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J. Ashot Kozak

Researcher at Wright State University

Publications -  33
Citations -  4911

J. Ashot Kozak is an academic researcher from Wright State University. The author has contributed to research in topics: Patch clamp & Transient receptor potential channel. The author has an hindex of 17, co-authored 31 publications receiving 4625 citations. Previous affiliations of J. Ashot Kozak include University of California, Irvine.

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STIM1, an essential and conserved component of store-operated Ca2+ channel function

TL;DR: It is proposed that STIM1, a ubiquitously expressed protein that is conserved from Drosophila to mammalian cells, plays an essential role in SOC influx and may be a common component of SOC and CRAC channels.
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STIM1 is a Ca2+ sensor that activates CRAC channels and migrates from the Ca2+ store to the plasma membrane

TL;DR: It is proposed that STIM1 functions as the missing link between Ca2+ store depletion and SOC influx, serving as aCa2+ sensor that translocates upon store depletion to the plasma membrane to activate CRAC channels.
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Orai1 and STIM1 Move to the Immunological Synapse and Are Up-Regulated during T Cell Activation

TL;DR: It is shown that STIM1 and Orai1 are recruited to the immunological synapse between primary human T cells and autologous dendritic cells, implying a positive feedback loop in which an initial TCR signal favors up-regulation of STIM 1 and ORAi proteins that would augment Ca2+ signaling during subsequent antigen encounter.
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Soluble amyloid oligomers increase bilayer conductance by altering dielectric structure

TL;DR: This paper addresses the mechanism of the amyloid hypothesis of Alzheimer's toxicity, and finds that only oligomers increase the conductance of lipid bilayers and patch-clamped mammalian cells, producing almost identical current–voltage curves in both preparations.
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Store-dependent and -independent Modes Regulating Ca2+ Release-activated Ca2+ Channel Activity of Human Orai1 and Orai3

TL;DR: Analysis of a series of Orai1-3 chimeras revealed the structural determinant responsible for 2-APB-induced current within the sequence from the second to third transmembrane segment of ORAi3 that may reflect a store-independent mode of CRAC channel activation that opens a relatively nonselective cation pore.