Loading…
Human diseases deficient in RecQ helicases
RecQ helicases are conserved from bacteria to man. Mutations in three of the human RecQ family members give rise to genetic disorders characterized by genomic instability and a predisposition to cancer. RecQ helicases are therefore caretakers of the genome, and although they do not directly regulate...
Saved in:
| Published in: | Biochimie 2003-11, Vol.85 (11), p.1185-1193 |
|---|---|
| Main Authors: | , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c389t-e42bb92738e4d8f271fa4d34b2c2a7dbef09cceaab58dc3cad1b79d6d6680f463 |
|---|---|
| cites | |
| container_end_page | 1193 |
| container_issue | 11 |
| container_start_page | 1185 |
| container_title | Biochimie |
| container_volume | 85 |
| creator | Harrigan, J.A Bohr, V.A |
| description | RecQ helicases are conserved from bacteria to man. Mutations in three of the human RecQ family members give rise to genetic disorders characterized by genomic instability and a predisposition to cancer. RecQ helicases are therefore caretakers of the genome, and although they do not directly regulate tumorigenesis, they influence stability and the rate of accumulation of genetic alterations, which in turn, result in tumorigenesis. Maintenance of genome stability by RecQ helicases likely involves their participation in DNA replication, recombination, and repair pathways. |
| doi_str_mv | 10.1016/j.biochi.2003.10.006 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71509415</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0300908403001822</els_id><sourcerecordid>71509415</sourcerecordid><originalsourceid>FETCH-LOGICAL-c389t-e42bb92738e4d8f271fa4d34b2c2a7dbef09cceaab58dc3cad1b79d6d6680f463</originalsourceid><addsrcrecordid>eNqFkE1Lw0AQhhdRbK3-A5GcPAipsx_d7F4EKWqFgih6XvZjQrckTc2mgv_ehBa86WngneedgYeQSwpTClTerqcuNn4VpwyA99EUQB6RMZVc5ZIqfkzGwAFyDUqMyFlKawCYAdOnZERFwSQwPiY3i11tN1mICW3ClAUso4-46bK4yd7Qv2YrrKIfdufkpLRVwovDnJCPx4f3-SJfvjw9z--XuedKdzkK5pxmBVcogipZQUsrAheOeWaL4LAE7T1a62YqeO5toK7QQQYpFZRC8gm53t_dts3nDlNn6pg8VpXdYLNLpqAz0ILO_gVpobmmagDFHvRtk1KLpdm2sbbtt6FgBplmbfYyzSBzSHuZfe3qcH_nagy_pYO9HrjbA9jr-IrYmjS48xhii74zoYl_f_gBN6aGgA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17939185</pqid></control><display><type>article</type><title>Human diseases deficient in RecQ helicases</title><source>ScienceDirect Freedom Collection 2022-2024</source><creator>Harrigan, J.A ; Bohr, V.A</creator><creatorcontrib>Harrigan, J.A ; Bohr, V.A</creatorcontrib><description>RecQ helicases are conserved from bacteria to man. Mutations in three of the human RecQ family members give rise to genetic disorders characterized by genomic instability and a predisposition to cancer. RecQ helicases are therefore caretakers of the genome, and although they do not directly regulate tumorigenesis, they influence stability and the rate of accumulation of genetic alterations, which in turn, result in tumorigenesis. Maintenance of genome stability by RecQ helicases likely involves their participation in DNA replication, recombination, and repair pathways.</description><identifier>ISSN: 0300-9084</identifier><identifier>EISSN: 1638-6183</identifier><identifier>DOI: 10.1016/j.biochi.2003.10.006</identifier><identifier>PMID: 14726023</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Adenosine Triphosphatases - chemistry ; Bloom syndrome ; Bloom Syndrome - genetics ; Bloom Syndrome - physiopathology ; DNA Helicases - chemistry ; DNA Helicases - deficiency ; DNA Helicases - genetics ; DNA Helicases - physiology ; Helicase ; Humans ; RecQ ; RecQ Helicases ; Rothmund-Thomson Syndrome - genetics ; Rothmund-Thomson Syndrome - physiopathology ; Rothmund–Thompson syndrome ; Werner syndrome ; Werner Syndrome - genetics ; Werner Syndrome - physiopathology</subject><ispartof>Biochimie, 2003-11, Vol.85 (11), p.1185-1193</ispartof><rights>2003 Éditions scientifiques et médicales Elsevier SAS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-e42bb92738e4d8f271fa4d34b2c2a7dbef09cceaab58dc3cad1b79d6d6680f463</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14726023$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Harrigan, J.A</creatorcontrib><creatorcontrib>Bohr, V.A</creatorcontrib><title>Human diseases deficient in RecQ helicases</title><title>Biochimie</title><addtitle>Biochimie</addtitle><description>RecQ helicases are conserved from bacteria to man. Mutations in three of the human RecQ family members give rise to genetic disorders characterized by genomic instability and a predisposition to cancer. RecQ helicases are therefore caretakers of the genome, and although they do not directly regulate tumorigenesis, they influence stability and the rate of accumulation of genetic alterations, which in turn, result in tumorigenesis. Maintenance of genome stability by RecQ helicases likely involves their participation in DNA replication, recombination, and repair pathways.