Loss of zinc finger protein multitype 1 (Zfpm1) activity resulted in over-activation of Neuregulin-ErbB signaling and abnormally elevated cardiomyocyte proliferation.
we observed the activation of Notch signaling in cardiomyocytes adjacent to those undergoing apical constriction and we showed that this activation is positively regulated by Neuregulin signaling.
these results suggest that Nrg1 is not the primary effector of trabeculation and/or that other EGF-like ligand(s) activates the ErbB2/ErbB4 pathway either through functioning as the primary ligand or acting in a redundant manner. Overall our work provides an example of cross-species differences in EGF family member requirements for an evolutionary conserved process.
Notch1 activation induces expression of ephrin b2a (efnb2a) and neuregulin 1 (nrg1) in the endocardium to promote trabeculation and forced Notch activation in the absence of cardiac contraction rescues efnb2a and nrg1 expression
These results demonstrate that Nrg1 type III is an essential signal that controls Schwann cell migration to ensure that these glia are present in the correct numbers and positions in developing nerves.
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