Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

C-Jun impedes somatic cell reprogramming by activating mesenchymal core regulators and suppressing pluripotent ones


ABSTRACT: The somatic cell fate can be converted to tumor or pluripotent ones by ectopic expression of transcription factors in vitro and in vivo. Many oncogenic transcription factors are known to mediate both fates as they share similar proliferative and metabolic properties. Paradoxically, we found c-Jun as the first oncogene that appears to specify a somatic fate, oppose the pluripotent one and impede reprogramming. We performed a series of high through out sequencing to understand the way cJun works. To understand how c-Jun drives mESCs differentiating, we obtained c-Jun TetOn mESCs, and performed RNAseq 36h later with dox inducing or not . To understand why c-Jun blocks reprogramming while c-JunDN and Jdp2 can replace Oct4, we overexpressed these factors with KSM during reprogramming and perfor

ORGANISM(S): Mus musculus

SUBMITTER: Xiaoshan Wang 

PROVIDER: E-GEOD-50776 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress