Dok2 likely down-regulates Klf1 in mouse erythroleukemia cells

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

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)4561-4568
Number of pages8
JournalAnticancer research
Issue number8
Publication statusPublished - Aug 1 2014

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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