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Richa Tyagi

Researcher at Johns Hopkins University School of Medicine

Publications -  34
Citations -  1468

Richa Tyagi is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Signal transduction & PI3K/AKT/mTOR pathway. The author has an hindex of 17, co-authored 30 publications receiving 1195 citations. Previous affiliations of Richa Tyagi include National Institutes of Health & University of California, Los Angeles.

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Journal ArticleDOI

Human endogenous retrovirus-K contributes to motor neuron disease

TL;DR: It is shown that HERV-K is activated in a subpopulation of patients with sporadic amyotrophic lateral sclerosis (ALS) and that its envelope (env) protein may contribute to neurodegeneration and disease pathogenesis.
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Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia.

TL;DR: It is found that Ras homolog enriched in striatum (Rhes), a striatal-specific protein, binds to and activates mTOR, and Rhes−/− mice showed reduced striatal mTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA treatment, suggesting a therapeutic benefit for Rhes-binding drugs.
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Inositol Pyrophosphates Mediate the DNA-PK/ATM-p53 Cell Death Pathway by Regulating CK2 Phosphorylation of Tti1/Tel2

TL;DR: It is demonstrated that IP7, formed by IP6K2, binds CK2 to enhance its phosphorylation of the TTT complex, thereby stabilizing DNA-PKcs and ATM and stimulating p53 phosphorylated at serine 15 to activate the cell death program in human cancer cells and in murine B cells.
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Antidepressant action of ketamine via mTOR is mediated by inhibition of nitrergic Rheb degradation.

TL;DR: A novel signaling pathway wherein NMDA receptor activation stimulates generation of nitric oxide, which S-nitrosylates glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which stabilizes Rheb that enhances mTOR signaling and drugs selectively targeting components of this pathway may offer novel approaches to the treatment of depression.