P160 steroid coactivator

Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs). Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.

The activation of gene transcription is a multistep process that is triggered by factors that recognize transcriptional enhancer sites in DNA . These factors work with co-activators to direct transcriptional initiation by the RNA polymerase II apparatus. The mediator of RNA polymerase II transcription subunit 1 protein is a subunit of the CRSP (cofactor required for SP1 activation) complex, which, along with TFIID , is required for efficient activation by SP1. This protein is also a component of other multisubunit complexes [., thyroid hormone receptor -(TR-) associated proteins that interact with TR and facilitate TR function on DNA templates in conjunction with initiation factors and cofactors]. It also regulates p53 -dependent apoptosis and it is essential for adipogenesis . This protein is known to have the ability to self-oligomerize. [7]

Using transient transfection assays, Fan et al. (1999) demonstrated that BRCA1 inhibits signaling by the ligand-activated estrogen receptor ESR-alpha through the estrogen-responsive enhancer element and blocks the C-terminal transcriptional activation function AF2 of ESR-alpha. These results suggested that wildtype BRCA1 protein may function, in part, to suppress estrogen-dependent mammary epithelial proliferation by inhibiting ESR-alpha-mediated transcriptional pathways related to cell proliferation, and that loss of this ability may contribute to tumorigenesis.

In a 29-year-old woman with selective pituitary thyroid hormone resistance ( 145650 ), Asteria et al. (1999) identified a mutation in exon 9 of the THRB gene (T337A; ). She presented with symptoms and signs of hyperthyroidism and was successfully treated with 3,5,3-prime-triiodothyroacetic acid (TRIAC) until the onset of pregnancy, when the therapy was discontinued to avoid possible adverse effects on fetal development. TRIAC therapy was reinstituted following recurrence of thyrotoxic features, and the fetus was shown also to be heterozygous for the T337A mutation. The authors advocated prenatal diagnosis of thyroid hormone resistance and adequate treatment of the disease in the case of maternal hyperthyroidism, to avoid fetal thyrotrope hyperplasia, reduce fetal goiter, and maintain maternal euthyroidism during pregnancy.

P160 steroid coactivator

p160 steroid coactivator

In a 29-year-old woman with selective pituitary thyroid hormone resistance ( 145650 ), Asteria et al. (1999) identified a mutation in exon 9 of the THRB gene (T337A; ). She presented with symptoms and signs of hyperthyroidism and was successfully treated with 3,5,3-prime-triiodothyroacetic acid (TRIAC) until the onset of pregnancy, when the therapy was discontinued to avoid possible adverse effects on fetal development. TRIAC therapy was reinstituted following recurrence of thyrotoxic features, and the fetus was shown also to be heterozygous for the T337A mutation. The authors advocated prenatal diagnosis of thyroid hormone resistance and adequate treatment of the disease in the case of maternal hyperthyroidism, to avoid fetal thyrotrope hyperplasia, reduce fetal goiter, and maintain maternal euthyroidism during pregnancy.

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