{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T22:32:01Z","timestamp":1790289121708,"version":"4.1.0"},"reference-count":24,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2000,3,1]],"date-time":"2000-03-01T00:00:00Z","timestamp":951868800000},"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":[[2000,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Wiskott-Aldrich syndrome protein (WASP)-interacting protein (WIP), specifically binds to a region of WASp that is frequently mutated in Wiskott-Aldrich syndrome. Due to the similar phenotypes of WASp- and Vav-deficient T cells, and the putative importance of the WIP\/WASp complex in mediating normal signals from the TCR, we investigated the role of WIP in regulating NF-AT\/AP-1-mediated gene transcription. We show that WIP has the ability to enhance Vav-mediated activation of NF-AT\/AP-1 gene transcription. In addition, we provide evidence that the interaction of WIP with WASp is necessary, but not sufficient for the ability of WIP to regulate NF-AT\/AP-1 activity. Finally, we have identified a region in WIP required for its regulation of NF-AT\/AP-1 activity. Our data suggests that the WIP-WASp interaction is important for NF-AT\/AP-1-mediated gene transcription, and that defects seen in the activation of T cells from WAS patients may be due to the inability of these cells to form a functional WIP\/WASp-signaling complex.<\/jats:p>","DOI":"10.4049\/jimmunol.164.6.2866","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T16:28:33Z","timestamp":1398184113000},"page":"2866-2870","source":"Crossref","is-referenced-by-count":26,"title":["Cutting Edge: WIP, a Binding Partner for Wiskott-Aldrich Syndrome Protein, Cooperates with Vav in the Regulation of T Cell Activation"],"prefix":"10.1093","volume":"164","author":[{"given":"Doris N","family":"Savoy","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Mayo Graduate and Medical Schools, Mayo Clinic , Rochester, MN 55905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel D","family":"Billadeau","sequence":"additional","affiliation":[{"name":"Department of Immunology, Mayo Graduate and Medical Schools, Mayo Clinic , Rochester, MN 55905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J","family":"Leibson","sequence":"additional","affiliation":[{"name":"Department of Immunology, Mayo Graduate and Medical Schools, Mayo Clinic , Rochester, MN 55905"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,3,15]]},"reference":[{"key":"2026020214024848200_R1","first-page":"635","volume-title":"Cell","year":"1994"},{"key":"2026020214024848200_R2","first-page":"905","volume-title":"Annu. 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