Mammalian SWI/SNF-A Subunit BAF250/ARID1 Is an E3 Ubiquitin Ligase That Targets Histone H2B

Li, Xuan Shirley; Trojer, Patrick; Matsumura, Tatsushi; Treisman, Jessica E.; Tanese, Naoko

doi:10.1128/mcb.00540-09

Cited by 99 publications

(87 citation statements)

References 44 publications

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“…and rapidly degrade histone H2B through the proteosomal complex (30). This process includes the pathway from aberrations in ARID1A to dysregulated (unubiquitinated) histone H2B, leading to downstream changes in transcription genes.…”

Section: Discussionmentioning

confidence: 99%

“…1, various BAF250a (ARID1A)-interacting proteins (transcription factor) exist, including HOXA9 and HIC1. ARID1A is a positive regulator of HOXA9 (30). HOXA9 expression is spatially and temporally regulated during hematopoiesis and embryonic development.…”

Section: Identification Of Arid-containing Proteins and Arid1a-interamentioning

confidence: 99%

“…Loss of the ARID1A tumor suppressor, which occurs with VHL mutations in ccRCC, promotes CCC tumorigenesis primarily through loss of the assembly of the Cullin-Elongin-Rbx1-E2 complex and subsequent ARID1A-mediated histone H2B regulation. The binding of H2B to ARID1 and to the ubiquitin ligase complex causes H2B to be ubiquitinated and degraded by the proteasomal complex (30). Mutated ARID1A may not bind to H2B, and consequently is not degraded.…”

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confidence: 99%

“…As with VHL, ARID1A exists in complex with a series of other proteins, including elongin B, elongin C, cullin2 and Rbx1, to form an ubiquitin ligase complex (30) (Fig. 2B).…”

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confidence: 99%

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The role of components of the chromatin modification machinery in carcinogenesis of clear cell carcinoma of the ovary (Review)

et al. 2011

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Abstract. Recent data have provided information regarding the profiles of clear cell carcinoma of the ovary (CCC) with adenine-thymine rich interactive domain 1A (ARID1A) mutations. The purpose of this review was to summarize current knowledge regarding the molecular mechanisms involved in CCC tumorigenesis and to describe the central role played by the aberrant chromatin remodeling. The present article reviews the English-language literature for biochemical studies on the ARID1A mutation and chromatin remodeling in CCC. ARID1A is responsible for directing the SWI/SNF complex to target promoters and regulates the transcription of certain genes by altering the chromatin structure around those genes. The mutation spectrum of ARID1A was enriched for C to T transitions. CCC and clear cell renal cell carcinoma (ccRCC) resemble each other pathogenetically. Dysfunction of the ARID1A protein, which occurs with VHL mutations in ccRCC, is responsible for loss of the assembly of the ARID1A-mediated histone H2B complex. Therefore, ARID1A acts as a chromatin remodeling modifier, which stimulates cell signaling that can lead to cell cycle arrest and cell death in the event of DNA damage. The dysfunction of ARID1A may result in susceptibility to CCC carcinogenesis through a defect in the repair or replication of damaged DNA. IntroductionEpithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy worldwide. Epidemiology calculations of lifetime risk for EOC are that 1 in 55 women is likely to develop EOC during their lifetime (1). Since EOC is more likely to be advanced stage with unfavorable tumor biology, there are serious limitations to the surgical and oncological treatment available. Therefore, it is crucial to determine the earliest possible diagnosis. Early diagnosis and surgical resection offer patients the best opportunity of excellent long-term survival. On the other hand, patients who either present with metastatic disease or develop distant relapse within 6 months after surgery and chemotherapy have a poor prognosis. Among EOC, clear cell carcinomas of the ovary (CCC) are frequently characterized by chemoresistance and recurrence, resulting in a poor prognosis (2). Since CCC are resistant to conventional cytotoxic (platinum plus taxan-based) chemotherapy, the prognosis is mostly poor (3). In the USA, the incidence of CCC is 5% of all EOC, but the incidence in Japan is reported to be over 20% of all EOC. Thus, Japanese oncologists have focused on investigating the molecular pathogenesis and treatment strategies of CCC.At present, little is known about the molecular genetic mechanisms that are involved in CCC tumorigenesis. Accumulated somatic mutations found in a subset of cancer genes are frequently noted. Such mutations include insertions/deletions (indels) and base substitutions that act as the 'driver mutations' in oncogenesis. These mutations result in the activation of proto-oncogenes (gain of function) or the inhibition of tumor suppressor genes (loss of function) during the process of carcinoge...

