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Rapid translocation and insertion of the epithelial Na+ channel in response to RhoA signaling.
J Biol Chem. 2006 Sep 08; 281(36):26520-7.JB

Abstract

Activity of the epithelial Na+ channel (ENaC) is limiting for Na+ absorption across many epithelia. Consequently, ENaC is a central effector impacting systemic blood volume and pressure. Two members of the Ras superfamily of small GTPases, K-Ras and RhoA, activate ENaC. K-Ras activates ENaC via a signaling pathway involving phosphatidylinositol 3-kinase and production of phosphatidylinositol 3,4,5-trisphosphate with the phospholipid directly interacting with the channel to increase open probability. How RhoA increases ENaC activity is less clear. Here we report that RhoA and K-Ras activate ENaC through independent signaling pathways and final mechanisms of action. Activation of RhoA signaling rapidly increases the membrane levels of ENaC likely by promoting channel insertion. This process dramatically increases functional ENaC current, resulting in tight spatial-temporal control of these channels. RhoA signals to ENaC via a transduction pathway, including the downstream effectors Rho kinase and phosphatidylinositol-4-phosphate 5-kinase. Phosphatidylinositol 4,5-biphosphate produced by activated phosphatidylinositol 4-phosphate 5-kinase may play a role in targeting vesicles containing ENaC to the plasma membrane.

Authors+Show Affiliations

Department of Physiology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16829523

Citation

Pochynyuk, Oleh, et al. "Rapid Translocation and Insertion of the Epithelial Na+ Channel in Response to RhoA Signaling." The Journal of Biological Chemistry, vol. 281, no. 36, 2006, pp. 26520-7.
Pochynyuk O, Medina J, Gamper N, et al. Rapid translocation and insertion of the epithelial Na+ channel in response to RhoA signaling. J Biol Chem. 2006;281(36):26520-7.
Pochynyuk, O., Medina, J., Gamper, N., Genth, H., Stockand, J. D., & Staruschenko, A. (2006). Rapid translocation and insertion of the epithelial Na+ channel in response to RhoA signaling. The Journal of Biological Chemistry, 281(36), 26520-7.
Pochynyuk O, et al. Rapid Translocation and Insertion of the Epithelial Na+ Channel in Response to RhoA Signaling. J Biol Chem. 2006 Sep 8;281(36):26520-7. PubMed PMID: 16829523.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rapid translocation and insertion of the epithelial Na+ channel in response to RhoA signaling. AU - Pochynyuk,Oleh, AU - Medina,Jorge, AU - Gamper,Nikita, AU - Genth,Harald, AU - Stockand,James D, AU - Staruschenko,Alexander, Y1 - 2006/07/07/ PY - 2006/7/11/pubmed PY - 2006/12/19/medline PY - 2006/7/11/entrez SP - 26520 EP - 7 JF - The Journal of biological chemistry JO - J. Biol. Chem. VL - 281 IS - 36 N2 - Activity of the epithelial Na+ channel (ENaC) is limiting for Na+ absorption across many epithelia. Consequently, ENaC is a central effector impacting systemic blood volume and pressure. Two members of the Ras superfamily of small GTPases, K-Ras and RhoA, activate ENaC. K-Ras activates ENaC via a signaling pathway involving phosphatidylinositol 3-kinase and production of phosphatidylinositol 3,4,5-trisphosphate with the phospholipid directly interacting with the channel to increase open probability. How RhoA increases ENaC activity is less clear. Here we report that RhoA and K-Ras activate ENaC through independent signaling pathways and final mechanisms of action. Activation of RhoA signaling rapidly increases the membrane levels of ENaC likely by promoting channel insertion. This process dramatically increases functional ENaC current, resulting in tight spatial-temporal control of these channels. RhoA signals to ENaC via a transduction pathway, including the downstream effectors Rho kinase and phosphatidylinositol-4-phosphate 5-kinase. Phosphatidylinositol 4,5-biphosphate produced by activated phosphatidylinositol 4-phosphate 5-kinase may play a role in targeting vesicles containing ENaC to the plasma membrane. SN - 0021-9258 UR - https://www.unboundmedicine.com/medline/citation/16829523/Rapid_translocation_and_insertion_of_the_epithelial_Na+_channel_in_response_to_RhoA_signaling_ L2 - http://www.jbc.org/cgi/pmidlookup?view=long&pmid=16829523 DB - PRIME DP - Unbound Medicine ER -