M
Michael Vetter
Researcher at Harvard University
Publications - 15
Citations - 507
Michael Vetter is an academic researcher from Harvard University. The author has contributed to research in topics: GUCY1B3 & Guanylate cyclase 2C. The author has an hindex of 12, co-authored 15 publications receiving 489 citations. Previous affiliations of Michael Vetter include Vanderbilt University & Case Western Reserve University.
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Inhibition of Nox‐4 activity by plumbagin, a plant‐derived bioactive naphthoquinone
TL;DR: Results indicated that plumbagin directly interacted with Nox‐4 and inhibited its activity, and inhibited the superoxide production in Nx‐4 transfected COS‐7 cells.
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The HIV-1 Vif PPLP motif is necessary for human APOBEC3G binding and degradation.
TL;DR: It is demonstrated that mutation of the Vif PPLP motif reduces Vif binding to A3G without affecting its interaction with ElonginC and Cullin5 and resulted in A 3G incorporation into assembling virions with loss of viral infectivity.
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Multitarget, quantitative nanoplasmonic electrical field-enhanced resonating device (NE2RD) for diagnostics.
Fatih Inci,Chiara Filippini,Murat Baday,Mehmet Ozgun Ozen,Semih Calamak,Naside Gozde Durmus,ShuQi Wang,Emily Hanhauser,Kristen S. Hobbs,Franceline Juillard,Ping Ping Kuang,Michael Vetter,Margot Carocci,Hidemi S. Yamamoto,Yuko Takagi,Umit Hakan Yildiz,Demir Akin,Duane R. Wesemann,Duane R. Wesemann,Amit Singhal,Priscilla L. Yang,Max L. Nibert,Raina N. Fichorova,Daryl T.-Y. Lau,Timothy J. Henrich,Kenneth M. Kaye,Steven C. Schachter,Daniel R. Kuritzkes,Lars M. Steinmetz,Sanjiv S. Gambhir,Ronald W. Davis,Utkan Demirci +31 more
TL;DR: The nanoplasmonic electrical field-enhanced resonating device (NE2RD) is demonstrated, a label-free, quantitative, portable, multitarget platform by rapidly detecting various protein biomarkers, drugs, protein allergens, bacteria, eukaryotic cells, and distinct viruses.
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Differences in APOBEC3G expression in CD4+ T helper lymphocyte subtypes modulate HIV-1 infectivity.
TL;DR: It is indicated that APOBEC3G and APOBec3F levels vary physiologically during CD4+ T lymphocyte differentiation, that interferon-γ contributes to this modulation, and that this physiological regulation can cause changes in infectivity of progeny virions, even in the presence of HIV-1 vif.
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Cyclosporin A Disrupts Bradykinin Signaling Through Superoxide
TL;DR: It is suggested that CsA activates a NADPH oxidase that releases O2− and disrupts the bradykinin/soluble guanylate cyclase pathway, probably by binding with NO to form peroxynitrite (ONOO−).