BRCA1 Is Associated with a Human SWI/SNF-Related Complex

Bochar, Daniel A.; Wang, Lai; Beniya, Hideo; Kinev, Alexander; Xue, Yutong; Lane, William S.; Wang, Weidong; Kashanchi, Fatah; Shiekhattar, Ramin

doi:10.1016/s0092-8674(00)00030-1

Cited by 496 publications

(335 citation statements)

References 34 publications

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“…The first one is built on the assumption that the promoter region of the gene to be activated by p53 is usually not accessible to the general transcription factors and RNA polymerase. In this scenario binding of p53 to its REs within a promoter would facilitate promoter opening via recruiting either chromatin remodeling factors (CRF) 91,92 (though see reference Hill et al 93 ) or histone transacetylases (HAT) [94][95][96][97] and/or methyltransferases 98 (Figure 2). This view has been validated recently in a significant number of studies.…”

Section: Transcription Regulation By P53mentioning

confidence: 99%

Transcriptional regulation by p53: one protein, many possibilities

2006

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The p53 tumor suppressor protein is a DNA sequence-specific transcriptional regulator that, in response to various forms of cellular stress, controls the expression of numerous genes involved in cellular outcomes including among others, cell cycle arrest and cell death. Two key features of the p53 protein are required for its transcriptional activities: its ability to recognize and bind specific DNA sequences and to recruit both general and specialized transcriptional co-regulators. In fact, multiple interactions with co-activators and corepressors as well as with the components of the general transcriptional machinery allow p53 to either promote or inhibit transcription of different target genes. This review focuses on some of the salient features of the interactions of p53 with DNA and with factors that regulate transcription. We discuss as well the complexities of the functional domains of p53 with respect to these interactions.

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Section: Transcription Regulation By P53mentioning

confidence: 99%

Transcriptional regulation by p53: one protein, many possibilities

2006

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“…In Drosophila the two forms of SWI/SNF called BAP (Brahma associated proteins) and PBAP (Polybromo-associated BAP) both contain the same catalytic subunit (Brahma), but are distinguished by BAP containing the OSA subunit and PBAF containing the Polybromo and BAP170 subunits [10]. Although human SWI/SNF can be characterized as being of two forms, namely BAF (BRG1/hBRM-Associated Factors) and PBAF (Polybromo-associated BAF), there are many forms of human SWI/SNF that acquire tissue-specific subunits [11] or additional sub-complexes in which the SWI/SNF-type remodelers are associated with other factors such as BRCA1 [12,13], components of the histone deacetylase Sin3 complex [14] and histone methylases [15,16]. Recently, Rtt102p was identified as the newest subunit of both SWI/SNF and RSC complexes by MudPIT or mass spectrometry analysis [17].…”

Section: Nucleosome Remodeling Complexes Swi/snf Familymentioning

confidence: 99%

Mechanisms of ATP dependent chromatin remodeling

Gangaraju

Bartholomew

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

127

159

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The inter-relationship between DNA repair and ATP dependent chromatin remodeling has begun to become very apparent with recent discoveries. ATP dependent remodeling complexes mobilize nucleosomes along DNA, promote the exchange of histones, or completely displace nucleosomes from DNA. These remodeling complexes are often categorized based on the domain organization of their catalytic subunit. The biochemical properties and structural information of several of these remodeling complexes are reviewed. The different models for how these complexes are able to mobilize nucleosomes and alter nucleosome structure are presented incorporating several recent findings. Finally the role of histone tails and their respective modifications in ATP-dependent remodeling are discussed.

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“…Various classes of proteins interact with BRCA1, including: (1) components of the basal transcription machinery [e.g., RNA helicase A and RNA pol II (Anderson et al, 1998;Schlegel et al, 2000a)]; (2) generalized transcriptional coactivators [p300, CBP, Brg1 (Bochar et al, 2000;Pao et al, 2000)] and corepressors [e.g., RbAp46, RbAp48, histone deacetylases-1,2, and CtIP (Yarden and Brody, 1998;Yu et al, 1998)]; (3) tumor suppressors [e.g., p53, RB1, BRCA2 (Chen et al, 1998;Ouichi et al, 1998;Yarden and Brody, 1998;Zhang et al, 1998;Aprelikova et al, 1999;Chai et al, 1999;Fan et al, 2001c)]; (4) steroid hormone receptors, estrogen receptor-a, and androgen receptor (Yeh et al, 2000;Fan et al, 2001a); (5) DNA repair proteins [e.g., Rad51, Rad50, hMSH2 (Scully et al, 1997b;Zhong et al, 1999;Wang et al, 2001a)]; (6) other sequence-specific transcription factors [e.g., c-Myc, Oct-1, and NF-YA Fan et al, 2002b)]; and (7) cell cycle regulatory proteins [e.g., BARD1, E2F1, cyclins (Wu et al, 1996;Wang et al, 1997)]. These interactions are summarized in Figure 1; and the significance of these interactions is discussed in ''Functional Activities of BRCA1''.…”

Section: Brca1 Protein: Protein Interactionsmentioning

confidence: 99%

“…The C-terminal BRCT domains of BRCA1 can interact with both CtIP and LMO4 [a LIM-only (LMO) transcriptional regulator]; and LMO4 represses BRCA1-mediated transcriptional activity (Sum et al, 2002). BRCA1 can also interact with Brg1, a component of the SWI/SNF chromatin remodeling complex with ATPase activity; and a proteomic analysis revealed that BRCA1 is associated with a SWI/ SNF-like macromolecular complex (Bochar et al, 2000). A chromatin unfolding activity has recently been ascribed to the C-terminus of BRCA1 (Ye et al, 2001).…”

Section: Regulation Of Transcriptionmentioning

confidence: 99%

BRCA1 gene in breast cancer

Rosen

Fan

Pestell

et al. 2003

Journal Cellular Physiology

234

195

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The BRCA1 gene was identified and cloned in 1994 based on its linkage to early onset breast cancer and breast-ovarian cancer syndromes in women. While inherited mutations of BRCA1 are responsible for about 40-45% of hereditary breast cancers, these mutations account for only 2-3% of all breast cancers, since the BRCA1 gene is rarely mutated in sporadic breast cancers. However, BRCA1 expression is frequently reduced or absent in sporadic cancers, suggesting a much wider role in mammary carcinogenesis. Since BRCA1 was cloned in 1994, its molecular function has been the subject of intense investigation. These studies have revealed multiple functions of the BRCA1 that may contribute to its tumor suppressor activity, including roles in: cell cycle progression, several highly specialized DNA repair processes, DNA damage-responsive cell cycle checkpoints, regulation of a set of specific transcriptional pathways, and apoptosis. Many of these functions are linked to protein:protein interactions involving different portions of the 1,863 amino acid (aa) BRCA1 protein. BRCA1 functions in cell cycle progression and the DNA damage response appear to be regulated by distinct and specific phosphorylation events, but the molecular pathways activated by these phosphorylations are only beginning to be unraveled. In addition, the reason that BRCA1 mutation carriers develop specific tumor types (breast and ovarian cancers in women and possibly prostate cancers in men) is not clearly understood. Elucidation of the precise molecular functions of the BRCA1 gene product will greatly enhance our understanding of the pathogenesis of hereditary as well as sporadic mammary carcinogenesis.

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BRCA1 Is Associated with a Human SWI/SNF-Related Complex

Cited by 496 publications

References 34 publications

Transcriptional regulation by p53: one protein, many possibilities

Transcriptional regulation by p53: one protein, many possibilities

Mechanisms of ATP dependent chromatin remodeling

BRCA1 gene in breast cancer

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