scispace - formally typeset
J

James R. Van Brocklyn

Researcher at Ohio State University

Publications -  45
Citations -  5549

James R. Van Brocklyn is an academic researcher from Ohio State University. The author has contributed to research in topics: Receptor & Sphingosine-1-phosphate. The author has an hindex of 32, co-authored 45 publications receiving 5357 citations. Previous affiliations of James R. Van Brocklyn include Max Delbrück Center for Molecular Medicine & University of Connecticut Health Center.

Papers
More filters
Journal ArticleDOI

Dual Actions of Sphingosine-1-Phosphate: Extracellular through the Gi-coupled Receptor Edg-1 and Intracellular to Regulate Proliferation and Survival

TL;DR: Sphingosine-1-phosphate is a prototype for a novel class of lipid mediators that act both extracellularly as ligands for cell surface receptors and intracellulary as second messengers.
Journal ArticleDOI

MicroRNA-451 regulates LKB1/AMPK signaling and allows adaptation to metabolic stress in glioma cells.

TL;DR: Overexpression of miR-451 sensitized cells to glucose deprivation, suggesting that its downregulation is necessary for robust activation of LKB1 in response to metabolic stress, and this may represent a fundamental mechanism that contributes to cellular adaptation in Response to altered energy availability.
Journal ArticleDOI

Sphingosine 1-Phosphate Stimulates Cell Migration through a Gi-coupled Cell Surface Receptor POTENTIAL INVOLVEMENT IN ANGIOGENESIS

TL;DR: The results suggest that SPP may play a role in angiogenesis through binding to endothelial cell Gi-coupled SPP receptors and checkerboard analysis indicated that sphingosine 1-phosphate stimulates both chemotaxis and chemokinesis.
Journal ArticleDOI

Sphingosine kinase-1 expression correlates with poor survival of patients with glioblastoma multiforme: roles of sphingosine kinase isoforms in growth of glioblastoma cell lines.

TL;DR: Surprisingly, RNA interference to knockdown SphK2 expression inhibited glioblastoma cell proliferation more potently than did SphK1 knockdown, and SphK knockdown prevented cells from exiting G1 phase of the cell cycle and marginally increased apoptosis.