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Your search keyword '"Selmi, Tommaso"' showing total 22 results
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22 results on '"Selmi, Tommaso"'

1. An aptamer-mediated base editing platform for simultaneous knockin and multiple gene knockout for allogeneic CAR-T cells generation

Author

Porreca, Immacolata, Blassberg, Robert, Harbottle, Jennifer, Joubert, Bronwyn, Mielczarek, Olga, Stombaugh, Jesse, Hemphill, Kevin, Sumner, Jonathan, Pazeraitis, Deividas, Touza, Julia Liz, Francescatto, Margherita, Firth, Mike, Selmi, Tommaso, Collantes, Juan Carlos, Strezoska, Zaklina, Taylor, Benjamin, Jin, Shengkan, Wiggins, Ceri M., van Brabant Smith, Anja, and Lambourne, John J.

Published
2024
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2. Targeting autophagy potentiates tyrosine kinase inhibitor�induced cell death in Philadelphia chromosome�positive cells, including primary CML stem cells

Author

Bellodi, Cristian, Lidonnici, Maria Rosa, Hamilton, Ashley, Helgason, G. Vignir, Soliera, Angela Rachele, Ronchetti, Mattia, Galavotti, Sara, Young, Kenneth W, Selmi, Tommaso, Yacobi, Rinat, Van Etten, Richard A, Donato, Nick, Hunter, Ann, Dinsdale, David, Tirrò, Elena, Vigneri, Paolo, Nicotera, Pierluigi, Dyer, Martin J, Holyoake, Tessa, Salomoni, Paolo, and Calabretta, Bruno

Published
2013

3. Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells.

Author

Bellodi, Cristian, Lidonnici, Maria Rosa, Hamilton, Ashley, Helgason, G Vignir, Soliera, Angela Rachele, Ronchetti, Mattia, Galavotti, Sara, Young, Kenneth W, Selmi, Tommaso, Yacobi, Rinat, Van Etten, Richard A, Donato, Nick, Hunter, Ann, Dinsdale, David, Tirrò, Elena, Vigneri, Paolo, Nicotera, Pierluigi, Dyer, Martin J, Holyoake, Tessa, Salomoni, Paolo, and Calabretta, Bruno

Subjects
Animals, Antineoplastic Agents: pharmacology, therapeutic use, Autophagy: drug effects, physiology, Benzamides, Calcium: metabolism, Cell Death: drug effects, physiology, Cell Line, Tumor, Chloroquine: pharmacology, therapeutic use, Endoplasmic Reticulum: drug effects, metabolism, Fusion Proteins, bcr-abl: antagonists & inhibitors, genetics, Gene Expression: drug effects, genetics, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive: drug therapy, metabolism, pathology, Macrolides: pharmacology, therapeutic use, Mice, Mice, Inbred C3H, Microtubule-Associated Proteins: metabolism, Neoplastic Stem Cells: cytology, drug effects, metabolism, Piperazines: pharmacology, therapeutic use, Protein Kinase Inhibitors: pharmacology, therapeutic use, Protein-Tyrosine Kinases: antagonists & inhibitors, Pyrimidines: pharmacology, therapeutic use, RNA Interference, Thiazoles: pharmacology, therapeutic use, Transcription Factor CHOP: genetics, Xenograft Model Antitumor Assays
Abstract

Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia (CML), but the frequency of resistance increases in advancing stages of disease. Elimination of BCR/ABL-dependent intracellular signals triggers apoptosis, but it is unclear whether this activates additional cell survival and/or death pathways. We have shown here that IM induces autophagy in CML blast crisis cell lines, CML primary cells, and p210BCR/ABL-expressing myeloid precursor cells. IM-induced autophagy did not involve c-Abl or Bcl-2 activity but was associated with ER stress and was suppressed by depletion of intracellular Ca2+, suggesting it is mechanistically nonoverlapping with IM-induced apoptosis. We further demonstrated that suppression of autophagy using either pharmacological inhibitors or RNA interference of essential autophagy genes enhanced cell death induced by IM in cell lines and primary CML cells. Critically, the combination of a tyrosine kinase inhibitor (TKI), i.e., IM, nilotinib, or dasatinib, with inhibitors of autophagy resulted in near complete elimination of phenotypically and functionally defined CML stem cells. Together, these findings suggest that autophagy inhibitors may enhance the therapeutic effects of TKIs in the treatment of CML.

Published
2009

9. miRNome and Proteome Profiling of Small Extracellular Vesicles Secreted by Human Glioblastoma Cell Lines and Primary Cancer Stem Cells

Author

Cifola, Ingrid, primary, Fratini, Federica, additional, Cardinali, Beatrice, additional, Palmieri, Valentina, additional, Gatti, Giuliana, additional, Selmi, Tommaso, additional, Donzelli, Sara, additional, Sacconi, Andrea, additional, Cesarini, Valeriana, additional, Marei, Hany E., additional, Papi, Massimilano, additional, Blandino, Giovanni, additional, Cenciarelli, Carlo, additional, Falcone, Germana, additional, and D’Agnano, Igea, additional

Published
2022
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13. Development and Characterization of a Modular CRISPR and RNA Aptamer Mediated Base Editing System

