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Article: Cre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4-CD8- to CD4 +CD8+ transition

TitleCre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4-CD8- to CD4 +CD8+ transition
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2007
PublisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.org
Citation
Neoplasia, 2007, v. 9 n. 4, p. 315-321 How to Cite?
AbstractIn the most common form of stem cell leukemia (SCL) gene rearrangement, an interstitial deletion of 82 kb brings SCL under the control of regulatory elements that normally govern expression of the ubiquitously expressed SCL interrupting locus (SIL) gene, which is located directly upstream of SCL. To investigate the effect of this fusion in a mouse model, a bacterial artificial chromosome (BAC) clone containing both human SIL and SCL genes was isolated, and loxP sites were inserted into intron 1 of both the SIL and SCL genes, corresponding to the sites at which recombination occurs in human T-cell acute lymphocytic leukemia patients. This BAC clone was used to generate transgenic SILloxloxSCL mice. These transgenic mice were subsequently bred to Lck-Cre mice that express the Cre recombinase specifically in the thymus. The BAC transgene was recombined between the two loxP sites in over 50% of the thymocytes from SILloxloxSCL/Cre double-transgenic mice, bringing the SCL gene under the direct control of SIL regulatory elements. Aberrant SCL gene expression in the thymus was verified by reverse transcription-polymerase chain reaction. Using FACS analysis, we found that mice carrying both SILloxloxSCL and Cre transgenes have increased CD4-/CD8- thymocytes compared with transgene-negative mice. In the spleen, these transgenic mice show a marked reduction in the number of mature CD4+ or CD8+ cells. These results demonstrate that conditional activation of SCL under control of SIL regulatory elements can impair normal T-cell development. Copyright © 2007 Neoplasia Press, Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/91267
ISSN
2014 Impact Factor: 4.252
2015 SCImago Journal Rankings: 2.541
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorZhang, Zen_HK
dc.contributor.authorSlape, Cen_HK
dc.contributor.authorAplan, PDen_HK
dc.date.accessioned2010-09-17T10:15:55Z-
dc.date.available2010-09-17T10:15:55Z-
dc.date.issued2007en_HK
dc.identifier.citationNeoplasia, 2007, v. 9 n. 4, p. 315-321en_HK
dc.identifier.issn1522-8002en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91267-
dc.description.abstractIn the most common form of stem cell leukemia (SCL) gene rearrangement, an interstitial deletion of 82 kb brings SCL under the control of regulatory elements that normally govern expression of the ubiquitously expressed SCL interrupting locus (SIL) gene, which is located directly upstream of SCL. To investigate the effect of this fusion in a mouse model, a bacterial artificial chromosome (BAC) clone containing both human SIL and SCL genes was isolated, and loxP sites were inserted into intron 1 of both the SIL and SCL genes, corresponding to the sites at which recombination occurs in human T-cell acute lymphocytic leukemia patients. This BAC clone was used to generate transgenic SILloxloxSCL mice. These transgenic mice were subsequently bred to Lck-Cre mice that express the Cre recombinase specifically in the thymus. The BAC transgene was recombined between the two loxP sites in over 50% of the thymocytes from SILloxloxSCL/Cre double-transgenic mice, bringing the SCL gene under the direct control of SIL regulatory elements. Aberrant SCL gene expression in the thymus was verified by reverse transcription-polymerase chain reaction. Using FACS analysis, we found that mice carrying both SILloxloxSCL and Cre transgenes have increased CD4-/CD8- thymocytes compared with transgene-negative mice. In the spleen, these transgenic mice show a marked reduction in the number of mature CD4+ or CD8+ cells. These results demonstrate that conditional activation of SCL under control of SIL regulatory elements can impair normal T-cell development. Copyright © 2007 Neoplasia Press, Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherNeoplasia Press. The Journal's web site is located at http://www.neoplasia.orgen_HK
dc.relation.ispartofNeoplasiaen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntigens, CD4 - biosynthesis - geneticsen_HK
dc.subject.meshAntigens, CD8 - biosynthesis - geneticsen_HK
dc.subject.meshBasic Helix-Loop-Helix Transcription Factors - biosynthesis - genetics - metabolismen_HK
dc.subject.meshCD4-Positive T-Lymphocytes - enzymology - immunology - pathologyen_HK
dc.subject.meshCD8-Positive T-Lymphocytes - enzymology - immunology - pathologyen_HK
dc.subject.meshCell Differentiation - geneticsen_HK
dc.subject.meshExtracellular Matrix Proteins - physiologyen_HK
dc.subject.meshGene Rearrangement, T-Lymphocyte - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntegrases - biosynthesis - geneticsen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteins - genetics - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, SCIDen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshProtein-Lysine 6-Oxidase - physiologyen_HK
dc.subject.meshProto-Oncogene Proteins - biosynthesis - genetics - metabolismen_HK
dc.subject.meshRecombination, Genetic - immunologyen_HK
dc.titleCre-loxP-mediated recombination between the SIL and SCL genes leads to a block in T-cell development at the CD4-CD8- to CD4 +CD8+ transitionen_HK
dc.typeArticleen_HK
dc.identifier.emailCheng, Y:yuecheng@hku.hken_HK
dc.identifier.authorityCheng, Y=rp01320en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1593/neo.07148en_HK
dc.identifier.pmid17460775-
dc.identifier.scopuseid_2-s2.0-34247181622en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247181622&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume9en_HK
dc.identifier.issue4en_HK
dc.identifier.spage315en_HK
dc.identifier.epage321en_HK
dc.identifier.eissn1476-5586-
dc.identifier.isiWOS:000245802000006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheng, Y=36131038300en_HK
dc.identifier.scopusauthoridZhang, Z=8511330100en_HK
dc.identifier.scopusauthoridSlape, C=8759250300en_HK
dc.identifier.scopusauthoridAplan, PD=35404812500en_HK
dc.identifier.citeulike1245263-

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