</description><subject>Adenosine Triphosphatases - chemistry</subject><subject>Bloom syndrome</subject><subject>Bloom Syndrome - genetics</subject><subject>Bloom Syndrome - physiopathology</subject><subject>DNA Helicases - chemistry</subject><subject>DNA Helicases - deficiency</subject><subject>DNA Helicases - genetics</subject><subject>DNA Helicases - physiology</subject><subject>Helicase</subject><subject>Humans</subject><subject>RecQ</subject><subject>RecQ Helicases</subject><subject>Rothmund-Thomson Syndrome - genetics</subject><subject>Rothmund-Thomson Syndrome - physiopathology</subject><subject>Rothmund–Thompson syndrome</subject><subject>Werner syndrome</subject><subject>Werner Syndrome - genetics</subject><subject>Werner Syndrome - physiopathology</subject><issn>0300-9084</issn><issn>1638-6183</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkE1Lw0AQhhdRbK3-A5GcPAipsx_d7F4EKWqFgih6XvZjQrckTc2mgv_ehBa86WngneedgYeQSwpTClTerqcuNn4VpwyA99EUQB6RMZVc5ZIqfkzGwAFyDUqMyFlKawCYAdOnZERFwSQwPiY3i11tN1mICW3ClAUso4-46bK4yd7Qv2YrrKIfdufkpLRVwovDnJCPx4f3-SJfvjw9z--XuedKdzkK5pxmBVcogipZQUsrAheOeWaL4LAE7T1a62YqeO5toK7QQQYpFZRC8gm53t_dts3nDlNn6pg8VpXdYLNLpqAz0ILO_gVpobmmagDFHvRtk1KLpdm2sbbtt6FgBplmbfYyzSBzSHuZfe3qcH_nagy_pYO9HrjbA9jr-IrYmjS48xhii74zoYl_f_gBN6aGgA</recordid><startdate>20031101</startdate><enddate>20031101</enddate><creator>Harrigan, J.A</creator><creator>Bohr, V.A</creator><general>Elsevier Masson SAS</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20031101</creationdate><title>Human diseases deficient in RecQ helicases</title><author>Harrigan, J.A ; Bohr, V.A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-e42bb92738e4d8f271fa4d34b2c2a7dbef09cceaab58dc3cad1b79d6d6680f463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adenosine Triphosphatases - chemistry</topic><topic>Bloom syndrome</topic><topic>Bloom Syndrome - genetics</topic><topic>Bloom Syndrome - physiopathology</topic><topic>DNA Helicases - chemistry</topic><topic>DNA Helicases - deficiency</topic><topic>DNA Helicases - genetics</topic><topic>DNA Helicases - physiology</topic><topic>Helicase</topic><topic>Humans</topic><topic>RecQ</topic><topic>RecQ Helicases</topic><topic>Rothmund-Thomson Syndrome - genetics</topic><topic>Rothmund-Thomson Syndrome - physiopathology</topic><topic>Rothmund–Thompson syndrome</topic><topic>Werner syndrome</topic><topic>Werner Syndrome - genetics</topic><topic>Werner Syndrome - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Harrigan, J.A</creatorcontrib><creatorcontrib>Bohr, V.A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochimie</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Harrigan, J.A</au><au>Bohr, V.A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human diseases deficient in RecQ helicases</atitle><jtitle>Biochimie</jtitle><addtitle>Biochimie</addtitle><date>2003-11-01</date><risdate>2003</risdate><volume>85</volume><issue>11</issue><spage>1185</spage><epage>1193</epage><pages>1185-1193</pages><issn>0300-9084</issn><eissn>1638-6183</eissn><abstract>RecQ helicases are conserved from bacteria to man. Mutations in three of the human RecQ family members give rise to genetic disorders characterized by genomic instability and a predisposition to cancer. RecQ helicases are therefore caretakers of the genome, and although they do not directly regulate tumorigenesis, they influence stability and the rate of accumulation of genetic alterations, which in turn, result in tumorigenesis. Maintenance of genome stability by RecQ helicases likely involves their participation in DNA replication, recombination, and repair pathways.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>14726023</pmid><doi>10.1016/j.biochi.2003.10.006</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-9084 |
| ispartof | Biochimie, 2003-11, Vol.85 (11), p.1185-1193 |
| issn | 0300-9084 1638-6183 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71509415 |
| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | Adenosine Triphosphatases - chemistry Bloom syndrome Bloom Syndrome - genetics Bloom Syndrome - physiopathology DNA Helicases - chemistry DNA Helicases - deficiency DNA Helicases - genetics DNA Helicases - physiology Helicase Humans RecQ RecQ Helicases Rothmund-Thomson Syndrome - genetics Rothmund-Thomson Syndrome - physiopathology Rothmund–Thompson syndrome Werner syndrome Werner Syndrome - genetics Werner Syndrome - physiopathology |
| title | Human diseases deficient in RecQ helicases |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-20T09%3A46%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Human%20diseases%20deficient%20in%20RecQ%20helicases&rft.jtitle=Biochimie&rft.au=Harrigan,%20J.A&rft.date=2003-11-01&rft.volume=85&rft.issue=11&rft.spage=1185&rft.epage=1193&rft.pages=1185-1193&rft.issn=0300-9084&rft.eissn=1638-6183&rft_id=info:doi/10.1016/j.biochi.2003.10.006&rft_dat=%3Cproquest_cross%3E71509415%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c389t-e42bb92738e4d8f271fa4d34b2c2a7dbef09cceaab58dc3cad1b79d6d6680f463%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=17939185&rft_id=info:pmid/14726023&rfr_iscdi=true |