The amount of secreted Pgk1 is sharply decreased in Rtn4al/NogoA-overexpressed muscle cells, leading to various manifestations of neurodegenerative disease, including denervated neuromuscular junction and failed neurite outgrowth of motoneurons.
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.
Quantitative live-cell microscopy and molecular perturbations in Drosophila and human cells reveal a crosstalk between molecular 'rulers' (Aurora B) and 'clocks' (Cdk1) that coordinates mitotic exit in space and time.
p27Kip1 directly controls invadopodia turnover by promoting the interaction of PAK1 with Cortactin, which induces Cortactin phosphorylation, invadopodia disassembly and facilitates invasion through extracellular matrix.
The gluconeogenic enzyme PCK1 and pyrimidine nucleotide biosynthetic enzyme DHODH drive hypoxic pyrimidine nucleotide biosynthesis and liver metastatic colonization in colorectal cancer, which is therapeutically exploitable by DHODH pharmacologic inhibition.