RGD Reference Report - Dephosphorylation of Akt in C6 cells grown in serum-free conditions corresponds with redistribution of p85/PI3K to the nucleus. - Rat Genome Database

Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models   new Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources

Dephosphorylation of Akt in C6 cells grown in serum-free conditions corresponds with redistribution of p85/PI3K to the nucleus.

Authors: Sephton, CF  Mousseau, DD 
Citation: Sephton CF and Mousseau DD, J Neurosci Res. 2008 Feb 15;86(3):675-82.
RGD ID: 4108495
Pubmed: PMID:17918740   (View Abstract at PubMed)
DOI: DOI:10.1002/jnr.21516   (Journal Full-text)

Withdrawal of serum from cell cultures constitutes a useful model for the study of mechanisms involved in the regulation of Akt function in vitro. However, there have been several reports of changes in Akt activity that are not fully explained by the current model of phosphatidylinositol 3'-kinase (PI3K)/Akt signaling. We demonstrate the expected loss of Akt phosphorylation in C6 glioma cells cultured in serum-free conditions, yet we also observed a paradoxical increase in PI3K-lipid kinase activity in the same cultures. These events corresponded with relocalization of p85, the regulatory subunit of PI3K, to the perinuclear region and a local increase in PI3K-lipid kinase products. Treatment with platelet-derived growth factor (PDGF) maintained the association between p85 and the PDGF receptor during serum withdrawal and restored PI3K-lipid production at the plasma membrane. Although this protected Akt from dephosphorylation, it only slightly reversed cell-cycle arrest. These effects were not sensitive to treatment with epidermal growth factor, thus precluding a generalized role for growth factors. Our data suggest that loss of growth factor signaling, including PDGF signaling, may disrupt recruitment and/or anchoring of an active p85(PI3K) complex at the plasma membrane during serum withdrawal, which could account for the concurrent loss of Akt function.

Objects referenced in this article
Gene Pik3r1 phosphoinositide-3-kinase regulatory subunit 1 Rattus norvegicus

Additional Information