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Titolo:
Cell-type specific differences in glutamate cysteine ligase transcriptional regulation demonstrate independent subunit control
Autore:
Dahl, EL; Mulcahy, RT;
Indirizzi:
Univ Wisconsin, Ctr Environm Toxicol, Madison, WI 53792 USA Univ Wisconsin Madison WI USA 53792 vironm Toxicol, Madison, WI 53792 USA Univ Wisconsin, Dept Pharmacol, Madison, WI 53792 USA Univ Wisconsin Madison WI USA 53792 Dept Pharmacol, Madison, WI 53792 USA
Titolo Testata:
TOXICOLOGICAL SCIENCES
fascicolo: 2, volume: 61, anno: 2001,
pagine: 265 - 272
SICI:
1096-6080(200106)61:2<265:CSDIGC>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAMMA-GLUTAMYLCYSTEINE SYNTHETASE; ANTIOXIDANT RESPONSE ELEMENT; NAPHTHOFLAVONE-INDUCED EXPRESSION; MESSENGER-RNA EXPRESSION; HEME OXYGENASE-1 GENE; EPITHELIAL L2 CELLS; OXIDATIVE STRESS; GLUTATHIONE SYNTHESIS; LIGHT SUBUNIT; HEAVY SUBUNIT;
Keywords:
glutathione; glutamate cysteine ligase; gamma-glutamylcysteine synthetase; liver; lung; kidney; skeletal muscle; human cell lines; gene expression; tissue specific;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Mulcahy, RT Univ Wisconsin, Ctr Environm Toxicol, 600 Highland Ave,K4-554 CSC, Madison, WI 53792 USA Univ Wisconsin 600 Highland Ave,K4-554 CSC Madison WI USA 53792
Citazione:
E.L. Dahl e R.T. Mulcahy, "Cell-type specific differences in glutamate cysteine ligase transcriptional regulation demonstrate independent subunit control", TOXICOL SCI, 61(2), 2001, pp. 265-272

Abstract

Glutamate cysteine ligase (GCL; also referred to as gamma -glutamyl-cysteine synthetase, GCS) catalyzes the rate-limiting step of glutathione synthesis. The GCL holoenzyme is composed of a catalytic (GCLC; also called GCS(h)) and a modifier (GCLM; also called GCS(l)) subunit, each encoded by a unique gene, Wild-type and mutant promoter/luciferase reporter transgenes containing the promoter region of each GCL subunit gene were transfected into A549 (lung carcinoma), HEK 293 (transformed embryonic kidney), HepG2 (hepatocellular carcinoma), and RD (skeletal muscle rhabdomyosarcoma) cells to examine potential cell-type related differences in transcriptional regulation, In A549, HepG2, and RD cells, maximal basal expression of the GCLC transgene required the full-length (-3802 bp) promoter. Maximal expression in HEK 293 cells was uniquely directed by cis-elements contained within the -2752 to -1286 bp fragment of the promoter, No differences in GLCM promoter function were detected among these 4 cell lines. GCL subunit induction in each cell line by pyrrolidine dithiocarbamate (PDTC), phenethyl isothiocyanate (PEITC), and beta -naphthoflavone (beta -NF) was examined by RNAse protection assays. Although both genes were similarly induced in HepG2 cells by beta -NF, PDTC, and PEITC, neither was induced by beta -NF in A549, HEK 293, and RD cells, PDTC and PEITC induced GCLM to a much greater extent than GCLC inHEK 293 cells and failed to induce GCLC in RD cells. Neither subunit was induced by any of the agents in A549 cells, These studies indicate that the GCL subunit genes are independently regulated and display cell-type specific differences in both basal and inducible expression.

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Documento generato il 04/04/20 alle ore 15:00:03