Loading…
Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene
CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock...
Saved in:
Published in: | Genesis (New York, N.Y. : 2000) N.Y. : 2000), 2010-02, Vol.48 (2), p.127-136 |
---|---|
Main Authors: | , , , , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites 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-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563 |
---|---|
cites | cdi_FETCH-LOGICAL-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563 |
container_end_page | 136 |
container_issue | 2 |
container_start_page | 127 |
container_title | Genesis (New York, N.Y. : 2000) |
container_volume | 48 |
creator | Qiu, Min Ru Jiang, Lele Matthaei, Klaus I. Schoenwaelder, Simone M. Kuffner, Tamara Mangin, Pierre Joseph, Joanne E. Low, Joyce Connor, David Valenzuela, Stella M. Curmi, Paul M.G. Brown, Louise J. Mahaut-Smith, Martyn Jackson, Shaun P. Breit, Samuel N. |
description | CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock‐out mice. This represents creation of the first gene knock‐out of a vertebrate CLIC protein family member. We first generated a Clic1 Knock‐in (Clic1FN) allele, followed by Clic1 knock‐out (Clic1−/−) mice by crossing Clic1FN allele with TNAP‐cre mice, resulting in germline gene deletion through Cre‐mediated recombination. Mice heterozygous or homozygous for these alleles are viable and fertile and appear normal. However, Clic1−/− mice show a mild platelet dysfunction characterized by prolonged bleeding times and decreased platelet activation in response to adenosine diphosphate stimulation linked to P2Y12 receptor signaling. genesis 48:127–136, 2010. © 2010 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/dvg.20590 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_754553908</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>754553908</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563</originalsourceid><addsrcrecordid>eNqNkc1u1DAURi1ERUthwQsg7xCLtNe_iZdQ6ICoWgkB7c5yPDczBidp7YRSnp4M6cwO0ZWvfM93bOkj5AWDIwbAj5c_V0cclIFH5IAprgujq6vH21nJq33yNOfvAKAqzp-QfQ4gjVHigKwW2GFyQ-g76rol9WuXnB8whd_zZd_QNnikt2FY026MkbbjsFsNa5wisU9hiTR0w5TFGMfo0sbUdRgpo6vpiWdkr3Ex4_P785B8PX3_5eRDcXax-Hjy5qzwUjMosGQcvBdcisaVqFklQYCEpmbomwaV1DXTDqGCsjaMq4pxxo1TXshaKC0OyavZe536mxHzYNuQN39yHfZjtqWSSgkD1f9JKbWp9ENIIQxjFZiJfD2TPvU5J2zsdQqtS3eWgd1UZaeq7N-qJvblvXWsW1zuyG03E3A8A7ch4t2_Tfbdt8VWWcyJkAf8tUu49MPqUpTKXp4v7Olb-flSiE9WiD8o1au_</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>733911809</pqid></control><display><type>article</type><title>Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene</title><source>Wiley</source><creator>Qiu, Min Ru ; Jiang, Lele ; Matthaei, Klaus I. ; Schoenwaelder, Simone M. ; Kuffner, Tamara ; Mangin, Pierre ; Joseph, Joanne E. ; Low, Joyce ; Connor, David ; Valenzuela, Stella M. ; Curmi, Paul M.G. ; Brown, Louise J. ; Mahaut-Smith, Martyn ; Jackson, Shaun P. ; Breit, Samuel N.</creator><creatorcontrib>Qiu, Min Ru ; Jiang, Lele ; Matthaei, Klaus I. ; Schoenwaelder, Simone M. ; Kuffner, Tamara ; Mangin, Pierre ; Joseph, Joanne E. ; Low, Joyce ; Connor, David ; Valenzuela, Stella M. ; Curmi, Paul M.G. ; Brown, Louise J. ; Mahaut-Smith, Martyn ; Jackson, Shaun P. ; Breit, Samuel N.