PMID- 9261171
OWN - NLM
STAT- MEDLINE
DCOM- 19970915
LR  - 20211203
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 272
IP  - 34
DP  - 1997 Aug 22
TI  - Regulation of protein kinase B in rat adipocytes by insulin, vanadate, and 
      peroxovanadate. Membrane translocation in response to peroxovanadate.
PG  - 21520-6
AB  - Protein kinase B (PKB) (also referred to as RAC/Akt kinase) has been shown to be 
      controlled by various growth factors, including insulin, using cell lines and 
      transfected cells. However, information is so far scarce regarding its regulation 
      in primary insulin-responsive cells. We have therefore used isolated rat 
      adipocytes to examine the mechanisms, including membrane translocation, whereby 
      insulin and the insulin-mimicking agents vanadate and peroxovanadate control PKB. 
      Stimulation of adipocytes with insulin, vanadate, or peroxovanadate caused 
      decreased PKB mobility on sodium dodecyl sulfate-polyacrylamide gels, indicative 
      of increased phosphorylation, which correlated with an increase in kinase 
      activity detected with the peptide KKRNRTLTK. This peptide was found to detect 
      activated PKB selectively in crude cytosol and partially purified cytosol 
      fractions from insulin-stimulated adipocytes. The decrease in electrophoretic 
      mobility and activation of PKB induced by insulin was reversed both in vitro by 
      treatment of the enzyme with alkaline phosphatase and in the intact adipocyte 
      upon removal of insulin or addition of the phosphatidylinositol 3-kinase (PI 
      3-kinase) inhibitor wortmannin. Significant translocation of PKB to membranes 
      could not be demonstrated after insulin stimulation, but peroxovanadate, which 
      appeared to activate PI 3-kinase to a higher extent than insulin, induced 
      substantial translocation. The translocation was prevented by wortmannin, 
      suggesting that PI 3-kinase and/or the 3-phosphorylated phosphoinositides 
      generated by PI 3-kinase are indeed involved in the membrane targeting of PKB.
FAU - Wijkander, J
AU  - Wijkander J
AD  - Section for Molecular Signaling, Department of Cell and Molecular Biology, Lund 
      University, S-221 00 Lund, Sweden. jonny wijkander@medkem.lu.se
FAU - Holst, L S
AU  - Holst LS
FAU - Rahn, T
AU  - Rahn T
FAU - Resjo, S
AU  - Resjo S
FAU - Castan, I
AU  - Castan I
FAU - Manganiello, V
AU  - Manganiello V
FAU - Belfrage, P
AU  - Belfrage P
FAU - Degerman, E
AU  - Degerman E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Insulin)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (peroxovanadate)
RN  - 3WHH0066W5 (Vanadates)
RN  - EC 2.7.11.1 (Akt1 protein, rat)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Adipocytes/*enzymology
MH  - Animals
MH  - Cell Compartmentation
MH  - Cell Membrane/enzymology
MH  - Cytosol/enzymology
MH  - Enzyme Activation/drug effects
MH  - Insulin/*physiology
MH  - Male
MH  - *Protein Serine-Threonine Kinases
MH  - Proto-Oncogene Proteins/*metabolism
MH  - Proto-Oncogene Proteins c-akt
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Vanadates/*pharmacology
EDAT- 1997/08/22 00:00
MHDA- 1997/08/22 00:01
CRDT- 1997/08/22 00:00
PHST- 1997/08/22 00:00 [pubmed]
PHST- 1997/08/22 00:01 [medline]
PHST- 1997/08/22 00:00 [entrez]
AID - S0021-9258(19)65786-8 [pii]
AID - 10.1074/jbc.272.34.21520 [doi]
PST - ppublish
SO  - J Biol Chem. 1997 Aug 22;272(34):21520-6. doi: 10.1074/jbc.272.34.21520.