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Asim Dasgupta
Researcher at University of California, Los Angeles
Publications - 85
Citations - 3838
Asim Dasgupta is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Transcription (biology) & RNA. The author has an hindex of 36, co-authored 85 publications receiving 3674 citations. Previous affiliations of Asim Dasgupta include University of California & University of California, Berkeley.
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A novel broad-spectrum antiviral targeting entry of enveloped viruses.
Michael Wolf,Alexander N. Freiberg,Tinghu Zhang,Zeynep Akyol-Ataman,Andrew Grock,Patrick Hong,Jianrong Li,Jianrong Li,Natalya F. Watson,Angela Q. Fang,Hector C. Aguilar,Matteo Porotto,Anna N. Honko,Robert Damoiseaux,John P. Miller,Sara E. Woodson,Steven Chantasirivisal,Vanessa Fontanes,Oscar A. Negrete,Paul Krogstad,Asim Dasgupta,Anne Moscona,Lisa E. Hensley,Sean P. J. Whelan,Kym F. Faull,Michael R. Holbrook,Michael E. Jung,Benhur Lee +27 more
TL;DR: A class of broad-spectrum antivirals effective against enveloped viruses that target the viral lipid membrane and compromises its ability to mediate virus–cell fusion are revealed.
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Direct cleavage of human TATA-binding protein by poliovirus protease 3C in vivo and in vitro.
TL;DR: It is demonstrated that a cellular transcription factor can be directly cleaved both in vitro and in vivo by a viral protease and suggested a role of the poliovirus proteinase 3C in host cell Pol II-mediated transcription shutoff.
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The Soluble Serum Protein Gas6 Bridges Virion Envelope Phosphatidylserine to the TAM Receptor Tyrosine Kinase Axl to Mediate Viral Entry
TL;DR: An alternative molecular mechanism of viral entry that can broaden host range and enhance infectivity of enveloped viruses is revealed, conferred by the soluble bovine protein S in fetal calf serum, or Gas6, its human homolog.
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Poliovirus proteinase 3C converts an active form of transcription factor IIIC to an inactive form: a mechanism for inhibition of host cell polymerase III transcription by poliovirus.
TL;DR: It is suggested that proteolysis of the transcriptionally active form of TFIIIC by poliovirus 3Cpro is a mechanism by which poliov virus inhibits host cell RNA pol III transcription.
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The heat shock protein inhibitor Quercetin attenuates hepatitis C virus production.
Oscar Gonzalez,Vanessa Fontanes,Santanu Raychaudhuri,Rachel R. Ogorzalek Loo,Joseph A. Loo,Vaithilingaraja Arumugaswami,Ren Sun,Asim Dasgupta,Samuel W. French +8 more
TL;DR: The marked inhibition of virus production by Quercetin may partially be related to reduction of HSP40 and HSP70 and their potential involvement in IRES translation, as well as viral morphogenesis or secretion.