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Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1.

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Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1. / Jafari, Claudia; Panzer, Ulf; Steinmetz, Oliver; Zahner, Gunther; Stahl, Rolf A.K.; Harendza, Sigrid.

In: CELL MOL BIOL LETT, Vol. 11, No. 3, 3, 2006, p. 424-437.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Jafari, C, Panzer, U, Steinmetz, O, Zahner, G, Stahl, RAK & Harendza, S 2006, 'Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1.', CELL MOL BIOL LETT, vol. 11, no. 3, 3, pp. 424-437. https://doi.org/10.2478/s11658-006-0035-1

APA

Jafari, C., Panzer, U., Steinmetz, O., Zahner, G., Stahl, R. A. K., & Harendza, S. (2006). Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1. CELL MOL BIOL LETT, 11(3), 424-437. [3]. https://doi.org/10.2478/s11658-006-0035-1

Vancouver

Jafari C, Panzer U, Steinmetz O, Zahner G, Stahl RAK, Harendza S. Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1. CELL MOL BIOL LETT. 2006;11(3):424-437. 3. https://doi.org/10.2478/s11658-006-0035-1

Bibtex

@article{3aef88116f3c46679a1cd5479f410857,
title = "Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1.",
abstract = "Acute glomerulonephritis can lead to chronic glomerulonephritis or resolve without permanent damage to the kidneys. Differential gene expression was studied in a model of acute and chronic glomerulonephritis to identify factors influencing the course of glomerulonephritis towards healing or chronification. One of the differentially expressed genes was identified as SCL, encoding selenocysteine lyase. Its expression was higher in acute glomerulonephritis and lower in chronic glomerulonephritis. The transcriptional regulation of SCL was studied in vitro in rat mesangial cells (MC). SCL RNA expression increased eight-fold compared to the baseline after stimulation with interleukin-1beta (IL-1beta) for three hours. Luciferase expression and gel shift experiments revealed an enhancer element between bp -152 and -298 of the SCL 5'-regulatory region, with protein binding to an AP-1 binding site that may be involved in the regulation of SCL-RNA in vivo in an endogenous feedback mechanism to the inflammatory reaction in acute glomerulonephritis, leading to resolution of this disease.",
author = "Claudia Jafari and Ulf Panzer and Oliver Steinmetz and Gunther Zahner and Stahl, {Rolf A.K.} and Sigrid Harendza",
year = "2006",
doi = "10.2478/s11658-006-0035-1",
language = "Deutsch",
volume = "11",
pages = "424--437",
journal = "CELL MOL BIOL LETT",
issn = "1425-8153",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1.

AU - Jafari, Claudia

AU - Panzer, Ulf

AU - Steinmetz, Oliver

AU - Zahner, Gunther

AU - Stahl, Rolf A.K.

AU - Harendza, Sigrid

PY - 2006

Y1 - 2006

N2 - Acute glomerulonephritis can lead to chronic glomerulonephritis or resolve without permanent damage to the kidneys. Differential gene expression was studied in a model of acute and chronic glomerulonephritis to identify factors influencing the course of glomerulonephritis towards healing or chronification. One of the differentially expressed genes was identified as SCL, encoding selenocysteine lyase. Its expression was higher in acute glomerulonephritis and lower in chronic glomerulonephritis. The transcriptional regulation of SCL was studied in vitro in rat mesangial cells (MC). SCL RNA expression increased eight-fold compared to the baseline after stimulation with interleukin-1beta (IL-1beta) for three hours. Luciferase expression and gel shift experiments revealed an enhancer element between bp -152 and -298 of the SCL 5'-regulatory region, with protein binding to an AP-1 binding site that may be involved in the regulation of SCL-RNA in vivo in an endogenous feedback mechanism to the inflammatory reaction in acute glomerulonephritis, leading to resolution of this disease.

AB - Acute glomerulonephritis can lead to chronic glomerulonephritis or resolve without permanent damage to the kidneys. Differential gene expression was studied in a model of acute and chronic glomerulonephritis to identify factors influencing the course of glomerulonephritis towards healing or chronification. One of the differentially expressed genes was identified as SCL, encoding selenocysteine lyase. Its expression was higher in acute glomerulonephritis and lower in chronic glomerulonephritis. The transcriptional regulation of SCL was studied in vitro in rat mesangial cells (MC). SCL RNA expression increased eight-fold compared to the baseline after stimulation with interleukin-1beta (IL-1beta) for three hours. Luciferase expression and gel shift experiments revealed an enhancer element between bp -152 and -298 of the SCL 5'-regulatory region, with protein binding to an AP-1 binding site that may be involved in the regulation of SCL-RNA in vivo in an endogenous feedback mechanism to the inflammatory reaction in acute glomerulonephritis, leading to resolution of this disease.

U2 - 10.2478/s11658-006-0035-1

DO - 10.2478/s11658-006-0035-1

M3 - SCORING: Zeitschriftenaufsatz

VL - 11

SP - 424

EP - 437

JO - CELL MOL BIOL LETT

JF - CELL MOL BIOL LETT

SN - 1425-8153

IS - 3

M1 - 3

ER -