J
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.
Papers
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Journal ArticleDOI
STIM1, an essential and conserved component of store-operated Ca2+ channel function
Jack Roos,Paul J. Digregorio,Andriy V. Yeromin,Kari Lynn Ohlsen,Maria I. Lioudyno,Shenyuan L. Zhang,Olga Safrina,J. Ashot Kozak,Steven L. Wagner,Michael D. Cahalan,Gonul Velicelebi,Kenneth A. Stauderman +11 more
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.
Journal ArticleDOI
STIM1 is a Ca2+ sensor that activates CRAC channels and migrates from the Ca2+ store to the plasma membrane
Shenyuan L. Zhang,Ying Yu,Jack Roos,J. Ashot Kozak,Thomas J. Deerinck,Mark H. Ellisman,Kenneth A. Stauderman,Michael D. Cahalan +7 more
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
Maria I. Lioudyno,J. Ashot Kozak,Aubin Penna,Olga Safrina,Shenyuan L. Zhang,Debasish Sen,Jack Roos,Kenneth A. Stauderman,Michael D. Cahalan +8 more
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.
Journal ArticleDOI
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.
Journal ArticleDOI
Store-dependent and -independent Modes Regulating Ca2+ Release-activated Ca2+ Channel Activity of Human Orai1 and Orai3
Shenyuan L. Zhang,J. Ashot Kozak,Weihua Jiang,Andriy V. Yeromin,Jing Chen,Ying Yu,Aubin Penna,Wei Shen,Victor Chi,Michael D. Cahalan +9 more
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.