論文

査読有り
2017年8月

GATA Factor-Regulated Samd14 Enhancer Confers Red Blood Cell Regeneration and Survival in Severe Anemia

DEVELOPMENTAL CELL
  • Kyle J. Hewitt
  • Koichi R. Katsumura
  • Daniel R. Matson
  • Prithvia Devadas
  • Nobuyuki Tanimura
  • Alexander S. Hebert
  • Joshua J. Coon
  • Jin-Soo Kim
  • Colin N. Dewey
  • Sunduz Keles
  • Siyang Hao
  • Robert F. Paulson
  • Emery H. Bresnick
  • 全て表示

42
3
開始ページ
213
終了ページ
+
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.devcel.2017.07.009
出版者・発行元
CELL PRESS

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 accessibility. Thus, a GATA-2/anemia-regulated enhancer controls expression of an SAM domain protein that confers survival in anemia. We propose that Samd14-Enh and an ensemble of anemia-responsive enhancers are essential for erythrocyte regeneration in stress erythropoiesis, a vital process in pathologies, including beta-thalassemia, myelodysplastic syndrome, and viral infection.

リンク情報
DOI
https://doi.org/10.1016/j.devcel.2017.07.009
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/28787589
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000407040900006&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.devcel.2017.07.009
  • ISSN : 1534-5807
  • eISSN : 1878-1551
  • PubMed ID : 28787589
  • Web of Science ID : WOS:000407040900006

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