Ana Maria G Dumitru, Scott F Rusin ... Duane A Compton
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.
PDK1 serves as a critical role for intrinsically promoting T follicular helper cell differentiation and effector functions via controlling expression level of TCF1.
Loss of hepatic Cdk1 leads to oxidative stress, increased fatty acids in blood, and hyperinsulinemia, which resulted in insulin resistance and hepatic steatosis, similar as in diabetes.
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.
In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.
Joaquim Grego-Bessa, Joshua Bloomekatz ... Kathryn V Anderson
In addition to its role in regulating proliferation and cell death, the PTEN tumor suppressor regulates epithelial morphogenesis through the PDK1 kinase.
Olga Afonso, Colleen M Castellani ... Helder Maiato
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.
Unbiased proteomics and molecular analysis revealed a new role for S6K1 in regulating DNA repair through the orchestrated phosphorylation of CDK1 and MSH6. The findings may explain why RPS6KB1 gene amplification contributed to breast cancer drug resistance.