Chromatin Remodeling and the Control of Gene Expression

Wu, Carl

doi:10.1074/jbc.272.45.28171

Cited by 215 publications

(129 citation statements)

References 108 publications

(45 reference statements)

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“…[3][4][5]. Two general classes of chromatin remodeling factors that appear to play critical roles in transcriptional activation by nuclear receptors have been identified.…”

Section: Atp-dependent Chromatin Remodeling Complexesmentioning

confidence: 99%

“…These are ATP-dependent nucleosome remodeling complexes and factors that contain histone acetyltransferase activity. The yeast SWI⅐SNF complex facilitates the binding of sequence-specific transcription factors to nucleosomal DNA and can cause local changes in chromatin structure in an ATP-dependent manner (3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Mammalian homologues of Drosophila SWI2/SNF2 such as BRG1/hBrm function as components of large multiprotein complexes.…”

Section: Atp-dependent Chromatin Remodeling Complexesmentioning

confidence: 99%

“…As the number of potential coregulators clearly exceeds the capacity for direct interaction by a single receptor, the most plausible hypothesis is that transcriptional activation by nuclear receptors involves the actions of multiple factors. These factors act in a sequential and/or combinatorial manner to reorganize chromatin templates and to modify and recruit basal factors and RNA polymerase II (3,4).…”

Section: Nuclear Receptor Coactivatorsmentioning

confidence: 99%

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Coregulator Codes of Transcriptional Regulation by Nuclear Receptors

Rosenfeld¹,

Glass²

2001

Journal of Biological Chemistry

467

371

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Members of the nuclear receptor superfamily directly activate or repress target genes by binding to hormone response elements (HREs) 1 in promoter or enhancer regions, and by binding to other DNA sequence-specific activators and can inhibit the transcriptional activities of other classes of transcription factors by transrepression. Hormone response elements provide specificity to receptor homodimer heterodimer binding (reviewed in Ref.2). Nuclear receptor functions are directed by specific activation domains, referred to as activation function 1 (AF-1), which resides in the N terminus, and activation function 2 (AF-2), which resides in the C-terminal ligand binding domain (LBD) (reviewed in Ref. 1). Regulation of gene transcription by nuclear receptors requires the recruitment of proteins characterized as coregulators, with liganddependent exchange of corepressors for coactivators serving as the basic mechanism for switching gene repression to activation. In this review, we discuss biochemical and genetic studies suggesting that coregulatory complexes are differentially utilized in both a cell-and promoter-specific fashion to activate or repress gene transcription. These coregulatory components, themselves targets of diverse intracellular signaling pathways, provide a combinatorial code for tissue-and gene-specific responses, utilizing both enzymatic and platform assembly functions to mediate the actions of nuclear receptor genetic programs critical for developmental and homeostatic processes in metazoan organisms. Nuclear Receptor CoactivatorsA diverse group of proteins have emerged as potential coactivators for nuclear receptors. Ligand-dependent recruitment of coactivators is dependent on AF-2, which consists of a short conserved helical sequence within the C terminus of the LBD (2). Biochemical and expression cloning approaches have been used to identify a large number of factors that interact with nuclear receptors in either a ligand-independent or a ligand-dependent manner and are often components of large multiprotein complexes. Many of these factors are capable of potentiating nuclear receptor activity in transient cotransfection assays. In addition, a distinct set of coactivators is associated with the AF-1 domain. As the number of potential coregulators clearly exceeds the capacity for direct interaction by a single receptor, the most plausible hypothesis is that transcriptional activation by nuclear receptors involves the actions of multiple factors. These factors act in a sequential and/or combinatorial manner to reorganize chromatin templates and to modify and recruit basal factors and RNA polymerase II (3, 4). ATP-dependent Chromatin Remodeling ComplexesAs chromatinized transcription units are "repressed" compared with naked DNA, a critical aspect of gene activation involves nucleosomal remodeling (reviewed in Refs. 3-5). Two general classes of chromatin remodeling factors that appear to play critical roles in transcriptional activation by nuclear receptors have been identified. These are ATP-depen...

