{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T22:49:01Z","timestamp":1787611741742,"version":"build-2736575974"},"reference-count":83,"publisher":"Rockefeller University Press","issue":"10","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,9,21]]},"abstract":"<jats:p>B cell antigen receptor (BCR) signaling is critical for B cell development and activation. Using mass spectrometry, we identified a protein kinase D\u2013interacting substrate of 220 kD (Kidins220)\/ankyrin repeat\u2013rich membrane-spanning protein (ARMS) as a novel interaction partner of resting and stimulated BCR. Upon BCR stimulation, the interaction increases in a Src kinase\u2013independent manner. By knocking down Kidins220 in a B cell line and generating a conditional B cell\u2013specific Kidins220 knockout (B-KO) mouse strain, we show that Kidins220 couples the BCR to PLC\u03b32, Ca2+, and extracellular signal-regulated kinase (Erk) signaling. Consequently, BCR-mediated B cell activation was reduced in vitro and in vivo upon Kidins220 deletion. Furthermore, B cell development was impaired at stages where pre-BCR or BCR signaling is required. Most strikingly, \u03bb light chain\u2013positive B cells were reduced sixfold in the B-KO mice, genetically placing Kidins220 in the PLC\u03b32 pathway. Thus, our data indicate that Kidins220 positively regulates pre-BCR and BCR functioning.<\/jats:p>","DOI":"10.1084\/jem.20141271","type":"journal-article","created":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T01:38:57Z","timestamp":1441071537000},"page":"1693-1708","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":19,"title":["Kidins220\/ARMS binds to the B cell antigen receptor and regulates B cell development and activation"],"prefix":"10.1084","volume":"212","author":[{"given":"Gina J.","family":"Fiala","sequence":"first","affiliation":[{"name":"Department of Molecular Immunology, BioIII, Faculty of Biology, University of Freiburg and Max Planck Institute of Immunobiology and Epigenetics, 79104 Freiburg, Germany 1"},{"name":"Centre for Biological Signaling Studies (BIOSS) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Spemann Graduate School of Biology and Medicine (SGBM) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Centre of Chronic Immunodeficiency (CCI) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Department of Dermatology 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Center for Biological Systems Analysis (ZBSA) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Institute of Molecular Medicine and Cell Research 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Comprehensive Cancer Centre Freiburg 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Institute of Pathology, University Medical Center Freiburg, University of Freiburg, 79104 Freiburg, Germany 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Centre for Biological Signaling Studies (BIOSS) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Spemann Graduate School of Biology and Medicine (SGBM) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Centre of Chronic Immunodeficiency (CCI) 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Department of Dermatology 2 , 3 , 4 , 5 , 6 , 7 , 8 , and 9"},{"name":"Center for Biological Systems Analysis (ZBSA) 2 , 3 , 4 , 5 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