title: Forcing FAK into Transcriptional Activity.
abstract: Focal adhesion kinase (FAK) has known signaling roles in cytoplasmic adhesion structures, but was recently shown to act as a transcriptional regulator in the nucleus. In this issue of Structure, Cardoso et al. (2016) report that mechanical forces translocate FAK to the nucleus of cardiomyocytes, and provide structural insights into how FAK interacts with the MEF2 transcription factor to control cardiac hypertrophy.
authors.affiliation: Cell Signalling and Adhesion Group, Structural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Calle Melchor Fernández Almagro 3, Madrid 28029, Spain. Electronic address: dlietha@cnio.es.
authors.forename: Daniel
authors.initials: D
authors.lastname: Lietha
mesh_terms: D006332:Cardiomegaly; D002467:Cell Nucleus; D002478:Cells, Cultured; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000737:chemistry*; D006801:Humans; D011505:Protein-Tyrosine Kinases; D015398:Signal Transduction
chemical_list: D011505:Protein-Tyrosine Kinases; D051416:Focal Adhesion Protein-Tyrosine Kinases