The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death.

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The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death. / Pedersen, Stine Falsig.

In: Pflügers Archiv: European Journal of Physiology, Vol. 452, No. 3, 2006, p. 249-59.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Pedersen, SF 2006, 'The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death.', Pflügers Archiv: European Journal of Physiology, vol. 452, no. 3, pp. 249-59. https://doi.org/10.1007/s00424-006-0044-y

APA

Pedersen, S. F. (2006). The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death. Pflügers Archiv: European Journal of Physiology, 452(3), 249-59. https://doi.org/10.1007/s00424-006-0044-y

Vancouver

Pedersen SF. The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death. Pflügers Archiv: European Journal of Physiology. 2006;452(3):249-59. https://doi.org/10.1007/s00424-006-0044-y

Author

Pedersen, Stine Falsig. / The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death. In: Pflügers Archiv: European Journal of Physiology. 2006 ; Vol. 452, No. 3. pp. 249-59.

Bibtex

@article{93d4e8a096d411dd86a6000ea68e967b,
title = "The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death.",
abstract = "The ubiquitous plasma membrane Na+/H+ exchanger NHE1 is highly conserved across vertebrate species and is extensively characterized as a major membrane transport mechanism in the regulation of cellular pH and volume. In recent years, the understanding of the role of NHE1 in regulating cell function has expanded from one of a household protein involved in ion homeostasis to that of a multifaceted regulator and/or modulator of a wide variety of cell functions. NHE1 plays pivotal roles in response to a number of important physiological stress conditions which, in addition to cell shrinkage and acidification, include hypoxia and mechanical stimuli, such as cell stretch. It has recently become apparent that NHE1-mediated modulation of, e.g., cell migration, morphology, proliferation, and death results not only from NHE1-mediated changes in pHi, cell volume, and/or [Na+]i, but also from direct protein-protein interactions with, e.g., ezrin/radixin/moesin (ERM) proteins and regulation of cellular signaling events, including the activity of mitogen-activated protein kinases (MAPKs) and Akt/protein kinase B (PKB). The aim of this review is to present and discuss new findings implicating NHE1 activation as a central signaling event activated by stress conditions and modulating cell proliferation and death. The pathophysiological importance of NHE1 in modulating the balance between cell proliferation and cell death in cancer and in ischemia/severe hypoxia will also be briefly addressed.",
author = "Pedersen, {Stine Falsig}",
note = "Keywords: Animals; Anoxia; Cell Death; Cell Proliferation; Cell Size; Erythrocytes; Neoplasms; Osmotic Pressure; Phosphotransferases; Signal Transduction; Sodium-Hydrogen Antiporter; Stress",
year = "2006",
doi = "10.1007/s00424-006-0044-y",
language = "English",
volume = "452",
pages = "249--59",
journal = "Pfl{\"u}gers Archiv - European Journal of Physiology",
issn = "0031-6768",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - The Na+/H+ exchanger NHE1 in stress-induced signal transduction: implications for cell proliferation and cell death.

AU - Pedersen, Stine Falsig

N1 - Keywords: Animals; Anoxia; Cell Death; Cell Proliferation; Cell Size; Erythrocytes; Neoplasms; Osmotic Pressure; Phosphotransferases; Signal Transduction; Sodium-Hydrogen Antiporter; Stress

PY - 2006

Y1 - 2006

N2 - The ubiquitous plasma membrane Na+/H+ exchanger NHE1 is highly conserved across vertebrate species and is extensively characterized as a major membrane transport mechanism in the regulation of cellular pH and volume. In recent years, the understanding of the role of NHE1 in regulating cell function has expanded from one of a household protein involved in ion homeostasis to that of a multifaceted regulator and/or modulator of a wide variety of cell functions. NHE1 plays pivotal roles in response to a number of important physiological stress conditions which, in addition to cell shrinkage and acidification, include hypoxia and mechanical stimuli, such as cell stretch. It has recently become apparent that NHE1-mediated modulation of, e.g., cell migration, morphology, proliferation, and death results not only from NHE1-mediated changes in pHi, cell volume, and/or [Na+]i, but also from direct protein-protein interactions with, e.g., ezrin/radixin/moesin (ERM) proteins and regulation of cellular signaling events, including the activity of mitogen-activated protein kinases (MAPKs) and Akt/protein kinase B (PKB). The aim of this review is to present and discuss new findings implicating NHE1 activation as a central signaling event activated by stress conditions and modulating cell proliferation and death. The pathophysiological importance of NHE1 in modulating the balance between cell proliferation and cell death in cancer and in ischemia/severe hypoxia will also be briefly addressed.

AB - The ubiquitous plasma membrane Na+/H+ exchanger NHE1 is highly conserved across vertebrate species and is extensively characterized as a major membrane transport mechanism in the regulation of cellular pH and volume. In recent years, the understanding of the role of NHE1 in regulating cell function has expanded from one of a household protein involved in ion homeostasis to that of a multifaceted regulator and/or modulator of a wide variety of cell functions. NHE1 plays pivotal roles in response to a number of important physiological stress conditions which, in addition to cell shrinkage and acidification, include hypoxia and mechanical stimuli, such as cell stretch. It has recently become apparent that NHE1-mediated modulation of, e.g., cell migration, morphology, proliferation, and death results not only from NHE1-mediated changes in pHi, cell volume, and/or [Na+]i, but also from direct protein-protein interactions with, e.g., ezrin/radixin/moesin (ERM) proteins and regulation of cellular signaling events, including the activity of mitogen-activated protein kinases (MAPKs) and Akt/protein kinase B (PKB). The aim of this review is to present and discuss new findings implicating NHE1 activation as a central signaling event activated by stress conditions and modulating cell proliferation and death. The pathophysiological importance of NHE1 in modulating the balance between cell proliferation and cell death in cancer and in ischemia/severe hypoxia will also be briefly addressed.

U2 - 10.1007/s00424-006-0044-y

DO - 10.1007/s00424-006-0044-y

M3 - Journal article

C2 - 16586098

VL - 452

SP - 249

EP - 259

JO - Pflügers Archiv - European Journal of Physiology

JF - Pflügers Archiv - European Journal of Physiology

SN - 0031-6768

IS - 3

ER -

ID: 6511451