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Literature DB >> 10691732

ATR disruption leads to chromosomal fragmentation and early embryonic lethality.

Abstract

Although a small decrease in survival and increase in tumor incidence was observed in ATR(+/-) mice, ATR(-/-) embryos die early in development, subsequent to the blastocyst stage and prior to 7.5 days p.c. In culture, ATR(-/-) blastocysts cells continue to cycle into mitosis for 2 days but subsequently fail to expand and die of caspase-dependent apoptosis. Importantly, caspase-independent chromosome breaks are observed in ATR(-/-) cells prior to widespread apoptosis, implying that apoptosis is caused by a loss of genomic integrity. These data show that ATR is essential for early embryonic development and must function in processes other than regulation of p53.

Entities: Disease Gene Mutation Species

Mesh：

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Year: 2000 PMID： 10691732 PMCID： PMC316378

Source DB: PubMed Journal: Genes Dev ISSN： 0890-9369 Impact factor: 11.361

36 in total

1. A role for ATR in the DNA damage-induced phosphorylation of p53.

Authors: R S Tibbetts; K M Brumbaugh; J M Williams; J N Sarkaria; W A Cliby; S Y Shieh; Y Taya; C Prives; R T Abraham
Journal: Genes Dev Date: 1999-01-15 Impact factor: 11.361

2. Caffeine-induced uncoupling of mitosis from the completion of DNA replication in mammalian cells.

Authors: R Schlegel; A B Pardee
Journal: Science Date: 1986-06-06 Impact factor: 47.728

3. Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells.

Authors: X Xu; Z Weaver; S P Linke; C Li; J Gotay; X W Wang; C C Harris; T Ried; C X Deng
Journal: Mol Cell Date: 1999-03 Impact factor: 17.970

ATR disruption leads to chromosomal fragmentation and early embryonic lethality.

1. A role for ATR in the DNA damage-induced phosphorylation of p53.

2. Caffeine-induced uncoupling of mitosis from the completion of DNA replication in mammalian cells.

3. Centrosome amplification and a defective G2-M cell cycle checkpoint induce genetic instability in BRCA1 exon 11 isoform-deficient cells.

4. Requirement of ATM-dependent phosphorylation of brca1 in the DNA damage response to double-strand breaks.

5. 14-3-3Sigma is required to prevent mitotic catastrophe after DNA damage.

6. Human wee1 maintains mitotic timing by protecting the nucleus from cytoplasmically activated Cdc2 kinase.

7. Tumor spectrum analysis in p53-mutant mice.

8. Mitotic checkpoint genes in budding yeast and the dependence of mitosis on DNA replication and repair.

9. The p53-dependent G1 cell cycle checkpoint pathway and ataxia-telangiectasia.

10. A mammalian protein targeted by G1-arresting rapamycin-receptor complex.

1. Suppression of genome instability by redundant S-phase checkpoint pathways in Saccharomyces cerevisiae.

2. ATR inhibition selectively sensitizes G1 checkpoint-deficient cells to lethal premature chromatin condensation.

3. Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance.

4. A subset of ATM- and ATR-dependent phosphorylation events requires the BRCA1 protein.

Review 5. Embryonic cleavage cycles: how is a mouse like a fly?

6. Apoptosis associated with deregulated E2F activity is dependent on E2F1 and Atm/Nbs1/Chk2.

7. Thresholds of replication stress signaling in cancer development and treatment.

Review 8. Stem cell ageing and non-random chromosome segregation.

9. ATR Plays a Direct Antiapoptotic Role at Mitochondria, which Is Regulated by Prolyl Isomerase Pin1.

10. Wild-type H- and N-Ras promote mutant K-Ras-driven tumorigenesis by modulating the DNA damage response.