RECQL4-deficient cells are hypersensitive to oxidative stress/damage: Insights for osteosarcoma prevalence and heterogeneity in Rothmund-Thomson syndrome
- 23 June 2006
- journal article
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 345 (1) , 403-409
- https://doi.org/10.1016/j.bbrc.2006.04.093
Abstract
No abstract availableKeywords
This publication has 26 references indexed in Scilit:
- Defective sister-chromatid cohesion, aneuploidy and cancer predisposition in a mouse model of type II Rothmund-Thomson syndromeHuman Molecular Genetics, 2005
- Tumor suppressor p53 represses transcription of RECQ4 helicaseOncogene, 2005
- The RAD51 gene family, genetic instability and cancerCancer Letters, 2004
- Association Between Osteosarcoma and Deleterious Mutations in the RECQL4 Gene in Rothmund-Thomson SyndromeJNCI Journal of the National Cancer Institute, 2003
- RecQ helicases: caretakers of the genomeNature Reviews Cancer, 2003
- Differential regulation of human RecQ family helicases in cell transformation and cell cycleOncogene, 2000
- Rothmund-Thomson syndrome due toRECQ4 helicase mutations: Report and clinical and molecular comparisons with Bloom syndrome and Werner syndromeAmerican Journal of Medical Genetics, 2000
- Mutations in RECQL4 cause a subset of cases of Rothmund-Thomson syndromeNature Genetics, 1999
- The Bloom's Syndrome Gene Product Is a 3′-5′ DNA HelicaseJournal of Biological Chemistry, 1997
- Bloom's syndrome and Fanconi's anemia: Demonstration of two distinctive patterns of chromosome disruption and rearrangementPublished by Springer Nature ,1974