Ronald J. Holewinski

This study identifies phosphorylation as a mechanism protecting oncogenic RAS from LZTR1-mediated degradation, with implications for targeting RAS stability in hematologic cancers.

The paper uses phosphoproteomic data and KMEA to identify tumor-specific kinase activity in GEP-NETs, revealing potential therapeutic targets.

This paper compares two 3D culture models for breast cancer cells, finding that the EmC model better mimics lung metastasis by altering metabolism and gene expression.

This paper develops a scalable method to generate pure CD103+ cDC1 from mouse bone marrow cultures, achieving high purity and yield for immunological studies.

This study shows that tRNA acetylation regulates stress signaling in mammals by affecting ribosome function and interacting with the Gcn2 kinase.

This study identifies acetylation of the Integrator complex as a key determinant of gene-specific transcriptional bursting patterns through high-throughput imaging screens.

This paper develops a 3D self-assembly system to engineer tumor stroma-like structures using decellularized ECM and cancer cells, showing effects on malignancy and metabolism.

The paper develops activity-based probes to selectively detect USP18 activity and screen for inhibitors, enabling analysis of USP18's role in disease states.

This study shows that NAT10 loss reduces lung metastasis by disrupting enhancer organization through p300 mislocalization and altering gene transcription related to metastasis.

This paper identifies key transcription and translation regulators affected by CDC treatment in rat HFpEF, correlating their levels with diastolic function improvements.

The paper introduces a method to quantify lysine and arginine PTMs in NASH using mass spectrometry and applies it to mouse liver lysates, finding altered methylation and acetylation in NASH.