Literature DB >> 8848099

Stress activated protein kinases, a novel family of mitogen-activated protein kinases, are heterogeneously expressed in the adult rat brain and differentially distributed from extracellular-signal-regulated protein kinases.

R Carletti1, S Tacconi, E Bettini, F Ferraguti.   

Abstract

Mitogen-activated protein kinases are important mediators of signal transduction from the cell surface to the nucleus and their activation has been implicated in a wide array of physiological processes. The extracellular-signal-regulated kinases are the archetypal and best studied members of the mitogen activated protein kinases. Recently, additional subgroups of mitogen activated protein kinases have been identified which exhibit distinct regulatory elements, substrate specificity and respond to diverse extracellular stimuli. Among these newly identified protein kinases are the rat stress-activated protein kinases. Despite a rapidly expanding literature on the biochemical properties of stress-activated protein kinases no anatomical data are yet available. In the present study, we have investigated the regional distribution of messenger RNA transcripts for stress-activated protein kinases in the adult rat central nervous system and compared this distribution to that observed for extracellular-signal-regulated kinases. Intense labelling for stress-activated protein kinases could be detected in discrete brain areas with high levels in hippocampus, neocortex and some nuclei of the brain stem. The apparent hybridization signal appeared to be selectively neuronal. Stress-activated protein kinases and extracellular-signal-regulated kinases hybridization patterns appeared generally dissimilar although a certain degree of co-expression in some brain areas, such as the hippocampal formation, could be observed. These results reveal an extreme complexity in the mitogen-activated protein kinase signalling pathway and suggest the existence of parallel mitogen-activated protein kinase cascades that can be activated independently or in some cases simultaneously, by extracellular stimuli.

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Year:  1995        PMID: 8848099     DOI: 10.1016/0306-4522(95)00284-p

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  7 in total

1.  In vivo expression and regulation of Elk-1, a target of the extracellular-regulated kinase signaling pathway, in the adult rat brain.

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2.  Intracellular signaling MAPK pathway after cerebral ischemia-reperfusion injury.

Authors:  Maria Kovalska; Libusa Kovalska; Martina Pavlikova; Maria Janickova; Katarina Mikuskova; Marian Adamkov; Peter Kaplan; Zuzana Tatarkova; Jan Lehotsky
Journal:  Neurochem Res       Date:  2012-03-20       Impact factor: 3.996

3.  Detection of MAPK signal transduction proteins in an ischemia/reperfusion model of mouse intestine using in vivo cryotechnique.

Authors:  Jiaorong Chen; Nobuo Terada; Yurika Saitoh; Zheng Huang; Nobuhiko Ohno; Shinichi Ohno
Journal:  Histochem Cell Biol       Date:  2013-06-23       Impact factor: 4.304

4.  Dynamic regulation of c-Jun N-terminal kinase activity in mouse brain by environmental stimuli.

Authors:  X Xu; J Raber; D Yang; B Su; L Mucke
Journal:  Proc Natl Acad Sci U S A       Date:  1997-11-11       Impact factor: 11.205

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Review 6.  MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.

Authors:  Nicola Origlia; Ottavio Arancio; Luciano Domenici; Shirley ShiDu Yan
Journal:  Expert Rev Neurother       Date:  2009-11       Impact factor: 4.618

7.  Lasting N-terminal phosphorylation of c-Jun and activation of c-Jun N-terminal kinases after neuronal injury.

Authors:  T Herdegen; F X Claret; T Kallunki; A Martin-Villalba; C Winter; T Hunter; M Karin
Journal:  J Neurosci       Date:  1998-07-15       Impact factor: 6.167

  7 in total

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