</creatorcontrib><description>CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock‐out mice. This represents creation of the first gene knock‐out of a vertebrate CLIC protein family member. We first generated a Clic1 Knock‐in (Clic1FN) allele, followed by Clic1 knock‐out (Clic1−/−) mice by crossing Clic1FN allele with TNAP‐cre mice, resulting in germline gene deletion through Cre‐mediated recombination. Mice heterozygous or homozygous for these alleles are viable and fertile and appear normal. However, Clic1−/− mice show a mild platelet dysfunction characterized by prolonged bleeding times and decreased platelet activation in response to adenosine diphosphate stimulation linked to P2Y12 receptor signaling. genesis 48:127–136, 2010. © 2010 Wiley‐Liss, Inc.</description><identifier>ISSN: 1526-954X</identifier><identifier>EISSN: 1526-968X</identifier><identifier>DOI: 10.1002/dvg.20590</identifier><identifier>PMID: 20049953</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Alleles ; Animals ; Blood Platelets - metabolism ; Chloride Channels - genetics ; chloride intracellular channel family ; CLIC1 ; Cre ; Crosses, Genetic ; Gene Deletion ; Gene Targeting - methods ; Genetic Engineering ; Hemorrhage ; Heterozygote ; Homozygote ; Immunohistochemistry ; Integrases - metabolism ; Mice ; Mice, Knockout ; Models, Genetic ; platelet ; Recombination, Genetic</subject><ispartof>Genesis (New York, N.Y. : 2000), 2010-02, Vol.48 (2), p.127-136</ispartof><rights>Copyright © 2010 Wiley‐Liss, Inc.</rights><rights>(c) 2010 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563</citedby><cites>FETCH-LOGICAL-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563</cites></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/20049953$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qiu, Min Ru</creatorcontrib><creatorcontrib>Jiang, Lele</creatorcontrib><creatorcontrib>Matthaei, Klaus I.</creatorcontrib><creatorcontrib>Schoenwaelder, Simone M.</creatorcontrib><creatorcontrib>Kuffner, Tamara</creatorcontrib><creatorcontrib>Mangin, Pierre</creatorcontrib><creatorcontrib>Joseph, Joanne E.</creatorcontrib><creatorcontrib>Low, Joyce</creatorcontrib><creatorcontrib>Connor, David</creatorcontrib><creatorcontrib>Valenzuela, Stella M.</creatorcontrib><creatorcontrib>Curmi, Paul M.G.</creatorcontrib><creatorcontrib>Brown, Louise J.</creatorcontrib><creatorcontrib>Mahaut-Smith, Martyn</creatorcontrib><creatorcontrib>Jackson, Shaun P.</creatorcontrib><creatorcontrib>Breit, Samuel N.</creatorcontrib><title>Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene</title><title>Genesis (New York, N.Y. : 2000)</title><addtitle>Genesis</addtitle><description>CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock‐out mice. This represents creation of the first gene knock‐out of a vertebrate CLIC protein family member. We first generated a Clic1 Knock‐in (Clic1FN) allele, followed by Clic1 knock‐out (Clic1−/−) mice by crossing Clic1FN allele with TNAP‐cre mice, resulting in germline gene deletion through Cre‐mediated recombination. Mice heterozygous or homozygous for these alleles are viable and fertile and appear normal. However, Clic1−/− mice show a mild platelet dysfunction characterized by prolonged bleeding times and decreased platelet activation in response to adenosine diphosphate stimulation linked to P2Y12 receptor signaling. genesis 48:127–136, 2010. © 2010 Wiley‐Liss, Inc.