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Accumulating evidence positions the\n                    <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>\n                    iskott\u2013\n                    <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                    ldrich syndrome protein (\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p), a scaffolding protein that promotes actin polymerization, at the center of actin cytoskeleton\u2010dependent T\u2010cell function. During the past decade, we and others have utilized multidisciplinary technologies, including live\u2010cell imaging, biochemical, and biophysical analyses, to gain insight into the mechanisms by which\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p and other cytoskeletal proteins control actin homeostasis. Following\n                    <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content>\n                    engagement,\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p is rapidly activated and recruited to\n                    <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content>\n                    microclusters, as part of multiprotein complexes, where it promotes actin remodeling. Late in the activation process,\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p is internalized and eventually degraded. In this review, we describe the dynamic interactions of\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p with signaling proteins, which regulate its activation and recruitment to the\n                    <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content>\n                    and to actin\u2010rich sites. Finally, we present the molecular mechanism of\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p downregulation. Some of the signaling proteins that mediate\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p activation eventually lead to its degradation. Thus, we focus here on the regulation of\n                    <jats:styled-content style=\"fixed-case\">WAS<\/jats:styled-content>\n                    p expression and function and the mechanisms whereby they control actin machinery and T\u2010cell effector functions.\n                  <\/jats:p>","DOI":"10.1111\/imr.12112","type":"journal-article","created":{"date-parts":[[2014,8,30]],"date-time":"2014-08-30T03:27:21Z","timestamp":1409369241000},"page":"10-29","source":"Crossref","is-referenced-by-count":51,"title":["<scp>W<\/scp>\n                    iskott\u2013\n                    <scp>A<\/scp>\n                    ldrich syndrome protein \u2013 dynamic regulation of actin homeostasis: from activation through function and signal termination in T lymphocytes"],"prefix":"10.1111","volume":"256","author":[{"given":"Omri","family":"Matalon","sequence":"first","affiliation":[{"name":"The Mina and Everard Goodman Faculty of Life Sciences Bar\u2010Ilan University Ramat\u2010Gan 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