F. McCormick

Ras-dependent RAF-MAPK hyperactivation by pathogenic RIT1 is a therapeutic target in Noonan syndrome-associated cardiac hypertrophy

This study identifies how pathogenic RIT1 mutations drive RAF-MAPK hyperactivation in Noonan syndrome, showing MEK inhibition can alleviate cardiac hypertrophy in a mouse model.

Structure of the SHOC2-MRAS-PP1C complex provides insights into RAF activation and Noonan syndrome

The paper presents the structure of the SHOC2-MRAS-PP1C complex and shows how it regulates RAF activation and is linked to Noonan syndrome mutations.

The RAS GTPase RIT1 compromises mitotic fidelity through spindle assembly checkpoint suppression

This study shows that RIT1, a Ras GTPase, suppresses the spindle assembly checkpoint, leading to mitotic errors and chromosome segregation defects.

UDP-glucose pyrophosphorylase 2, a regulator of glycosylation and glycogen, is essential for pancreatic cancer growth

This study identifies UGP2 as essential for pancreatic cancer growth by regulating glycogen and N-glycosylation, with potential therapeutic implications.

KRAS interaction with RAF1 RAS-binding domain and cysteine-rich domain provides insights into RAS-mediated RAF activation

The paper determines crystal structures of KRAS mutants bound to RAF1 domains, revealing molecular interactions critical for RAS-mediated RAF activation.

Biochemical and structural analysis reveals the Neurofibromin (NF1) protein forms a high-affinity dimer

This study shows Neurofibromin forms a high-affinity dimer through biochemical and structural analysis, with implications for its function in RAS-MAPK signaling.

Targeted phosphoproteomics of the Ras signaling network reveal regulatory mechanisms mediated by oncogenic KRAS

This study uses targeted phosphoproteomics to analyze KRAS signaling network regulation in lung cancer cells, identifying unique phosphorylation changes and their roles in transcriptional silencing.

Integration of pathway, cellular and genetic context reveals principles of synthetic lethality that affect reproducibility

The paper identifies principles for improving synthetic lethality reproducibility by integrating pathway, cellular, and genetic context in KRAS-mutant cells.

Facile real time detection of membrane colocalization of RAS superfamily GTPase proteins in living cells

This study uses ReBiL2.0 to show that the C-terminal HVR-CAAX domain directs KRAS to colocalize with other prenylated proteins, impacting its signaling.