β-Actin knock-out mouse embryonic fibroblasts show increased expression of LIM-, CH-, EFh-domain containing proteins...

β-actin depletion from mouse embryonic fibroblasts results in an altered transcriptional response rendering these cells a myofibroblast like phenotype. The proteins and upstream regulatory factors responsible for this acquired phenotype, with prominent focal adhesions and stress fibres, are unknown. Data-mining of the changed proteome revealed that actin binding proteins associated with stress fiber or focal adhesion formation are overexpressed in the β-actin knock-out cells and that many of these contain CH-, LIM- or EFh- domains. Furthermore in silico analysis predicts potential common upstream regulators that may, at least partly, coordinate the altered transcriptional response.