biostudies-literatureHewitt KJInstitute for Basic ScienceUSDA-NIFANIDDK NIH HHSUW Skin Disease Research CenterNHLBI NIH HHSNCI NIH HHSTraining Program in Translational Cardiovascular ScienceNIHAmerican Heart Association Postdoctoral FellowshipNIGMS NIH HHSCancer Center213-225.e4https://www.ebi.ac.uk/biostudies/studies/S-EPMC5578808biostudies-literatureUnknown42(3)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^-/- 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 accessiDevelopmental cellGATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia.PMC5578808IBS-R021-D1T32 HL0079364581R01 DK080040R37 DK050107T32 HL-007936-16K01 DK113117P30 CA014520P30CA014520DK50107R01 DK050107R56 DK068634DK68634P41 GM108538DK080040R01 DK068634K01DK113117Devadas PHao SBresnick EHCoon JJKim JSHewitt KJTanimura NKatsumura KRMatson DRHebert ASDewey CNKeles SPaulson RFfalseGATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia.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^-/- 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 accessi2017-01-01T00:00:00Z2017 Aug2025-04-26T11:06:22.98Z2019-03-26T23:49:38ZS-EPMC55788082878758910.1016/j.devcel.2017.07.009