Author

C. Bonnemann

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

Biology Disciplines

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Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:human· 2 Research Focus:cell-cell communication· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Approach:genetic perturbation / CRISPR· 1 Assay:multiome· 1

Frequent Co-Authors

A. Beltran· 1 shared A. Zidell· 1 shared D. Armao· 1 shared D. Bharucha-Goebel· 1 shared E. A. Shoubridge· 1 shared H. F. Pedro· 1 shared J. A. Ezzell· 1 shared J. A. M. Saute· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCell Biology

A. Beltran

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Intermediate filament dysregulation and astrocytopathy in the human disease model of KLHL16 mutation in giant axonal neuropathy (GAN)

R. Battaglia, M. Faridounnia, A. Beltran, J. Robinson, K. Kinghorn, J. A. Ezzell, D. Bharucha-Goebel, C. Bonnemann, J. E. Hooper, P. Opal, T. W. Bouldin, D. Armao, N. Snider

This study investigates KLHL16 mutations in GAN using patient-derived iPSCs, revealing dysregulated intermediate filaments and astrocytic pathology.

bioRxiv · Mar 13, 2023 · 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