Differential effects of protein kinase C on the levels of epithelial Na+ channel subunit proteins

James D Stockand, B. Hui-Fang, J. Schenck, B. Malik, P. Middleton, L. E. Schlanger, D. C. Eaton

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

Original languageEnglish
Pages (from-to)25760-25765
Number of pages6
JournalJournal of Biological Chemistry
Volume275
Issue number33
DOIs
StatePublished - Aug 18 2000

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Epithelial Sodium Channels
Protein Subunits
Protein Kinase C
Chemical activation
Protein C Inhibitor
Protein Kinase Inhibitors
Proteins

ASJC Scopus subject areas

  • Biochemistry

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Stockand, J. D., Hui-Fang, B., Schenck, J., Malik, B., Middleton, P., Schlanger, L. E., & Eaton, D. C. (2000). Differential effects of protein kinase C on the levels of epithelial Na+ channel subunit proteins. Journal of Biological Chemistry, 275(33), 25760-25765. https://doi.org/10.1074/jbc.M003615200

Differential effects of protein kinase C on the levels of epithelial Na+ channel subunit proteins. / Stockand, James D; Hui-Fang, B.; Schenck, J.; Malik, B.; Middleton, P.; Schlanger, L. E.; Eaton, D. C.

In: Journal of Biological Chemistry, Vol. 275, No. 33, 18.08.2000, p. 25760-25765.

Research output: Contribution to journalArticle

Stockand, JD, Hui-Fang, B, Schenck, J, Malik, B, Middleton, P, Schlanger, LE & Eaton, DC 2000, 'Differential effects of protein kinase C on the levels of epithelial Na+ channel subunit proteins', Journal of Biological Chemistry, vol. 275, no. 33, pp. 25760-25765. https://doi.org/10.1074/jbc.M003615200
Stockand, James D ; Hui-Fang, B. ; Schenck, J. ; Malik, B. ; Middleton, P. ; Schlanger, L. E. ; Eaton, D. C. / Differential effects of protein kinase C on the levels of epithelial Na+ channel subunit proteins. In: Journal of Biological Chemistry. 2000 ; Vol. 275, No. 33. pp. 25760-25765.
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abstract = "Regulation of epithelial Na+ channel (ENaC) subunit levels by protein kinase C (PKC) was investigated in A6 cells. PKC activation altered ENaC subunit levels, differentially decreasing the levels of both β and γ, but not αENaC. Temporal regulation of β and γENaC by PKC differed; γENaC decreased with a time constant of3.7 ± 1.0 h, whereas βENaC decreased in 13.9 ±3.0h. Activation of PKC also resulted in a decrease in trans-epithelial Na+ reabsorption for up to 48h. PMA activation of PKC resulted in negative feedback inhibition of PKC protein levels beginning within 4h. Both β and γENaC levels, as well as transport tended toward pretreatment values after 48 h of PMA treatment. PKC inhibitors attenuated the effects of PMA on ENaC subunit levels and Na+ transport. These results directly show for the first time that PKC differentially regulates ENaC subunit levels by decreasing the levels of β and γ but not αENaC protein. These results imply a PKC-dependent, long term decrease in Na+ reabsorption.",
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AU - Hui-Fang, B.

AU - Schenck, J.

AU - Malik, B.

AU - Middleton, P.

AU - Schlanger, L. E.

AU - Eaton, D. C.

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N2 - Regulation of epithelial Na+ channel (ENaC) subunit levels by protein kinase C (PKC) was investigated in A6 cells. PKC activation altered ENaC subunit levels, differentially decreasing the levels of both β and γ, but not αENaC. Temporal regulation of β and γENaC by PKC differed; γENaC decreased with a time constant of3.7 ± 1.0 h, whereas βENaC decreased in 13.9 ±3.0h. Activation of PKC also resulted in a decrease in trans-epithelial Na+ reabsorption for up to 48h. PMA activation of PKC resulted in negative feedback inhibition of PKC protein levels beginning within 4h. Both β and γENaC levels, as well as transport tended toward pretreatment values after 48 h of PMA treatment. PKC inhibitors attenuated the effects of PMA on ENaC subunit levels and Na+ transport. These results directly show for the first time that PKC differentially regulates ENaC subunit levels by decreasing the levels of β and γ but not αENaC protein. These results imply a PKC-dependent, long term decrease in Na+ reabsorption.

AB - Regulation of epithelial Na+ channel (ENaC) subunit levels by protein kinase C (PKC) was investigated in A6 cells. PKC activation altered ENaC subunit levels, differentially decreasing the levels of both β and γ, but not αENaC. Temporal regulation of β and γENaC by PKC differed; γENaC decreased with a time constant of3.7 ± 1.0 h, whereas βENaC decreased in 13.9 ±3.0h. Activation of PKC also resulted in a decrease in trans-epithelial Na+ reabsorption for up to 48h. PMA activation of PKC resulted in negative feedback inhibition of PKC protein levels beginning within 4h. Both β and γENaC levels, as well as transport tended toward pretreatment values after 48 h of PMA treatment. PKC inhibitors attenuated the effects of PMA on ENaC subunit levels and Na+ transport. These results directly show for the first time that PKC differentially regulates ENaC subunit levels by decreasing the levels of β and γ but not αENaC protein. These results imply a PKC-dependent, long term decrease in Na+ reabsorption.

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