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Items: 1 to 20 of 173

1.

Regulation of the DNA damage response and gene expression by the Dot1L histone methyltransferase and the 53Bp1 tumour suppressor.

FitzGerald J, Moureau S, Drogaris P, O'Connell E, Abshiru N, Verreault A, Thibault P, Grenon M, Lowndes NF.

PLoS One. 2011 Feb 24;6(2):e14714. doi: 10.1371/journal.pone.0014714.

2.

Impact of histone H4 lysine 20 methylation on 53BP1 responses to chromosomal double strand breaks.

Hartlerode AJ, Guan Y, Rajendran A, Ura K, Schotta G, Xie A, Shah JV, Scully R.

PLoS One. 2012;7(11):e49211. doi: 10.1371/journal.pone.0049211. Epub 2012 Nov 28.

3.

Bat3 facilitates H3K79 dimethylation by DOT1L and promotes DNA damage-induced 53BP1 foci at G1/G2 cell-cycle phases.

Wakeman TP, Wang Q, Feng J, Wang XF.

EMBO J. 2012 May 2;31(9):2169-81. doi: 10.1038/emboj.2012.50. Epub 2012 Feb 28.

4.

Methylated lysine 79 of histone H3 targets 53BP1 to DNA double-strand breaks.

Huyen Y, Zgheib O, Ditullio RA Jr, Gorgoulis VG, Zacharatos P, Petty TJ, Sheston EA, Mellert HS, Stavridi ES, Halazonetis TD.

Nature. 2004 Nov 18;432(7015):406-11. Epub 2004 Nov 3.

PMID:
15525939
5.

The histone H3K79 methyltransferase Dot1L is essential for mammalian development and heterochromatin structure.

Jones B, Su H, Bhat A, Lei H, Bajko J, Hevi S, Baltus GA, Kadam S, Zhai H, Valdez R, Gonzalo S, Zhang Y, Li E, Chen T.

PLoS Genet. 2008 Sep 12;4(9):e1000190. doi: 10.1371/journal.pgen.1000190.

6.

The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle.

Kim W, Choi M, Kim JE.

Cell Cycle. 2014;13(5):726-38. doi: 10.4161/cc.28104. Epub 2014 Feb 6. Review.

7.

Histone H4 deacetylation facilitates 53BP1 DNA damage signaling and double-strand break repair.

Hsiao KY, Mizzen CA.

J Mol Cell Biol. 2013 Jun;5(3):157-65. doi: 10.1093/jmcb/mjs066. Epub 2013 Jan 16.

PMID:
23329852
8.

MMSET regulates histone H4K20 methylation and 53BP1 accumulation at DNA damage sites.

Pei H, Zhang L, Luo K, Qin Y, Chesi M, Fei F, Bergsagel PL, Wang L, You Z, Lou Z.

Nature. 2011 Feb 3;470(7332):124-8. doi: 10.1038/nature09658.

9.

DOT1L/KMT4 recruitment and H3K79 methylation are ubiquitously coupled with gene transcription in mammalian cells.

Steger DJ, Lefterova MI, Ying L, Stonestrom AJ, Schupp M, Zhuo D, Vakoc AL, Kim JE, Chen J, Lazar MA, Blobel GA, Vakoc CR.

Mol Cell Biol. 2008 Apr;28(8):2825-39. doi: 10.1128/MCB.02076-07. Epub 2008 Feb 19.

10.

Leukemic transformation by the MLL-AF6 fusion oncogene requires the H3K79 methyltransferase Dot1l.

Deshpande AJ, Chen L, Fazio M, Sinha AU, Bernt KM, Banka D, Dias S, Chang J, Olhava EJ, Daigle SR, Richon VM, Pollock RM, Armstrong SA.

Blood. 2013 Mar 28;121(13):2533-41. doi: 10.1182/blood-2012-11-465120. Epub 2013 Jan 29.

11.

53BP1 is a reader of the DNA-damage-induced H2A Lys 15 ubiquitin mark.

