Author

M. J. Aaltonen

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 Biochemistry· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1

Frequent Co-Authors

E. A. Shoubridge· 2 shared A. Eiyama· 1 shared A. Janer· 1 shared A. Zidell· 1 shared A.-C. Gingras· 1 shared C. Bonnemann· 1 shared H. Antonicka· 1 shared H. F. Pedro· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 17 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

E. A. Shoubridge

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

ESYT1 tethers the endoplasmic reticulum to mitochondria and is required for mitochondrial lipid and calcium homeostasis

A. Janer, J. L. Morris, M. Krols, H. Antonicka, M. J. Aaltonen, Z.-Y. Lin, A.-C. Gingras, J. Prudent, E. A. Shoubridge

This study identifies ESYT1 as a key protein tethering ER and mitochondria at MERCs, showing its role in calcium and lipid homeostasis.

bioRxiv · Nov 14, 2022 · PreprintCell Biology

SPTLC1 variants associated with childhood onset amyotrophic lateral sclerosis produce distinct sphingolipid signatures through impaired interaction with ORMDL proteins

M. A. Lone, M. J. Aaltonen, A. Zidell, H. F. Pedro, J. A. M. Saute, S. Mathew, P. Mohassel, C. Bonnemann, E. A. Shoubridge, T. Hornemann

The paper shows that SPTLC1 variants causing childhood ALS disrupt ORMDL interactions, leading to altered sphingolipid synthesis and distinct lipid signatures, modifiable by L-serine availability.

bioRxiv · Apr 29, 2022 · PreprintBiochemistry

Disturbed intramitochondrial phosphatidic acid transport impairs cellular stress signaling

A. Eiyama, M. J. Aaltonen, H. Nolte, T. Tatsuta, T. Langer

This study shows that impaired phosphatidic acid transport into mitochondria disrupts ER membrane homeostasis and impairs glycolytic growth and stress signaling.

bioRxiv · Nov 5, 2020Cell Biology