V
Vanessa Taupin
Researcher at University of California, San Diego
Publications - 17
Citations - 1066
Vanessa Taupin is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Encephalitozoon cuniculi & Endosome. The author has an hindex of 11, co-authored 14 publications receiving 967 citations. Previous affiliations of Vanessa Taupin include Children's Hospital Los Angeles & Blaise Pascal University.
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Journal ArticleDOI
Human hematopoietic stem/progenitor cells modified by zinc-finger nucleases targeted to CCR5 control HIV-1 in vivo
Nathalia Holt,Jianbin Wang,Kenneth Kim,Geoffrey Friedman,Xingchao Wang,Vanessa Taupin,Donald B. Kohn,Philip D. Gregory,Michael C. Holmes,Paula M. Cannon +9 more
TL;DR: The demonstration that a minority of CCR5−/− HSPCs can populate an infected animal with HIV-1-resistant, CCR4+/− progeny supports the use of ZFN-modified autologous hematopoietic stem cells as a clinical approach to treating HIV- 1.
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ARH directs megalin to the endocytic recycling compartment to regulate its proteolysis and gene expression
TL;DR: ARH is required for the trafficking of megalin from early endosomes to the endocytic recycling compartment, where megal in undergoes intramembrane proteolysis, releasing a tail fragment that represses megalIn transcription.
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Gαs Promotes EEA1 Endosome Maturation and Shuts down Proliferative Signaling through Interaction with GIV (Girdin)
Anthony Beas,Vanessa Taupin,Carmen Teodorof,Lien T. Nguyen,Mikel Garcia-Marcos,Marilyn G. Farquhar +5 more
TL;DR: Evidence is given that EGF-induced, proliferative signaling occurs from EEA1 endosomes and is regulated by interaction between the signal-transducing protein GIV and the trimeric G protein Gαs.
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GIV/Girdin Links Vascular Endothelial Growth Factor Signaling to Akt Survival Signaling in Podocytes Independent of Nephrin
TL;DR: It is shown that Gα-interacting, vesicle-associated protein (GIV)/girdin mediates VEGF receptor 2 (VEGFR2) signaling and compensates for nephrin loss in podocyte survival and may represent a novel target for therapeutic intervention in the nephrotic syndrome and other proteinuric diseases.
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Activation of Gαi at the Golgi by GIV/Girdin imposes finiteness in Arf1 signaling.
I-Chung Lo,Vijay Gupta,Krishna Midde,Vanessa Taupin,Inmaculada Lopez-Sanchez,Irina Kufareva,Ruben Abagyan,Paul A. Randazzo,Marilyn G. Farquhar,Pradipta Ghosh +9 more
TL;DR: It is demonstrated that Gi is activated in the Golgi by GIV/Girdin, a non-receptor guanine-nucleotide exchange factor (GEF), which places GIV-GEF at the crossroads between signals gated by the trimeric G proteins and the Arf family of monomeric GTPases.