A
Anurag Tandon
Researcher at University of Toronto
Publications - 64
Citations - 6958
Anurag Tandon is an academic researcher from University of Toronto. The author has contributed to research in topics: Presenilin & APH-1. The author has an hindex of 31, co-authored 63 publications receiving 6437 citations. Previous affiliations of Anurag Tandon include McGill University & University Health Network.
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Journal ArticleDOI
Quantitative assessment on the cloning efficiencies of lentiviral transfer vectors with a unique clone site.
Gang Zhang,Anurag Tandon +1 more
TL;DR: A combinatorial strategy to efficiently construct LVs using EGFP, hPlk2 wild type (WT) and mutant genes as inserts using BamH I site for the inserts and the amounts and ratios of the insert and vector DNA were optimized to increase monomeric ligation.
Journal ArticleDOI
Nicastrin modulates presenilin-mediated notch/glp-1 signal transduction and βAPP processing
Gang Yu,Masaki Nishimura,Shigeki Arawaka,Shigeki Arawaka,Diane Levitan,Lili Zhang,Anurag Tandon,Anurag Tandon,You-Qiang Song,You-Qiang Song,Ekaterina Rogaeva,Ekaterina Rogaeva,Fusheng Chen,Fusheng Chen,Toshitaka Kawarai,Toshitaka Kawarai,Agnes Supala,Agnes Supala,Lyne Levesque,Lyne Levesque,Haung Yu,Haung Yu,Dun-Sheng Yang,Dun-Sheng Yang,Erin Holmes,Erin Holmes,Paul Milman,Paul Milman,Yan Liang,Yan Liang,Dong Mel Zhang,Dong Mel Zhang,Dong Hong Xu,Dong Hong Xu,Christine Sato,Christine Sato,Evgeny I. Rogaev,Evgeny I. Rogaev,Marsha Smith,Christopher Janus,Christopher Janus,Yanni Zhang,Ruedl Aebersold,Lindsay A. Farrer,Sandro Sorbl,Amalia C. Bruni,Paul E. Fraser,Paul E. Fraser,Peter St George-Hyslop,Peter St George-Hyslop +49 more
TL;DR: Nicastrin and presenilins are likely to be functional components of a multimeric complex necessary for the intramembranous proteolysis of proteins such as Notch/GLP-1 and βAPP.
Journal ArticleDOI
Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission
Ruben K. Dagda,Salvatore J. Cherra,Scott M. Kulich,Scott M. Kulich,Anurag Tandon,David S. Park,Charleen T. Chu +6 more
TL;DR: It is found that loss of PINK1 function elicits oxidative stress and mitochondrial turnover coordinated by the autophagic and fission/fusion machineries, and Pink1 and Parkin may cooperate through different mechanisms to maintain mitochondrial homeostasis.
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Wild-type PINK1 prevents basal and induced neuronal apoptosis, a protective effect abrogated by Parkinson disease-related mutations.
Agnes Petit,Toshitaka Kawarai,Erwan Paitel,Nobuo Sanjo,Mary C. Maj,Michael P. Scheid,Fusheng Chen,Yongjun Gu,Hiroshi Hasegawa,Shabnam Salehi-Rad,Linda Wang,Ekaterina Rogaeva,Paul E. Fraser,Brian D. Robinson,Peter St George-Hyslop,Anurag Tandon +15 more
TL;DR: Results suggest that PINK1 reduces the basal neuronal pro-apoptotic activity and protects neurons from staurosporine-induced apoptosis, and loss of this protective function may underlie the degeneration of nigral dopaminergic neurons in patients with Pink1 mutations.
Journal ArticleDOI
Mutations in GDI1 are responsible for X-linked non-specific mental retardation
Pio D'Adamo,Andrea Menegon,C Lo Nigro,Margherita Grasso,Massimo Gulisano,Filippo Tamanini,Thierry Bienvenu,Agi K. Gedeon,Ben A. Oostra,Shih-Kwang Wu,Anurag Tandon,Flavia Valtorta,William E. Balch,Jamel Chelly,Daniela Toniolo +14 more
TL;DR: The results show that both functional and developmental alterations in the neuron may account for the severe impairment of learning abilities as a consequence of mutations in GDI1, emphasizing its critical role in development of human intellectual and learning abilities.