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Alliance"],"accepted":{"date-parts":[[2025,3,31]]},"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:p>\n                    STAT5B is a vital transcription factor for lymphocytes. Here, the function of two STAT5B mutations from human T-cell leukemias: one substituting tyrosine 665 with phenylalanine (STAT5B\n                    <jats:sup>Y665F<\/jats:sup>\n                    ) and the other with histidine (STAT5B\n                    <jats:sup>Y665H<\/jats:sup>\n                    ), was interrogated. In silico modeling predicted divergent energetic effects on homodimerization with a range of pathogenicity. In primary T cells in vitro, STAT5B\n                    <jats:sup>Y665F<\/jats:sup>\n                    showed gain-of-function, whereas STAT5B\n                    <jats:sup>Y665H<\/jats:sup>\n                    demonstrated loss-of-function. Introducing the mutation into the mouse genome illustrated that the gain-of-function\n                    <jats:italic>Stat5b<\/jats:italic>\n                    <jats:sup>Y665F<\/jats:sup>\n                    mutation resulted in accumulation of CD8\n                    <jats:sup>+<\/jats:sup>\n                    effector and memory and CD4\n                    <jats:sup>+<\/jats:sup>\n                    regulatory T cells, altering CD8\n                    <jats:sup>+<\/jats:sup>\n                    \/CD4\n                    <jats:sup>+<\/jats:sup>\n                    ratios. In contrast, STAT5B\n                    <jats:sup>Y665H<\/jats:sup>\n                    \u201cknock-in\u201d mice showed diminished CD8\n                    <jats:sup>+<\/jats:sup>\n                    effector and memory and CD4\n                    <jats:sup>+<\/jats:sup>\n                    regulatory T cells. In contrast to WT STAT5B, the STAT5B\n                    <jats:sup>Y665F<\/jats:sup>\n                    variant displayed greater STAT5 phosphorylation, DNA binding, and transcriptional activity after cytokine activation, whereas the STAT5B\n                    <jats:sup>Y665H<\/jats:sup>\n                    variant resembled a null. The work exemplifies how joining in silico and in vivo studies of single nucleotides deepens our understanding of disease-associated variants, revealing structural determinants of altered function, defining mechanistic roles, and, specifically here, identifying a gain-of-function variant that does not directly induce hematopoietic malignancy.\n                  <\/jats:p>","DOI":"10.26508\/lsa.202503222","type":"journal-article","created":{"date-parts":[[2025,4,14]],"date-time":"2025-04-14T15:50:13Z","timestamp":1744645813000},"page":"e202503222","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["STAT5B leukemic mutations, altering SH2 tyrosine 665, have opposing impacts on immune gene programs"],"prefix":"10.26508","volume":"8","author":[{"given":"Hye Kyung","family":"Lee","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00adh9b73","id-type":"ROR","asserted-by":"publisher"}],"name":"Laboratory 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