SMRT (silencing mediator of retinoid and thyroid hormone receptors) is recruited by numerous transcription factors to mediate lineage and signal dependent transcriptional repression. We generated a knock-in mutation in the receptor interaction domain (RID) of SMRT (SMRTmRID) that solely disrupts its interaction with nuclear hormone receptors. SMRTmRID-derived 3T3-MEFs display a dramatically increased adipogenic capacity and accelerated differentiation rate. We measured global gene expression in wild-type versus SMRTmRID-derived 3T3-MEFs in the undifferentiated state to examine which pathways were altered. Our results demonstrate that SMRT-RID dependent repression is a key determinant of the adipogenic set point.
SMRT repression of nuclear receptors controls the adipogenic set point and metabolic homeostasis.
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View SamplesCompared transccriptome of breast cancer in young women to those arising in two mature groups to characterize the underlying biological mechanisms of the breast cancer in Middle Eastern young women.
Age-specific gene expression signatures for breast tumors and cross-species conserved potential cancer progression markers in young women.
Age, Specimen part, Disease, Disease stage
View SamplesGEP class prediction in association with CI-FISH (42 candidate genes) and patient MRD stratification
Linking genomic lesions with minimal residual disease improves prognostic stratification in children with T-cell acute lymphoblastic leukaemia.
Specimen part, Disease, Disease stage
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