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.

SAK1, a novel cytoplasmic phosphoprotein, is a key intermediate component of the retrograde signaling pathway controlling nuclear gene expression during acclimation of Chlamydomonas cells to singlet oxygen stress.

A novel retinal ganglion cell requires a cell adhesion molecule to grow its dendrites, collect synaptic inputs, and become selective to edges placed in its receptive field.

Overexpression of inhibitor of Bruton's tyrosine kinase contributes to the process of tumorigenesis by amplifying translation, represents a promising target for anti-cancer therapies.

LARP1 turns off and on the translation of an essential class of mRNAs by acting as a key effecter and regulator for mTORC1.

A new mechanism linking lysosomes to mTOR regulation and synaptic plasticity involves p18 ubiquitination by Ube3a, and underlies some of the pathology observed in Angelman syndrome.

The kinase AKT acts as a nodal point that coordinates both positive and negative cues to regulate the regeneration of central nervous system axons in adult mice.

Protein kinase A (PKA) phosphorylates Raptor and inhibits mammalian target of rapamycin complex 1 (mTORC1) activity.

Transcription profiling of activated cells using Phospho-Trap, a new method for identifying activated cells, reveals a critical role for mTOR signaling in red blood cell development and the pathogenesis of anemia

Single-cell data on cell signaling responses to nutrient variation enable quantitative models of cellular control over protein synthesis, formalizing the concept of mTOR as a homeostatic controller of cellular metabolism.