Anti-Mesp1: Mouse Mesp1 Antibody

For the cellular and the molecular mechanism by which Mesp1 acts during cardiac specification, it was shown that Mesp1 acts as a cardiovascular master regulator during specification of MCPs during ESC differentiation. Embryonic stem cell (ESC) differentiation is a good model to study the cardiovascular progenitor specification. Mesp1 both directly activated many key genes belonging to the core cardiac transcriptional machinery and directly repressed genes promoting early mesoderm and endoderm cell-fate specification. Mesp1 first transiently stimulated its own endogenous expression through a direct positive autoregulatory loop and then inhibited its own expression, therefore, acting as a molecular switch during cardiac specification. Altogether, our results provide compelling evidence that Mesp1 acts as a cardiovascular master regulator during specification of MCPs during ESC differentiation.⁴ In addition, it was further demonstrated that Mesp1 promoted mesoderm development independently of Wnt signaling. Transient Mesp1 expression in ESCs promotes changes associated with epithelial-mesenchymal transition (EMT) and induction of Snai1, consistent with a role in gastrulation. Mesp1 expression also restricted the potential fates derived from ESCs, generating mesoderm progenitors with cardiovascular, but not hematopoietic, potential. Thus, in addition to its effects on EMT, Mesp1 may be capable of generating the multipotent cardiovascular progenitor from ESCs in vitro.⁵