Vincenza Vigorito

ORCID: 0009-0006-7274-756X
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About
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Research Areas
  • Microtubule and mitosis dynamics
  • Cancer Immunotherapy and Biomarkers
  • Immune Cell Function and Interaction
  • Immune cells in cancer
  • Cell death mechanisms and regulation
  • Cancer-related Molecular Pathways
  • DNA Repair Mechanisms
  • Immunotherapy and Immune Responses
  • RNA Research and Splicing
  • RNA modifications and cancer
  • Mitochondrial Function and Pathology
  • Signaling Pathways in Disease
  • T-cell and B-cell Immunology
  • PARP inhibition in cancer therapy
  • RNA and protein synthesis mechanisms
  • Cancer Cells and Metastasis
  • CAR-T cell therapy research
  • Hippo pathway signaling and YAP/TAZ

University of Trento
2023-2024

University of Naples Federico II
2018-2020

Relatively few studies have examined the link between SNPs and mRNA translation, despite established importance of translational regulation in shaping cell phenotypes. We developed a pipeline analyzing allelic imbalance total polysome-bound mRNAs from paired RNA-seq data HCT116 cells identified 40 candidate tranSNPs, i.e. associated with allele-specific translation. Among them, SNP rs1053639 (T/A) on DNA damage-inducible transcript 4 (DDIT4) 3UTR was identified, reference T allele showing...

10.1101/2025.04.02.646512 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2025-04-04

Abstract 53BP1 acts at the crossroads between DNA repair and p53‐mediated stress response. With its interactors p53 USP28, it is part of mitotic surveillance (or stopwatch) pathway (MSP), a sensor that monitors duration cell division, promoting p53‐dependent cycle arrest when critical time threshold surpassed. Here, we show Polo‐like kinase 1 (PLK1) activity essential for time‐dependent release from kinetochores. PLK1 inhibition, which leads to persistence kinetochores, prevents cytosolic...

10.15252/embr.202357234 article EN cc-by EMBO Reports 2023-10-27

Abstract Gliomas aberrantly express programmed cell death ligand-1 (PD-L1), which has a pivotal role in immunoevasion. The splicing isoform of FKBP5 , termed FKBP51s, is PD-L1 foldase, assisting the immune checkpoint molecule maturation and expression on plasma membrane. concept that supports tumor-intrinsic properties increasingly emerging. aim present work was to confirm pro-tumoral effect human glioma survival, stemness capacity resistance, address issue whether, by targeting its foldase...

10.1038/s41420-019-0216-0 article EN cc-by Cell Death Discovery 2019-09-24

FKBP51 immunophilin is abundantly expressed by immune cells. Co-inhibitory receptor signalling generates the splicing isoform FKBP51s. Tregs stained FKBP51s are increased in melanoma patients and their counts associated with anti-CTLA-4 response. An expansion of FKBP51s+PD-L1+ monocytes was measured a group non-responding to anti-CTLA-4. The aim this work confirm predictive value response FKBP51s+Tregs cohort undergoing anti-PD1 treatment shed light on monocyte subset co-expressing...

10.1038/s41416-020-0840-8 article EN cc-by British Journal of Cancer 2020-04-21

Centrosomes are membrane-less organelles that orchestrate a wide array of biological functions by acting as microtubule organizing centers. Here, we report caspase-2-driven apoptosis is elicited in blood cells failing cytokinesis and extra centrosomes necessary to trigger this cell death. Activation caspase-2 depends on the PIDDosome multi-protein complex priming PIDD1 at for pathway. Accordingly, loss its centrosomal adapter, ANKRD26, allows survival unrestricted polyploidization response...

10.1101/2024.02.13.580097 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-02-14

Centrosomes are membrane-less organelles that orchestrate a wide array of biological functions by acting as microtubule organizing centers. Here, we report caspase-2–driven apoptosis is elicited in blood cells failing cytokinesis and extra centrosomes necessary to trigger this cell death. Activation caspase-2 depends on the PIDDosome multi-protein complex, priming PIDD1 at for pathway activation. Accordingly, loss its centrosomal adapter, ANKRD26, allows survival unrestricted...

10.1126/sciadv.ado6607 article EN cc-by-nc Science Advances 2024-10-30

Abstract 53BP1 acts at the crossroads between DNA repair and p53-mediated stress response. With its interactor USP28, it is part of mitotic surveillance pathway (MSP), a sensor that monitors duration cell division, promoting p53-dependent cycle arrest when critical time threshold surpassed. dynamically associates with kinetochores, being recruited during prophase, then undergoing time-dependent loss affinity. However, relevance this behaviour remains unclear. Here, we identify CENP-F as an...

10.1101/2023.03.27.534346 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-03-27

Abstract Melanoma often exploits Treg to avoid immune attack. is a heterogeneous population with respect immunosuppressive capability. Lymphocytes are particularly rich in FKBP51 (encoded by FKBP5 gene), known as the receptor for FK506. aberrantly expresses this protein, which sustains resistance and invasion. Melanoma/immune cell interaction, through PD-L1/PD1, bidirectionally generates splicing inducing lower molecular weight form termed FKBP51s. In 64 advanced melanoma patient PBMCs, we...

10.1158/1538-7445.am2018-5712 article EN Cancer Research 2018-07-01
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