دورية أكاديمية
أعرض في EDS

Regulation of GTP-binding protein (Gαs) expression in human myometrial cells: a role for tumor necrosis factor in modulating Gαs promoter acetylation by transcriptional complexes.

التفاصيل البيبلوغرافية
العنوان: Regulation of GTP-binding protein (Gαs) expression in human myometrial cells: a role for tumor necrosis factor in modulating Gαs promoter acetylation by transcriptional complexes.
المؤلفون: Webster SJ; Academic Unit of Reproductive and Developmental Medicine, Department of Human Metabolism, University of Sheffield, Level 4, Jessop Wing, Tree Root Walk, Sheffield S10 2SF, United Kingdom., Waite SL, Cookson VJ, Warren A, Khan R, Gandhi SV, Europe-Finner GN, Chapman NR
المصدر: The Journal of biological chemistry [J Biol Chem] 2013 Mar 01; Vol. 288 (9), pp. 6704-16. Date of Electronic Publication: 2013 Jan 07.
نوع المنشور: Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Country of Publication: United States NLM ID: 2985121R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1083-351X (Electronic) Linking ISSN: 00219258 NLM ISO Abbreviation: J Biol Chem Subsets: MEDLINE
أسماء مطبوعة: Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology
Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology
مواضيع طبية MeSH: GTP-Binding Protein alpha Subunits/*metabolism , Gene Expression Regulation/*physiology , Multiprotein Complexes/*metabolism , Muscle Proteins/*metabolism , Myometrium/*metabolism , Response Elements/*physiology , Transcription Factors/*metabolism , Tumor Necrosis Factor-alpha/*pharmacology, Acetylation/drug effects ; Adolescent ; Adult ; Cells, Cultured ; Female ; GTP-Binding Protein alpha Subunits/genetics ; Histone Deacetylase 1/genetics ; Histone Deacetylase 1/metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Histones/genetics ; Histones/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Multiprotein Complexes/genetics ; Muscle Proteins/genetics ; Myometrium/cytology ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism ; Transcription Factors/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Uterine Contraction/drug effects ; Uterine Contraction/physiology
مستخلص: The onset of parturition is associated with a number of proinflammatory mediators that are themselves regulated by the nuclear factor κB (NF-κB) family of transcription factors. In this context, we previously reported that the RelA NF-κB subunit represses transcription and mRNA expression of the proquiescent Gαs gene in human myometrial cells following stimulation with the proinflammatory cytokine TNF. In the present study, we initially defined the functional consequence of this on myometrial contractility. Here we show that, contrary to our initial expectations, TNF did not induce myometrial contractility but did inhibit the relaxation produced by the histone deacetylase inhibitor trichostatin A, an effect that in turn was abolished by the NF-κB inhibitor N(4)-[2-(4-phenoxyphenyl)ethyl]-4,6-quinazolinediamine. This result suggested a role for TNF in regulating Gαs expression via activating NF-κB and modifying histone acetylation associated with the promoter region of the gene. In this context, we show that the -837 to -618 region of the endogenous Gαs promoter is occupied by cAMP-response element-binding protein (CREB), Egr-1, and Sp1 transcription factors and that CREB-binding protein (CBP) transcriptional complexes form within this region where they induce histone acetylation, resulting in increased Gαs expression. TNF, acting via NF-κB, did not change the levels of CREB, Sp1, or Egr-1 binding to the Gαs promoter, but it induced a significant reduction in the level of CBP. This was associated with increased levels of histone deacetylase-1 and surprisingly an increase in H4K8 acetylation. The latter is discussed herein.
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معلومات مُعتمدة: G0701322 United Kingdom Medical Research Council
المشرفين على المادة: 0 (GTP-Binding Protein alpha Subunits)
0 (Histone Deacetylase Inhibitors)
0 (Histones)
0 (Hydroxamic Acids)
0 (Multiprotein Complexes)
0 (Muscle Proteins)
0 (RELA protein, human)
0 (Transcription Factor RelA)
0 (Transcription Factors)
0 (Tumor Necrosis Factor-alpha)
3X2S926L3Z (trichostatin A)
EC 3.5.1.98 (HDAC1 protein, human)
EC 3.5.1.98 (Histone Deacetylase 1)
تواريخ الأحداث: Date Created: 20130109 Date Completed: 20130509 Latest Revision: 20211021
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3585108
DOI: 10.1074/jbc.M112.440602
PMID: 23297421
قاعدة البيانات: MEDLINE
الوصف
تدمد:1083-351X
DOI:10.1074/jbc.M112.440602