{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T06:17:42Z","timestamp":1790835462004,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,1,14]],"date-time":"2016-01-14T00:00:00Z","timestamp":1452729600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","award":["P30CA16672"],"award-info":[{"award-number":["P30CA16672"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Heterozygous mutations in the transcriptional regulator <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 associate with multilineage immunodeficiency, myelodysplastic syndrome (<jats:styled-content style=\"fixed-case\">MDS<\/jats:styled-content>), and acute myeloid leukemia (<jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content>). The majority of these mutations localize in the zinc finger (ZnF) domains, which mediate <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> binding. Deregulated hematopoiesis with <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 mutation frequently develops in adulthood, yet <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 function in the bone marrow remains unresolved. To investigate this, we conditionally deleted the <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 C\u2010terminal ZnF (C\u2010ZnF) coding sequences in adult mice. Upon <jats:italic>Gata2 C\u2010ZnF<\/jats:italic> deletion, we observed rapid peripheral cytopenia, bone marrow failure, and decreased c\u2010Kit expression on hematopoietic progenitors. Transplant studies indicated <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 has a cell\u2010autonomous role in bone marrow hematopoiesis. Moreover, myeloid lineage populations were particularly sensitive to <jats:italic>Gata2<\/jats:italic> hemizygosity, while molecular assays indicated <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 regulates c\u2010Kit expression in multilineage progenitor cells. Enforced c\u2010Kit expression in <jats:italic>Gata2 C\u2010ZnF\u2010<\/jats:italic>deficient hematopoietic progenitors enhanced myeloid colony activity, suggesting <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 sustains myelopoiesis via a cell intrinsic role involving maintenance of c\u2010Kit expression. Our results provide insight into mechanisms regulating hematopoiesis in bone marrow and may contribute to a better understanding of immunodeficiency and bone marrow failure associated with <jats:styled-content style=\"fixed-case\">GATA<\/jats:styled-content>\u20102 mutation.<\/jats:p>","DOI":"10.1111\/ejh.12719","type":"journal-article","created":{"date-parts":[[2015,12,11]],"date-time":"2015-12-11T08:16:48Z","timestamp":1449821808000},"page":"261-270","source":"Crossref","is-referenced-by-count":11,"title":["Loss of c\u2010Kit and bone marrow failure upon conditional removal of the <scp>GATA<\/scp>\u20102 C\u2010terminal zinc finger domain in adult mice"],"prefix":"10.1111","volume":"97","author":[{"given":"Haiyan S.","family":"Li","sequence":"first","affiliation":[{"name":"Department of Immunology The University of Texas MD Anderson Cancer Center Houston TX 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