Author

D. C. Gorecki

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 Pathology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Organism:mouse· 3 Research Focus:differential expression· 2 Approach:experimental assay· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

J. Rog· 2 shared A. L. Giuliani· 1 shared A. Occhipinti· 1 shared A. Oksiejuk· 1 shared C. Angione· 1 shared C. Pinset· 1 shared E. Adinolfi· 1 shared F. Di Virgilio· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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2 shared papersBiochemistry

J. Rog

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

P2X7-dependent exchange of extracellular microparticles and mitochondria by mouse microglia

S. Falzoni, P. Chiozzi, V. Vultaggio-Poma, M. Tarantini, E. Adinolfi, P. Boldrini, A. L. Giuliani, D. C. Gorecki, F. Di Virgilio

This study shows that P2X7R-dependent release of microparticles containing mitochondria and other molecules modulates energy metabolism and inflammation in mouse microglia.

bioRxiv · Apr 18, 2023 · PreprintCell Biology

Metabotropic purinergic receptor profiles and calcium signalling in primary mice myoblasts differ depending on their muscle origin and are altered in cells with mutated dystrophin gene (mdx mice)

J. Rog, A. Oksiejuk, D. C. Gorecki, K. O. Zablocki

The paper investigates metabotropic purinergic receptor profiles and calcium signaling in primary myoblasts from different muscles of normal and mdx mice, finding differences in P2Y receptor expression and calcium signaling proteins between muscle origins and mdx mutations.

bioRxiv · Feb 16, 2022 · PreprintBiochemistry

Loss of full-length dystrophin expression results in major cell-autonomous abnormalities in proliferating myoblasts

M. R. Gosselin, V. Mournetas, M. Borczyk, S. Verma, A. Occhipinti, J. Rog, L. Bozycki, M. Korostynski, S. Robson, C. Angione, C. Pinset, D. C. Gorecki

This study shows that loss of full-length dystrophin in myoblasts causes cell-autonomous defects in gene expression, proliferation, chemotaxis, and differentiation, contributing to muscle regeneration failure in Duchenne muscular dystrophy.

bioRxiv · Aug 24, 2021Pathology