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Article: β-Catenin directly regulates Islet1 expression in cardiovascular progenitors and is required for multiple aspects of cardiogenesis

Titleβ-Catenin directly regulates Islet1 expression in cardiovascular progenitors and is required for multiple aspects of cardiogenesis
Authors
KeywordsCardiac morphogenesis
Cardiac progenitors
Direct target
Isl1
Issue Date2007
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2007, v. 104 n. 22, p. 9313-9318 How to Cite?
AbstractRecent studies have demonstrated that the LIM homeodomain transcription factor Islet1 (Isl1) marks pluripotent cardiovascular progenitor cells and is required for proliferation, survival, and migration of recently defined second heart field progenitors. Factors that are upstream of Isl1 in cardiovascular progenitors have not yet been defined. Here we demonstrate that β-catenin is required for Isl1 expression in cardiac progenitors, directly regulating the Isl1 promoter. Ablation of β-catenin in Isl1-expressing progenitors disrupts multiple aspects of cardiogenesis, resulting in embryonic lethality at E13. β-Catenin is also required upstream of a number of genes required for pharyngeal arch, outflow tract, and/or atrial septal morphogenesis, including Tbx2, Tbx3, Wnt11, Shh, and Pitx2. Our findings demonstrate that β-catenin signaling regulates proliferation and survival of cardiac progenitors. © 2007 by The National Academy of Sciences of the USA.
Persistent Identifierhttp://hdl.handle.net/10722/141712
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLin, Len_HK
dc.contributor.authorCui, Len_HK
dc.contributor.authorZhou, Wen_HK
dc.contributor.authorDufort, Den_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorCai, CLen_HK
dc.contributor.authorBu, Len_HK
dc.contributor.authorYang, Len_HK
dc.contributor.authorMartin, Jen_HK
dc.contributor.authorKemler, Ren_HK
dc.contributor.authorRosenfeld, MGen_HK
dc.contributor.authorChen, Jen_HK
dc.contributor.authorEvans, SMen_HK
dc.date.accessioned2011-09-27T02:58:42Z-
dc.date.available2011-09-27T02:58:42Z-
dc.date.issued2007en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2007, v. 104 n. 22, p. 9313-9318en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/141712-
dc.description.abstractRecent studies have demonstrated that the LIM homeodomain transcription factor Islet1 (Isl1) marks pluripotent cardiovascular progenitor cells and is required for proliferation, survival, and migration of recently defined second heart field progenitors. Factors that are upstream of Isl1 in cardiovascular progenitors have not yet been defined. Here we demonstrate that β-catenin is required for Isl1 expression in cardiac progenitors, directly regulating the Isl1 promoter. Ablation of β-catenin in Isl1-expressing progenitors disrupts multiple aspects of cardiogenesis, resulting in embryonic lethality at E13. β-Catenin is also required upstream of a number of genes required for pharyngeal arch, outflow tract, and/or atrial septal morphogenesis, including Tbx2, Tbx3, Wnt11, Shh, and Pitx2. Our findings demonstrate that β-catenin signaling regulates proliferation and survival of cardiac progenitors. © 2007 by The National Academy of Sciences of the USA.en_HK
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_HK
dc.subjectCardiac morphogenesisen_HK
dc.subjectCardiac progenitorsen_HK
dc.subjectDirect targeten_HK
dc.subjectIsl1en_HK
dc.titleβ-Catenin directly regulates Islet1 expression in cardiovascular progenitors and is required for multiple aspects of cardiogenesisen_HK
dc.typeArticleen_HK
dc.identifier.emailBu, L:leibu@hku.hken_HK
dc.identifier.authorityBu, L=rp01534en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1073/pnas.0700923104en_HK
dc.identifier.pmid17519333-
dc.identifier.pmcidPMC1890491-
dc.identifier.scopuseid_2-s2.0-34250888462en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34250888462&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume104en_HK
dc.identifier.issue22en_HK
dc.identifier.spage9313en_HK
dc.identifier.epage9318en_HK
dc.identifier.isiWOS:000246935700042-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLin, L=13606302000en_HK
dc.identifier.scopusauthoridCui, L=36518491200en_HK
dc.identifier.scopusauthoridZhou, W=8510445100en_HK
dc.identifier.scopusauthoridDufort, D=6602714795en_HK
dc.identifier.scopusauthoridZhang, X=8510445700en_HK
dc.identifier.scopusauthoridCai, CL=7202874136en_HK
dc.identifier.scopusauthoridBu, L=8510445400en_HK
dc.identifier.scopusauthoridYang, L=8303959000en_HK
dc.identifier.scopusauthoridMartin, J=7501557320en_HK
dc.identifier.scopusauthoridKemler, R=7006736886en_HK
dc.identifier.scopusauthoridRosenfeld, MG=35356018800en_HK
dc.identifier.scopusauthoridChen, J=7501887040en_HK
dc.identifier.scopusauthoridEvans, SM=35583946900en_HK

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