title: Dok2 likely down-regulates Klf1 in mouse erythroleukemia cells.
abstract: OBJECTIVE
  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.
  
  
  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.
  
  
  CONCLUSIONS
  Dok2 is able to control Klf1 expression by transcriptional regulation through directly binding to its promoter region.
authors: Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan Center for Clinical and Translational Research, Kyushu University Hospital, Fukuoka, Japan.
authors: Yuka
authors: Y
authors: Tanaka
authors: Department of Research and Development of Next Generation Medicine, Kyushu University Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors: Kasem
authors: K
authors: Kulkeaw
authors: Department of Research and Development of Next Generation Medicine, Kyushu University Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors: Tomoko
authors: T
authors: Inoue
authors: Department of Research and Development of Next Generation Medicine, Kyushu University Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors: Keai Sinn
authors: KS
authors: Tan
authors: Center for Clinical and Translational Research, Kyushu University Hospital, Fukuoka, Japan.
authors: Yoichi
authors: Y
authors: Nakanishi
authors: Department of Cell Biology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors: Senji
authors: S
authors: Shirasawa
authors: Department of Research and Development of Next Generation Medicine, Kyushu University Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan ds-mons@yb3.so-net.ne.jp.
authors: Daisuke
authors: D
authors: Sugiyama
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000502:physiology*; D000818:Animals; D045744:Cell Line, Tumor; D015536:Down-Regulation; D015973:Gene Expression Regulation, Leukemic; D051741:Kruppel-Like Transcription Factors / Q000235:genetics*; D004915:Leukemia, Erythroblastic, Acute / Q000235:genetics* / Q000473:pathology; D051379:Mice; D010750:Phosphoproteins / Q000502:physiology*; D011401:Promoter Regions, Genetic
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C498444:Dok2 protein, mouse; D051741:Kruppel-Like Transcription Factors; D010750:Phosphoproteins; C080774:erythroid Kruppel-like factor
keywords: Dok2; KIf1; Mouse erythroleukemia cells; docking protein 2; erythropoiesis