M
Minzhen He
Researcher at Rutgers University
Publications - 20
Citations - 1766
Minzhen He is an academic researcher from Rutgers University. The author has contributed to research in topics: Gene expression & Chromatin. The author has an hindex of 9, co-authored 17 publications receiving 1613 citations. Previous affiliations of Minzhen He include University of Medicine and Dentistry of New Jersey.
Papers
More filters
Journal ArticleDOI
Downregulation of MiR-199a Derepresses Hypoxia-Inducible Factor-1α and Sirtuin 1 and Recapitulates Hypoxia Preconditioning in Cardiac Myocytes
Shweta Rane,Minzhen He,Danish Sayed,Himanshu Vashistha,Ashwani Malhotra,Junichi Sadoshima,Dorothy E. Vatner,Stephen F. Vatner,Maha Abdellatif +8 more
TL;DR: It is reported here that miR-199a is acutely downregulated in cardiac myocytes on a decline in oxygen tension and this reduction is required for the rapid upregulation of its target, hypoxia-inducible factor (Hif)-1α.
Journal ArticleDOI
MicroRNA-21 Targets Sprouty2 and Promotes Cellular Outgrowths
Danish Sayed,Shweta Rane,Jacqueline Lypowy,Minzhen He,Ieng-Yi Chen,Himanshu Vashistha,Lin Yan,Ashwani Malhotra,Dorothy E. Vatner,Maha Abdellatif +9 more
TL;DR: It is proposed that an increase in miR-21 enhances the formation of various types of cellular protrusions through directly targeting and down-regulating SPRY2.
Journal ArticleDOI
MicroRNA-21 Is a Downstream Effector of AKT That Mediates Its Antiapoptotic Effects via Suppression of Fas Ligand
TL;DR: It is demonstrated here for the first time that miR-21 is positively regulated via an AKT-dependent pathway, which is depressed during prolonged hypoxia, and identified a unique aspect of the function of AKT by which it inhibits apoptosis through mi R-21-dependent suppression of FasL.
Journal ArticleDOI
Mitochondrial complex II is a source of the reserve respiratory capacity that is regulated by metabolic sensors and promotes cell survival
TL;DR: The results show that activation of metabolic sensors, including pyruvate dehydrogenase and AMP-dependent kinase, increases cardiac myocyte RRC via a Sirt3-dependent mechanism, and for the first time, it is shown that metabolic sensors via SIRT3 maximize the cellular RRC through activating cII, which enhances cell survival after hypoxia.
Journal ArticleDOI
An antagonism between the AKT and beta-adrenergic signaling pathways mediated through their reciprocal effects on miR-199a-5p.
TL;DR: Activation of beta-adrenergic signaling counteracts the survival effects of the AKT pathway via upregulating miR-199a-5p and their role in myocyte survival during hypoxia is delineated.