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

Am J Physiol Renal Physiol. 2004 Dec;287(6):F1102-10. doi: 10.1152/ajprenal.00225.2004.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Humans
  • Hypertonic Solutions
  • Kidney / physiology
  • Kidney Concentrating Ability
  • Mitogen-Activated Protein Kinases / physiology*
  • Osmolar Concentration
  • Saccharomyces cerevisiae / physiology
  • Saccharomyces cerevisiae Proteins / physiology
  • Water-Electrolyte Balance / physiology*
  • p38 Mitogen-Activated Protein Kinases / physiology

Substances

  • Hypertonic Solutions
  • Saccharomyces cerevisiae Proteins
  • HOG1 protein, S cerevisiae
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases