomeres. These results implicate the NBs in the maintenance of genomic stability and suggest that p95 and MRE11 may have roles in telomere maintenance in mammals, analogous to the role their homologues play in yeast.

Related Organizations
Keywords

Cell Nucleus, Endodeoxyribonucleases, Saccharomyces cerevisiae Proteins, Neutrophils, Fluorescent Antibody Technique, Nuclear Proteins, Cell Cycle Proteins, Fibroblasts, Telomere, Cell Line, Fungal Proteins, Meiosis, Mice, Exodeoxyribonucleases, Mutation, Animals, Humans

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Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
91
Top 10%
Top 10%
Top 1%
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