title: Activation of kinase phosphorylation by heat-shift and mild heat-shock.
abstract: Most cells activate intracellular signalling to recover from heat damage. An increase of temperature, known as HS (heat shock), induces two major signalling events: the transcriptional induction of HSPs (heat-shock proteins) and the activation of the MAPK (mitogen-activated protein kinase) cascade. We performed the present study to examine the effects of HS, induced by different experimental conditions, on various kinases [ERK (extracellular-signal-regulated kinase), JNK (c-Jun N-terminal kinase), p38, Akt, AMPK (AMP-activated protein kinase) and PKC (protein kinase C)]. We investigated by Western blot analysis the phosphorylation of MAPK as a measure of cellular responsiveness to heat shift (37°C) and mild HS (40°C) in different cell lines. The results of the study indicate that every cell line responded to heat shift, and to a greater extent to HS, increasing ERK and JNK phosphorylation, whereas variable effects on activation or inhibition of PKC, AMPK, Akt and p38 were observed. Besides the implications of intracellular signalling activated by heat variations, these data may be of technical relevance, indicating possible sources of error due to different experimental temperature conditions.
authors.affiliation: Institute of Neurobiology and Molecular Medicine, CNR, Via del Fosso di Fiorano 65, 00143 Rome, Italy.
authors.forename: Pamela
authors.initials: P
authors.lastname: Petrocchi
authors.forename: Stefania
authors.initials: S
authors.lastname: Quaresima
authors.forename: Maria Patrizia
authors.initials: MP
authors.lastname: Mongiardi
authors.forename: Cinzia
authors.initials: C
authors.lastname: Severini
authors.forename: Roberta
authors.initials: R
authors.lastname: Possenti
keywords: AMPK, AMP-activated protein kinase; CGC, cerebellar granule cell; CHO, Chinese-hamster ovary; ERK, extracellular-signal-regulated kinase; HS, heat shock; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; PKC, protein kinase C; cell culture; heat damage; signal transduction