Anterior Hox Genes in Cardiac Development and Great Artery Patterning
AbstractDuring early development, the heart tube grows by progressive addition of progenitor cells to the arterial and venous poles. These cardiac progenitor cells, originally identified in 2001, are located in the splanchnic mesoderm in a region termed the second heart field (SHF). Since its discovery, our view of heart development has been refined and it is well established that perturbation in the addition of SHF cells results in a spectrum of congenital heart defects. We have previously shown that anterior Hox genes, including Hoxb1, Hoxa1 and Hoxa3, are expressed in distinct subdomains of the SHF that contribute to atrial and subpulmonary myocardium. It is well known that Hox proteins exert their function through interaction with members of the TALE family, including Pbx and Meis factors. The expression profile of Pbx and Meis factors overlaps with that of anterior Hox factors in the embryonic heart, and recent data suggest that they may interact together during cardiac development. This review aims to bring together recent findings in vertebrates that strongly suggest an important function for Hox, Pbx and Meis factors in heart development and disease. View Full-Text
Scifeed alert for new publicationsNever miss any articles matching your research from any publisher
- Get alerts for new papers matching your research
- Find out the new papers from selected authors
- Updated daily for 49'000+ journals and 6000+ publishers
- Define your Scifeed now
Laforest, B.; Bertrand, N.; Zaffran, S. Anterior Hox Genes in Cardiac Development and Great Artery Patterning. J. Cardiovasc. Dev. Dis. 2014, 1, 3-13.
Laforest B, Bertrand N, Zaffran S. Anterior Hox Genes in Cardiac Development and Great Artery Patterning. Journal of Cardiovascular Development and Disease. 2014; 1(1):3-13.Chicago/Turabian Style
Laforest, Brigitte; Bertrand, Nicolas; Zaffran, Stéphane. 2014. "Anterior Hox Genes in Cardiac Development and Great Artery Patterning." J. Cardiovasc. Dev. Dis. 1, no. 1: 3-13.