Protein Kinase C
Insulin-like growth factor-I inhibits transcriptional responses of transforming growth factor-beta by phosphatidylinositol 3-kinase/Akt-dependent suppression of the activation of Smad3 but not Smad2.
In PLoS ONE, 2002
... (Abcam, ab15309), IGFR (Cell Signaling, 111A9), EGFR, (Santacruz, sc 03, 1005), Glucose-6-P dehydrogenase (Abcam, ab34436), Protein Kinase C-zeta (Cell signaling, ab51157), P-PKC-zeta (Abcam, ab76129), ...
Protein Kinase C
Apocynin prevents mitochondrial burdens, microglial activation, and pro-apoptosis induced by a toxic dose of methamphetamine in the striatum of mice via inhibition of p47phox activation by ERK.
South Korea. In J Neuroinflammation, Dec 2015
METHODS: We examined changes in mitogen-activated protein kinases (MAPKs), mitochondrial function [i.e., mitochondrial membrane potential, intramitochondrial Ca(2+) accumulation, mitochondrial oxidative burdens, mitochondrial superoxide dismutase expression, and mitochondrial translocation of the cleaved form of protein kinase C delta type (cleaved PKCδ)], microglial activity, and pro-apoptotic changes [i.e., cytosolic cytochrome c release, cleaved caspase 3, and terminal deoxynucleotidyl transferase dUDP nick-end labeling (TUNEL) positive populations] after a neurotoxic dose of MA in the striatum of mice to achieve a better understanding of the effects of apocynin, a non-specific PHOX inhibitor, or genetic inhibition of p47phox (by using p47phox knockout mice or p47phox antisense oligonucleotide) against MA-induced dopaminergic neurotoxicity.
Transcriptional regulation of hepatic lipogenesis.
Berkeley, United States. In Nat Rev Mol Cell Biol, Nov 2015
After feeding, high blood glucose and insulin levels activate lipogenic genes through several pathways, including the DNA-dependent protein kinase (DNA-PK), atypical protein kinase C (aPKC) and AKT-mTOR pathways.
Mobile Phone Radiation: Physiological & Pathophysiologcal Considerations.
In Indian J Physiol Pharmacol, Apr 2015
Pathophysiological mechanisms of interaction of EMR at plasma membrane are calcium efflux from cell membranes, increased expression of stress proteins, influence on channels/gap junctions in cell membrane, overproduction of reactive oxygen species, ornithine decarboxylase activation, reduction in melatonin levels, decrease in protein kinase C activity, damage to DNA and change in gene expression in brain cells and altered blood-brain barrier.