DNA Ligase IV Deficiency in Mice Leads to Defective Neurogenesis and Embryonic Lethality via the p53 Pathway
Karen M. Frank,Norman E. Sharpless,Yijie Gao,JoAnn Sekiguchi,David O. Ferguson,Chengming Zhu,John P. Manis,James W. Horner,Ronald A. DePinho,Frederick W. Alt +9 more
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TLDR
In the context of Lig4 deficiency, embryonic lethality and neuronal apoptosis likely result from a p53-dependent response to unrepaired DNA damage, and neurons apoptosis and lymphocyte developmental defects can be mechanistically dissociated.About:
This article is published in Molecular Cell.The article was published on 2000-06-01 and is currently open access. It has received 491 citations till now. The article focuses on the topics: DNA repair & DNA damage.read more
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DNA double-strand breaks: signaling, repair and the cancer connection.
TL;DR: Recent progress is described in understanding of how cells detect and signal the presence and repair of one particularly important form of DNA damage induced by ionizing radiation—the DNA double-strand break (DSB).
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Chromosomal stability and the DNA double-stranded break connection.
TL;DR: Interactions between both double-stranded break-repair pathways and other cellular processes, such as cell-cycle regulation and replication, are being unveiled.
Journal ArticleDOI
Sensing and repairing DNA double-strand breaks.
TL;DR: An increased knowledge of DSB repair and of other DNA DSB responses may provide opportunities for developing more effective treatments for cancer, with particular emphasis on non-homologous end-joining and homologous recombination.
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Developmental defects and p53 hyperacetylation in Sir2 homolog (SIRT1)-deficient mice
Hwei-Ling Cheng,Raul Mostoslavsky,Shin'ichi Saito,John P. Manis,Yansong Gu,Parin Patel,Roderick T. Bronson,Ettore Appella,Frederick W. Alt,Katrin F. Chua +9 more
TL;DR: Observations provide direct evidence that endogenous SIRT1 protein regulates p53 acetylation and p53-dependent apoptosis, and show that the function of this enzyme is required for specific developmental processes.
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The signals and pathways activating cellular senescence.
TL;DR: Recent advances in understanding of the stimuli that trigger senescence, the molecular pathways activated by these stimuli, and the manner by which these signals determine the entry of a population of cells intosenescence are reviewed.
References
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Journal ArticleDOI
p53, the Cellular Gatekeeper for Growth and Division
TL;DR: The author regrets the lack of citations for many important observations mentioned in the text, but their omission is made necessary by restrictions in the preparation of review manuscripts.
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo
Goberdhan P. Dimri,X Lee,G Basile,Meileen Acosta,G Scott,C Roskelley,E E Medrano,Maarten H.K. Linskens,Ivica Rubelj,Olivia M. Pereira-Smith +9 more
TL;DR: It is shown that several human cells express a beta-galactosidase, histochemically detectable at pH 6, upon senescence in culture, which provides in situ evidence that senescent cells may exist and accumulate with age in vivo.
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Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
TL;DR: It is shown that expression of oncogenic ras in primary human or rodent cells results in a permanent G1 arrest, and that the onset of cellular senescence does not simply reflect the accumulation of cell divisions, but can be prematurely activated in response to an onCogenic stimulus.
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Lawrence A. Donehower,Michele Harvey,Betty L. Slagle,Mark J. McArthur,Charles A. Montgomery,Janet S. Butel,Allan Bradley +6 more
TL;DR: Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
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RAG-1-deficient mice have no mature B and T lymphocytes
Peter Mombaerts,John Iacomini,Randall S. Johnson,Karl Herrup,Susumu Tonegawa,Virginia E. Papaioannou +5 more
TL;DR: The introduction of a mutation in RAG-1 into the germline of mice via gene targeting in embryonic stem cells is described and it is shown that this mutation either activates or catalyzes the V(D)J recombination reaction of immunoglobulin and T cell receptor genes.
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