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Olga Safrina

Researcher at University of California, Irvine

Publications -  18
Citations -  4395

Olga Safrina is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Mutation (genetic algorithm) & Voltage-dependent calcium channel. The author has an hindex of 11, co-authored 18 publications receiving 4209 citations. Previous affiliations of Olga Safrina include University of California, Berkeley.

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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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Genome-wide RNAi screen of Ca(2+) influx identifies genes that regulate Ca(2+) release-activated Ca(2+) channel activity.

TL;DR: Using an unbiased genome-wide RNA interference screen in Drosophila S2 cells, 75 hits are identified that strongly inhibited Ca(2+) influx upon store emptying by thapsigargin, including Stim and olf186-F, a member of a highly conserved family of four-transmembrane spanning proteins with homologs from Caenorhabditis elegans to human.
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Imaging the Single Cell Dynamics of CD4+ T Cell Activation by Dendritic Cells in Lymph Nodes

TL;DR: Observations suggest that the immunological synapse in native tissues is remarkably fluid, and that stable synapses form only at specific stages of antigen presentation to T cells, which implies that T cells activate by way of multiple antigen recognition events.
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The CRAC channel consists of a tetramer formed by Stim-induced dimerization of Orai dimers

TL;DR: It is shown that Orai is predominantly a dimer in the plasma membrane under resting conditions, which represents a new mechanism in which assembly and activation of the functional ion channel are mediated by the same triggering molecule.
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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.