Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from mouse liver over-expressing either GFP alone or biotinylated-TRb1 and GFP


ABSTRACT: We over-expressed biotinylated-thyroid hormone receptor beta 1 (TRb1) in mouse liver using an adenovirus in order to perform ChIP-seq experiments. These microarrays were performed to determine gene expression changes in response to tri-iodothyronine (thyroid hormone; T3) stimulation. A control GFP adenovirus was used and gene expression from these livers was also done as a comparison. We performed microarrays from Ad-GFP-infected propylthiouracil (PTU)-fed livers injected with either saline or T3 and Ad-TRb1-GFP infected livers injected with either saline or T3. RNA was extracted from livers of biotin ligase (BirA)-expressing mice that had been infected with either Ad-GFP or Ad-TRb1, fed with PTU for 3 weeks followed by saline or T3 injections for 4 consecutive days.

ORGANISM(S): Mus musculus

SUBMITTER: Preeti Ramados 

PROVIDER: E-GEOD-52433 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Novel mechanism of positive versus negative regulation by thyroid hormone receptor β1 (TRβ1) identified by genome-wide profiling of binding sites in mouse liver.

Ramadoss Preeti P   Abraham Brian J BJ   Tsai Linus L   Zhou Yiming Y   Costa-e-Sousa Ricardo H RH   Ye Felix F   Bilban Martin M   Zhao Keji K   Hollenberg Anthony N AN  

The Journal of biological chemistry 20131127 3


Triiodothyronine (T3) regulates key metabolic processes in the liver through the thyroid hormone receptor, TRβ1. However, the number of known target genes directly regulated by TRβ1 is limited, and the mechanisms by which positive and especially negative transcriptional regulation occur are not well understood. To characterize the TRβ1 cistrome in vivo, we expressed a biotinylated TRβ1 in hypo- and hyperthyroid mouse livers, used ChIP-seq to identify genomic TRβ1 targets, and correlated these da  ...[more]

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