A unified view of the DNA-damage checkpoint

Melo, Justine A.; Toczyski, David P.

doi:10.1016/s0955-0674(02)00312-5

Cited by 436 publications

(414 citation statements)

References 67 publications

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“…(Bartek and Lukas, 2003) For example, ATR was proven to be activated in response to various genotoxic agents and chemicals which stall replication folks such as topoisomerase inhibitors and hydroxyurea (HU) (Melo and Toczyski, 2002).…”

Section: Figure15 Two Conserved Pathways Involved In Checkpoint Sysmentioning

confidence: 99%

Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors

2014

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Section: Figure15 Two Conserved Pathways Involved In Checkpoint Sysmentioning

confidence: 99%

Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors

2014

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“…The DNA damage checkpoint is initiated by the recruitment of multiple checkpoint components to the DSB by the DNA repair machinery, including the PI3family kinase ATR in mammals and its homolog Mec1 in yeast [80]. Once recruited to the DNA, ATR / Mec1 phosphorylates and activates downstream targets in the DNA damage checkpoint signaling cascade.…”

Section: Regulation Of Histone Chaperones By the Dna Damage Checkpointmentioning

confidence: 99%

Chromatin disassembly and reassembly during DNA repair

Linger

Tyler

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Current research is demonstrating that the packaging of the eukaryotic genome together with histone proteins into chromatin is playing a fundamental role in DNA repair and the maintenance of genomic integrity. As is well established to be the case for transcription, the chromatin structure dynamically changes during DNA repair. Recent studies indicate that the complete removal of histones from DNA and their subsequent reassembly onto DNA accompanies DNA repair. This review will present evidence indicating that chromatin disassembly and reassembly occur during DNA repair and that these are critical processes for cell survival after DNA repair. Concomitantly, candidate proteins utilized for these processes will be highlighted.

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“…DNA damage activated nuclear kinases (e.g., ATM, ATR, chk1, chk2) promote survival, in part, by activating specific DNA damage-responsive cell cycle checkpoints, including those in G1/S, intra-S, and G2/M (reviewed in McGowan, 2002;Melo and Toczyski, 2002). These checkpoints play an important protective function by preventing the propagation of DNA damage by cell cycle progression occurring before the DNA is repaired.…”

Section: Functional Activities Of Brca1 Cell Cycle Regulation and Gromentioning

confidence: 99%

BRCA1 gene in breast cancer

Rosen

Fan

Pestell

et al. 2003

Journal Cellular Physiology

241

195

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The BRCA1 gene was identified and cloned in 1994 based on its linkage to early onset breast cancer and breast-ovarian cancer syndromes in women. While inherited mutations of BRCA1 are responsible for about 40-45% of hereditary breast cancers, these mutations account for only 2-3% of all breast cancers, since the BRCA1 gene is rarely mutated in sporadic breast cancers. However, BRCA1 expression is frequently reduced or absent in sporadic cancers, suggesting a much wider role in mammary carcinogenesis. Since BRCA1 was cloned in 1994, its molecular function has been the subject of intense investigation. These studies have revealed multiple functions of the BRCA1 that may contribute to its tumor suppressor activity, including roles in: cell cycle progression, several highly specialized DNA repair processes, DNA damage-responsive cell cycle checkpoints, regulation of a set of specific transcriptional pathways, and apoptosis. Many of these functions are linked to protein:protein interactions involving different portions of the 1,863 amino acid (aa) BRCA1 protein. BRCA1 functions in cell cycle progression and the DNA damage response appear to be regulated by distinct and specific phosphorylation events, but the molecular pathways activated by these phosphorylations are only beginning to be unraveled. In addition, the reason that BRCA1 mutation carriers develop specific tumor types (breast and ovarian cancers in women and possibly prostate cancers in men) is not clearly understood. Elucidation of the precise molecular functions of the BRCA1 gene product will greatly enhance our understanding of the pathogenesis of hereditary as well as sporadic mammary carcinogenesis.

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A unified view of the DNA-damage checkpoint

Cited by 436 publications

References 67 publications

Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors

Differential response of normal and malignant urothelial cells to CHK1 and ATM inhibitors

Chromatin disassembly and reassembly during DNA repair

BRCA1 gene in breast cancer

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