Michael J. Kruhlak

This study shows that deep vein thrombosis primes neutrophils to promote brain metastasis in triple-negative breast cancer by enhancing their recruitment and NET formation.

This study identifies SAC competency as the determinant of sensitivity to KIF18A inhibition in SCLC, offering a predictive biomarker for targeted therapies.

The paper uses intravital imaging in zebrafish to show age-dependent changes in collective T cell migration patterns in fins, linking tissue structure and immune function.

This study demonstrates that cell penetrating thyclotides enhance the cellular uptake and endosomal escape of bioactive peptides, improving their therapeutic potential.

This paper identifies RRP1B as a stress-responsive regulator of RNA processing and splicing in breast cancer, showing its role in splicing programs and tumor aggressiveness.

This study shows that EWSR1 forms a ribonucleoprotein network with nascent RNA, and its loss leads to compensatory reorganization of FUS and TAF15, revealing functional redundancy in maintaining nascent RNA homeostasis.

Imaging of mitochondria and lipid droplets (LDs) across mouse liver lobules shows fasting, not Western diet, expands mitochondria-LD contacts; PLIN5 phosphomutants tune contacts and lipid storage.

This study identifies immune-tumor interactions that drive tumor dormancy in a mouse model, highlighting IFN-γ-KLF4-SLURP1 and CD200-CD200R1 pathways.

The paper quantifies CDK activity in mouse embryos and shows it decreases in trophectoderm cells before implantation, correlating with FGF4 signaling, but does not determine cell fate.

This study shows cancer stem cells (CSCs) have distinct population dynamics and are hyper-responsive to microenvironmental cues, which regulate metastasis and therapy response via the YAP/TAZ/TEAD pathway.

This study shows pericyte-tumor interactions promote metastatic tumor cell dormancy via PIEZO1-mediated lysophospholipid transfer, enhancing persistence and relapse risk.

The paper shows AGO2 localizes to the nucleus in quiescent cells to silence mobile transposons via RNA interference.

This study identifies ERF as a key transcription factor that facilitates the exit from naive pluripotency by regulating enhancer activity and DNMT3B expression during the transition to primed pluripotency.

This study identifies CTCF as a barrier to 2C-like reprogramming in ESCs, showing its role in maintaining chromatin structure and that its depletion promotes totipotent-like state conversion.