Dok2 likely down-regulates Klf1 in mouse erythroleukemia cells

Yuka Tanaka, Kasem Kulkeaw, Tomoko Inoue, Keai Sinn Tan, Yoichi Nakanishi, Senji Shirasawa, Daisuke Sugiyama

研究成果: ジャーナルへの寄稿学術誌査読

2 被引用数 (Scopus)

抄録

Background/Aim: Docking protein 2 (Dok2) is an adapter protein which is involved in hematopoiesis. However, it still remains unclear how Dok2 functions in regulation of transcription of hematopoietic genes. To address this issue, we knocked-down Dok2 mRNA in mouse erythroleukemia cells which highly express Dok2 intrinsically. Materials and Methods: Mouse erythroleukemia cells were transfected with Dok2 siRNA for 24 h and gene expression of erythroid differentiation-related genes, such as GATA binding protein 1 (Gata1), Krüppel-like factor 1 (Klf1), α-globin and β-globin were assessed by real-time polymerase chain reaction. Results: Among the tested genes, expression of Klf1 exhibited a 1.94-fold increase when compared to the control 24 h after transfection. Immunocytochemistry and chromatin immunoprecipitation assays revealed that Dok2 protein localizes in the nucleus and binds to the promoter region of Klf1 gene. Conclusion: Dok2 is able to control Klf1 expression by transcriptional regulation through directly binding to its promoter region.

本文言語英語
ページ(範囲)4561-4568
ページ数8
ジャーナルAnticancer research
34
8
出版ステータス出版済み - 8月 1 2014

!!!All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 癌研究

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