BRG1 Promotes chromatin remodeling around DNA damage sites

Qi, Wenjing; Chen, Hongyu; Lü, Chao; Bu, Qingpan; Wang, Xiaoguang; Han, Liping

doi:10.1080/19768354.2018.1525429

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…3a , orange trace), indicating that BET proteins play a role in remodeling chromatin at DSBs. Brahma-Related Gene 1 (BRG1) is an ATPase subunit of the SWI/SNF chromatin remodeling complex, and has been linked to both DNA repair 51 – 53 and BET proteins 54 , 55 . To test whether BET proteins regulate binding of BRG1 during DSB repair, DNA-bound proteins were analyzed by plasmid pull-down.…”

Section: Resultsmentioning

confidence: 99%

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

et al. 2022

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Double-strand breaks (DSBs) are one of the most toxic forms of DNA damage and represent a major source of genomic instability. Members of the bromodomain and extra-terminal (BET) protein family are characterized as epigenetic readers that regulate gene expression. However, evidence suggests that BET proteins also play a more direct role in DNA repair. Here, we establish a cell-free system using Xenopus egg extracts to elucidate the gene expression-independent functions of BET proteins in DSB repair. We identify the BET protein BRD4 as a critical regulator of homologous recombination and describe its role in stimulating DNA processing through interactions with the SWI/SNF chromatin remodeling complex and resection machinery. These results establish BRD4 as a multifunctional regulator of chromatin binding that links transcriptional activity and homology-directed repair.

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Section: Resultsmentioning

confidence: 99%

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

et al. 2022

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“…In addition to transcription, BRG1 also has roles in DNA processes which further contribute to its importance in cancer [13][14][15]. BRG1 has been shown to promote DNA repair at doublestranded breaks through nucleosome repositioning and recruitment of repair factors [13][14][15], whilst its absence has been demonstrated to induce replication stress which is a major cause of genome instability [16,17]. The associations between BRG1 and cancer, and the types of genetic alterations that are observed are highly dependent on the cancer type.…”

Section: Smarca4 As An Epigenetic Regulator In Cancermentioning

confidence: 99%

The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target

Navickas,

Giles,

Brettingham-Moore

et al. 2023

Oncogene

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The chromatin remodeler SMARCA4/BRG1 is a key epigenetic regulator with diverse roles in coordinating the molecular programs that underlie brain tumour development. BRG1 function in brain cancer is largely specific to the tumour type and varies further between tumour subtypes, highlighting its complexity. Altered SMARCA4 expression has been linked to medulloblastoma, low-grade gliomas such as oligodendroglioma, high-grade gliomas such as glioblastoma and atypical/teratoid rhabdoid tumours. SMARCA4 mutations in brain cancer predominantly occur in the crucial catalytic ATPase domain, which is associated with tumour suppressor activity. However, SMARCA4 is opposingly seen to promote tumourigenesis in the absence of mutation and through overexpression in other brain tumours. This review explores the multifaceted interaction between SMARCA4 and various brain cancer types, highlighting its roles in tumour pathogenesis, the pathways it regulates, and the advances that have been made in understanding the functional relevance of mutations. We discuss developments made in targeting SMARCA4 and the potential to translate these to adjuvant therapies able to enhance current methods of brain cancer treatment.

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“…Qi et al [56,57] found that BRG1 decreases the nucleosomes stability at DSBs and creates an open and relaxed chromatin structure in SW13 and U2OS cells. It shows that BRG1 is crucial in early damage repair by remodeling the chromatin structure near DNA damage sites.…”

Section: Chromatin Modifications In Dsb Repairmentioning

confidence: 99%

Epigenetics and DNA Repair in Cancer

López-Ibarra¹,

Hernández-Caballero²

2021

DNA - Damages and Repair Mechanisms

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Cells can use chemical modifications in chromatin to regulate accessibility to DNA to the repair complexes and to prevent transcription in case of damage. We analyzed the relationship between repair systems and epigenetic mechanisms in DNA and RNA. We searched the PubMed database for genes involved in DNA damage response (DDR) and methylation in mRNA and DNA repair, in cancer. Epigenetic modifications, particularly histone modifications and nucleosome remodeling, trigger a signaling cascade of kinases in DNA damage response (DDR) toward efficient repair. SWI/SNF remodelers promote the recruitment of repair factors in DNA, such as DNA double-strand breaks (DSBs) that activate kinases in DDR. RNA methylation via m6A has recently attracted attention as a possible alternative pathway for repairing DNA damage. m6A is a dynamic methylation mark on mRNA that accumulates after UV irradiation and regulates transcription to facilitate DNA repair. Currently, studies seek to understand how signaling pathways activate proteins in the early response to damage. The repair maintains DNA integrity, which is a challenge in cancer because this process also represents a potential barrier to anticancer agents. The impact that epigenetic regulation can have on DNA repair is beginning to be understood.

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BRG1 Promotes chromatin remodeling around DNA damage sites

Cited by 7 publications

References 23 publications

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks

The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target

Epigenetics and DNA Repair in Cancer

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