Structural and functional striatal synaptic plasticity abnormalities occur early in a sensitive developmental period, representing a potential unique endophenotypic traits that increase the risk of manifesting clinical symptoms in DYT1 mutation carriers.
A structural analysis of the transcription regulator Mot1 in complex with promoter DNA and the proteins TBP and NC2 provides a first structural framework for how a Swi2/Snf2 type remodeler interacts with a histone fold protein:DNA complex.
First comprehensive genetic analysis of a Myt1 family protein reveals that neurogenesis requires direct repression of non-neuronal identities by the Myt1 family protein through MuvB co-repressor complex.
Unfair competition, in which a phosphatase and a phosphoprotein inhibitor/substrate mutually sequester each other from competing substrates and enzymes, is a conserved mechanism for the control of PPP family phosphatases.
Quantitative phosphoproteomics defines the substrates for Cyclin A/Cdk1 kinase during early mitosis and follow up studies validate that one identified substrate, MYPT1, influences the stability of k-MT attachments by regulating Plk1.