M. Varjosalo

This study shows that KEAP1 mutations in lung cancer activate TRAF2-NFκB signaling, enhancing cell survival by preventing apoptosis.

This study identifies NERCLIN as a mitochondrial protein that regulates cardiolipin homeostasis and ultrastructure, with implications for stress-induced mitochondrial adaptation.

This study identifies GTPBP8 as a critical factor for mitoribosomal assembly and mitochondrial translation, showing its depletion impairs subunit maturation and function.

This study determines the structure of the endogenous human Commander complex using cryo-EM and proteomics, revealing its asymmetric organization and novel interactions involved in cellular processes.

This study investigates how canine parvovirus infection alters nucleolar structure and ribosome biogenesis using advanced imaging and biochemical techniques.

The paper shows that transient DUX4 expression in hESCs generates iBM cells with EGA-like profiles, resembling 8-cell blastomeres and can be enriched using SLC34A2.

This study identifies PROX1 as a master regulator of myogenic and oncogenic features in rhabdomyosarcoma, showing its role in stemness, tumor growth, and therapeutic potential through HDAC interactions.

This study shows that multiple antidepressants disrupt the TRKB:AP2M interaction, affecting TRKB surface expression and BDNF signaling.

The paper introduces tissue-ABPP, a method for high-resolution imaging of serine hydrolase activity in tissue sections, revealing activity hotspots in glioma tumors linked to neutrophils.

The paper identifies novel nuclear actin binding partners and functional roles in chromatin remodeling, transcription, and RNA splicing using mass spectrometry techniques.

This study identifies FGFR4 as a kinase that phosphorylates MST1, thereby inhibiting MST1/2-dependent apoptosis and promoting breast cancer cell survival.

The paper reports a novel gain-of-function TMEM173 mutation and its additive effects with IFIH1 risk allele on clinical phenotype in a multigeneration family.

The paper uses proteomics to analyze age-related retinal diseases, identifying inflammation and neurodegeneration as key factors in their pathogenesis.