{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:39:58Z","timestamp":1790746798235,"version":"4.1.0"},"reference-count":50,"publisher":"American Society of Hematology","issue":"11","license":[{"start":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T00:00:00Z","timestamp":1780012800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,9,10]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Glanzmann thrombasthenia (GT) is characterized by absent platelet aggregation in response to all agonists except ristocetin and is caused by recessive inactivating variants in ITGA2B or ITGB3. Although patients with GT typically are described as having normal platelet counts, autosomal dominant activating variants in ITGA2B or ITGB3 cause macrothrombocytopenia. Interestingly, in our cohort of 16 patients with GT, 8 consistently exhibited platelet counts at the lower end of the normal range. We studied the role of integrin \u03b1IIb\u03b23 in platelet formation using megakaryocytes (MKs) derived from genetically modified immortalized MK cell lines (imMKCLs), focusing on 2 modifications of ITGB3: ITGB3\u2212\/\u2212 (inactivating) and ITGB3WT\/D673_E713del (activating). In static differentiation cultures, ITGB3\u2212\/\u2212 and ITGB3WT\/D673_E713del imMKCLs exhibited normal MK differentiation but reduced proplatelet formation. Platelet production was also impaired in a 3-dimensional silk-based bone marrow system and in shaking cultures, confirming a quantitative role for ITGB3 in platelet production independent of the type of variant. Although thrombin receptor activating protein\u2013activated, in vitro\u2013generated platelets lacking \u03b1IIb\u03b23 failed to bind the activation-dependent PAC-1 antibody, ITGB3WT\/D673_E713del platelets bound PAC-1 before activation, mimicking the patient\u2019s phenotype. Transcriptome profiling and metabolomic analyses of integrin \u03b1IIb\u03b23\u2013deficient MKs revealed impaired serine metabolism and downregulation of SLC3A2 (CD98hc), an amino acid transporter chaperon known to interact with the \u03b23 subunit. Flow cytometry confirmed decreased CD98hc in mutant MKs, whereas reexpression of wild-type ITGB3 in ITGB3\u2212\/\u2212 MKs restored \u03b1IIb\u03b23 and CD98hc expression, normalized proplatelet formation, and enhanced serine uptake. These results uncover a previously unrecognized role of integrin \u03b1IIb\u03b23 in coupling serine metabolism to platelet biogenesis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2025031904","type":"journal-article","created":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T17:20:17Z","timestamp":1780075217000},"page":"1466-1480","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":2,"title":["Reduced platelet formation associated with serine metabolic dysregulation in integrin \u03b1IIb\u03b23\u2013deficient megakaryocytes"],"prefix":"10.1182","volume":"148","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0023-7940","authenticated-orcid":false,"given":"Kato","family":"Ramaekers","sequence":"first","affiliation":[{"name":"1Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Leuven, 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