PMID:10772775

Citation	Maroni, P, Bendinelli, P, Zuccorononno, C, Schiaffonati, L and Piccoletti, R (2000) Cellular signalling after in vivo heat shock in the liver. Cell Biol. Int. 24:145-52
Abstract	In an experimental model of in vivo hyperthermia, we investigated the involvement of a number of signalling events in rat liver. We report that in vivo heat shock causes a powerful activation of c-Jun N-terminal kinase and p38 kinase but does not trigger poly(ADP-ribose) polymerase cleavage, a signature event of apoptosis. Among the upstream regulators of the kinases, we show that stress-activated protein kinase/extracellular signal-regulated kinase/nitrogen-activated protein kinase kinase 4 SEK1/MKK4 is not involved whereas MKK3 and/or MKK6 are activated. PAK activity displays a transient rise, whereas GCK does not change. PI3-kinase activity increases in anti-phosphotyrosine immunoprecipitates, suggesting a tyrosine kinase-dependent induction mechanism, and the co-immunoprecipitation of PI3-kinase with p60 Src kinase supports the involvement of this latter. GSK3, which may act downstream to PI3-kinase through AKT, undergoes hyperphosphorylation, thus playing a possible role in the protection from apoptosis and in the modulation of heat-shock transcription factor activity.
Links	PubMed Online version:10.1006/cbir.1999.0493
Keywords	Animals; Heat-Shock Response/physiology; Liver/enzymology; Male; Mitogen-Activated Protein Kinase 8; Mitogen-Activated Protein Kinases/metabolism; Phosphatidylinositol 3-Kinases/metabolism; Poly(ADP-ribose) Polymerases/metabolism; Rats; Rats, Wistar; Signal Transduction/physiology; Up-Regulation; p38 Mitogen-Activated Protein Kinases
edit table

Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
RAT:MK08	involved_in	GO:0009408: response to heat	ECO:0000314: direct assay evidence used in manual assertion		P		Seeded From UniProt	complete

References

See Help:References for how to manage references in GONUTS.