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Deletion of Ku86 causes early onset of senescence in mice

Deletion of Ku86 causes early onset of senescence in mice

http://www.wikidata.org/entity/Q28144342

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The progeroid phenotype of Ku80 deficiency is dominant over DNA-PKCS deficiency Knock-in reporter mice demonstrate that DNA repair by non-homologous end joining declines with age Altered hematopoiesis in mice lacking DNA polymerase mu is due to inefficient double-strand break repair Overexpression of eIF-5A2 in mice causes accelerated organismal aging by increasing chromosome instability Web-based analysis of the mouse transcriptome using Genevestigator Ku complex interacts with and stimulates the Werner protein A functional interaction of Ku with Werner exonuclease facilitates digestion of damaged DNA WRN interacts physically and functionally with the recombination mediator protein RAD52 Regulation of osteocalcin gene expression by a novel Ku antigen transcription factor complex Identification and biochemical characterization of a Werner's syndrome protein complex with Ku70/80 and poly(ADP-ribose) polymerase-1 Ku86 autoantigen related protein-1 transcription initiates from a CpG island and is induced by p53 through a nearby p53 response element Mammalian Ku86 mediates chromosomal fusions and apoptosis caused by critically short telomeres.Subnuclear localization of Ku protein: functional association with RNA polymerase II elongation sites.Two faces of p53: aging and tumor suppression Deletion of Ku70, Ku80, or both causes early aging without substantially increased cancer Adaptive stress response in segmental progeria resembles long-lived dwarfism and calorie restriction in mice Stem cells, senescence, neosis and self-renewal in cancer.Functional interaction between Ku and the werner syndrome protein in DNA end processing DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation Werner protein is a target of DNA-dependent protein kinase in vivo and in vitro, and its catalytic activities are regulated by phosphorylation Accelerating aging by mouse reverse genetics: a rational approach to understanding longevity Loss of a single allele for Ku80 leads to progenitor dysfunction and accelerated aging in skeletal muscle ERCC1-XPF endonuclease facilitates DNA double-strand break repair Progeria of stem cells: stem cell exhaustion in Hutchinson-Gilford progeria syndrome Growth conditions that increase or decrease lifespan in Saccharomyces cerevisiae lead to corresponding decreases or increases in rates of interstitial deletions and non-reciprocal translocations p53-dependent inhibition of FKHRL1 in response to DNA damage through protein kinase SGK1 Reduced hematopoietic reserves in DNA interstrand crosslink repair-deficient Ercc1-/- mice DNA-dependent protein kinase catalytic subunit is not required for dysfunctional telomere fusion and checkpoint response in the telomerase-deficient mouse The African Turquoise Killifish Genome Provides Insights into Evolution and Genetic Architecture of Lifespan.WRN regulates pathway choice between classical and alternative non-homologous end joining Increased insensible water loss contributes to aging related dehydration.High preservation of CpG cytosine methylation patterns at imprinted gene loci in liver and brain of aged mice Requirements for the nucleolytic processing of DNA ends by the Werner syndrome protein-Ku70/80 complex.Effect of Ku80 deficiency on mutation frequencies and spectra at a LacZ reporter locus in mouse tissues and cells Mouse models of telomere dysfunction phenocopy skeletal changes found in human age-related osteoporosis.Ku80 deletion suppresses spontaneous tumors and induces a p53-mediated DNA damage response.Senescent cells: a novel therapeutic target for aging and age-related diseases Mammalian Ku86 protein prevents telomeric fusions independently of the length of TTAGGG repeats and the G-strand overhang.An alternate form of Ku80 is required for DNA end-binding activity in mammalian mitochondria.DNA-PK and P38 MAPK: A Kinase Collusion in Alzheimer's Disease?

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P2860

Deletion of Ku86 causes early onset of senescence in mice

http://www.wikidata.org/entity/Q28144342

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1999 nî lūn-bûn

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1999 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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1999 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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1999年の論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年论文

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name

Deletion of Ku86 causes early onset of senescence in mice

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Deletion of Ku86 causes early onset of senescence in mice

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Deletion of Ku86 causes early onset of senescence in mice

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type

label

Deletion of Ku86 causes early onset of senescence in mice

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Deletion of Ku86 causes early onset of senescence in mice

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Deletion of Ku86 causes early onset of senescence in mice

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prefLabel

Deletion of Ku86 causes early onset of senescence in mice

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Deletion of Ku86 causes early onset of senescence in mice

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Deletion of Ku86 causes early onset of senescence in mice

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Proceedings of the National Academy of Sciences of the United States of America

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Deletion of Ku86 causes early onset of senescence in mice

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G Karsenty

http://www.w3.org/2001/XMLSchema#string

M Finegold

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P2860

The Werner syndrome protein is a DNA helicase

Aging: a theory based on free radical and radiation chemistry

Redistribution of silencing proteins from telomeres to the nucleolus is associated with extension of life span in S. cerevisiae.

Accelerated aging and nucleolar fragmentation in yeast sgs1 mutants.

Relocalization of telomeric Ku and SIR proteins in response to DNA strand breaks in yeast.

Genetic instabilities in human cancers

MEC1-dependent redistribution of the Sir3 silencing protein from telomeres to DNA double-strand breaks

THE LIMITED IN VITRO LIFETIME OF HUMAN DIPLOID CELL STRAINS

Ku70-deficient embryonic stem cells have increased ionizing radiosensitivity, defective DNA end-binding activity, and inability to support V(D)J recombination

A critical role for DNA end-joining proteins in both lymphogenesis and neurogenesis

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2864492

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19

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Otto Hannes Vogel

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12814106

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10485901

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17958

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