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1
DNA resection in eukaryotes: deciding how to fix the break.
Nat Struct Mol Biol. 2010 Jan;17(1):11-6. doi: 10.1038/nsmb.1710.
2
End resection at double-strand breaks: mechanism and regulation.
Cold Spring Harb Perspect Biol. 2014 Aug 1;6(8):a016436. doi: 10.1101/cshperspect.a016436.
3
Regulation of DNA double-strand break repair pathway choice.
Cell Res. 2008 Jan;18(1):134-47. doi: 10.1038/cr.2007.111.
4
The Determinant of DNA Repair Pathway Choices in Ionising Radiation-Induced DNA Double-Strand Breaks.
Biomed Res Int. 2020 Aug 25;2020:4834965. doi: 10.1155/2020/4834965. eCollection 2020.
6
Double-strand break end resection and repair pathway choice.
Annu Rev Genet. 2011;45:247-71. doi: 10.1146/annurev-genet-110410-132435. Epub 2011 Sep 12.
7
Coupling end resection with the checkpoint response at DNA double-strand breaks.
Cell Mol Life Sci. 2016 Oct;73(19):3655-63. doi: 10.1007/s00018-016-2262-6. Epub 2016 May 3.
8
Break dosage, cell cycle stage and DNA replication influence DNA double strand break response.
EMBO J. 2008 Jul 9;27(13):1875-85. doi: 10.1038/emboj.2008.111. Epub 2008 May 29.
9
DNA repair in mammalian cells: DNA double-strand break repair: how to fix a broken relationship.
Cell Mol Life Sci. 2009 Mar;66(6):1039-56. doi: 10.1007/s00018-009-8740-3.
10
The role of RNA and RNA-related proteins in the regulation of DNA double strand break repair pathway choice.
DNA Repair (Amst). 2019 Sep;81:102662. doi: 10.1016/j.dnarep.2019.102662. Epub 2019 Jul 8.

引用本文的文献

1
Phase separation of ERCC6L2-CtIP regulates the extent of DNA end resection.
Nat Cell Biol. 2025 Sep 5. doi: 10.1038/s41556-025-01760-4.
2
DNA2 protein destruction dictates DNA hyperexcision, cGAS-STING activation, and innate immune response in CDK12-deregulated cancers.
Proc Natl Acad Sci U S A. 2025 Jul 15;122(28):e2413732122. doi: 10.1073/pnas.2413732122. Epub 2025 Jul 7.
4
Mechanisms of HDACs in cancer development.
Front Immunol. 2025 Apr 7;16:1529239. doi: 10.3389/fimmu.2025.1529239. eCollection 2025.
9
Structure-specific nucleases in genome dynamics and strategies for targeting cancers.
J Mol Cell Biol. 2024 Oct 21;16(5). doi: 10.1093/jmcb/mjae019.

本文引用的文献

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Human Dna2 is a nuclear and mitochondrial DNA maintenance protein.
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Cell cycle-dependent processing of DNA lesions controls localization of Rad9 to sites of genotoxic stress.
Cell Cycle. 2009 Jun 1;8(11):1765-74. doi: 10.4161/cc.8.11.8721. Epub 2009 Jun 10.
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Human RAD50 deficiency in a Nijmegen breakage syndrome-like disorder.
Am J Hum Genet. 2009 May;84(5):605-16. doi: 10.1016/j.ajhg.2009.04.010. Epub 2009 Apr 30.
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CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle.
Nature. 2009 May 21;459(7245):460-3. doi: 10.1038/nature07955. Epub 2009 Apr 8.
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MRE11 complex links RECQ5 helicase to sites of DNA damage.
Nucleic Acids Res. 2009 May;37(8):2645-57. doi: 10.1093/nar/gkp147. Epub 2009 Mar 6.
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Human CtIP mediates cell cycle control of DNA end resection and double strand break repair.
J Biol Chem. 2009 Apr 3;284(14):9558-65. doi: 10.1074/jbc.M808906200. Epub 2009 Feb 7.
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Human exonuclease 1 and BLM helicase interact to resect DNA and initiate DNA repair.
Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):16906-11. doi: 10.1073/pnas.0809380105. Epub 2008 Oct 29.
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The P. furiosus mre11/rad50 complex promotes 5' strand resection at a DNA double-strand break.
Cell. 2008 Oct 17;135(2):250-60. doi: 10.1016/j.cell.2008.09.054.
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DNA helicases Sgs1 and BLM promote DNA double-strand break resection.
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