D
Davide Zella
Researcher at University of Maryland, Baltimore
Publications - 100
Citations - 4555
Davide Zella is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: T cell & Virus. The author has an hindex of 31, co-authored 94 publications receiving 3753 citations. Previous affiliations of Davide Zella include Medical Research Council & University of Maryland Biotechnology Institute.
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Journal ArticleDOI
Emerging SARS-CoV-2 mutation hot spots include a novel RNA-dependent-RNA polymerase variant.
Maria Pachetti,Maria Pachetti,Bruna Marini,Francesca Benedetti,Fabiola Giudici,Elisabetta Mauro,Paola Storici,Claudio Masciovecchio,Silvia Angeletti,Massimo Ciccozzi,Robert C. Gallo,Robert C. Gallo,Davide Zella,Davide Zella,Rudy Ippodrino +14 more
TL;DR: The findings suggest that the virus is evolving and European, North American and Asian strains might coexist, each of them characterized by a different mutation pattern.
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Structural basis for high-affinity peptide inhibition of p53 interactions with MDM2 and MDMX
Marzena Pazgier,Min Liu,Guozhang Zou,Weirong Yuan,Changqing Li,Chong Li,Jing Li,Juahdi Monbo,Davide Zella,Sergey G. Tarasov,Wuyuan Lu +10 more
TL;DR: The structural basis for high-affinity peptide inhibition of p53 interactions with MDM2 and MDMX is deciphered, shedding new light on structure-based rational design of different classes of p 53 activators for potential therapeutic use.
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Modulation of Nrf2/ARE Pathway by Food Polyphenols: A Nutritional Neuroprotective Strategy for Cognitive and Neurodegenerative Disorders
TL;DR: Low concentrations of epigallocatechin-3-gallate, the major green tea catechin, induces HO-1 by ARE/Nrf2 pathway in hippocampal neurons, and by this induction, it is able to protect neurons against different models of oxidative damages and identify a novel class of compounds that could be used for therapeutic purposes as preventive agents against cognitive decline.
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TRAIL promotes the survival and proliferation of primary human vascular endothelial cells by activating the Akt and ERK pathways.
Paola Secchiero,Arianna Gonelli,Edvige Carnevale,Daniela Milani,Assunta Pandolfi,Davide Zella,Giorgio Zauli +6 more
TL;DR: The ability of TRAIL to promote the survival/proliferation of endothelial cells without inducing NF-&kgr;B activation and inflammatory markers suggests that the TRAIL/TRAIL-R system plays an important role in endothelial cell physiology.
Journal Article
Extracellular HIV-1 Tat Protein Up-Regulates the Expression of Surface CXC-Chemokine Receptor 4 in Resting CD4+ T Cells
TL;DR: The data indicate a potentially important role for extracellular Tat in rendering bystander CD4+ T cells more susceptible to infection with X4-tropic HIV-1 isolates.