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Ligand-dependent contribution of RXRbeta to cholesterol homeostasis in Sertoli cells.

EMBO reports | Dec 3, 2004

We show that mice expressing retinoid X receptor beta (RXRbeta) impaired in its transcriptional activation function AF-2 (Rxrb(af20) mutation) do not display the spermatid release defects observed in RXRbeta-null mutants, indicating that the role of RXRbeta in spermatid release is ligand-independent. In contrast, like RXRbeta-null mutants, Rxrb(af20) mice accumulate cholesteryl esters in Sertoli cells (SCs) due to reduced ABCA1 transporter-mediated cholesterol efflux. We provide genetic and molecular evidence that cholesterol homeostasis in SCs does not require PPARalpha and beta, but depends upon the TIF2 coactivator and RXRbeta/LXRbeta heterodimers, in which RXRbeta AF-2 is transcriptionally active. Our results also indicate that RXRbeta may be activated by a ligand distinct from 9-cis retinoic acid.

Pubmed ID: 14993927 RIS Download

Mesh terms: ATP-Binding Cassette Transporters | Animals | Cholesterol | DNA-Binding Proteins | Dimerization | Electrophoretic Mobility Shift Assay | Gene Expression Regulation | Gene Silencing | Histone Acetyltransferases | Homeostasis | Immunochemistry | Ligands | Liver X Receptors | Male | Mice | Mice, Knockout | Nuclear Receptor Coactivator 1 | Nuclear Receptor Coactivator 2 | Orphan Nuclear Receptors | Protein Binding | Receptors, Cytoplasmic and Nuclear | Retinoid X Receptor beta | Sertoli Cells | Spermatids | Transcription Factors

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Associated grants

  • Agency: NIDDK NIH HHS, Id: P01 DK059820
  • Agency: NIDDK NIH HHS, Id: 1-P01-DK59820-01

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