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Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells. / Mogilenko, Denis A.; Kudriavtsev, Igor V.; Shavva, Vladimir S.; Dizhe, Ella B.; Vilenskaya, Ekaterina G.; Efremov, Alexander M.; Perevozchikov, Andrej P.; Orlov, Sergey V.

In: Journal of Biological Chemistry, Vol. 288, No. 3, 2013, p. 1726-1738.

Research output: Contribution to journal › Article

Harvard

Mogilenko, DA, Kudriavtsev, IV, Shavva, VS, Dizhe, EB, Vilenskaya, EG, Efremov, AM, Perevozchikov, AP & Orlov, SV 2013, 'Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells', Journal of Biological Chemistry, vol. 288, no. 3, pp. 1726-1738. https://doi.org/10.1074/jbc.M112.437525

APA

Mogilenko, D. A., Kudriavtsev, I. V., Shavva, V. S., Dizhe, E. B., Vilenskaya, E. G., Efremov, A. M., Perevozchikov, A. P., & Orlov, S. V. (2013). Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells. Journal of Biological Chemistry, 288(3), 1726-1738. https://doi.org/10.1074/jbc.M112.437525

Vancouver

Mogilenko DA, Kudriavtsev IV, Shavva VS, Dizhe EB, Vilenskaya EG, Efremov AM et al. Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells. Journal of Biological Chemistry. 2013;288(3):1726-1738. https://doi.org/10.1074/jbc.M112.437525

Author

Mogilenko, Denis A. ; Kudriavtsev, Igor V. ; Shavva, Vladimir S. ; Dizhe, Ella B. ; Vilenskaya, Ekaterina G. ; Efremov, Alexander M. ; Perevozchikov, Andrej P. ; Orlov, Sergey V. / Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells. In: Journal of Biological Chemistry. 2013 ; Vol. 288, No. 3. pp. 1726-1738.

BibTeX

@article{826c7bf792aa4938ae2a25c5eb14fb7e,
title = "Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells",
abstract = "Complement C3 is a pivotal component of three cascades of complement activation. The liver is the main source of C3 in circulation and expression and secretion of C3 by hepatocytes is increased during acute inflammation. However, the mechanism of the regulation of the C3 gene in hepatocytes is not well elucidated. We showed that the C3 gene is the direct target for peroxisome proliferator-activated receptor alpha (PPAR alpha) in human hepatoma HepG2 cells and mouse liver. Using PPAR alpha siRNA and synthetic PPAR alpha agonist WY-14643 and antagonist MK886 we showed that activation of PPAR alpha results in up-regulation of C3 gene expression and protein secretion by HepG2 cells. The PPAR response element (PPRE), which is able to bind PPAR alpha in vitro and in vivo, was found in the human C3 promoter. PPRE is conserved between human and mouse, and WY-14643 stimulates mouse C3 expression in the liver. TNF alpha increases C3 gene via NF-kappa B and, to a lesser extent, MEK1/2 signaling pathways, whereas TNF alp",
author = "Mogilenko, {Denis A.} and Kudriavtsev, {Igor V.} and Shavva, {Vladimir S.} and Dizhe, {Ella B.} and Vilenskaya, {Ekaterina G.} and Efremov, {Alexander M.} and Perevozchikov, {Andrej P.} and Orlov, {Sergey V.}",
year = "2013",
doi = "10.1074/jbc.M112.437525",
language = "English",
volume = "288",
pages = "1726--1738",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "3",

}

RIS

TY - JOUR

T1 - Peroxisome Proliferator-activated Receptor α Positively Regulates Complement C3 Expression but Inhibits Tumor Necrosis Factor α-mediated Activation of C3 Gene in Mammalian Hepatic-derived Cells

AU - Mogilenko, Denis A.

AU - Kudriavtsev, Igor V.

AU - Shavva, Vladimir S.

AU - Dizhe, Ella B.

AU - Vilenskaya, Ekaterina G.

AU - Efremov, Alexander M.

AU - Perevozchikov, Andrej P.

AU - Orlov, Sergey V.

PY - 2013

Y1 - 2013

N2 - Complement C3 is a pivotal component of three cascades of complement activation. The liver is the main source of C3 in circulation and expression and secretion of C3 by hepatocytes is increased during acute inflammation. However, the mechanism of the regulation of the C3 gene in hepatocytes is not well elucidated. We showed that the C3 gene is the direct target for peroxisome proliferator-activated receptor alpha (PPAR alpha) in human hepatoma HepG2 cells and mouse liver. Using PPAR alpha siRNA and synthetic PPAR alpha agonist WY-14643 and antagonist MK886 we showed that activation of PPAR alpha results in up-regulation of C3 gene expression and protein secretion by HepG2 cells. The PPAR response element (PPRE), which is able to bind PPAR alpha in vitro and in vivo, was found in the human C3 promoter. PPRE is conserved between human and mouse, and WY-14643 stimulates mouse C3 expression in the liver. TNF alpha increases C3 gene via NF-kappa B and, to a lesser extent, MEK1/2 signaling pathways, whereas TNF alp

AB - Complement C3 is a pivotal component of three cascades of complement activation. The liver is the main source of C3 in circulation and expression and secretion of C3 by hepatocytes is increased during acute inflammation. However, the mechanism of the regulation of the C3 gene in hepatocytes is not well elucidated. We showed that the C3 gene is the direct target for peroxisome proliferator-activated receptor alpha (PPAR alpha) in human hepatoma HepG2 cells and mouse liver. Using PPAR alpha siRNA and synthetic PPAR alpha agonist WY-14643 and antagonist MK886 we showed that activation of PPAR alpha results in up-regulation of C3 gene expression and protein secretion by HepG2 cells. The PPAR response element (PPRE), which is able to bind PPAR alpha in vitro and in vivo, was found in the human C3 promoter. PPRE is conserved between human and mouse, and WY-14643 stimulates mouse C3 expression in the liver. TNF alpha increases C3 gene via NF-kappa B and, to a lesser extent, MEK1/2 signaling pathways, whereas TNF alp

U2 - 10.1074/jbc.M112.437525

DO - 10.1074/jbc.M112.437525

M3 - Article

VL - 288

SP - 1726

EP - 1738

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 3

ER -

ID: 7380022