{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hewitt KJ"],"funding":["Institute for Basic Science","USDA-NIFA","NIDDK NIH HHS","UW Skin Disease Research Center","NHLBI NIH HHS","NCI NIH HHS","Training Program in Translational Cardiovascular Science","NIH","American Heart Association Postdoctoral Fellowship","NIGMS NIH HHS","Cancer Center"],"pagination":["213-225.e4"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5578808"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["42(3)"],"pubmed_abstract":["An enhancer with amalgamated E-box and GATA motifs (+9.5) controls expression of the regulator of hematopoiesis GATA-2. While similar GATA-2-occupied elements are common in the genome, occupancy does not predict function, and GATA-2-dependent genetic networks are incompletely defined. A \"+9.5-like\" element resides in an intron of Samd14 (Samd14-Enh) encoding a sterile alpha motif (SAM) domain protein. Deletion of Samd14-Enh in mice strongly decreased Samd14 expression in bone marrow and spleen. Although steady-state hematopoiesis was normal, Samd14-Enh<sup>-/-</sup> mice died in response to severe anemia. Samd14-Enh stimulated stem cell factor/c-Kit signaling, which promotes erythrocyte regeneration. Anemia activated Samd14-Enh by inducing enhancer components and enhancer chromatin accessi"],"journal":["Developmental cell"],"pubmed_title":["GATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia."],"pmcid":["PMC5578808"],"funding_grant_id":["IBS-R021-D1","T32 HL007936","4581","R01 DK080040","R37 DK050107","T32 HL-007936-16","K01 DK113117","P30 CA014520","P30CA014520","DK50107","R01 DK050107","R56 DK068634","DK68634","P41 GM108538","DK080040","R01 DK068634","K01DK113117"],"pubmed_authors":["Devadas P","Hao S","Bresnick EH","Coon JJ","Kim JS","Hewitt KJ","Tanimura N","Katsumura KR","Matson DR","Hebert AS","Dewey CN","Keles S","Paulson RF"],"additional_accession":[]},"is_claimable":false,"name":"GATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia.","description":"An enhancer with amalgamated E-box and GATA motifs (+9.5) controls expression of the regulator of hematopoiesis GATA-2. While similar GATA-2-occupied elements are common in the genome, occupancy does not predict function, and GATA-2-dependent genetic networks are incompletely defined. A \"+9.5-like\" element resides in an intron of Samd14 (Samd14-Enh) encoding a sterile alpha motif (SAM) domain protein. Deletion of Samd14-Enh in mice strongly decreased Samd14 expression in bone marrow and spleen. Although steady-state hematopoiesis was normal, Samd14-Enh<sup>-/-</sup> mice died in response to severe anemia. Samd14-Enh stimulated stem cell factor/c-Kit signaling, which promotes erythrocyte regeneration. Anemia activated Samd14-Enh by inducing enhancer components and enhancer chromatin accessi","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Aug","modification":"2025-04-26T11:06:22.98Z","creation":"2019-03-26T23:49:38Z"},"accession":"S-EPMC5578808","cross_references":{"pubmed":["28787589"],"doi":["10.1016/j.devcel.2017.07.009"]}}