C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells

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C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells. / Galuska, Dana; Pirkmajer, Sergej; Barres, Romain; Ekberg, Karin; Wahren, John; Chibalin, Alexander V.

In: P L o S One, Vol. 6, No. 12, 2011, p. e28294.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Galuska, D, Pirkmajer, S, Barres, R, Ekberg, K, Wahren, J & Chibalin, AV 2011, 'C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells', P L o S One, vol. 6, no. 12, pp. e28294. https://doi.org/10.1371/journal.pone.0028294

APA

Galuska, D., Pirkmajer, S., Barres, R., Ekberg, K., Wahren, J., & Chibalin, A. V. (2011). C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells. P L o S One, 6(12), e28294. https://doi.org/10.1371/journal.pone.0028294

Vancouver

Galuska D, Pirkmajer S, Barres R, Ekberg K, Wahren J, Chibalin AV. C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells. P L o S One. 2011;6(12):e28294. https://doi.org/10.1371/journal.pone.0028294

Author

Galuska, Dana ; Pirkmajer, Sergej ; Barres, Romain ; Ekberg, Karin ; Wahren, John ; Chibalin, Alexander V. / C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells. In: P L o S One. 2011 ; Vol. 6, No. 12. pp. e28294.

Bibtex

@article{7dcd6d17a0234f2db4243814f17213ae,
title = "C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells",
abstract = "Replacement of proinsulin C-peptide in type 1 diabetes ameliorates nerve and kidney dysfunction, conditions which are associated with a decrease in Na,K-ATPase activity. We determined the molecular mechanism by which long term exposure to C-peptide stimulates Na,K-ATPase expression and activity in primary human renal tubular cells (HRTC) in control and hyperglycemic conditions.",
keywords = "C-Peptide, Cell Nucleus, Extracellular Signal-Regulated MAP Kinases, Gene Expression Regulation, Enzymologic, Gene Silencing, Homeodomain Proteins, Humans, Hyperglycemia, Kidney Tubules, MAP Kinase Signaling System, Models, Biological, Ouabain, Peptides, Phosphorylation, Protein Isoforms, Protein Kinase C, Protein Kinase C-alpha, Protein Kinase C-delta, Protein Kinase C-epsilon, Signal Transduction, Sodium, Sodium-Potassium-Exchanging ATPase, Transcription Factors",
author = "Dana Galuska and Sergej Pirkmajer and Romain Barres and Karin Ekberg and John Wahren and Chibalin, {Alexander V}",
year = "2011",
doi = "10.1371/journal.pone.0028294",
language = "English",
volume = "6",
pages = "e28294",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "12",

}

RIS

TY - JOUR

T1 - C-peptide increases Na,K-ATPase expression via PKC- and MAP kinase-dependent activation of transcription factor ZEB in human renal tubular cells

AU - Galuska, Dana

AU - Pirkmajer, Sergej

AU - Barres, Romain

AU - Ekberg, Karin

AU - Wahren, John

AU - Chibalin, Alexander V

PY - 2011

Y1 - 2011

N2 - Replacement of proinsulin C-peptide in type 1 diabetes ameliorates nerve and kidney dysfunction, conditions which are associated with a decrease in Na,K-ATPase activity. We determined the molecular mechanism by which long term exposure to C-peptide stimulates Na,K-ATPase expression and activity in primary human renal tubular cells (HRTC) in control and hyperglycemic conditions.

AB - Replacement of proinsulin C-peptide in type 1 diabetes ameliorates nerve and kidney dysfunction, conditions which are associated with a decrease in Na,K-ATPase activity. We determined the molecular mechanism by which long term exposure to C-peptide stimulates Na,K-ATPase expression and activity in primary human renal tubular cells (HRTC) in control and hyperglycemic conditions.

KW - C-Peptide

KW - Cell Nucleus

KW - Extracellular Signal-Regulated MAP Kinases

KW - Gene Expression Regulation, Enzymologic

KW - Gene Silencing

KW - Homeodomain Proteins

KW - Humans

KW - Hyperglycemia

KW - Kidney Tubules

KW - MAP Kinase Signaling System

KW - Models, Biological

KW - Ouabain

KW - Peptides

KW - Phosphorylation

KW - Protein Isoforms

KW - Protein Kinase C

KW - Protein Kinase C-alpha

KW - Protein Kinase C-delta

KW - Protein Kinase C-epsilon

KW - Signal Transduction

KW - Sodium

KW - Sodium-Potassium-Exchanging ATPase

KW - Transcription Factors

U2 - 10.1371/journal.pone.0028294

DO - 10.1371/journal.pone.0028294

M3 - Journal article

C2 - 22162761

VL - 6

SP - e28294

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 12

ER -

ID: 45577193