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Rad51 antibody [14B4]

RRID:AB_302856

Antibody ID

AB_302856

Target Antigen

Rad51 human

Proper Citation

(Abcam Cat# ab213, RRID:AB_302856)

Clonality

monoclonal antibody

Comments

validation status unknown, seller recommendations provided in 2012: Immunofluorescence; Immunoprecipitation; Western Blot; Immunocytochemistry/Immunofluorescence, Immunoprecipitation, Western Blot

Clone ID

Clone 14B4

Host Organism

mouse

Vendor

Abcam

Cat Num

ab213

Publications that use this research resource

The Histone Chaperones ASF1 and CAF-1 Promote MMS22L-TONSL-Mediated Rad51 Loading onto ssDNA during Homologous Recombination in Human Cells.

  • Huang TH
  • Mol. Cell
  • 2018 Mar 1

Literature context:


Abstract:

The access-repair-restore model for the role of chromatin in DNA repair infers that chromatin is a mere obstacle to DNA repair. However, here we show that blocking chromatin assembly, via knockdown of the histone chaperones ASF1 or CAF-1 or a mutation that prevents ASF1A binding to histones, hinders Rad51 loading onto ssDNA during homologous recombination. This is a consequence of reduced recruitment of the Rad51 loader MMS22L-TONSL to ssDNA, resulting in persistent RPA foci, extensive DNA end resection, persistent activation of the ATR-Chk1 pathway, and cell cycle arrest. In agreement, histones occupy ssDNA during DNA repair in yeast. We also uncovered DNA-PKcs-dependent DNA damage-induced ASF1A phosphorylation, which enhances chromatin assembly, promoting MMS22L-TONSL recruitment and, hence, Rad51 loading. We propose that transient assembly of newly synthesized histones onto ssDNA serves to recruit MMS22L-TONSL to efficiently form the Rad51 nucleofilament for strand invasion, suggesting an active role of chromatin assembly in homologous recombination.

Funding information:
  • Intramural NIH HHS - (United States)
  • NCI NIH HHS - R01 CA095641()

p53 orchestrates DNA replication restart homeostasis by suppressing mutagenic RAD52 and POLθ pathways.

  • Roy S
  • Elife
  • 2018 Jan 15

Literature context:


Abstract:

Classically, p53 tumor suppressor acts in transcription, apoptosis, and cell cycle arrest. Yet, replication-mediated genomic instability is integral to oncogenesis, and p53 mutations promote tumor progression and drug-resistance. By delineating human and murine separation-of-function p53 alleles, we find that p53 null and gain-of-function (GOF) mutations exhibit defects in restart of stalled or damaged DNA replication forks that drive genomic instability, which isgenetically separable from transcription activation. By assaying protein-DNA fork interactions in single cells, we unveil a p53-MLL3-enabled recruitment of MRE11 DNA replication restart nuclease. Importantly, p53 defects or depletion unexpectedly allow mutagenic RAD52 and POLθ pathways to hijack stalled forks, which we find reflected in p53 defective breast-cancer patient COSMIC mutational signatures. These data uncover p53 as a keystone regulator of replication homeostasis within a DNA restart network. Mechanistically, this has important implications for development of resistance in cancer therapy. Combined, these results define an unexpected role for p53-mediated suppression of replication genome instability.

Funding information:
  • NIAID NIH HHS - R01 AI038382(United States)