<--- Back to Details
First PageDocument Content
Cell cycle / Cellular processes / Tumor suppressor genes / DNA repair / BRCT domain / Nibrin / Ataxia telangiectasia mutated / H2AFX / TOPBP1 / Biology / Cell biology / Proteins
Date: 2011-06-08 05:03:16
Cell cycle
Cellular processes
Tumor suppressor genes
DNA repair
BRCT domain
Nibrin
Ataxia telangiectasia mutated
H2AFX
TOPBP1
Biology
Cell biology
Proteins

The EMBO Journal, 3723–3732 www.embojournal.org |& 2010 European Molecular Biology Organization | All Rights Reserved

Add to Reading List

Source URL: molbio.unige.ch

Download Document from Source Website

File Size: 1,65 MB

Share Document on Facebook

Similar Documents

Genome-wide methylation analysis A common hallmark in tumorigenesis is the silencing of tumor suppressor genes by hypermethylation of promoter CpG islands. To facilitate the identification of novel hypermethylated  tumor

Genome-wide methylation analysis A common hallmark in tumorigenesis is the silencing of tumor suppressor genes by hypermethylation of promoter CpG islands. To facilitate the identification of novel hypermethylated tumor

DocID: 1sY7v - View Document

Profiling of UV-induced ATM/ATR signaling pathways -- Stokes et a…nasProceedings of the National Academy of Sciences:41 AM Institution: CELL SIGNALING TECH Sign In as Member / Individual

Profiling of UV-induced ATM/ATR signaling pathways -- Stokes et a…nasProceedings of the National Academy of Sciences:41 AM Institution: CELL SIGNALING TECH Sign In as Member / Individual

DocID: 1r1uz - View Document

Outlaw Human Gene Patents Because Human Genes Belong to Human Beings NOT Corporations. The US Supreme Court is currently considering the question

Outlaw Human Gene Patents Because Human Genes Belong to Human Beings NOT Corporations. The US Supreme Court is currently considering the question

DocID: 1qIXp - View Document

ISP2014 Poster Presentations (Updated) Registration ID Date  Time

ISP2014 Poster Presentations (Updated) Registration ID Date Time

DocID: 1qHwB - View Document

Microsoft Word - Document1

Microsoft Word - Document1

DocID: 1qrWU - View Document