{"@type": "dcat:Dataset", "accessLevel": "public", "bureauCode": ["009:25"], "contactPoint": {"@type": "vcard:Contact", "fn": "NIH", "hasEmail": "mailto:info@nih.gov"}, "description": "Background\n          Bruton's tyrosine kinase (Btk) is essential for B cell development and function. Mutations of Btk elicit X-linked agammaglobulinemia in humans and X-linked immunodeficiency in the mouse. Btk has been proposed to participate in B cell antigen receptor-induced signaling events leading to activation of phospholipase C-\u03b32 (PLC\u03b32) and calcium mobilization. However it is unclear whether Btk activation is alone sufficient for these signaling events, and whether Btk can activate additional pathways that do not involve PLC\u03b32. To address such issues we have generated Btk:ER, a conditionally active form of the kinase, and expressed it in the PLC\u03b32-deficient DT40 B cell line.\n        \n        \n          Results\n          Activation of Btk:ER was sufficient to induce multiple B cell signaling pathways in PLC\u03b32-sufficient DT40 cells. These included tyrosine phosphorylation of PLC\u03b32, mobilization of intracellular calcium, activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) pathways, and apoptosis. In DT40 B cells deficient for PLC\u03b32, Btk:ER activation failed to induce the signaling events described above with the consequence that the cells failed to undergo apoptosis.\n        \n        \n          Conclusions\n          These data suggest that Btk:ER regulates downstream signaling pathways primarily via PLC\u03b32 in B cells. While it is not known whether activated Btk:ER precisely mimics activated Btk, this conditional system will likely facilitate the dissection of the role of Btk and its family members in a variety of biological processes in many different cell types.", "distribution": [{"@type": "dcat:Distribution", "description": "Visit the original government dataset for complete information, documentation, and data access.", "downloadURL": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC32313/", "mediaType": "text/html", "title": "Official Government Data Source"}], "identifier": "https://healthdata.gov/api/views/x8i4-br95", "issued": "2025-07-14", "keyword": ["b-cell-signaling", "btk-kinase", "nih", "plc-gamma-2", "x-linked-agammaglobulinemia"], "landingPage": "https://healthdata.gov/d/x8i4-br95", "modified": "2025-09-06", "programCode": ["009:033"], "publisher": {"@type": "org:Organization", "name": "National Institutes of Health"}, "theme": ["NIH"], "title": "A conditional form of Bruton's tyrosine kinase is sufficient to activate multiple downstream signaling pathways via PLC Gamma 2 in B cells"}