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您的检索式：作者名="Stefania Berton"
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| 1 | Early CPAP prevents evolution of acute lung injury in patients with hematologic malignancy显示文摘 | Vincenzo Squadrone Massimo Massaia Benedetto Bruno Filippo Marmont Michele Falda Carlotta Bagna Stefania Bertone Claudia Filippini Arthur S. Slutsky Umberto Vitolo Mario Boccadoro V. Marco Ranieri | 2010 | Intensive Care Medicine2010，，10： | 1 |
| 2 | SUMOylation regulates p27^(Kip1) stability and localization in response to TGFβ显示文摘Exposure of normal and tumor-derived cells to TGFbresults in different outcomes,depending on the regulation of key targets.The CDK inhibitor p27^(Kip1) is one of these TGFβ targets and is essential for the TGFβ-induced cell cycle arrest.TGFb treatment inhibits p27^(Kip1) degradation and induces its nuclear translocation,through mechanisms that are still unknown.Recent evidences suggest that SUMOylation,a post-translational modification able to modulate the stability and subcellular localization of target proteins,critically modifies members of the TGFβ signaling pathway.Here,we demonstrate that p27^(Kip1) is SUMOylated in response to TGFβ treatment.Using different p27^(Kip1) point mutants,we identified lysine 134(K134)as the residue modified by small ubiquitin-like modifier 1(SUMO1)in response to TGFb treatment.TGFβ-induced K134 SUMOylation increased protein stability and nuclear localization of both endogenous and exogenously expressed p27^(Kip1).We observed thatSUMOylation regulated p27^(Kip1) binding to CDK2,thereby governing its nuclear proteasomal degradation through the phosphorylation of threonine 187.Importantly,p27^(Kip1) SUMOylation was necessary for proper cell cycle exit following TGFbtreatment.These data indicate thatSUMOylation is a novel regulatory mechanism that modulates p27^(Kip1) function in response to TGFβ stimulation.Given the involvement of TGFb signaling in cancer cell proliferation and invasion,our data may shed light on an important aspect of this pathway during tumor progression. | Sara Lovisa Simona Citro Maura Sonego Alessandra Dall’Acqua Valentina Ranzuglia Stefania Berton Alfonso Colombatti Barbara Belletti Susanna Chiocca Monica Schiappacassi Gustavo Baldassarre | 2016 | Journal of Molecular Cell Biology2016，8，1： | 0 |
| 3 | Loss of CDKN1B induces an age-related clonal hematopoietic disorder via Notch2 activity dysregulation显示文摘Dear Editor,The tumor suppressor gene CDKN1B,encoding for the p27^(Kip1)(p27)protein,defines the smallest region of deletion on chromosome 12p13 described in clonal hematopoietic disorders(CHDs)[1].Among them,myelodysplastic syndromes(MDSs)display typical onset in the elderly and an indolent behavior that may evolve in acute myeloid leukemia(AML)[2].Recent evidences support a model of parallel clonal evolution at the stem or progenitor cell level and implicate the need of more preclinical,translational and clinical research to identify better ways to timely target clones that may evolve toward malignancy[3,4]. | Ilenia Segatto Gian Luca Rampioni Vinciguerra Ilenia Pellarin Alessandra Dall’Acqua Stefania Berton Francesca Citron Sara D’Andrea Giorgia Mungo Davide Viotto Lorena Musco Arianna Di Napoli Maria Antonietta Aloe Spiriti Vincenzo Canzonieri Valter Gattei Andrea Vecchione Barbara Belletti Gustavo Baldassarre | 2023 | Cancer Communications2023，43，7： | 0 |
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