</description><subject>Alleles</subject><subject>Animals</subject><subject>Blood Platelets - metabolism</subject><subject>Chloride Channels - genetics</subject><subject>chloride intracellular channel family</subject><subject>CLIC1</subject><subject>Cre</subject><subject>Crosses, Genetic</subject><subject>Gene Deletion</subject><subject>Gene Targeting - methods</subject><subject>Genetic Engineering</subject><subject>Hemorrhage</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Immunohistochemistry</subject><subject>Integrases - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Models, Genetic</subject><subject>platelet</subject><subject>Recombination, Genetic</subject><issn>1526-954X</issn><issn>1526-968X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqNkc1u1DAURi1ERUthwQsg7xCLtNe_iZdQ6ICoWgkB7c5yPDczBidp7YRSnp4M6cwO0ZWvfM93bOkj5AWDIwbAj5c_V0cclIFH5IAprgujq6vH21nJq33yNOfvAKAqzp-QfQ4gjVHigKwW2GFyQ-g76rol9WuXnB8whd_zZd_QNnikt2FY026MkbbjsFsNa5wisU9hiTR0w5TFGMfo0sbUdRgpo6vpiWdkr3Ex4_P785B8PX3_5eRDcXax-Hjy5qzwUjMosGQcvBdcisaVqFklQYCEpmbomwaV1DXTDqGCsjaMq4pxxo1TXshaKC0OyavZe536mxHzYNuQN39yHfZjtqWSSgkD1f9JKbWp9ENIIQxjFZiJfD2TPvU5J2zsdQqtS3eWgd1UZaeq7N-qJvblvXWsW1zuyG03E3A8A7ch4t2_Tfbdt8VWWcyJkAf8tUu49MPqUpTKXp4v7Olb-flSiE9WiD8o1au_</recordid><startdate>201002</startdate><enddate>201002</enddate><creator>Qiu, Min Ru</creator><creator>Jiang, Lele</creator><creator>Matthaei, Klaus I.</creator><creator>Schoenwaelder, Simone M.</creator><creator>Kuffner, Tamara</creator><creator>Mangin, Pierre</creator><creator>Joseph, Joanne E.</creator><creator>Low, Joyce</creator><creator>Connor, David</creator><creator>Valenzuela, Stella M.</creator><creator>Curmi, Paul M.G.</creator><creator>Brown, Louise J.</creator><creator>Mahaut-Smith, Martyn</creator><creator>Jackson, Shaun P.</creator><creator>Breit, Samuel N.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>201002</creationdate><title>Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene</title><author>Qiu, Min Ru ; Jiang, Lele ; Matthaei, Klaus I. ; Schoenwaelder, Simone M. ; Kuffner, Tamara ; Mangin, Pierre ; Joseph, Joanne E. ; Low, Joyce ; Connor, David ; Valenzuela, Stella M. ; Curmi, Paul M.G. ; Brown, Louise J. ; Mahaut-Smith, Martyn ; Jackson, Shaun P. ; Breit, Samuel N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Alleles</topic><topic>Animals</topic><topic>Blood Platelets - metabolism</topic><topic>Chloride Channels - genetics</topic><topic>chloride intracellular channel family</topic><topic>CLIC1</topic><topic>Cre</topic><topic>Crosses, Genetic</topic><topic>Gene Deletion</topic><topic>Gene Targeting - methods</topic><topic>Genetic Engineering</topic><topic>Hemorrhage</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Immunohistochemistry</topic><topic>Integrases - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Models, Genetic</topic><topic>platelet</topic><topic>Recombination, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qiu, Min Ru</creatorcontrib><creatorcontrib>Jiang, Lele</creatorcontrib><creatorcontrib>Matthaei, Klaus I.</creatorcontrib><creatorcontrib>Schoenwaelder, Simone M.</creatorcontrib><creatorcontrib>Kuffner, Tamara</creatorcontrib><creatorcontrib>Mangin, Pierre</creatorcontrib><creatorcontrib>Joseph, Joanne E.</creatorcontrib><creatorcontrib>Low, Joyce</creatorcontrib><creatorcontrib>Connor, David</creatorcontrib><creatorcontrib>Valenzuela, Stella M.</creatorcontrib><creatorcontrib>Curmi, Paul M.G.</creatorcontrib><creatorcontrib>Brown, Louise J.</creatorcontrib><creatorcontrib>Mahaut-Smith, Martyn</creatorcontrib><creatorcontrib>Jackson, Shaun P.