Transcriptomics

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Transcription profiling of mouse Bmi1-overexpressing Ink4a-Arf-null hepatoblasts


ABSTRACT: Forced expression of Bmi1 accelerated the self-renewal of hepatic stem/progenitor cells and eventually induced their transformation in an in vivo transplant model. The Ink4a/Arf locus, which encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf, is a pivotal target of Bmi1. Therefore, it would be of importance to understand the contribution of the Ink4a/Arf locus to Bmi1 oncogenic functions in cancer and search for as-yet-unknown Bmi1 target genes other than Ink4a/Arf. We used microarrays to explore novel candidate downstream targets for Bmi1 in hepatic stem/progenitor cells Experiment Overall Design: Purified Dlk-positive hepatoblasts at day 28 of culture were subjected to RNA extraction and hybridization on Affymetrix microarrays. Data were obtained for quadrant samples from four independent experiments.

ORGANISM(S): Mus musculus  

SUBMITTER: Tetsuhiro Chiba  

PROVIDER: E-GEOD-17462 | ArrayExpress | 2009-08-07

SECONDARY ACCESSION(S): GSE17462PRJNA118739

REPOSITORIES: GEO, ArrayExpress

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