Markus Räschle

This study shows that mitochondrial presequences function in cytosolic quality control and trigger a heat shock response when mitochondrial import is inhibited.

The paper shows that Vms1 protects mitochondrial import and homeostasis during translation stress by interacting with Msp1.

The paper identifies a phospho-switch mechanism that reprograms TRAIP to ubiquitylate replisomes in mitosis, enabling disassembly of unreplicated DNA.

The paper identifies stress-induced changes in the surfaceome, revealing osmotic stress causes surface accumulation of CI-M6PR through reduced endocytosis and increased lysosomal exocytosis.

This study shows that BLM helicase is essential for resolving ultrafine DNA bridges during mitosis, preventing genomic instability.

This study uses explainable machine learning to identify factors that buffer protein levels in aneuploid cancer cells, finding key predictors and implications for therapy.

The paper identifies the cohibitin complex, including Aim11, as a quality control factor that supports TIM22-mediated insertion of carrier proteins into the mitochondrial inner membrane.

The paper classifies mitochondrial presequences into seven groups and identifies group A presequences as enhancing import efficiency through a specific targeting mechanism involving TOMM34.

This study shows that aneuploidy disrupts proteostasis, leading to mitochondrial dysfunction and accumulation of mitochondrial precursor proteins in cytosolic p62 bodies.

This study shows that BTRR complex deficiency increases genomic instability through copy number alterations, enriched at fragile sites, using CRISPR-edited iPSC models.

This study identifies Pex30's role in maintaining ER lipid homeostasis through membrane contact sites with peroxisomes and vacuoles in budding yeast.

The paper identifies adaptation strategies in aneuploid cancer cells through in vitro evolution and multi-omics analysis, revealing key transcription factors and genomic changes that improve proliferation and survival.

This study shows TopBP1 interacts with GINS via two distinct sites to support replication origin firing and predicts coordination of molecular processes in origin activation.

This study uses single-cell transcriptome analysis to show that BLM deficiency in Bloom syndrome patients alters gene expression related to mitosis, genomic instability, and condensin complexes.

This study shows that both SPRTN and the proteasome degrade DNA-protein crosslinks during DNA replication, using distinct mechanisms involving ubiquitylation and polymerase extension.