Author

Collantes, Juan Carlos, primary, Tan, Victor M., additional, Xu, Huiting, additional, Ruiz-Urigüen, Melany, additional, Alasadi, Amer, additional, Guo, Jingjing, additional, Tao, Hanlin, additional, Su, Chi, additional, Tyc, Katarzyna M., additional, Selmi, Tommaso, additional, Lambourne, John J., additional, Harbottle, Jennifer A., additional, Stombaugh, Jesse, additional, Xing, Jinchuan, additional, Wiggins, Ceri M., additional, and Jin, Shengkan, additional

Published
2021
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14. Sequence- and structure-specific cytosine-5 mRNA methylation by NSUN6

Author

Selmi, Tommaso, primary, Hussain, Shobbir, additional, Dietmann, Sabine, additional, Heiß, Matthias, additional, Borland, Kayla, additional, Flad, Sophia, additional, Carter, Jean-Michel, additional, Dennison, Rebecca, additional, Huang, Ya-Lin, additional, Kellner, Stefanie, additional, Bornelöv, Susanne, additional, and Frye, Michaela, additional

Published
2020
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17. ZFP36 stabilizes RIP1 via degradation of XIAP and cIAP2 thereby promoting ripoptosome assembly

Author

Selmi, Tommaso, primary, Alecci, Claudia, additional, dell’ Aquila, Miriam, additional, Montorsi, Lucia, additional, Martello, Andrea, additional, Guizzetti, Filippo, additional, Volpi, Nicola, additional, Parenti, Sandra, additional, Ferrari, Sergio, additional, Salomoni, Paolo, additional, Grande, Alexis, additional, and Zanocco-Marani, Tommaso, additional

Published
2015
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18. Targeting autophagy potentiates tyrosine kinase inhibitor–induced cell death in Philadelphia chromosome–positive cells, including primary CML stem cells

Author

Bellodi, Cristian, primary, Lidonnici, Maria Rosa, additional, Hamilton, Ashley, additional, Helgason, G. Vignir, additional, Soliera, Angela Rachele, additional, Ronchetti, Mattia, additional, Galavotti, Sara, additional, Young, Kenneth W., additional, Selmi, Tommaso, additional, Yacobi, Rinat, additional, Van Etten, Richard A., additional, Donato, Nick, additional, Hunter, Ann, additional, Dinsdale, David, additional, Tirrò, Elena, additional, Vigneri, Paolo, additional, Nicotera, Pierluigi, additional, Dyer, Martin J., additional, Holyoake, Tessa, additional, Salomoni, Paolo, additional, and Calabretta, Bruno, additional

Published
2013
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21. Targeting Autophagy Potentiates Imatinib-Induced Cell Death in Philadelphia Positive Cells Including Primary CML Stem Cells.

Author

Bellodi, Cristian, primary, Lidonnici, Maria Rosa, primary, Hamilton, Ashley, primary, Helgason, Gudmundur V, primary, Soliera, Angela R, primary, Ronchetti, Mattia, primary, Galavotti, Sara, primary, Young, Kenneth W, primary, Selmi, Tommaso, primary, Van Etten, Richard A., primary, Donato, Nicholas, primary, Hunter, Ann, primary, Dinsdale, David, primary, Tirro’, Elena, primary, Vigneri, Paolo, primary, Nicotera, Pierluigi, primary, Dyer, Martin J.S., primary, Holyoake, Tessa, primary, Calabretta, Bruno, primary, and Salomoni, Paolo, primary

Published
2008
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22. Sequence- and structure-specific cytosine-5 mRNA methylation by NSUN6.

Author

Selmi T, Hussain S, Dietmann S, Heiß M, Borland K, Flad S, Carter JM, Dennison R, Huang YL, Kellner S, Bornelöv S, and Frye M

Subjects
3' Untranslated Regions, Animals, Base Sequence, Cell Line, Tumor, Codon Usage, Consensus Sequence, Cytidine metabolism, Embryonic Stem Cells, Gene Knockout Techniques, Genes, Reporter, HEK293 Cells, Humans, Immunoprecipitation, Methylation, Mice, Mice, Knockout, Mutagenesis, Site-Directed, RNA, Messenger genetics, Transcriptome, tRNA Methyltransferases deficiency, Cytidine analogs & derivatives, RNA Processing, Post-Transcriptional, RNA, Messenger metabolism, tRNA Methyltransferases metabolism
Abstract

The highly abundant N6-methyladenosine (m6A) RNA modification affects most aspects of mRNA function, yet the precise function of the rarer 5-methylcytidine (m5C) remains largely unknown. Here, we map m5C in the human transcriptome using methylation-dependent individual-nucleotide resolution cross-linking and immunoprecipitation (miCLIP) combined with RNA bisulfite sequencing. We identify NSUN6 as a methyltransferase with strong substrate specificity towards mRNA. NSUN6 primarily targeted three prime untranslated regions (3'UTR) at the consensus sequence motif CTCCA, located in loops of hairpin structures. Knockout and rescue experiments revealed enhanced mRNA and translation levels when NSUN6-targeted mRNAs were methylated. Ribosome profiling further demonstrated that NSUN6-specific methylation correlated with translation termination. While NSUN6 was dispensable for mouse embryonic development, it was down-regulated in human tumours and high expression of NSUN6 indicated better patient outcome of certain cancer types. In summary, our study identifies NSUN6 as a methyltransferase targeting mRNA, potentially as part of a quality control mechanism involved in translation termination fidelity., (© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.)

Published
2021
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