A requirement for PARP-1 for the assembly or stability of XRCC1 nuclear foci at sites of oxidative DNA damage.

By S. El-khamisy, M. Masutani, Hiroshi Suzuki, K. Caldecott. Nucleic Acids Research, 2003

714 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/85d9a5b121893f5882014c345452dfef26cc40a3

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Citations in the corpus

The expanding field of poly(ADP-ribosyl)ation reactions. ‘Protein Modifications: Beyond the Usual Suspects' Review Series (2008, background): “Here, we discuss some of these processes, with a particular emphasis on those that have been described recently. the role of par in the regulation of chromatin structure, DNa repair, replication, transcription, insulation and telomere homeostasis has been described in several recent in-depth reviews”
PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination (2009, background): “It is well established that PARP is activated by DNA single-strand breaks (SSBs), produced directly or as a base excision repair intermediate (Satoh and Lindahl, 1992), and that this attracts SSB repair proteins for repair (El-Khamisy et al, 2003).”
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase (2005, positive): “dtd" [ ]> Poly(ADP-ribose) polymerase (PARP1) facilitates DNA repair by binding to DNA breaks and attracting DNA repair proteins to the site of damag”
PARP-1 cleavage fragments: signatures of cell-death proteases in neurodegeneration (2010, background): “AMD contains a BRCT fold (a motif also found in many DNA repair proteins) that is involved in protein-protein interactions which promotes the recruitment of DNA repair enzymes to the site of DNA damage [48,49].”
PARP inhibition: PARP1 and beyond (2010, background): “Some of these recruited proteins — typified by XRCC1 , the scaffolding protein that assembles and activates the DNA base excision repair (BER) machiner”
The PARP Side of the Nucleus: Molecular Actions, Physiological Outcomes, and Clinical Targets (2010, neutral): “…(3) function as insulators (e.g., CTCF), and (4) methylate DNA (e.g., DNMT-1) (Figure 5) (Caiafa et al., 2009; Caiafa and Zlatanova, 2009; El-Khamisy et al., 2003; Farrar et al., 2010; Guastafierro et al., 2008; Hassa et al., 2005; Heale et al., 2006; Ju et al., 2004; Malanga and…”
Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “Through the use of anti-PAR antibodies, PARylation can be detected locally at sites of DNA breaks in mammalian cells (Tartier et al. 2003), where it promotes recruitment of the DNA break repair factors XRCC1 (El-Khamisy et al. 2003; Okano et al. 2003) and APLF (Bekker-Jensen et al. 2007; Kanno et al”
Genomic instability and aging-like phenotype in the absence of mammalian SIRT6. (2006, neutral): “In this regard, XRCC1 forms foci upon MMS and H 2 O 2 treatment that colocalize with sites of poly-ADP ribose (PAR) formation (El-Khamisy et al., 2003).”