Author

M. Frieden

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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Physiology· 2 Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:cell type annotation· 2 Organism:human· 2 Organism:mouse· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1

Frequent Co-Authors

S. Koenig· 2 shared A. Carreras-Sureda· 1 shared A. Prola· 1 shared A. Ruiz· 1 shared A. Schmidt· 1 shared B. Domingo· 1 shared C. Ferec· 1 shared C. Le Marechal· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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2 shared papersPhysiology

S. Koenig

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4 papers

Recent·Most cited

mTORC1-dependent SOCE activity regulates synaptic gene expression and muscle response to denervation

A. Prola, O. Dupont, J. Rajendran, F. Chabry, S. Koenig, M. Frieden, P. Castets

The paper identifies SOCE's role in synaptic gene regulation and muscle response to denervation, showing mTORC1's involvement in this process.

bioRxiv · Apr 1, 2024 · PreprintPhysiology

Quantitative proteomic analysis of skeletal muscles from wild type and transgenic mice carrying recessive Ryr1 mutations linked to congenital myopathies

J. Eckhardt, A. Ruiz, S. Koenig, M. Frieden, A. Schmidt, S. Treves, F. Zorzato

The paper quantitatively analyzes proteomic differences in skeletal muscles of wild type and Ryr1 mutant mice, revealing reduced RyR1 and altered protein content linked to congenital myopathies.

bioRxiv · Sep 26, 2022Physiology

S-acylation targets ORAI1 channels to lipid rafts for efficient Ca2+ signaling by T cell receptors at the immune synapse

A. Carreras-Sureda, L. Abrami, K. JI-Hee, M. Frieden, M. Didier, F. G. van der Goot, N. Demaurex

This study shows that S-acylation of ORAI1 channels at Cys143 by ZDHHC20 is essential for TCR signaling and Ca2+ flux at the immune synapse.

bioRxiv · Feb 3, 2021Biochemistry

p.E152K-STIM1 mutation deregulates Ca2+ signaling contributing to chronic pancreatitis.

M. Burgos, R. Phillipe, F. Antigny, P. Buscaglia, E. Masson, S. Mukherjee, P. Dubar, C. Le Marechal, F. Campeotto, N. Lebonvallet, M. Frieden, J. Llopis, B. Domingo, P. B. Stathopulos, M. Ikura, , O. Mignen

The paper identifies a p.E152K-STIM1 mutation that disrupts Ca2+ signaling in pancreatic acinar cells, leading to trypsin activation and cell death in pancreatitis patients.

bioRxiv · Jan 22, 2020Cell Biology