BMI-1 regulates DNA end resection and homologous recombination repair

Fitieh, Amira; Locke, Andrew J.; Mashayekhi, Fatemeh; Khaliqdina, Fajr; Sharma, Ajit; Ismail, Ismail Hassan

doi:10.1016/j.celrep.2022.110536

Cited by 18 publications

(28 citation statements)

References 86 publications

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“…Of these regulatory mechanisms, PRC1 and PRC2 are well known to be recruited to the damage site and induce H2AK119ub and H3K27me3, respectively [ 124 ]. Consequently, transcription is repressed in the chromatin proximal to the damage site, and binding to H2AK119ub recruits the DNA end resection factor CtIP to promote HR repair [ 76 ]. Therefore, histone modification, which functions in the DNA damage repair response, is also associated with transcription and replication.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, BMI-mediated H2AK119 ubiquitylation induces DNA end resection, allowing the recruitment of downstream factors, such as replication protein A (RPA), BRCA1, and RAD51, at DNA damage sites, as well as the progression of HR. H2AK119ub could recruit the resection factor CtIP, interacting with ubiquitin moieties at the DSB site [ 36 , 76 , 112 ].…”

Section: Histone Ubiquitination Regulates Dna Repairmentioning

confidence: 99%

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DNA Damage Response Regulation by Histone Ubiquitination

Sekiguchi

Matsushita

2022

IJMS

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Cells are constantly exposed to numerous genotoxic stresses that induce DNA damage. DNA double-strand breaks (DSBs) are among the most serious damages and should be systematically repaired to preserve genomic integrity. The efficiency of repair is closely associated with chromatin structure, which is regulated by posttranslational modifications of histones, including ubiquitination. Recent evidence shows crosstalk between histone ubiquitination and DNA damage responses, suggesting an integrated model for the systematic regulation of DNA repair. There are two major pathways for DSB repair, viz., nonhomologous end joining and homologous recombination, and the choice of the pathway is partially controlled by posttranslational modifications of histones, including ubiquitination. Histone ubiquitination changes chromatin structure in the vicinity of DSBs and serves as a platform to select and recruit repair proteins; the removal of these modifications by deubiquitinating enzymes suppresses the recruitment of repair proteins and promotes the convergence of repair reactions. This article provides a comprehensive overview of the DNA damage response regulated by histone ubiquitination in response to DSBs.

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Section: Discussionmentioning

confidence: 99%

Section: Histone Ubiquitination Regulates Dna Repairmentioning

confidence: 99%

DNA Damage Response Regulation by Histone Ubiquitination

Sekiguchi

Matsushita

2022

IJMS

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“… 9 , 10 This reporter, in combination with mCherry-LacI- Fok I, has been used to study transcription in the context of local DSBs. 1 , 9 ) …”

Section: Before You Beginmentioning

confidence: 99%

Quantification of protein enrichment at site-specific DNA double-strand breaks by chromatin immunoprecipitation in cultured human cells

et al. 2023

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“…We use an SYBR-based master mix that contains all the reagents for qPCR. 1 Other qPCR protocols require sequence-specific fluorescent probes, such as TaqMan probes can also be used. 2 To calculate ΔCt for each sample, ΔCt is calculated by subtracting the Ct value of the mock-digested sample from the Ct value of the restriction enzyme (BsrGI-HF or Ban1) digested sample.…”

Section: Quantification and Statistical Analysismentioning

confidence: 99%

“…We use an SYBR-based master mix that contains all the reagents for qPCR. 1 Other qPCR protocols require sequence-specific fluorescent probes, such as TaqMan probes can also be used. 2 …”

Section: Quantification and Statistical Analysismentioning

confidence: 99%