Sort by
Items per page

Send to

Choose Destination

Links from PubMed

Items: 1 to 20 of 82


Ku's essential role in keeping telomeres intact.

Indiviglio SM, Bertuch AA.

Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12217-8. doi: 10.1073/pnas.0906427106. Epub 2009 Jul 21. No abstract available.


Processing of human telomeres by the Werner syndrome protein.

Reddy S, Li B, Comai L.

Cell Cycle. 2010 Aug 15;9(16):3137-8. doi: 10.4161/cc.9.16.12952. Epub 2010 Aug 9. No abstract available.


TRF2 interaction with Ku heterotetramerization interface gives insight into c-NHEJ prevention at human telomeres.

Ribes-Zamora A, Indiviglio SM, Mihalek I, Williams CL, Bertuch AA.

Cell Rep. 2013 Oct 17;5(1):194-206. doi: 10.1016/j.celrep.2013.08.040. Epub 2013 Oct 3.


Ku86 represses lethal telomere deletion events in human somatic cells.

Wang Y, Ghosh G, Hendrickson EA.

Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12430-5. doi: 10.1073/pnas.0903362106. Epub 2009 Jul 6.


Ku interacts with telomerase RNA to promote telomere addition at native and broken chromosome ends.

Stellwagen AE, Haimberger ZW, Veatch JR, Gottschling DE.

Genes Dev. 2003 Oct 1;17(19):2384-95. Epub 2003 Sep 15.


Coordinate action of the helicase and 3' to 5' exonuclease of Werner syndrome protein.

Opresko PL, Laine JP, Brosh RM Jr, Seidman MM, Bohr VA.

J Biol Chem. 2001 Nov 30;276(48):44677-87. Epub 2001 Sep 25.


The Ku-binding motif is a conserved module for recruitment and stimulation of non-homologous end-joining proteins.

Grundy GJ, Rulten SL, Arribas-Bosacoma R, Davidson K, Kozik Z, Oliver AW, Pearl LH, Caldecott KW.

Nat Commun. 2016 Apr 11;7:11242. doi: 10.1038/ncomms11242.


[Biological functions of DNA helicase responsible for Werner syndrome].

Sakamoto S, Shimamoto A, Furuichi Y.

Tanpakushitsu Kakusan Koso. 2001 Jun;46(8 Suppl):1073-81. Review. Japanese. No abstract available.


Molecular biology. DNA ends ReQ-uire attention.

Wu L, Hickson ID.

Science. 2001 Apr 13;292(5515):229-30. No abstract available.


Unraveling the roles of WRN and DNA-PKcs at telomeres.

Beattie TL, Lees-Miller SP.

Aging (Albany NY). 2010 May;2(5):257-8. No abstract available.


Which end: dissecting Ku's function at telomeres and double-strand breaks.

Bertuch AA, Lundblad V.

Genes Dev. 2003 Oct 1;17(19):2347-50. Review. No abstract available.


Telomere maintenance is dependent on activities required for end repair of double-strand breaks.

Nugent CI, Bosco G, Ross LO, Evans SK, Salinger AP, Moore JK, Haber JE, Lundblad V.

Curr Biol. 1998 May 21;8(11):657-60.


A means to a DNA end: the many roles of Ku.

Downs JA, Jackson SP.

Nat Rev Mol Cell Biol. 2004 May;5(5):367-78. Review. No abstract available.


WRN Exonuclease activity is blocked by specific oxidatively induced base lesions positioned in either DNA strand.

Bukowy Z, Harrigan JA, Ramsden DA, Tudek B, Bohr VA, Stevnsner T.

Nucleic Acids Res. 2008 Sep;36(15):4975-87. doi: 10.1093/nar/gkn468. Epub 2008 Jul 25.


Requirements for the nucleolytic processing of DNA ends by the Werner syndrome protein-Ku70/80 complex.

Li B, Comai L.

J Biol Chem. 2001 Mar 30;276(13):9896-902. Epub 2001 Jan 4.


Functional interaction between Ku and the werner syndrome protein in DNA end processing.

Li B, Comai L.

J Biol Chem. 2000 Sep 15;275(37):28349-52. Erratum in: J Biol Chem 2000 Dec 15;275(50):39800.


Werner protein cooperates with the XRCC4-DNA ligase IV complex in end-processing.

Kusumoto R, Dawut L, Marchetti C, Wan Lee J, Vindigni A, Ramsden D, Bohr VA.

Biochemistry. 2008 Jul 15;47(28):7548-56. doi: 10.1021/bi702325t. Epub 2008 Jun 18.


Fission yeast Rhp51 is required for the maintenance of telomere structure in the absence of the Ku heterodimer.

Kibe T, Tomita K, Matsuura A, Izawa D, Kodaira T, Ushimaru T, Uritani M, Ueno M.

Nucleic Acids Res. 2003 Sep 1;31(17):5054-63.

Supplemental Content

Support Center