(Q24291371)

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J A Sommers

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Q Yang

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X W Wang

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E A Spillare

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C C Harris

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V A Bohr

Journal of Biological Chemistry

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language of work or name

English

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publication date

14 September 2001

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published in

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volume

276

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issue

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page(s)

35093-102

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cites work

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A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

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WAF1, a potential mediator of p53 tumor suppression

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p53, the cellular gatekeeper for growth and division

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A Review of its Symptomatology, Natural History, Pathologic Features, Genetics And Relationship to the Natural Aging Process

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Werner's syndrome: a review of recent research with an analysis of connective tissue metabolism, growth control of cultured cells, and chromosomal aberrations

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Positional cloning of the Werner's syndrome gene

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The Werner syndrome protein is a DNA helicase

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Characterization of Werner syndrome protein DNA helicase activity: directionality, substrate dependence and stimulation by replication protein A

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Functional and physical interaction between WRN helicase and human replication protein A

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The premature ageing syndrome protein, WRN, is a 3'-->5' exonuclease

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Werner syndrome protein. I. DNA helicase and dna exonuclease reside on the same polypeptide.

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Characterization of the human and mouse WRN 3'-->5' exonuclease

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p53-mediated apoptosis is attenuated in Werner syndrome cells

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Physical and functional interaction between p53 and the Werner's syndrome protein

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Sp1-mediated transcription of the Werner helicase gene is modulated by Rb and p53.

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Mutations in the WRN gene in mice accelerate mortality in a p53-null background

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Enzymatic and DNA binding properties of purified WRN protein: high affinity binding to single-stranded DNA but not to DNA damage induced by 4NQO.

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p53 modulation of TFIIH–associated nucleotide excision repair activity

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Replication protein A physically interacts with the Bloom's syndrome protein and stimulates its helicase activity

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p53 binds single-stranded DNA ends and catalyzes DNA renaturation and strand transfer.

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Selective blockage of the 3'-->5' exonuclease activity of WRN protein by certain oxidative modifications and bulky lesions in DNA.

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A functional interaction of Ku with Werner exonuclease facilitates digestion of damaged DNA

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Effects of the cellular p53 protein on Simian-virus-40-T-antigen-catalyzed DNA unwinding in vitro

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Wild-type, but not mutant, human p53 proteins inhibit the replication activities of simian virus 40 large tumor antigen

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Nucleolar localization of the Werner syndrome protein in human cells

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Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest

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The Werner syndrome gene product co-purifies with the DNA replication complex and interacts with PCNA and topoisomerase I.

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Impaired S-phase transit of Werner syndrome cells expressed in lymphoblastoid cell lines

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Myc-mediated apoptosis requires wild-type p53 in a manner independent of cell cycle arrest and the ability of p53 to induce p21waf1/cip1.

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p53-dependent apoptosis in the absence of transcriptional activation of p53-target genes

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A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis

21 January 2018

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The XPB and XPD DNA helicases are components of the p53-mediated apoptosis pathway

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Drug-induced apoptosis is delayed and reduced in XPD lymphoblastoid cell lines: possible role of TFIIH in p53-mediated apoptotic cell death

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Werner syndrome protein. II. Characterization of the integral 3' --> 5' DNA exonuclease

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The DNA-binding domain of p53 contains the four conserved regions and the major mutation hot spots

21 January 2018

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Altered frequency of initiation sites of DNA replication in Werner's syndrome cells

21 January 2018

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Autoradiographic studies of DNA replication in Werner's syndrome cells

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Conformational shifts propagate from the oligomerization domain of p53 to its tetrameric DNA binding domain and restore DNA binding to select p53 mutants.

21 January 2018

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inferred from DOI database lookup

7 January 2021

based on heuristic

Werner's syndrome a review of its symptomatology, natural history, pathologic features, genetics and relationship to the natural aging process

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M103332200

inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1074/JBC.M103332200

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

11427532

1 reference

Consolidated OpenCitations Corpus – April 2017