Transcription profiling of Cockayne Syndrome human fibroblasts lacking functional CSB, a SWI/SNF-like ATPase, to determine the molecular defect in CS

ABSTRACT: Cockayne syndrome (CS) is an inherited neurodevelopmental disorder with progeroid features. Although the genes responsible for CS have been implicated in a variety of DNA repair- and transcription-related pathways, the nature of the molecular defect in CS remains mysterious. We sought to define this defect by expression analysis of cells lacking functional CSB, a SWI/SNF-like ATPase that is responsible for most CS cases.

ORGANISM(S): Homo sapiens

SUBMITTER: John Newman 

PROVIDER: E-GEOD-3407 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress