Literature DB >> 17292118

Modifying the function of DNA repair nanomachines for therapeutic benefit.

William S Dynan1, Yoshihiko Takeda, Shuyi Li.   

Abstract

This article, which is based on a presentation at the First Annual Meeting of the American Academy of Nanomedicine, is divided into three parts. First, we describe naturally occurring DNA repair nanomachines, using as an example the nanomachine that executes the nonhomologous end-joining (NHEJ) reaction for DNA double-strand break (DSB) repair. Second, we discuss therapeutic benefits that may be derived from the ability to modify the behavior of naturally occurring nanomachines, using as an example the concept of delaying DSB repair in rapidly dividing cancer cells to increase their natural sensitivity to radiation therapy. Third, we discuss similarities in the overall size, shape, and design of different nanomachines that manipulate DNA and RNA, and the possibility of developing nanomachines with new specificities not found in nature.

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Year:  2006        PMID: 17292118      PMCID: PMC2792907          DOI: 10.1016/j.nano.2006.04.004

Source DB:  PubMed          Journal:  Nanomedicine        ISSN: 1549-9634            Impact factor:   5.307


  49 in total

1.  Synapsis of DNA ends by DNA-dependent protein kinase.

Authors:  Lisa G DeFazio; Rachel M Stansel; Jack D Griffith; Gilbert Chu
Journal:  EMBO J       Date:  2002-06-17       Impact factor: 11.598

2.  Subnuclear localization of Ku protein: functional association with RNA polymerase II elongation sites.

Authors:  Xianming Mo; William S Dynan
Journal:  Mol Cell Biol       Date:  2002-11       Impact factor: 4.272

3.  Ku autoantigen is the regulatory component of a template-associated protein kinase that phosphorylates RNA polymerase II.

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Journal:  Proc Natl Acad Sci U S A       Date:  1992-12-15       Impact factor: 11.205

4.  Nibrin, a novel DNA double-strand break repair protein, is mutated in Nijmegen breakage syndrome.

Authors:  R Varon; C Vissinga; M Platzer; K M Cerosaletti; K H Chrzanowska; K Saar; G Beckmann; E Seemanová; P R Cooper; N J Nowak; M Stumm; C M Weemaes; R A Gatti; R K Wilson; M Digweed; A Rosenthal; K Sperling; P Concannon; A Reis
Journal:  Cell       Date:  1998-05-01       Impact factor: 41.582

5.  MDC1 is a mediator of the mammalian DNA damage checkpoint.

Authors:  Grant S Stewart; Bin Wang; Colin R Bignell; A Malcolm R Taylor; Stephen J Elledge
Journal:  Nature       Date:  2003-02-27       Impact factor: 49.962

6.  Autophosphorylation of the DNA-dependent protein kinase catalytic subunit is required for rejoining of DNA double-strand breaks.

Authors:  Doug W Chan; Benjamin Ping-Chi Chen; Sheela Prithivirajsingh; Akihiro Kurimasa; Michael D Story; Jun Qin; David J Chen
Journal:  Genes Dev       Date:  2002-09-15       Impact factor: 11.361

7.  NFBD1/MDC1 regulates ionizing radiation-induced focus formation by DNA checkpoint signaling and repair factors.

Authors:  Xingzhi Xu; David F Stern
Journal:  FASEB J       Date:  2003-10       Impact factor: 5.191

8.  Autophosphorylation of the catalytic subunit of the DNA-dependent protein kinase is required for efficient end processing during DNA double-strand break repair.

Authors:  Qi Ding; Yeturu V R Reddy; Wei Wang; Timothy Woods; Pauline Douglas; Dale A Ramsden; Susan P Lees-Miller; Katheryn Meek
Journal:  Mol Cell Biol       Date:  2003-08       Impact factor: 4.272

9.  The DNA-dependent protein kinase: requirement for DNA ends and association with Ku antigen.

Authors:  T M Gottlieb; S P Jackson
Journal:  Cell       Date:  1993-01-15       Impact factor: 41.582

10.  Histone deacetylase 4 interacts with 53BP1 to mediate the DNA damage response.

Authors:  Gary D Kao; W Gillies McKenna; Matthew G Guenther; Ruth J Muschel; Mitchell A Lazar; Tim J Yen
Journal:  J Cell Biol       Date:  2003-03-31       Impact factor: 10.539

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