Oliver Mühlemann

The paper identifies USP9X as a deubiquitinase that regulates the degradation of trapped translation factors on stalled ribosomes, showing its role in trimming K6-linked ubiquitin chains and modulating translation feedback mechanisms.

This study examines how full-length and C-terminally truncated progranulin affects cell proliferation, colony formation, and migration in HepG2 and U87 cells.

This study shows UPF1 shuttles between nucleus and cytoplasm without needing its RNA binding or ATPase activities, with RNA binding causing cytoplasmic retention.

The paper presents a scalable method for preparing cell-type-specific lysates from human cell lines to improve cell-free translation systems.

The paper introduces two novel readthrough promoters that induce eRF1 degradation, leading to PTC suppression and revealing a new ribosome quality control mechanism.

This study shows that inhibiting NMD reduces tumorigenicity in HT1080 fibrosarcoma cells by lowering MMP9 expression, suggesting NMD inhibition as a potential cancer therapy.

This paper introduces a dual centrifugation method to produce human translation-competent lysates, enabling efficient mRNA translation in both cap-dependent and IRES-mediated ways.

The paper uses long-read sequencing to identify novel NMD-sensitive mRNAs and reveals features of their biogenesis and biological role.

The paper develops a method to purify phase-separated FUS droplets and shows that LLPS alters FUS interactome composition, linking it to chromatin remodeling and mitochondrial function in ALS.

This study identifies the SFV capsid protein as an inhibitor of nonsense-mediated mRNA decay by mapping viral-host protein interactions.

This study shows that FUS-dependent liquid-liquid phase separation is essential for early DNA damage response activation and repair complex assembly.

This study shows SARS-CoV-2 Nsp1 binds to the 40S ribosomal subunit to inhibit translation by blocking mRNA entry, while viral mRNA enhances its own translation.

This study challenges the prevailing model of NMD by showing that ribosome stalling at stop codons does not occur during NMD activation in vitro or in vivo.

This study shows that ABCE1 depletion inhibits NMD by promoting stop codon readthrough, which displaces NMD factors from the 3' UTR.

This study identifies how ALS-causative FUS mutations disrupt RNA processing and autoregulation, with implications for broader ALS genetic interactions.