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Arati Tripathi

Researcher at Brigham and Women's Hospital

Publications -  8
Citations -  318

Arati Tripathi is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Endoplasmic reticulum & Medicine. The author has an hindex of 4, co-authored 5 publications receiving 278 citations. Previous affiliations of Arati Tripathi include Princeton University & Howard Hughes Medical Institute.

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Journal ArticleDOI

A Structure-Based Mechanism for Vesicle Capture by the Multisubunit Tethering Complex Dsl1

TL;DR: To elucidate structural principles underlying MTC function, the structure of the Dsl1 complex is determined, revealing a tower containing at its base the binding sites for two ER SNAREs and at its tip a flexible lasso for capturing vesicles.
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Structural characterization of Tip20p and Dsl1p, subunits of the Dsl1p vesicle tethering complex.

TL;DR: Crystal structures reveal that two of the three subunits, Tip20p and Dsl1p, resemble known subunits of the exocyst complex, establishing a structural connection among several multisubunit tethering complexes and implying that many of their subunits are derived from a common progenitor.
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Two alternative binding mechanisms connect the protein translocation Sec71-Sec72 complex with heat shock proteins.

TL;DR: A crystal structure of the Sec71-Sec72 complex revealed that Sec72 contains a tetratricopeptide repeat (TPR) domain that is anchored to the endoplasmic reticulum membrane by Sec71, and it is demonstrated that Ssb1 binds through its ATPase domain to the TPR domain, an interaction that leads to inhibition of nucleotide exchange.
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Rapid Alpha-Synuclein Toxicity in a Neural Cell Model and Its Rescue by a Stearoyl-CoA Desaturase Inhibitor.

TL;DR: A cellular model of αS neurotoxicity after transducing human neuroblastoma cells to express yellow fluorescent protein (YFP)-tagged αS 3K in a doxycycline-dependent manner is presented, and the αS bioassay will be useful for elucidating compound mechanisms, for pharmacokinetic studies, and for compound/genetic screens.
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Pathogenic Mechanisms of Cytosolic and Membrane-Enriched α-Synuclein Converge on Fatty Acid Homeostasis

TL;DR: It is suggested that, despite divergent cytosol/membrane partitioning, both G51D and E46K neurotoxicity can be prevented by decreasing fatty-acid unsaturation as a common therapeutic approach.