MAP kinases and the adaptive response to hypertonicity: functional preservation from yeast to mammals

The adaptation to hypertonicity in mammalian cells is driven by multiple signaling pathways that include p38 kinase, Fyn, the catalytic subunit of PKA, ATM, and JNK2. In addition to the well-characterized tonicity enhancer (TonE)-TonE binding protein interaction, other transcription factors (and the...

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Bibliographic Details
Published inAmerican journal of physiology. Renal physiology Vol. 287; no. 6; pp. F1102 - F1110
Main Authors Sheikh-Hamad, David, Gustin, Michael C
Format Journal Article
LanguageEnglish
Published United States 01.12.2004
Subjects
Animals
Humans
Hypertonic Solutions
Kidney - physiology
Kidney Concentrating Ability
Mitogen-Activated Protein Kinases - physiology
Osmolar Concentration
p38 Mitogen-Activated Protein Kinases - physiology
Saccharomyces cerevisiae - physiology
Saccharomyces cerevisiae Proteins - physiology
Water-Electrolyte Balance - physiology
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Summary:The adaptation to hypertonicity in mammalian cells is driven by multiple signaling pathways that include p38 kinase, Fyn, the catalytic subunit of PKA, ATM, and JNK2. In addition to the well-characterized tonicity enhancer (TonE)-TonE binding protein interaction, other transcription factors (and their respective cis elements) can potentially respond to hypertonicity. This review summarizes the current knowledge about the signaling pathways that regulate the adaptive response to osmotic stress and discusses new insights from yeast that could be relevant to the osmostress response in mammals.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ObjectType-Review-2
ISSN:1931-857X
1522-1466
DOI:10.1152/ajprenal.00225.2004