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<jats:title>One, Two, Three, Remember Me</jats:title> <jats:p> When a stimulus (such as a word or a face) is presented for the second, third, or fourth time, do the neural representations differ? And, if they do, are multiply represented stimuli remembered better? These questions and related ones have fascinated psychologists for decades, but only recently has it become feasible to begin tackling them using neuroimaging. <jats:bold> Xue <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="97" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1193125">97</jats:related-article> , published online 9 September) provide evidence that the greater the similarity in the patterns of neural activity during encoding of the item, the greater the likelihood that the item will be remembered. </jats:p>

<jats:title>Channel STIMulation</jats:title> <jats:p> The STIM1 protein functions as a calcium sensor and regulates entry of calcium into cells across the plasma membrane. When cell surface receptors are stimulated and cause release of calcium from internal stores in the endoplasmic reticulum (ER), STIM proteins in the ER membrane interact with the Orai channel pore protein in the plasma membrane to allow calcium entry from the outside of the cell (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6000" page="43" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1196348">Cahalan</jats:related-article> </jats:bold> ). <jats:bold> Park <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="101" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1191027">101</jats:related-article> ) and <jats:bold> Wang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="105" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1191086">105</jats:related-article> ) now show that STIM also acts to suppress conductance by another calcium channel—the voltage-operated Ca <jats:sub>V</jats:sub> 1.2 channel. STIM1 appeared to interact directly with Ca <jats:sub>V</jats:sub> 1.2 channels in multiple cell types, including vascular smooth muscle cells, neurons, and cultured cells derived from T lymphocytes. The interaction inhibited opening of the Ca <jats:sub>V</jats:sub> 1.2 channels and caused depletion of the channel from the cell surface. </jats:p>

<jats:title>Channel STIMulation</jats:title> <jats:p> The STIM1 protein functions as a calcium sensor and regulates entry of calcium into cells across the plasma membrane. When cell surface receptors are stimulated and cause release of calcium from internal stores in the endoplasmic reticulum (ER), STIM proteins in the ER membrane interact with the Orai channel pore protein in the plasma membrane to allow calcium entry from the outside of the cell (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6000" page="43" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1196348">Cahalan</jats:related-article> </jats:bold> ). <jats:bold> Park <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="101" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1191027">101</jats:related-article> ) and <jats:bold> Wang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="105" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1191086">105</jats:related-article> ) now show that STIM also acts to suppress conductance by another calcium channel—the voltage-operated Ca <jats:sub>V</jats:sub> 1.2 channel. STIM1 appeared to interact directly with Ca <jats:sub>V</jats:sub> 1.2 channels in multiple cell types, including vascular smooth muscle cells, neurons, and cultured cells derived from T lymphocytes. The interaction inhibited opening of the Ca <jats:sub>V</jats:sub> 1.2 channels and caused depletion of the channel from the cell surface. </jats:p>

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