</creatorcontrib><creatorcontrib>Breit, Samuel N.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Genesis (New York, N.Y. : 2000)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qiu, Min Ru</au><au>Jiang, Lele</au><au>Matthaei, Klaus I.</au><au>Schoenwaelder, Simone M.</au><au>Kuffner, Tamara</au><au>Mangin, Pierre</au><au>Joseph, Joanne E.</au><au>Low, Joyce</au><au>Connor, David</au><au>Valenzuela, Stella M.</au><au>Curmi, Paul M.G.</au><au>Brown, Louise J.</au><au>Mahaut-Smith, Martyn</au><au>Jackson, Shaun P.</au><au>Breit, Samuel N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene</atitle><jtitle>Genesis (New York, N.Y. : 2000)</jtitle><addtitle>Genesis</addtitle><date>2010-02</date><risdate>2010</risdate><volume>48</volume><issue>2</issue><spage>127</spage><epage>136</epage><pages>127-136</pages><issn>1526-954X</issn><eissn>1526-968X</eissn><abstract>CLIC1 belongs to a family of highly conserved and widely expressed intracellular chloride ion channel proteins existing in both soluble and membrane integrated forms. To study the physiological and biological role of CLIC1 in vivo, we undertook conditional gene targeting to engineer Clic1 gene knock‐out mice. This represents creation of the first gene knock‐out of a vertebrate CLIC protein family member. We first generated a Clic1 Knock‐in (Clic1FN) allele, followed by Clic1 knock‐out (Clic1−/−) mice by crossing Clic1FN allele with TNAP‐cre mice, resulting in germline gene deletion through Cre‐mediated recombination. Mice heterozygous or homozygous for these alleles are viable and fertile and appear normal. However, Clic1−/− mice show a mild platelet dysfunction characterized by prolonged bleeding times and decreased platelet activation in response to adenosine diphosphate stimulation linked to P2Y12 receptor signaling. genesis 48:127–136, 2010. © 2010 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20049953</pmid><doi>10.1002/dvg.20590</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1526-954X |
ispartof | Genesis (New York, N.Y. : 2000), 2010-02, Vol.48 (2), p.127-136 |
issn | 1526-954X 1526-968X |
language | eng |
recordid | cdi_proquest_miscellaneous_754553908 |
source | Wiley |
subjects | Alleles Animals Blood Platelets - metabolism Chloride Channels - genetics chloride intracellular channel family CLIC1 Cre Crosses, Genetic Gene Deletion Gene Targeting - methods Genetic Engineering Hemorrhage Heterozygote Homozygote Immunohistochemistry Integrases - metabolism Mice Mice, Knockout Models, Genetic platelet Recombination, Genetic |
title | Generation and characterization of mice with null mutation of the chloride intracellular channel 1 gene |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T03%3A23%3A28IST&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=Generation%20and%20characterization%20of%20mice%20with%20null%20mutation%20of%20the%20chloride%20intracellular%20channel%201%20gene&rft.jtitle=Genesis%20(New%20York,%20N.Y.%20:%202000)&rft.au=Qiu,%20Min%20Ru&rft.date=2010-02&rft.volume=48&rft.issue=2&rft.spage=127&rft.epage=136&rft.pages=127-136&rft.issn=1526-954X&rft.eissn=1526-968X&rft_id=info:doi/10.1002/dvg.20590&rft_dat=%3Cproquest_cross%3E754553908%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4610-e7120cc3243fa7e618403040fb1ecffe546b16ae0807b9125812129a5c34b3563%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=733911809&rft_id=info:pmid/20049953&rfr_iscdi=true |