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Variable RXR requirements for thyroid hormone responsiveness of endogenous genes.

机译:内源基因对甲状腺激素反应性的RXR要求不同。

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摘要

Thyroid hormone receptors heterodimerize with retinoid X receptors in vitro and it is widely assumed that these heterodimers mediate the T3 induction of target genes. However, the importance of RXR for the T3 induction of endogenous genes has not been assessed. We used cDNA microarrays to identify 54 genes induced by T3 in Neuro2a cells that express thyroid hormone receptor beta. RNA interference-mediated knock down of endogenous RXRs showed that these genes vary from being highly dependent on RXR for T3 induction to being independent of RXR. Thus, the availability of RXR may differentially regulate the T3 induction of subsets of genes within a cell. Furthermore, coregulatory proteins that preferentially interact with TR homodimers or RXR-TR heterodimers may further expand the range of T3 response for genes within the same cell.
机译:甲状腺激素受体在体外与类维生素X受体异源二聚体,并且广泛认为这些异源二聚体介导了靶基因的T3诱导。但是,尚未评估RXR对T3诱导内源基因的重要性。我们使用cDNA微阵列识别T3诱导表达甲状腺激素受体β的Neuro2a细胞中的54个基因。 RNA干扰介导的内源性RXR敲低表明,这些基因从高度依赖RXR进行T3诱导变化到独立于RXR。因此,RXR的可用性可能会差异性地调节细胞内基因子集的T3诱导。此外,优先与TR同二聚体或RXR-TR异二聚体相互作用的核心调节蛋白可以进一步扩大同一细胞内基因的T3反应范围。

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