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Sofia Falzarano

Researcher at University of Ferrara

Publications -  23
Citations -  589

Sofia Falzarano is an academic researcher from University of Ferrara. The author has contributed to research in topics: Protein kinase C & Chemotaxis. The author has an hindex of 11, co-authored 23 publications receiving 562 citations.

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Signal transduction pathways triggered by selective formylpeptide analogues in human neutrophils

TL;DR: This review will consider the ability of selective analogues (ligands able to discriminate between different biological responses) to activate a single spectrum of signal transduction pathways capable of producing a unique set of cellular responses, hypothesising that a distinctive imprint of signal protein activation may exist.
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Exon skipping-mediated dystrophin reading frame restoration for small mutations.

TL;DR: The obtained results confirm cell‐free splicing assay as an alternative system to test exon skipping propensity when patients' cells are unavailable and highlights the complexity of identifying optimal AONs for skipping exons with small mutations.
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Dystrophin restoration in skeletal, heart and skin arrector pili smooth muscle of mdx mice by ZM2 NP–AON complexes

TL;DR: It is shown that PMMA/N-isopropil-acrylamide+ (NIPAM) nanoparticles (ZM2) bind and convey antisense oligoribonucleotides (AONs) very efficiently and this finding reveals arrector pili smooth muscle to be an appealing biomarker candidate and a novel low-invasive treatment end point.
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Nociceptin/orphanin FQ stimulates human monocyte chemotaxis via NOP receptor activation.

TL;DR: It is demonstrated that N/OFQ stimulates human monocyte chemotaxis via NOP receptor activation through the order of potency of agonists and the antagonist selectivity.
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Sodium Azide Induced Neuronal Damage In Vitro: Evidence for Non-Apoptotic Cell Death

TL;DR: The mitochondrial dysfunction induced by NaN3 provides a common platform for investigating the mechanisms of both ischemic and degenerative neuronal injury, useful for screening potential protective agents against neuronal death.