Identification of Domains of Ataxia-telangiectasia Mutated Required for Nuclear Localization and Chromatin Association
Open Access
- 1 July 2005
- journal article
- Published by Elsevier BV in Journal of Biological Chemistry
- Vol. 280 (30), 27587-27594
- https://doi.org/10.1074/jbc.m411689200
Abstract
No abstract availableKeywords
This publication has 22 references indexed in Scilit:
- DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociationNature, 2003
- ATM, a central controller of cellular responses to DNA damageCell Death & Differentiation, 2001
- The Human Origin Recognition Complex Protein 1 Dissociates from Chromatin during S Phase in HeLa CellsJournal of Biological Chemistry, 2001
- ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulationProceedings of the National Academy of Sciences, 2000
- Expression of the ataxia-telangiectasia gene (ATM) product in human cerebellar neurons during developmentNeuroscience Letters, 1998
- Transport into and out of the cell nucleusThe EMBO Journal, 1998
- Isolation of full-length ATM cDNA and correction of the ataxia-telangiectasia cellular phenotypeProceedings of the National Academy of Sciences of the United States of America, 1997
- Cellular localisation of the ataxia-telangiectasia (ATM) gene product and discrimination between mutated and normal formsOncogene, 1997
- Nucleocytoplasmic transport: signals, mechanisms and regulationNature, 1997
- The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not up-regulated following genome damageProceedings of the National Academy of Sciences of the United States of America, 1997