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Tip60- and Sirtuin 2-Regulated MARCKS Acetylation and Phosphorylation Are Required for Diabetic Embryopathy
UMB Dataset

UID: 60

Author(s): Penghua Yang*, Cheng Xu, E. Albert Reece, Xi Chen, Jianxiang Zhong, Min Zhan, Deborah J. Stumpo, Perry J. Blackshear, Peixin Yang * Corresponding Author
A high glucose level associated with maternal diabetes has been identified as a risk factor for fetal neural tube defects (NTD). The failure to successfully complete the complex neurulation process is possibly related to the loss of protection for cellular homeostasis resulting in organelle stress. Mitochondrial dysfunction and endoplasmic reticulum stress in the developing endothelium have been identified as significant components in diabetic embryopathy. Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) is a critical protein involved in fetal neural development. This study investigated the regulation and biological activity of MARCKS and its role in protecting neuroepithelial cell organelles during neurulation. Furthermore, the effects of the acetylation/phosphorylation/deacetylation of MARCKs by Tip60 and sirtuin 2 were examined with respect to the protein’s protective functionality. The dataset includes immunoblot/immunofluorescent/electronmicroscopy images and graphs.
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