The Interplay between Nonhomologous End-joining and Cell Cycle Checkpoint Factors in Development, Genomic Stability, and Tumorigenesis-Reference-Cited by-同舟云学术

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The Interplay between Nonhomologous End-joining and Cell Cycle Checkpoint Factors in Development, Genomic Stability, and Tumorigenesis

Published:2000-01-01 Issue:0 Volume:65 Page:395-404
ISSN:0091-7451
Container-title:Cold Spring Harbor Symposia on Quantitative Biology
language:en
Short-container-title:Cold Spring Harbor Symposia on Quantitative Biology

Author:

FERGUSON D.O.,SEKIGUCHI J.M.,FRANK K.M.,GAO Y.,SHARPLESS N.E.,GU Y.,MANIS J.,DEPINHO R.A.,ALT F.W.

Publisher

Cold Spring Harbor Laboratory

Subject

Genetics,Molecular Biology,Biochemistry

Reference46 articles.

1. DNA double-strand break repair proteins are required to cap the ends of mammalian chromosomes

2. RAD51 Is Required for the Repair of Plasmid Double-Stranded DNA Gaps from Either Plasmid or Chromosomal Templates

3. Chromosome Break-Induced DNA Replication Leads to Nonreciprocal Translocations and Telomere Capture

4. DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation

5. Recombinational repair of gaps in DNA is asymmetric in Ustilago maydis and can be explained by a migrating D-loop model.

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5. Sodium glycididazole enhances the radiosensitivity of laryngeal cancer cells through downregulation of ATM signaling pathway;Tumor Biology;2015-11-09

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