Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-seq of NuRD components and pluripotency factors in wild-type, Mbd3 and Sall4/1 mutant embryonic stem cells


ABSTRACT: Members of the Nucleosome Remodeling and Deacetylase (NuRD) complex Mbd3 and Mi2beta (Chd4) along with pluripotency regulators Nanog, Oct4, Klf4 and Esrrb were profiled for chromatin association by ChIP-seq in mouse embryonic stem cells mutant for Mbd3, Sall4 and/or the related Sall1 pluripotency-associated factors.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Paul Bertone 

PROVIDER: E-MTAB-4565 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex.

Miller Anzy A   Ralser Meryem M   Kloet Susan L SL   Loos Remco R   Loos Remco R   Nishinakamura Ryuichi R   Bertone Paul P   Vermeulen Michiel M   Hendrich Brian B  

Development (Cambridge, England) 20160728 17


Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Although it is reported to play an important role in embryonic stem cell (ESC) self-renewal, whether it is an essential pluripotency factor has been disputed. Here, we show that Sall4 is dispensable for mouse ESC pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ESCs but is not required for maintenanc  ...[more]

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