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Austin K. Mircheff

Researcher at University of Southern California

Publications -  167
Citations -  5559

Austin K. Mircheff is an academic researcher from University of Southern California. The author has contributed to research in topics: Lacrimal gland & Acinar cell. The author has an hindex of 39, co-authored 167 publications receiving 5371 citations. Previous affiliations of Austin K. Mircheff include United States Department of Veterans Affairs & Cedars-Sinai Medical Center.

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Journal ArticleDOI

The Pathology of Dry Eye: The Interaction Between the Ocular Surface and Lacrimal Glands

TL;DR: Although the etiologies of dry eye are varied, common to all ocular-surface disease is an underlying cytokine/receptor-mediated inflammatory process, by treating this process, it may be possible to normalize the ocular surface/lacrimal neural reflex and facilitate ocularsurface healing.
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Hepatitis C virus RNA polymerase and NS5A complex with a SNARE-like protein.

TL;DR: Cell fractionation analysis revealed that hVAP-33 is predominantly associated with the ER, the Golgi complex, and the prelysosomal membrane, consistent with its potential role in intracellular membrane trafficking.
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Analytical isolation of plasma membranes of intestinal epithelial cells: identification of Na, K-ATPase rich membranes and the distribution of enzyme activities.

TL;DR: Na, K-ATPase rich membranes are shown to originate from the basal lateral plasma membranes by the patterns of labeling that were produced when either isolated cells or everted gut sacs were incubated with the slowly permeating reagent35S-p-(diazonium)-benzenesulfonic acid.
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MHC class II molecules, cathepsins, and La/SSB proteins in lacrimal acinar cell endomembranes

TL;DR: Observations support the thesis that lacrimal gland acinar cells that have been induced to express MHC class II molecules function as autoantigen processing and presenting cells.
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Calcium-activated endoplasmic reticulum stress as a major component of tumor cell death induced by 2,5-dimethyl-celecoxib, a non-coxib analogue of celecoxib.

TL;DR: DMC increases intracellular free calcium levels and potently triggers the ESR in various tumor cell lines, as indicated by transient inhibition of protein synthesis, activation of ER stress–associated proteins GRP78/BiP, CHOP/GADD153, and caspase-4, and subsequent tumor cell death.