The stem cells of the postnatal muscle allow postnatal muscle growth and repair and withdraw from the cell cycle when the tyrosine phosphatase Ptpn11 (Shp2) is inhibited or mutated in mice.

The tandem SH2 domains of Spt6 use novel mechanisms to bind unexpected phosphorylated serine and threonine residues in the RNA polymerase II linker to recruit Spt6 to sites of transcription and maintain repressive chromatin.

The recruitment of SH2-containing proteins to Epidermal Growth Factor in cells happens more slowly than predicted by in vitro techniques.

By binding to Fc gamma receptor IIb, amyloid beta induces a series of phosphorylation events that mediate the damaging effects of hyperphosphorylated tau proteins in Alzheimer's disease.

The SHIP2 inositol phosphatase is an important upstream regulator of the Akt signaling pathway, which requires a catalytic core formed by the phosphatase domain tightly packed to a C2 domain for its function.

Crk proteins are critical mediators of FGF signaling to control cell shape changes.

Based on its nucleotide-bound state, the Chd1 chromatin remodeler can locally alter DNA twist on the nucleosome, which either pulls in or expels ~1 bp of DNA at the internal SHL2 binding site.

Chronic engagement of Natural killer cell inhibitory receptors by MHC-I molecules maintains a high activity of the mTOR pathway allowing subsequent amplification of signaling through activating receptors upon acute stimulation.

Local presynaptic protein synthesis occurring at established nerve terminals in the mammalian brain provides a mechanism for rapidly controlling or restoring presynaptic proteins that affect neurotransmitter release and presynaptic efficiency.