Jiangbo Tang, Nam Woo Cho, Gaofeng Cui, Erica M Manion, Niraj M Shanbhag, Maria Victoria Botuyan, Georges Mer, Roger A Greenberg. Nat Struct Mol Biol 2013
Times Cited: 327
Times Cited: 327
Times Cited
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The TIP60 Complex Regulates Bivalent Chromatin Recognition by 53BP1 through Direct H4K20me Binding and H2AK15 Acetylation.
Karine Jacquet, Amélie Fradet-Turcotte, Nikita Avvakumov, Jean-Philippe Lambert, Céline Roques, Raj K Pandita, Eric Paquet, Pauline Herst, Anne-Claude Gingras, Tej K Pandita,[...]. Mol Cell 2016
Karine Jacquet, Amélie Fradet-Turcotte, Nikita Avvakumov, Jean-Philippe Lambert, Céline Roques, Raj K Pandita, Eric Paquet, Pauline Herst, Anne-Claude Gingras, Tej K Pandita,[...]. Mol Cell 2016
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Structural basis for the methylation state-specific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair.
Maria Victoria Botuyan, Joseph Lee, Irene M Ward, Ja-Eun Kim, James R Thompson, Junjie Chen, Georges Mer. Cell 2006
Maria Victoria Botuyan, Joseph Lee, Irene M Ward, Ja-Eun Kim, James R Thompson, Junjie Chen, Georges Mer. Cell 2006
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Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks.
François Aymard, Beatrix Bugler, Christine K Schmidt, Emmanuelle Guillou, Pierre Caron, Sébastien Briois, Jason S Iacovoni, Virginie Daburon, Kyle M Miller, Stephen P Jackson,[...]. Nat Struct Mol Biol 2014
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53BP1 is a reader of the DNA-damage-induced H2A Lys 15 ubiquitin mark.
Amélie Fradet-Turcotte, Marella D Canny, Cristina Escribano-Díaz, Alexandre Orthwein, Charles C Y Leung, Hao Huang, Marie-Claude Landry, Julianne Kitevski-LeBlanc, Sylvie M Noordermeer, Frank Sicheri,[...]. Nature 2013
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ATM-dependent chromatin changes silence transcription in cis to DNA double-strand breaks.
Niraj M Shanbhag, Ilona U Rafalska-Metcalf, Carlo Balane-Bolivar, Susan M Janicki, Roger A Greenberg. Cell 2010
Niraj M Shanbhag, Ilona U Rafalska-Metcalf, Carlo Balane-Bolivar, Susan M Janicki, Roger A Greenberg. Cell 2010
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Screen identifies bromodomain protein ZMYND8 in chromatin recognition of transcription-associated DNA damage that promotes homologous recombination.
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A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice.
Cristina Escribano-Díaz, Alexandre Orthwein, Amélie Fradet-Turcotte, Mengtan Xing, Jordan T F Young, Ján Tkáč, Michael A Cook, Adam P Rosebrock, Meagan Munro, Marella D Canny,[...]. Mol Cell 2013
Cristina Escribano-Díaz, Alexandre Orthwein, Amélie Fradet-Turcotte, Mengtan Xing, Jordan T F Young, Ján Tkáč, Michael A Cook, Adam P Rosebrock, Meagan Munro, Marella D Canny,[...]. Mol Cell 2013
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53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks.
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DNA double-strand breaks promote methylation of histone H3 on lysine 9 and transient formation of repressive chromatin.
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Comprehensive Mapping of Histone Modifications at DNA Double-Strand Breaks Deciphers Repair Pathway Chromatin Signatures.
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The DNA damage response: making it safe to play with knives.
Alberto Ciccia, Stephen J Elledge. Mol Cell 2010
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RNF168 ubiquitinates K13-15 on H2A/H2AX to drive DNA damage signaling.
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Histone H4 deacetylation facilitates 53BP1 DNA damage signaling and double-strand break repair.
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RNF168 binds and amplifies ubiquitin conjugates on damaged chromosomes to allow accumulation of repair proteins.
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SETD2-dependent histone H3K36 trimethylation is required for homologous recombination repair and genome stability.
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A role for the Tip60 histone acetyltransferase in the acetylation and activation of ATM.
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The shieldin complex mediates 53BP1-dependent DNA repair.
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Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA nonhomologous end-joining.
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Histone acetylation by Trrap-Tip60 modulates loading of repair proteins and repair of DNA double-strand breaks.
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Histone demethylase KDM5A regulates the ZMYND8-NuRD chromatin remodeler to promote DNA repair.
Fade Gong, Thomas Clouaire, Marion Aguirrebengoa, Gaëlle Legube, Kyle M Miller. J Cell Biol 2017
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Double-strand break repair: 53BP1 comes into focus.
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A chromatin localization screen reveals poly (ADP ribose)-regulated recruitment of the repressive polycomb and NuRD complexes to sites of DNA damage.
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PARP1 Links CHD2-Mediated Chromatin Expansion and H3.3 Deposition to DNA Repair by Non-homologous End-Joining.
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53BP1 regulates DSB repair using Rif1 to control 5' end resection.
Michal Zimmermann, Francisca Lottersberger, Sara B Buonomo, Agnel Sfeir, Titia de Lange. Science 2013
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A macrohistone variant links dynamic chromatin compaction to BRCA1-dependent genome maintenance.
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Playing the end game: DNA double-strand break repair pathway choice.
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Histone H3 methylation links DNA damage detection to activation of the tumour suppressor Tip60.
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ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response.
Andrew N Blackford, Stephen P Jackson. Mol Cell 2017
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53BP1-RIF1-shieldin counteracts DSB resection through CST- and Polα-dependent fill-in.
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LEDGF (p75) promotes DNA-end resection and homologous recombination.
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RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection.
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Orchestration of the DNA-damage response by the RNF8 ubiquitin ligase.
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RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins.
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Bon voyage: A transcriptional journey around DNA breaks.
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H4K20me0 recognition by BRCA1-BARD1 directs homologous recombination to sister chromatids.
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RNF8- and RNF168-dependent degradation of KDM4A/JMJD2A triggers 53BP1 recruitment to DNA damage sites.
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MMSET regulates histone H4K20 methylation and 53BP1 accumulation at DNA damage sites.
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Histone H2A.Z controls a critical chromatin remodeling step required for DNA double-strand break repair.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.