J. M. Drake

The paper characterizes the proteome and phosphoproteome of prostate cancer patient-derived xenografts to identify differences between neuroendocrine-like and adenocarcinoma subtypes.

This study identifies ATGL as a CAMKK2-AMPK target that promotes CRPC progression by enhancing lipase activity and metabolic plasticity, suggesting it as a therapeutic target.

The paper uses an integrative approach to study mosquito dynamics in urban areas, finding differences in people's experiences with mosquitoes despite no difference in abundance.

This study identifies CREB5 as a key driver of resistance to androgen receptor targeting therapies by reprogramming nuclear interactions and activating TGFβ and Wnt signaling pathways.

The paper identifies predictors of zoonotic potential in helminths using a global dataset, finding that transmission and geographic traits are more important than morphology or epidemiology.

This paper designs pro-enzymes using computational methods and validates their activity regulation through protease cleavage.

The paper analyzes the spatial spread of white-nose syndrome in North America from 2006-2018, finding changing factors influencing its spread over time.

This study identifies a synergistic combination of cabozantinib and dasatinib that reduces viability and induces tumor regression in NCCRCC, with mechanisms involving MAPK-ERK pathway suppression.

This study assesses temperature-dependent competition between Aedes aegypti and Anopheles stephensi, finding Ae. aegypti dominates due to higher larval survival and growth rates across temperatures.

This study identifies p38/MAPK pathway activation as a convergent mechanism driving survival, immune evasion, and metastasis in hormone-resistant prostate cancer.

The paper analyzes changes in removal rates and hospitalization times during outbreaks of EVD, SARS, and MERS to assess population behavior changes.

The paper identifies how LynA is selectively degraded in macrophages via c-Cbl targeting tyrosine 32, while mast cells, with low c-Cbl, maintain high LynA levels, affecting signaling.

The paper identifies RET kinase as a targetable driver in neuroendocrine prostate cancer (NEPC) through phosphoproteomics and pharmacological inhibition studies, showing reduced tumor growth in models.