Author

M. E. Pasini

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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Cell Biology· 2 Physiology· 1

Signature Assays, Organisms & Methods

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Organism:Drosophila· 3 Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

P. Bellosta· 3 shared S. Santarelli· 2 shared S. Zola· 2 shared A. M. Valenza· 1 shared C. Bonfanti· 1 shared C. Gellera· 1 shared C. Paiardi· 1 shared D. Grifoni· 1 shared

Activity by Year

2019-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersCell Biology

P. Bellosta

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Author profile →

3 papers

Recent·Most cited

A Novel Drosophila Model to Investigate Adipose Tissue Macrophage Infiltration (ATM) and Obesity highlights the Therapeutic Potential of Attenuating Eiger/TNF Signaling to Ameliorate Insulin Resistance and ATM.

Z. Mirzoyan, A. M. Valenza, S. Zola, C. Bonfanti, L. Arnaboldi, N. Ferrari, J. Pollard, V. Lupi, M. Cassinelli, M. Frattaroli, M. Sahin, M. E. Pasini, P. Bellosta

This study develops a Drosophila model to investigate adipose tissue macrophage infiltration and obesity, showing that reducing Eiger/TNF signaling improves insulin resistance and reduces immune cell infiltration.

bioRxiv · Jul 6, 2023Physiology

Reduction of nucleolar NOC1 accumulates pre-rRNAs and induces Xrp1 affecting growth and resulting in cell competition in Drosophila

F. Destefanis, V. Manara, S. Santarelli, S. Zola, M. Brambilla, G. Viola, P. Maragno, I. Signoria, G. Viero, M. E. Pasini, M. Penzo, P. Bellosta

This study shows that reducing NOC1 in Drosophila leads to defects in ribosome biogenesis, growth, and cell competition through increased Xrp1 and eiger-JNK pathway activation.

bioRxiv · Jul 6, 2021Cell Biology

Glutamine Synthetase-1 induces autophagy-lysosomal degradation of huntingtin aggregates and ameliorates animal motility in a Drosophila model for Huntington’s disease

L. Vernizzi, C. Paiardi, G. Licata, T. Vitali, S. Santarelli, M. Raneli, V. Manelli, M. Rizzetto, M. Gioria, M. E. Pasini, D. Grifoni, M. A. Vanoni, C. Gellera, F. Taroni, P. Bellosta

This study shows that GS1 expression in Drosophila neurons reduces huntingtin aggregates and improves motility in a Huntington’s disease model by enhancing autophagy and inhibiting TOR signaling.

bioRxiv · Apr 30, 2019Cell Biology