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Rachele Bigi

Researcher at Sapienza University of Rome

Publications -  25
Citations -  350

Rachele Bigi is an academic researcher from Sapienza University of Rome. The author has contributed to research in topics: Medicine & Genome-wide association study. The author has an hindex of 8, co-authored 21 publications receiving 233 citations. Previous affiliations of Rachele Bigi include University of North Carolina at Chapel Hill.

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Differential regulation of miR-21 and miR-146a by Epstein-Barr virus-encoded EBNA2.

TL;DR: The present data suggest that EBNA2 might contribute to EBV-induced B-cell transformation by altering miR expression and in particular by increasing oncomiR-like miR-21 and by affecting the antiviral responses of the innate immune system through downregulation of its key regulator MiR-146a.
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Extracellular vesicles from Kaposi Sarcoma-associated herpesvirus lymphoma induce long-term endothelial cell reprogramming

TL;DR: It is proposed that the tumor virus Kaposi’s Sarcoma-associated herpesvirus (KSHV) establishes a niche favorable for viral spread and cell transformation through cell-derived vesicles, all while avoiding detection.
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Epstein-Barr virus enhances genome maintenance of Kaposi sarcoma-associated herpesvirus

TL;DR: It is demonstrated that EBV EBNA-1 plays an essential role in the pathogenesis of PEL by increasing KSHV viral load and LANA expression and adding exogenous EBV to K SHV+ single-positive PEL leads to increased KSHVs genome maintenance and KSHv latency-associated nuclear antigen (LANA) expression.
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Multiple Sclerosis and SARS-CoV-2: Has the Interplay Started?

TL;DR: In this article, the authors look over 18 months of the SARS-CoV-2 pandemic from the perspective of MS, dissect neuroinflammatory and demyelinating mechanisms associated with COVID-19, summarize pathophysiological crossroads between MS and SARS CoV2 infection, and discuss present evidence on COVID19 and its vaccination in people with MS.
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Targeting mTOR with MLN0128 Overcomes Rapamycin and Chemoresistant Primary Effusion Lymphoma

TL;DR: The results demonstrated that MLN0128 has a greater effect on inhibiting proliferation than the allosteric mTOR inhibitor rapamycin, and suggest that MLn0128 might offer a new approach to the treatment of chemotherapy-resistant PEL.