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Journal Abstract Search

244 related items for PubMed ID: 11809892

  • 1. Differential requirement for the ATPase domain of the Cockayne syndrome group B gene in the processing of UV-induced DNA damage and 8-oxoguanine lesions in human cells.
    Selzer RR, Nyaga S, Tuo J, May A, Muftuoglu M, Christiansen M, Citterio E, Brosh RM, Bohr VA.
    Nucleic Acids Res; 2002 Feb 01; 30(3):782-93. PubMed ID: 11809892
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  • 2. The ATPase domain but not the acidic region of Cockayne syndrome group B gene product is essential for DNA repair.
    Brosh RM, Balajee AS, Selzer RR, Sunesen M, Proietti De Santis L, Bohr VA.
    Mol Biol Cell; 1999 Nov 01; 10(11):3583-94. PubMed ID: 10564257
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  • 3. Role of the ATPase domain of the Cockayne syndrome group B protein in UV induced apoptosis.
    Balajee AS, Proietti De Santis L, Brosh RM, Selzer R, Bohr VA.
    Oncogene; 2000 Jan 27; 19(4):477-89. PubMed ID: 10698517
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  • 4. Phenotypic consequences of mutations in the conserved motifs of the putative helicase domain of the human Cockayne syndrome group B gene.
    Muftuoglu M, Selzer R, Tuo J, Brosh RM, Bohr VA.
    Gene; 2002 Jan 23; 283(1-2):27-40. PubMed ID: 11867210
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  • 5. The transcriptional response after oxidative stress is defective in Cockayne syndrome group B cells.
    Kyng KJ, May A, Brosh RM, Cheng WH, Chen C, Becker KG, Bohr VA.
    Oncogene; 2003 Feb 27; 22(8):1135-49. PubMed ID: 12606941
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  • 8. Functional consequences of mutations in the conserved SF2 motifs and post-translational phosphorylation of the CSB protein.
    Christiansen M, Stevnsner T, Modin C, Martensen PM, Brosh RM, Bohr VA.
    Nucleic Acids Res; 2003 Feb 01; 31(3):963-73. PubMed ID: 12560492
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  • 9. Functional crosstalk between hOgg1 and the helicase domain of Cockayne syndrome group B protein.
    Tuo J, Chen C, Zeng X, Christiansen M, Bohr VA.
    DNA Repair (Amst); 2002 Nov 03; 1(11):913-27. PubMed ID: 12531019
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  • 13. The C-terminal Region and SUMOylation of Cockayne Syndrome Group B Protein Play Critical Roles in Transcription-coupled Nucleotide Excision Repair.
    Sin Y, Tanaka K, Saijo M.
    J Biol Chem; 2016 Jan 15; 291(3):1387-97. PubMed ID: 26620705
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  • 14. Host cell reactivation of plasmids containing oxidative DNA lesions is defective in Cockayne syndrome but normal in UV-sensitive syndrome fibroblasts.
    Spivak G, Hanawalt PC.
    DNA Repair (Amst); 2006 Jan 05; 5(1):13-22. PubMed ID: 16129663
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  • 15. Structural basis of ubiquitin recognition by the winged-helix domain of Cockayne syndrome group B protein.
    Takahashi TS, Sato Y, Yamagata A, Goto-Ito S, Saijo M, Fukai S.
    Nucleic Acids Res; 2019 Apr 23; 47(7):3784-3794. PubMed ID: 30753618
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  • 17. Efficient UV repair requires disengagement of the CSB winged helix domain from the CSB ATPase domain.
    Batenburg NL, Qin J, Walker JR, Zhu XD.
    DNA Repair (Amst); 2018 Aug 23; 68():58-67. PubMed ID: 29957539
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  • 18. Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress.
    Kristensen U, Epanchintsev A, Rauschendorf MA, Laugel V, Stevnsner T, Bohr VA, Coin F, Egly JM.
    Proc Natl Acad Sci U S A; 2013 Jun 18; 110(25):E2261-70. PubMed ID: 23733932
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  • 19. A ubiquitin-binding domain in Cockayne syndrome B required for transcription-coupled nucleotide excision repair.
    Anindya R, Mari PO, Kristensen U, Kool H, Giglia-Mari G, Mullenders LH, Fousteri M, Vermeulen W, Egly JM, Svejstrup JQ.
    Mol Cell; 2010 Jun 11; 38(5):637-48. PubMed ID: 20541997
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