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HIC2 regulates isoform switching during maturation of the cardiovascular system

Research output: Contribution to journalArticle

  • Iain M. Dykes
  • Kelly Lammerts van Bueren
  • Peter J. Scambler
Original languageEnglish
Pages (from-to)29-37
Number of pages9
JournalJournal of Molecular and Cellular Cardiology
Early online date20 Oct 2017
DateAccepted/In press - 19 Oct 2017
DateE-pub ahead of print - 20 Oct 2017
DatePublished (current) - Jan 2018


Physiological changes during embryonic development are associated with changes in the isoform expression of both myocyte sarcomeric proteins and of erythrocyte haemoglobins. Cell type-specific isoform expression of these genes also occurs. Although these changes appear to be coordinated, it is unclear how changes in these disparate cell types may be linked. The transcription factor Hic2 is required for normal cardiac development and the mutant is embryonic lethal. Hic2 embryos exhibit precocious expression of the definitive-lineage haemoglobin Hbb-bt in circulating primitive erythrocytes and of foetal isoforms of cardiomyocyte genes (creatine kinase, Ckm, and eukaryotic elongation factor Eef1a2) as well as ectopic cardiac expression of fast-twitch skeletal muscle troponin isoforms. We propose that HIC2 regulates a switching event within both the contractile machinery of cardiomyocytes and the oxygen carrying systems during the developmental period where demands on cardiac loading change rapidly.

    Research areas

  • Congenital heart disease, Embryonic development, Haemoglobin, Troponin, Creatine kinase, Myoglobin

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    Licence: CC BY


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