M
Mohammad Z. Hossain
Researcher at University of Hawaii
Publications - 13
Citations - 920
Mohammad Z. Hossain is an academic researcher from University of Hawaii. The author has contributed to research in topics: Platelet-derived growth factor receptor & Protein kinase C. The author has an hindex of 11, co-authored 12 publications receiving 905 citations.
Papers
More filters
Journal Article
Reversion of the neoplastic phenotype of human glioblastoma cells by connexin 43 (cx43)
TL;DR: It is concluded that the loss of cx43 expression may play a role in the development of human gliomas and that cx43 acts as a tumor suppressor gene to humanglioblastoma.
Journal ArticleDOI
Enhancement of gap junctional communication by retinoids correlates with their ability to inhibit neoplastic transformation.
Mohammad Z. Hossain,Lynne R. Wilkens,Parmender P. Mehta,Werner R. Loewenstein,John S. Bertram +4 more
TL;DR: It is proposed that much of the chemopreventive action of retinoids can be explained by the enhanced junctional communication of growth regulatory signals.
Journal ArticleDOI
Reduced connexin43 expression in high-grade human brain glioma cells
TL;DR: The role of cx43 in the development of human gliomas is investigated by analyzing the expression of this gap junction protein in glioma grades I–IV and its role in tumor cell growth is investigated.
Journal ArticleDOI
Platelet-derived growth factor-induced disruption of gap junctional communication and phosphorylation of connexin43 involves protein kinase C and mitogen-activated protein kinase
TL;DR: It is postulate that the activation of PKC and MAPK are required in PDGF‐mediated Cx43 phosphorylation and junctional closure and elimination of GJC recovery by cycloheximide was associated with a sustained activated‐MAPK level.
Journal ArticleDOI
Rapid disruption of gap junctional communication and phosphorylation of connexin43 by platelet‐derived growth factor in T51B rat liver epithelial cells expressing platelet‐derived growth factor receptor
TL;DR: A suitable cell system is described which is currently being utilized for the characterization of the PDGF signaling pathway responsible for the inhibition of GJC.