Please use this identifier to cite or link to this item: https://doi.org/10.1074/jbc.M109.038539
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dc.titleGata4 and Gata5 Cooperatively Regulate Cardiac Myocyte Proliferation in Mice
dc.contributor.authorSingh, Manvendra K
dc.contributor.authorLi, Yan
dc.contributor.authorLi, Shanru
dc.contributor.authorCobb, Ryan M
dc.contributor.authorZhou, Diane
dc.contributor.authorLu, Min Min
dc.contributor.authorEpstein, Jonathan A
dc.contributor.authorMorrisey, Edward E
dc.contributor.authorGruber, Peter J
dc.date.accessioned2021-09-28T04:49:57Z
dc.date.available2021-09-28T04:49:57Z
dc.date.issued2010-01-15
dc.identifier.citationSingh, Manvendra K, Li, Yan, Li, Shanru, Cobb, Ryan M, Zhou, Diane, Lu, Min Min, Epstein, Jonathan A, Morrisey, Edward E, Gruber, Peter J (2010-01-15). Gata4 and Gata5 Cooperatively Regulate Cardiac Myocyte Proliferation in Mice. JOURNAL OF BIOLOGICAL CHEMISTRY 285 (3) : 1765-1772. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M109.038539
dc.identifier.issn00219258
dc.identifier.issn1083351X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/201349
dc.description.abstractGATA5 is a member of the zinc finger transcription factor GATA family (GATA1-6) that plays a wide variety of roles in embryonic and adult development. Experiments in multiple model systems have emphasized the importance of the GATA family members 4-6 in the development of the endoderm and mesoderm. Yet despite overlapping expression patterns, there is little evidence of an important role for GATA5 in mammalian cardiac development. We have generated a new Gata5 mutant allele lacking exons 2 and 3 that encodes both zinc finger domains (Gata5tm2Eem), and we show that although Gata5-/- mice are viable, Gata4+/-5-/- mutants die at mid-gestation and exhibit profound cardiovascular defects, including abnormalities of cardiomyocyte proliferation and cardiac chamber maturation. These results demonstrate functional redundancy between Gata4 and Gata5 during cardiac development and implicate Gata5 as a candidate modifier gene for congenital heart disease. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
dc.language.isoen
dc.publisherAMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectBiochemistry & Molecular Biology
dc.subjectCARDIOMYOCYTE CELL-CYCLE
dc.subjectHEART TUBE FORMATION
dc.subjectTRANSCRIPTION FACTOR
dc.subjectGENE-EXPRESSION
dc.subjectCARDIOVASCULAR-SYSTEM
dc.subjectVENTRAL MORPHOGENESIS
dc.subjectHEMATOPOIETIC-CELLS
dc.subjectMOUSE EMBRYO
dc.subjectDIFFERENTIATION
dc.subjectZEBRAFISH
dc.typeArticle
dc.date.updated2021-09-22T02:36:02Z
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.contributor.departmentInstitute of Data Science
dc.description.doi10.1074/jbc.M109.038539
dc.description.sourcetitleJOURNAL OF BIOLOGICAL CHEMISTRY
dc.description.volume285
dc.description.issue3
dc.description.page1765-1772
dc.published.statePublished
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