Cardiac neural crest: Difference between revisions

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=== GATA ===
[[GATA transcription factor]]s, which are complex molecules that bind to the DNA sequence ''GATA'', play a critical role in cell lineage differentiation restriction during cardiac development. The primary function of [[GATA6]] in cardiovascular development is to regulate the morphogenetic patterning of the outflow tract and aortic arch. When [[GATA6]] is inactivated in CNCCs, various cardiovascular defects such as persistent truncus arteriorusarteriosus and interrupted aortic arch may occur. This phenotype (anomaly) was also observed when GATA6 was inactivated within vascular smooth muscle cells.<ref name="Lepore (2006)">Lepore J. J. et al [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1409743/pdf/JCI0627363.pdf "GATA-6 regulates semaphorin 3C and is required in cardiac neural crest for cardiovascular morphogenesis."] Journal of Clinical Investigation 3 April 2006, 116(4) p929 - 939 {{PMID|16557299}} {{PMC|1409743}} {{doi|10.1172/JCI27363}}. Accessed 19 November 2012.</ref> GATA6 in combination with Wnt (Wnt2-GATA6) plays a role in the development of the posterior pole of the heart (the inflow tract).<ref name="Tian (2010)">Tian Y. et al [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846539/pdf/nihms177061.pdf "Characterization and in vivo pharmacological rescue of a Wnt2-GATA6 pathway required for cardiac inflow tract development."] Developmental Cell 16 February 2010 18(2) p275 - 287 pm =2846539 {{PMID|20159597}} {{doi|10.1016/j.devcel.2010.01.008}} Accessed 19 November 2012.</ref>
 
== CNCCS and ischaemic heart disease ==