Literature DB >> 24582502

Non-homologous end joining: emerging themes and unanswered questions.

Sarvan Kumar Radhakrishnan1, Nicholas Jette1, Susan P Lees-Miller2.   

Abstract

Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation induced DNA double strand breaks in human cells. Here, we discuss current insights into the mechanism of NHEJ and the interplay between NHEJ and other pathways for repair of IR-induced DNA damage.
Copyright © 2014 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  DNA double strand break repair; Ionizing radiation; Non-homologous end joining

Mesh:

Substances:

Year:  2014        PMID: 24582502      PMCID: PMC4084493          DOI: 10.1016/j.dnarep.2014.01.009

Source DB:  PubMed          Journal:  DNA Repair (Amst)        ISSN: 1568-7856


  129 in total

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2.  Purification and characterization of a template-associated protein kinase that phosphorylates RNA polymerase II.

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3.  PARP-3 and APLF function together to accelerate nonhomologous end-joining.

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

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7.  APLF promotes the assembly and activity of non-homologous end joining protein complexes.

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Review 9.  Induction and repair of clustered DNA lesions: what do we know so far?

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Journal:  Radiat Res       Date:  2013-05-17       Impact factor: 2.841

10.  A noncatalytic function of the ligation complex during nonhomologous end joining.

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  57 in total

1.  DNA Damage Repair Inhibitor for Breast Cancer Treatment.

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Review 6.  What Combined Measurements From Structures and Imaging Tell Us About DNA Damage Responses.

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7.  Characterization of Cardiac Glycoside Natural Products as Potent Inhibitors of DNA Double-Strand Break Repair by a Whole-Cell Double Immunofluorescence Assay.

Authors:  Yulia V Surovtseva; Vikram Jairam; Ahmed F Salem; Ranjini K Sundaram; Ranjit S Bindra; Seth B Herzon
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8.  The human DNA ends proteome uncovers an unexpected entanglement of functional pathways.

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9.  Probing Enhanced Double-Strand Break Formation at Abasic Sites within Clustered Lesions in Nucleosome Core Particles.

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10.  DNA repair factor APLF acts as a H2A-H2B histone chaperone through binding its DNA interaction surface.

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