Author

F. Martelli

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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Cancer Biology· 1 Cell Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 3 Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Approach:experimental assay· 3 Organism:mouse· 2 Approach:genetic perturbation / CRISPR· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

A. R. Migliaccio· 3 shared F. Gobbo· 2 shared M. Mazzarini· 2 shared P. Verachi· 2 shared A. C. Dueck· 1 shared A. Dunbar· 1 shared A. Karzai· 1 shared A. Krishnan· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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3 shared papersCell Biology

A. R. Migliaccio

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent

M. Mazzarini, J. Cherone, T. Nguyen, F. Martelli, L. Varricchio, A. P. W. Funnell, T. Papayannopoulou, A. R. Migliaccio

The paper shows BCL11A is required for glucocorticoid-induced erythroid expansion in human cells.

bioRxiv · Feb 5, 2024Cell Biology

GATA1-defective immune-megakaryocytes as possible drivers of idiopathic pulmonary fibrosis

F. Gobbo, M. Zingariello, P. Verachi, M. Falchi, F. Arciprete, F. Martelli, A. Peli, M. Mazzarini, J. Vierstra, C. Mead-Harvey, A. C. Dueck, G. Sarli, S. Nava, G. Sgalla, L. Richeldi, A. R. Migliaccio

The paper identifies GATA1-defective immune-megakaryocytes in IPF patients and mice, showing their role in lung fibrosis through TGF-β1, CXCL1, and P-selectin mechanisms.

bioRxiv · Jun 20, 2023 · PreprintImmunology

CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

A. Dunbar, D. Kim, M. Lu, M. Farina, J. L. Yang, Y. Park, F. Gobbo, P. Verachi, F. Martelli, A. Karzai, W. Xiao, L. Xia, N. Elmansy, M. Kleppe, Z. Chen, , R. Hoffman

This study identifies CXCL8/CXCR2 signaling as a driver of bone marrow fibrosis in myelofibrosis and shows its therapeutic potential through genetic and pharmacologic inhibition.

bioRxiv · Dec 8, 2021Cancer Biology