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Antonio Filippini
Researcher at Sapienza University of Rome
Publications - 117
Citations - 4505
Antonio Filippini is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Sertoli cell & Apoptosis. The author has an hindex of 36, co-authored 111 publications receiving 3880 citations. Previous affiliations of Antonio Filippini include National Institutes of Health & University of L'Aquila.
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Ecto-ATPase activity in cytolytic T-lymphocytes. Protection from the cytolytic effects of extracellular ATP.
TL;DR: Inactivation of CTL ecto-ATPase by pretreatment with FSBA makes CTL susceptible to lytic effects of extracellular ATP, as was hypothesized for the functional role of this enzyme in CTL.
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Extracellular ATP in T-lymphocyte activation: possible role in effector functions.
TL;DR: Cloned helper T lymphocytes also accumulate ATPo after incubation with anti-TCR mAb or Con A, suggesting the possibility that ATPo, which acts in concert with ectoprotein kinases and/or purinergic receptors, may be of general use as a messenger in cellular interactions of T lymphocyte.
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Toll-like receptor 3 triggers apoptosis of human prostate cancer cells through a PKC-α-dependent mechanism
Alessio Paone,Donatella Starace,Roberta Galli,Fabrizio Padula,Paola De Cesaris,Antonio Filippini,Elio Ziparo,Anna Riccioli +7 more
TL;DR: It is shown that a novel interferon-independent pathway involving protein kinase C (PKC)-alpha activation, upstream of p38 and c-jun N-terminal kinase, is responsible for poly (I:C) pro-apoptotic effects on LNCaP cells.
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Multifaceted Roles of GSK-3 in Cancer and Autophagy-Related Diseases
Romina Mancinelli,Guido Carpino,Simonetta Petrungaro,Caterina Loredana Mammola,Luana Tomaipitinca,Antonio Filippini,Antonio Facchiano,Elio Ziparo,Claudia Giampietri +8 more
TL;DR: The studies summarized here underline the GSK-3 multifaceted role and indicate such kinase as a molecular target in different pathologies, including diseases associated with autophagy dysregulation.
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VEGF-induced neoangiogenesis is mediated by NAADP and two-pore channel-2-dependent Ca2+ signaling
Annarita Favia,Marianna Desideri,Guido Gambara,Alessio D'Alessio,Margarida Ruas,Bianca Esposito,Donatella Del Bufalo,John Parrington,Elio Ziparo,Fioretta Palombi,Antony Galione,Antonio Filippini +11 more
TL;DR: It is demonstrated that a VEGFR2/NAADP/TPC2/Ca2+ signaling pathway is critical for VEGF-induced angiogenesis in vitro and in vivo, and that the angiogenic response can be abolished, in cultured cells and in vitro, by inhibiting components of this signaling cascade.