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Data in support of DPF2 regulates OCT4 protein level and nuclear distribution.
Liu, Chao; Zhang, Dijuan; Shen, Yuxian; Tao, Xiaofang; Liu, Lihua; Zhong, Yongwang; Fang, Shengyun.
Afiliação
  • Liu C; Department of Histology and Embryology, Institute of Stem Cell and Tissue Engineering, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui 230032, China; Center for Biomedical Engineering and Technology (BioMET), University of Maryland, Baltimore, MD 21201, USA.
  • Zhang D; Department of Histology and Embryology, Institute of Stem Cell and Tissue Engineering, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui 230032, China.
  • Shen Y; School of Basic Medical Sciences, Institute of Biopharmaceuticals, Anhui Medical University, Hefei, Anhui 230032, China.
  • Tao X; School of Basic Medical Sciences, Institute of Biopharmaceuticals, Anhui Medical University, Hefei, Anhui 230032, China.
  • Liu L; Institute of Clinical Pharmacology, Anhui Medical University, Hefei, Anhui 230032, China.
  • Zhong Y; Center for Biomedical Engineering and Technology (BioMET), University of Maryland, Baltimore, MD 21201, USA.
  • Fang S; Center for Biomedical Engineering and Technology (BioMET), University of Maryland, Baltimore, MD 21201, USA.
Data Brief ; 5: 599-604, 2015 Dec.
Article em En | MEDLINE | ID: mdl-26958616
ABSTRACT
DPF2, also named ubi-d4/requiem (REQU), interacts with a protein complex containing OCT4. This paper provides data in support of the research article entitled "DPF2 regulates OCT4 protein level and nuclear distribution". The highlights include (1) Denature-immunoprecipitation assay revealed ubiquitination of OCT4 in pluripotent H9 cells, which was enhancedby MG132, a proteasome inhibitor. (2) Well colocalization of ectopic OCT4 and FLAG-Ub was found in HeLa cells, which was also increased by MG132. (3) MG132 treatment decreased DPF2 cytoplasmic expression in vivo. These data give insights into how proteasome inhibition contributes to studying ubiquitnation of OCT4.

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2015 Tipo de documento: Article