Mutational dynamics between primary and relapse neuroblastomas.
Essen, Germany. In Nat Genet, Aug 2015
Recurrent alterations at relapse included mutations in the putative CHD5 neuroblastoma tumor suppressor, chromosome 9p losses, DOCK8 mutations, inactivating mutations in PTPN14 and a relapse-specific activity pattern for the PTPN14 target YAP.
Towards elucidating the stability, dynamics and architecture of the nucleosome remodeling and deacetylase complex by using quantitative interaction proteomics.
Nijmegen, Netherlands. In Febs J, May 2015
STRUCTURED DIGITAL ABSTRACT: MBD3 physically interacts with ZNF512B, HDAC1, ZMYND8, GATAD2B, SALL4, GATAD2A, ZNF592, MTA3, ZNF687, CDK2AP1, CHD3, ZNF532, HDAC2, MTA2, CHD4, MTA1, KPNA2, CHD5, RBBP4 and RBBP7 by pull down (View interaction) CDK2AP1 physically interacts with MBD3, MTA3, HDAC2, GATAD2A, CHD4, CDK2AP1, MTA2, HDAC1, MTA1, CHD3, GATAD2B, MBD2, RBBP4 and RBBP7 by pull down (View interaction) MBD3 physically interacts with MTA2, MTA3, RBBP4, RBBP7, HDAC2, HDAC1, CHD4, CHD3 and MTA1 by cross-linking study (View interaction).
CHD chromatin remodelling enzymes and the DNA damage response.
Calgary, Canada. In Mutat Res, 2013
We will first touch upon all four major chromatin remodelling enzyme families and then focus chiefly on the nine members of the Chromodomain, Helicase, DNA-binding (CHD) family, particularly CHD3, CHD4, CHD5 and CHD6.
1p36 tumor suppression--a matter of dosage?
Heidelberg, Germany. In Cancer Res, 2013
We discuss recent data derived from both human tumors and functional cancer models indicating that the 1p36 genes CHD5, CAMTA1, KIF1B, CASZ1, and miR-34a contribute to cancer development when reduced in dosage by genomic copy number loss or other mechanisms.
Mechanisms of CHD5 Inactivation in neuroblastomas.
Philadelphia, United States. In Clin Cancer Res, 2012
We conclude that (i) somatically acquired CHD5 mutations are rare in primary NBs, so inactivation probably occurs by deletion and epigenetic silencing.