Data in support of DPF2 regulates OCT4 protein level and nuclear distribution
Chao Liu,
Dijuan Zhang,
Yuxian Shen,
Xiaofang Tao,
Lihua Liu,
Yongwang Zhong,
Shengyun Fang
Affiliations
Chao Liu
Department of Histology and Embryology, Institute of Stem Cell and Tissue Engineering, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui 230032, China
Dijuan Zhang
Department of Histology and Embryology, Institute of Stem Cell and Tissue Engineering, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui 230032, China
Yuxian Shen
School of Basic Medical Sciences, Institute of Biopharmaceuticals, Anhui Medical University, Hefei, Anhui 230032, China
Xiaofang Tao
School of Basic Medical Sciences, Institute of Biopharmaceuticals, Anhui Medical University, Hefei, Anhui 230032, China
Lihua Liu
Institute of Clinical Pharmacology, Anhui Medical University, Hefei, Anhui 230032, China
Yongwang Zhong
Center for Biomedical Engineering and Technology (BioMET), University of Maryland, Baltimore, MD 21201, USA
Shengyun Fang
Center for Biomedical Engineering and Technology (BioMET), University of Maryland, Baltimore, MD 21201, USA
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.