scholarly journals Evidence that protein kinase Cα interacts with and regulates the glial glutamate transporter GLT-1

2005 ◽  
Vol 94 (5) ◽  
pp. 1180-1188 ◽  
Author(s):  
Marco I. González ◽  
Bala T. S. Susarla ◽  
Michael B. Robinson
Keyword(s):  
Protein Kinase ◽  
Glutamate Transporter ◽  
Glial Glutamate Transporter ◽  
Protein Kinase Cα

Antisense knockdown of the glial glutamate transporter GLT-1 exacerbates hippocampal neuronal damage following traumatic injury to rat brain

2001 ◽  
Vol 13 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Vemuganti L. Raghavendra Rao ◽  
Aclan Dogan ◽  
Kellie K. Bowen ◽  
Kathryn G. Todd ◽  
Robert J. Dempsey
Keyword(s):  
Rat Brain ◽  
Neuronal Damage ◽  
Traumatic Injury ◽  
Glutamate Transporter ◽  
Glial Glutamate Transporter ◽  
Antisense Knockdown

Loss of gap junctions in biliary atresia occurs simultaneously with declined expression of Protein kinase Cα

2015 ◽  
Vol 53 (01) ◽  
Author(s):  
JHK Andruszkow ◽  
S Groos ◽  
C Klaus ◽  
U Schneider ◽  
C Petersen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Gap Junctions ◽  
Biliary Atresia ◽  
Protein Kinase Cα

Transfection with Protein Kinase Cα Confers Increased Multidrug Resistance to MCF-7 Cells Expressing P-Glycoprotein

1991 ◽  
Vol 3 (6) ◽  
pp. 181-189 ◽  
Author(s):  
Gang Yu ◽  
Shakeel Ahmad ◽  
Angelo Aquino ◽  
Craig R. Fairchild ◽  
Jane B. Trepel ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Protein Kinase ◽  
P Glycoprotein ◽  
Protein Kinase Cα ◽  
Mcf 7

scholarly journals Novel Therapeutic Targets in Heart Failure: The Phospholipase Cβ1b–Shank3 Interface

2015 ◽  
Vol 7 ◽  
pp. CMT.S18480
Author(s):  
Elizabeth A. Woodcock ◽  
David R. Grubb
Keyword(s):  
Heart Failure ◽  
Protein Kinase ◽  
Inotropic Agents ◽  
Specific Enzyme ◽  
Pump Performance ◽  
New Class ◽  
Promising Target ◽  
Protein Kinase Cα ◽  
Myocyte Contractility ◽  
Contractile Performance

Inotropic agents are often used to improve the contractile performance of the failing myocardium, but this is often at a cost of increased myocardial ischemia and arrhythmia. Myocyte contractility depends on the release of Ca2+ from the sarcoplasmic reticulum, and this Ca2+ is subject to regulation by the phosphorylation status of phospholamban (PLN). Many currently used inotropic agents function by increasing the phosphorylation of PLN, but these also heighten the risk of ischemia. Another approach is to reduce the dephosphorylation of PLN, which can be achieved by inhibiting pathways upstream or downstream of the protein kinase Cα. Phospholipase Cβ1b is responsible for activating protein kinase Cα, and its activity is substantially heightened in failing myocardium. We propose phospholipase Cβ1b, a cardiac-specific enzyme, as a promising target for the development of a new class of inotropic agents. By reversing changes that accompany the transition to heart failure, it may be possible to provide well-tolerated improvement in pump performance.

scholarly journals Alcohol/Cholecystokinin-evoked Pancreatic Acinar Basolateral Exocytosis Is Mediated by Protein Kinase Cα Phosphorylation of Munc18c

2007 ◽  
Vol 282 (17) ◽  
pp. 13047-13058 ◽  
Author(s):  
Laura I. Cosen-Binker ◽  
Patrick P. L. Lam ◽  
Marcelo G. Binker ◽  
Joseph Reeve ◽  
Stephen Pandol ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase Cα

scholarly journals Phosphorylation by Protein Kinase Cα Regulates RalB Small GTPase Protein Activation, Subcellular Localization, and Effector Utilization

2012 ◽  
Vol 287 (18) ◽  
pp. 14827-14836 ◽  
Author(s):  
Timothy D. Martin ◽  
Natalia Mitin ◽  
Adrienne D. Cox ◽  
Jen Jen Yeh ◽  
Channing J. Der
Keyword(s):  
Protein Kinase ◽  
Subcellular Localization ◽  
Small Gtpase ◽  
Protein Activation ◽  
Protein Kinase Cα
Sign in / Sign up

Export Citation Format

Share Document