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“…[3][4][5]. Two general classes of chromatin remodeling factors that appear to play critical roles in transcriptional activation by nuclear receptors have been identified.…”

Section: Atp-dependent Chromatin Remodeling Complexesmentioning

confidence: 99%

Section: Atp-dependent Chromatin Remodeling Complexesmentioning

confidence: 99%

Section: Nuclear Receptor Coactivatorsmentioning

confidence: 99%

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Coregulator Codes of Transcriptional Regulation by Nuclear Receptors

Rosenfeld¹,

Glass²

2001

Journal of Biological Chemistry

467

371

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“…Unwinding of the closed DNA structure during active transcription of genes permits accessibility to transcription factors and allows them to exert regulatory control. Enhanced transcription of a restricted set of genes is associated with increased histone acetylation, governed by histone acetyltransferases (HAT), whereas gene silencing is commonly correlated with histone hypoacetylation, the result of histone deacetylase (HDAC) activity (14). HDAC are a family of proteins highly conserved during evolution (15).…”

mentioning

confidence: 99%

Histone Deacetylases Augment Cytokine Induction of the iNOS Gene

Zhang

Kone

2002

Journal of the American Society of Nephrology

102

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Abstract. The inducible nitric oxide synthase (iNOS) gene plays an important role in renal diseases. Transcription is the principal mode of regulation. This study explores the role of acetylation in cytokine-mediated iNOS induction in cultured murine mesangial cells and RAW 264.7 cells. Nitric oxide production was measured by the Griess reaction. The activity of the iNOS promoter and a nuclear factor-B (NF-B) element promoter were assessed in transient transfection assays. Gel shift and supershift assays were used to identify NF-B in nuclear extracts. Protein-protein interactions were assayed by co-immunoprecipitation and GST pull-down assays. Treatment with the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) and overexpression of HDAC isoforms were used to assess the impact of acetylation status on iNOS and NF-B element promoter activity. TSA inhibited induction of endogenous NO production and iNOS as well as NF-B element promoter activity in response to interleukin-1␤ (IL-1␤) or lipopolysaccharide (LPS) ϩ interferon-␥ (IFN-␥) in both cell types without altering NF-B DNA binding activity. Overexpression of specific HDAC isoforms enhanced cytokine induction of both the iNOS and the NF-B element promoter. HDAC2 and NF-B p65 co-immunoprecipitated from mesangial cell nuclear extracts, and in vitro translated HDAC2 specifically interacted with an NF-B p65 GST fusion protein.Hyperacetylation diminishes cytokine induction of iNOS transcription activity, at least partially, by limiting the functional efficacy of NF-B. The specific recruitment of HDAC2 to NF-B at target promoters and the consequent effects on acetylation status may play an important role in regulating iNOS as well as other NF-B-dependent genes involved in inflammation.

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“…Nucleosomes can impede DNA binding of transcription factors and GTFs and form a transcriptional barrier for RNAP. Thus, chromatin structure can significantly reduce the efficiency of transcription at both the initiation and elongation steps (Wu, 1997;Peterson and Workman, 2000;Wu and Grunstein, 2000;Narlikar et al, 2002;Li et al, 2007). It is well established that genes can be de-repressed when histones are depleted from cells (Han and Grunstein, 1988).…”

Section: Chromatin Remodeling and Modificationsmentioning

confidence: 99%

Transcriptional activators and activation mechanisms

2011

Protein Cell

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Chromatin Remodeling and the Control of Gene Expression

Cited by 215 publications

References 108 publications

Coregulator Codes of Transcriptional Regulation by Nuclear Receptors

Coregulator Codes of Transcriptional Regulation by Nuclear Receptors

Histone Deacetylases Augment Cytokine Induction of the iNOS Gene

Transcriptional activators and activation mechanisms

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