figshare
Browse

Christoph Schweingruber

Researcher (Biological sciences; Biomedical and clinical sciences)

Stockholm

Publications

  • Interactions of CstF-64, CstF-77, and symplekin: implications on localisation and function.
  • Nonsense-mediated mRNA decay - mechanisms of substrate mRNA recognition and degradation in mammalian cells.
  • The host nonsense-mediated mRNA decay pathway restricts Mammalian RNA virus replication.
  • Identification of Interactions in the NMD Complex Using Proximity-Dependent Biotinylation (BioID).
  • Minor intron splicing is regulated by FUS and affected by ALS-associated FUS mutants.
  • LCM-seq reveals unique transcriptional adaption mechanisms of resistant neurons in spinal muscular atrophy
  • A radical switch in clonality reveals a stem cell niche in the epiphyseal growth plate.
  • Modeling motor neuron resilience in ALS using stem cells
  • Modeling Motor Neuron Resilience in ALS Using Stem Cells
  • LCM-seq reveals unique transcriptional adaptation mechanisms of resistant neurons and identifies protective pathways in spinal muscular atrophy
  • Aberrant interaction of FUS with the U1 snRNA provides a molecular mechanism of FUS induced amyotrophic lateral sclerosis
  • The Cell Autonomous and Non-Cell Autonomous Aspects of Neuronal Vulnerability and Resilience in Amyotrophic Lateral Sclerosis
  • Single cell RNA sequencing in isogenic FUS and TARDBP mutant ALS lines reveals early mitochondrial dysfunction as a common pathway in motor neurons
  • Single cell RNA sequencing in isogenicFUSandTARDBPmutant ALS lines reveals early mitochondrial dysfunction as a common pathway in motor neurons
  • Human motor neurons are rare and can be transcriptomically divided into known subtypes
  • Challenges of profiling motor neuron transcriptomes from human spinal cord
  • Single-cell RNA sequencing across isogenic FUS and TARDBP ALS lines reveals a shared early mitochondrial dysfunction unique to motor neurons.
  • Single-cell RNA sequencing across isogenicFUSandTARDBPALS lines reveals a shared early mitochondrial dysfunction unique to motor neurons

Usage metrics

Co-workers & collaborators

Christoph Schweingruber's public data