Quantitative proteomic mass spectrometry of protein kinases to determine dynamic heterogeneity of the human kinome.

The kinome is a dynamic system of kinases regulating signaling networks in cells and dysfunction of protein kinases contributes to many diseases. Regulation of the protein expression of kinases alters cellular responses to environmental changes and perturbations. We configured a library of 672 proteotypic peptides to quantify >300 kinases in a single LC-MS experiment using ten micrograms protein from human tissues including biopsies.

Text "HEALER": Using Text Mentorship to Engage American Indians and Alaska Natives Interested in the Health Professions.

ProblemThe persistent underrepresentation of American Indians and Alaska Natives (AIANs) in the health professions and the decline of AIAN matriculants into health-related programs suggest interventions are needed. The authors developed Healers, a text message mentoring service, to engage and support AIANs interested in the health professions.ApproachHealers, launched in 2018, seeks to reach urban and rural high school/college-aged AIANs and other AIANs.

The unique catalytic properties of PSAT1 mediate metabolic adaptation to glutamine blockade.

Cultured cancer cells frequently rely on the consumption of glutamine and its subsequent hydrolysis by glutaminase (GLS). However, this metabolic addiction can be lost in the tumour microenvironment, rendering GLS inhibitors ineffective in the clinic. Here we show that glutamine-addicted breast cancer cells adapt to chronic glutamine starvation, or GLS inhibition, via AMPK-mediated upregulation of the serine synthesis pathway (SSP).

MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer.

The Hippo signaling pathway is commonly dysregulated in human cancer, which leads to a powerful tumor dependency on the YAP/TAZ transcriptional coactivators. In this study, we used paralog cotargeting CRISPR screens to identify kinases MARK2/3 as absolute catalytic requirements for YAP/TAZ function in diverse carcinoma and sarcoma contexts. Underlying this observation is the direct MARK2/3-dependent phosphorylation of NF2 and YAP/TAZ, which effectively reverses the tumor suppressive activity of the Hippo module kinases LATS1/2.