The Werner syndrome protein: an update
Identifieur interne : 000F86 ( Istex/Checkpoint ); précédent : 000F85; suivant : 000F87The Werner syndrome protein: an update
Auteurs : Junko Oshima [États-Unis]Source :
- BioEssays [ 0265-9247 ] ; 2000-10.
English descriptors
- Teeft :
- Biochemical studies, Bioessays, Biol, Biol chem, Cell biol, Central region, Coli, Coli recq, Common mutation, Escherichia coli, Exonuclease, Exonuclease activity, Exonuclease domains, Fibroblast, Functional domains, Furuichi, Gene product, Genet, Goto, Helicase, Helicase activity, Helicase domains, Helicases, Homolog, Human diseases, Localized, Mouse models, Mutation, Nuclear localization signal, Nucleic acids, Oshima, Phenotype, Proc natl acad, Recombination, Recq, Recq helicases, Replication, Replicative, Replicative senescence, Review articles, Syndrome, Syndrome gene, Telomere, Telomere length, Topoisomerase, Transcriptional, Transcriptional activation, Werner, Werner helicase gene, Werner syndrome, Werner syndrome cells, Werner syndrome gene product, Werner syndrome protein.
Abstract
Progeria and progeroid syndromes are characterized by the earlier onset of complex senescent phenotypes. WRN was originally identified as a gene responsible for Werner syndrome (WS; “Progeria of Adults”). The WRN gene product has RecQ‐type helicase domains in the central region of the protein. Subsequent studies also revealed that the WRN protein displays exonuclease activity and acts as a transcriptional activation factor. These biochemical studies, combined with cell biological studies, suggested that this protein is likely to be involved in the response to DNA damage during replication, as well as recombination and transcription processes. However, the precise molecular mechanisms by which mutations in WRN cause the WS phenotype remain unknown. Recent progress in the understanding of the WRN protein and its implication in the normal aging process are discussed. BioEssays 22:894–901, 2000. © 2000 John Wiley & Sons, Inc.
Url:
DOI: 10.1002/1521-1878(200010)22:10<894::AID-BIES4>3.0.CO;2-B
Affiliations:
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University of Washington, 1959 NE Pacific Ave., Seattle</wicri:cityArea></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Correspondence address: Department of Pathology, Box 357470, HSB K‐543. University of Washington, 1959 NE Pacific Ave., Seattle</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">BioEssays</title><title level="j" type="alt">BIOESSAYS</title><idno type="ISSN">0265-9247</idno><idno type="eISSN">1521-1878</idno><imprint><biblScope unit="vol">22</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="894">894</biblScope><biblScope unit="page" to="901">901</biblScope><biblScope unit="page-count">8</biblScope><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000-10">2000-10</date></imprint><idno type="ISSN">0265-9247</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0265-9247</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Biochemical studies</term><term>Bioessays</term><term>Biol</term><term>Biol chem</term><term>Cell biol</term><term>Central region</term><term>Coli</term><term>Coli recq</term><term>Common mutation</term><term>Escherichia coli</term><term>Exonuclease</term><term>Exonuclease activity</term><term>Exonuclease domains</term><term>Fibroblast</term><term>Functional domains</term><term>Furuichi</term><term>Gene product</term><term>Genet</term><term>Goto</term><term>Helicase</term><term>Helicase activity</term><term>Helicase domains</term><term>Helicases</term><term>Homolog</term><term>Human diseases</term><term>Localized</term><term>Mouse models</term><term>Mutation</term><term>Nuclear localization signal</term><term>Nucleic acids</term><term>Oshima</term><term>Phenotype</term><term>Proc natl acad</term><term>Recombination</term><term>Recq</term><term>Recq helicases</term><term>Replication</term><term>Replicative</term><term>Replicative senescence</term><term>Review articles</term><term>Syndrome</term><term>Syndrome gene</term><term>Telomere</term><term>Telomere length</term><term>Topoisomerase</term><term>Transcriptional</term><term>Transcriptional activation</term><term>Werner</term><term>Werner helicase gene</term><term>Werner syndrome</term><term>Werner syndrome cells</term><term>Werner syndrome gene product</term><term>Werner syndrome protein</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Progeria and progeroid syndromes are characterized by the earlier onset of complex senescent phenotypes. WRN was originally identified as a gene responsible for Werner syndrome (WS; “Progeria of Adults”). The WRN gene product has RecQ‐type helicase domains in the central region of the protein. Subsequent studies also revealed that the WRN protein displays exonuclease activity and acts as a transcriptional activation factor. These biochemical studies, combined with cell biological studies, suggested that this protein is likely to be involved in the response to DNA damage during replication, as well as recombination and transcription processes. However, the precise molecular mechanisms by which mutations in WRN cause the WS phenotype remain unknown. Recent progress in the understanding of the WRN protein and its implication in the normal aging process are discussed. BioEssays 22:894–901, 2000. © 2000 John Wiley & Sons, Inc.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Oshima, Junko" sort="Oshima, Junko" uniqKey="Oshima J" first="Junko" last="Oshima">Junko Oshima</name></region><name sortKey="Oshima, Junko" sort="Oshima, Junko" uniqKey="Oshima J" first="Junko" last="Oshima">Junko Oshima</name><name sortKey="Oshima, Junko" sort="Oshima, Junko" uniqKey="Oshima J" first="Junko" last="Oshima">Junko Oshima</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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