Deletion of PDK1 Caused Cardiac Malmorphogenesis and Heart Defects Due to Profound Protein Phosphorylation Changes Mediated by SHP2-Reference-Cited by-同舟云学术

Deletion of PDK1 Caused Cardiac Malmorphogenesis and Heart Defects Due to Profound Protein Phosphorylation Changes Mediated by SHP2

Published:2023-03-29 Issue:5 Volume:16 Page:1220-1231
ISSN:1937-5387
Container-title:Journal of Cardiovascular Translational Research
language:en
Short-container-title:J. of Cardiovasc. Trans. Res.

Author:

Luo Hongmei^ORCID,Yang Zhongzhou,Li Jie,Jin Hengwei,Jiang Mingyang,Shan Congjia

Funder

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Subject

Genetics (clinical),Cardiology and Cardiovascular Medicine,Pharmaceutical Science,Genetics,Molecular Medicine

Link

https://link.springer.com/content/pdf/10.1007/s12265-023-10380-y.pdf

Reference36 articles.

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3. Bruneau BG. The developmental genetics of congenital heart disease. Nature. 2008;451:943–8.

4. Kelly RG, Brown NA, Buckingham ME. The arterial pole of the mouse heart forms from Fgf10-expressing cells in pharyngeal mesoderm. Dev. 2001;1:435–40.

5. Plein A, Calmont A, Fantin A, Denti L, Anderson NA, Scambler PJ, Ruhrberg C. Neural crest–derived SEMA3C activates endothelial NRP1 for cardiac outflow tract septation. J Clin Investig. 2015;125(7):2661–76.

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