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Section: Discussionmentioning

confidence: 99%

Section: Identification Of Arid-containing Proteins and Arid1a-interamentioning

confidence: 99%

mentioning

confidence: 99%

“…As with VHL, ARID1A exists in complex with a series of other proteins, including elongin B, elongin C, cullin2 and Rbx1, to form an ubiquitin ligase complex (30) (Fig. 2B).…”

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confidence: 99%

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The role of components of the chromatin modification machinery in carcinogenesis of clear cell carcinoma of the ovary (Review)

et al. 2011

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“…This is consistent with our finding that ARID1A RNA levels are significantly lower in high-Ki67-expressing breast tumors (Figure 2). More recent evidence also implicates ARID1A in the regulation of histone modifications, specifically in the targeting of histone H2B for ubiquitination (Li et al, 2010), with consequent effects on E2F, histone deacetylase and Myc-dependent transcription.…”

Section: Inactivation Of Arid1a In Breast Cancermentioning

confidence: 99%

An integrated genomic approach identifies ARID1A as a candidate tumor-suppressor gene in breast cancer

et al. 2011

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Tumor-suppressor genes (TSGs) have been classically defined as genes whose loss of function in tumor cells contributes to the formation and/or maintenance of the tumor phenotype. TSGs containing nonsense mutations may not be expressed because of nonsense-mediated RNA decay (NMD). We combined inhibition of the NMD process, which clears transcripts that contain nonsense mutations, with the application of high-density single-nucleotide polymorphism arrays analysis to discriminate allelic content in order to identify candidate TSGs in five breast cancer cell lines. We identified ARID1A as a target of NMD in the T47D breast cancer cell line, likely as a consequence of a mutation in exon-9, which introduces a premature stop codon at position Q944. ARID1A encodes a human homolog of yeast SWI1, which is an integral member of the hSWI/SNF complex, an ATPdependent, chromatin-remodeling, multiple-subunit enzyme. Although we did not find any somatic mutations in 11 breast tumors, which show DNA copy-number loss at the 1p36 locus adjacent to ARID1A, we show that low ARID1A RNA or nuclear protein expression is associated with more aggressive breast cancer phenotypes, such as high tumor grade, in two independent cohorts of over 200 human breast cancer cases each. We also found that low ARID1A nuclear expression becomes more prevalent during the later stages of breast tumor progression. Finally, we found that ARID1A reexpression in the T47D cell line results in significant inhibition of colony formation in soft agar. These results suggest that ARID1A may be a candidate TSG in breast cancer.

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Modulation of Developmentally Regulated Gene Expression Programs through Targeting of Polycomb and Trithorax Group Proteins

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Dilworth

2012

Toxicology and Epigenetics

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Mammalian SWI/SNF-A Subunit BAF250/ARID1 Is an E3 Ubiquitin Ligase That Targets Histone H2B

Cited by 99 publications

References 44 publications

The role of components of the chromatin modification machinery in carcinogenesis of clear cell carcinoma of the ovary (Review)

The role of components of the chromatin modification machinery in carcinogenesis of clear cell carcinoma of the ovary (Review)

An integrated genomic approach identifies ARID1A as a candidate tumor-suppressor gene in breast cancer

Modulation of Developmentally Regulated Gene Expression Programs through Targeting of Polycomb and Trithorax Group Proteins

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