Reuben J. Shaw

HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery

This study shows HDAC inhibition reduces DDR gene expression in pancreatic tumors by altering transcriptional machinery distribution, enhancing sensitivity to DNA damage, and introduces a nanoparticle delivery system to reduce toxicity.

Med14 phosphorylation shapes genomic response to GLP-1 Agonist

The paper identifies Med14 phosphorylation as essential for sustained GLP-1 agonist-induced gene regulation in beta cells.

Modeling Compound Lipid Homeostasis Using Stable Isotope Tracing

This study introduces CL-MFA to quantify lipid metabolic fluxes in NSCLC models, revealing LKB1 regulation of sphingolipid recycling and fatty acid synthase upregulation under standard culture conditions.

Synthesis and Characterization of ULK1/2 Kinase Inhibitors that Inhibit Autophagy and Upregulate Expression of Major Histocompatibility Complex I for the Treatment of Non-Small Cell Lung Cancer

The paper reports the design, synthesis, and characterization of new ULK1/2 inhibitors that inhibit autophagy and upregulate MHC I in NSCLC cells, supporting their potential as cancer therapeutics.

ULK1/2 Inhibitors that Degrade ATG13 Effectively Target KRAS-Mutant Cancers

The paper identifies SBP-1750, a ULK inhibitor that degrades ATG13 and kills KRAS-mutant cancer cells, showing efficacy in vivo and immune enhancement.

Multi-site phosphorylation of BCL2L13 in a TBK1- and AMPK-dependent manner reveals new modes of mitophagy regulation

This study identifies phosphorylation sites in BCL2L13 regulated by AMPK and TBK1, revealing a novel mechanism for mitophagy regulation.

Leveraging autophagy and pyrimidine metabolism to target pancreatic cancer

This study identifies metabolic adaptations in pancreatic cancer cells resistant to autophagy inhibitors and shows that targeting pyrimidine salvage can enhance treatment efficacy.

Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy

This study shows Aβ42 oligomers cause synaptic loss by activating CAMKK2-AMPK, which coordinates mitochondrial fission and mitophagy in neurons.

Spatial regulation of AMPK signaling revealed by a sensitive kinase activity reporter

The paper develops a sensitive AMPK activity reporter, ExRai AMPKAR, to study subcellular AMPK dynamics and reveals differential regulation of AMPK activity at lysosomes, mitochondria, and the nucleus.