Author

J. Schuettpelz

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cell Biology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell type annotation· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

a. janer· 2 shared H. Antonicka· 2 shared E. A. Shoubridge· 1 shared E. Shoubridge· 1 shared K. Watt· 1 shared O. Larsson· 1 shared

Activity by Year

2022-2024 · peak 1/yr

Co-Author Collaboration Network

6 top collaborators · 12 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCell Biology

a. janer

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

SLC25A46 is in contact with lysosomes and plays a role in mitochondrial cholesterol homeostasis

J. Schuettpelz, K. Watt, H. Antonicka, a. janer, O. Larsson, E. A. Shoubridge

This study shows SLC25A46 is required for stress-induced mitochondrial hyperfusion and involved in mitochondrial cholesterol homeostasis.

bioRxiv · Apr 1, 2024 · PreprintCell Biology

SLC25A46 localizes to sites of mitochondrial fission and fusion and loss of function variants alter the oligomerization states of MFN2 and OPA1

J. Schuettpelz, A. Janer, H. Antonicka, E. Shoubridge

This study investigates the role of SLC25A46 in mitochondrial dynamics, showing that its loss causes mitochondrial fragmentation and altered oligomerization of fusion proteins.

bioRxiv · Sep 16, 2022 · PreprintCell Biology