Whitney R. Smith-Kinnaman

The paper investigates how EXOSC3 p.G191 variants affect RNA processing by analyzing transcriptomic, proteomic, and structural data in human cell models.

This study shows that suppressing PP2A-B56α promotes EMT in EGFR mutant NSCLC by reducing epithelial markers and increasing mesenchymal markers, leading to migratory and invasive phenotypes.

This study identifies changes in non-histone lysine methylation during neuronal differentiation of LUHMES cells using quantitative proteomics.

This study shows that spinophilin enhances D2R interaction with cytosolic proteins, contributing to D2R agonist-induced locomotor suppression in Parkinson's disease.

This study shows that activating PP2A-B56 in PDAC increases EGFR signaling and promotes tumor growth, suggesting a new therapeutic target.

The paper investigates how EXOSC3 S1-domain variants disrupt RNA exosome function, leading to altered rRNA processing and mRNA targeting.

The paper uses proteomics and PISA analysis to study PERK-dependent changes in protein homeostasis during ER stress induced by tunicamycin.

The paper quantifies non-histone lysine methylation sites and lysine demethylases in breast cancer cell lines using TMT labeling without antibody enrichment, identifying differentially abundant sites and enzymes.

This study defines the Hrq1 interactome in yeast using multi-omics approaches, revealing its role in DNA repair, transcription, and ICL repair, and linking it to human RECQL4 disease mechanisms.

This paper shows that Rtr1 prevents premature transcription termination by restricting the NNS-dependent termination pathway and facilitating low-level elongation of noncoding transcripts.