Fradet-Turcotte A, Canny MD, Escribano-Díaz C, Orthwein A, Leung CC, Huang H, Landry MC, Kitevski-LeBlanc J, Noordermeer SM, Sicheri F, Durocher D.

Nature. 2013 Jul 4;499(7456):50-4. doi: 10.1038/nature12318. Epub 2013 Jun 12.

12.

Deficiency of H3K79 histone methyltransferase Dot1-like protein (DOT1L) inhibits cell proliferation.

Kim W, Kim R, Park G, Park JW, Kim JE.

J Biol Chem. 2012 Feb 17;287(8):5588-99. doi: 10.1074/jbc.M111.328138. Epub 2011 Dec 21.

13.

PTIP regulates 53BP1 and SMC1 at the DNA damage sites.

Wu J, Prindle MJ, Dressler GR, Yu X.

J Biol Chem. 2009 Jul 3;284(27):18078-84. doi: 10.1074/jbc.M109.002527. Epub 2009 May 4.

14.

DOT1L-mediated H3K79 methylation in chromatin is dispensable for Wnt pathway-specific and other intestinal epithelial functions.

Ho LL, Sinha A, Verzi M, Bernt KM, Armstrong SA, Shivdasani RA.

Mol Cell Biol. 2013 May;33(9):1735-45. doi: 10.1128/MCB.01463-12. Epub 2013 Feb 19.

15.

Dot1L mediated histone H3 lysine79 methylation is essential to meiosis progression in mouse oocytes.

Wang X, Gao W, Ma X, Wang X, Song C, Huang X, Liu H.

Neuro Endocrinol Lett. 2014;35(6):523-30.

PMID:
25433842
16.

The Histone Methyltransferase DOT1L Promotes Neuroblastoma by Regulating Gene Transcription.

Wong M, Tee AEL, Milazzo G, Bell JL, Poulos RC, Atmadibrata B, Sun Y, Jing D, Ho N, Ling D, Liu PY, Zhang XD, Hüttelmaier S, Wong JWH, Wang J, Polly P, Perini G, Scarlett CJ, Liu T.

Cancer Res. 2017 May 1;77(9):2522-2533. doi: 10.1158/0008-5472.CAN-16-1663. Epub 2017 Feb 16.

17.

Overlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte development.

Liu X, Jiang W, Dubois RL, Yamamoto K, Wolner Z, Zha S.

Proc Natl Acad Sci U S A. 2012 Mar 6;109(10):3903-8. doi: 10.1073/pnas.1120160109. Epub 2012 Feb 21.

18.

Prognostic and therapeutic value of disruptor of telomeric silencing-1-like (DOT1L) expression in patients with ovarian cancer.

Zhang X, Liu D, Li M, Cao C, Wan D, Xi B, Li W, Tan J, Wang J, Wu Z, Ma D, Gao Q.

J Hematol Oncol. 2017 Jan 23;10(1):29. doi: 10.1186/s13045-017-0400-8.

19.

Purkinje cell degeneration in pcd mice reveals large scale chromatin reorganization and gene silencing linked to defective DNA repair.

Baltanás FC, Casafont I, Lafarga V, Weruaga E, Alonso JR, Berciano MT, Lafarga M.

J Biol Chem. 2011 Aug 12;286(32):28287-302. doi: 10.1074/jbc.M111.246041. Epub 2011 Jun 23.

20.

DOT1L inhibits SIRT1-mediated epigenetic silencing to maintain leukemic gene expression in MLL-rearranged leukemia.

Chen CW, Koche RP, Sinha AU, Deshpande AJ, Zhu N, Eng R, Doench JG, Xu H, Chu SH, Qi J, Wang X, Delaney C, Bernt KM, Root DE, Hahn WC, Bradner JE, Armstrong SA.

Nat Med. 2015 Apr;21(4):335-43. doi: 10.1038/nm.3832. Epub 2015 Mar 30.

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