{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T07:22:31Z","timestamp":1770103351652,"version":"3.49.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2005,3,1]],"date-time":"2005-03-01T00:00:00Z","timestamp":1109635200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Effector functions mediated by NK cells involve cytotoxicity and transcription-dependent production and release of cytokines and chemokines. Although the JAK\/STAT pathway mediates lymphokine-induced transcriptional regulation in NK cells, very little is known about transcriptional regulation induced during cell-cell contact. We demonstrate that the Wiskott-Aldrich syndrome protein (WASp) is an important component for integration of signals leading to nuclear translocation of NFAT2 and NF-\u03baB (RelA) during cell-cell contact and NKp46-dependent signaling. This WASp function is independent of its known role in F-actin polymerization and cytoskeletal rearrangement. Absence of WASp results in decreased accumulation of calcineurin, WASp-interacting protein, and molecules upstream of calcium mobilization, i.e., activated ZAP70 and phospholipase C-\u03b31, in the disorganized NK cell immune synapse. Production of GM-CSF, but not IFN-\u03b3, is decreased, while natural cytotoxicity of Wiskott-Aldrich syndrome-NK cells is maintained. Our results indicate that WASp independently regulates its dual functions, i.e., actin cytoskeletal remodeling and transcription in NK cells.<\/jats:p>","DOI":"10.4049\/jimmunol.174.5.2602","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:48:17Z","timestamp":1398023297000},"page":"2602-2611","source":"Crossref","is-referenced-by-count":51,"title":["The Wiskott-Aldrich Syndrome Protein Regulates Nuclear Translocation of NFAT2 and NF-\u03baB (RelA) Independently of Its Role in Filamentous Actin Polymerization and Actin Cytoskeletal Rearrangement"],"prefix":"10.1093","volume":"174","author":[{"given":"Winifred","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans D","family":"Ochs","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Washington , Seattle, WA 98195"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bo","family":"Dupont","sequence":"additional","affiliation":[{"name":"Immunology Program, Sloan-Kettering Institute for Cancer Research , New York, NY 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yatin M","family":"Vyas","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Memorial Sloan-Kettering Cancer Center , New York, NY 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,3,1]]},"reference":[{"key":"2026020214094566200_R1","first-page":"189","volume-title":"Annu. 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