(Q28209901)

English

Molecular mechanism of transforming growth factor (TGF)-beta1-induced glutathione depletion in alveolar epithelial cells. Involvement of AP-1/ARE and Fra-1

scientific article (publication date: 14 June 2002)

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Molecular mechanism of transforming growth factor (TGF)-beta1-induced glutathione depletion in alveolar epithelial cells. Involvement of AP-1/ARE and Fra-1 (English)

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William MacNee

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author name string

Hazel Jardine

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Kenneth Donaldson

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Irfan Rahman

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publication date

14 June 2002

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Journal of Biological Chemistry

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277

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24

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21158-66

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1 reference

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Transforming growth factor-beta1 is a potent inhibitor of glutathione synthesis in the lung epithelial cell line A549: transcriptional effect on the GSH rate-limiting enzyme gamma-glutamylcysteine synthetase

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Characterisation of gamma-glutamylcysteine synthetase-heavy subunit promoter: a critical role for AP-1.

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Molecular mechanism of the regulation of glutathione synthesis by tumor necrosis factor-alpha and dexamethasone in human alveolar epithelial cells

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Induction of Oxidative Stress by Okadaic Acid Is Required for Activation of Transcription Factor NF-κB

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Constitutive and beta-naphthoflavone-induced expression of the human gamma-glutamylcysteine synthetase heavy subunit gene is regulated by a distal antioxidant response element/TRE sequence

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Overlapping antioxidant response element and PMA response element sequences mediate basal and beta-naphthoflavone-induced expression of the human gamma-glutamylcysteine synthetase catalytic subunit gene

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Nrf1 and Nrf2 positively and c-Fos and Fra1 negatively regulate the human antioxidant response element-mediated expression of NAD(P)H:quinone oxidoreductase1 gene

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Single-Step Method of RNA Isolation by Acid Guanidinium Thiocyanate–Phenol–Chloroform Extraction

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Intracellular thiols regulate activation of nuclear factor kappa B and transcription of human immunodeficiency virus

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TGF-beta is a critical mediator of acute lung injury

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Overexpression of gamma-glutamylcysteine synthetase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-kappa B and activator protein-1

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Activation of an H2O2-generating NADH oxidase in human lung fibroblasts by transforming growth factor beta 1.

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c-Jun transactivates the promoter of the human p21(WAF1/Cip1) gene by acting as a superactivator of the ubiquitous transcription factor Sp1.

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ATF-2 is a common nuclear target of Smad and TAK1 pathways in transforming growth factor-beta signaling

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Activation of mitogen-activated protein kinase pathways induces antioxidant response element-mediated gene expression via a Nrf2-dependent mechanism

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Antitumor promotion by phenolic antioxidants: inhibition of AP-1 activity through induction of Fra expression

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Regulation of gamma-glutamylcysteine synthetase subunit gene expression by the transcription factor Nrf2.

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Nrf2 and c-Jun regulation of antioxidant response element (ARE)-mediated expression and induction of gamma-glutamylcysteine synthetase heavy subunit gene

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c-Ski acts as a transcriptional co-repressor in transforming growth factor-beta signaling through interaction with smads

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Negative feedback regulation of TGF-beta signaling by the SnoN oncoprotein

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The rat quinone reductase antioxidant response element. Identification of the nucleotide sequence required for basal and inducible activity and detection of antioxidant response element-binding proteins in hepatoma and non-hepatoma cell lines

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Two adjacent AP-1-like binding sites form the electrophile-responsive element of the murine glutathione S-transferase Ya subunit gene

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21 January 2018

Identifiers

10.1074/JBC.M112145200

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

PubMed publication ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

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