basal flux of Akt in the mitochondria is mediated by heat shock protein 90

Akt is a known client protein of heat shock protein 90 (HSP90). We have found that HSP90 is responsible for Akt accumulation in the mitochondria in unstimulated cells. Treatment of SH-SY5Y neuroblastoma cells and human embryonic kidney cells with the HSP90 inhibitors novobiocin and geldanamycin caus...

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Veröffentlicht in:	Journal of neurochemistry 2009-03, Vol.108 (5), p.1289-1299
Hauptverfasser:	Barksdale, Keri A, Bijur, Gautam N
Format:	Artikel
Sprache:	eng
Schlagworte:	Ageing, cell death Akt Animals Benzoquinones - pharmacology Biochemistry Biological and medical sciences Cell Line Cell physiology Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology glycogen synthase kinase-3β heat shock protein 90 Heat shock proteins HSP90 Heat-Shock Proteins - antagonists & inhibitors HSP90 Heat-Shock Proteins - metabolism Humans Inhibitor drugs Injections, Intraventricular - methods insulin-like growth factor-1 Intercellular Signaling Peptides and Proteins - pharmacology Lactams, Macrocyclic - pharmacology Medical sciences Mice Mice, Inbred C57BL Microscopy, Electron, Transmission - methods Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondria - ultrastructure Molecular and cellular biology Neuroblastoma - ultrastructure Neurology Novobiocin - pharmacology Oncogene Protein v-akt - metabolism phosphatidylinositol 3 kinase Pyruvate Dehydrogenase (Lipoamide) - metabolism Ribonucleic acid RNA RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Transfection - methods Tumors of the nervous system. Phacomatoses
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