期刊
MOLECULAR ENDOCRINOLOGY
卷 16, 期 11, 页码 2439-2451出版社
ENDOCRINE SOC
DOI: 10.1210/me.2001-0324
关键词
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资金
- NCI NIH HHS [R01-CA-89364] Funding Source: Medline
Ca2+/Calmodulin-dependent protein kinase IV (CaMKIV) is regulated by T-3 in a time- and concentration-dependent manner in the developing rat brain and plays an important role in neuronal-specific gene regulation. T-3 treatment, but not retinoic acid (RA), stimulated endogenous CaMKIV mRNA 5-fold in mouse embryonic stem (ES) cells differentiated into neurons. We localized a region -750 to -700 in the CaMKIV gene 5'-flanking region that conferred T-3 responsiveness and bound thyroid hormone receptor (TR), retinoic acid receptor (RAR), and chicken ovalbumin upstream promoter-transcription factor 1 (COUP-TF1). T-3 and RA treatment stimulated the CaMKIV hormone response element. Cotransfection of a COUP-TF1 expression vector repressed the T-3 response and augmented the RA response. Mutational analysis identified three half-sites arranged in a direct repeat (AB) and overlapping inverted repeat (BC), required for functional induction and receptor binding. TR and RAR bound predominantly to the BC portion of the element and COUP-TF1 to the AB region, with a close correlation of binding and functional studies. COUP-TF1 binding did not influence TR/retinoid X receptor binding but modestly augmented RAR/retinoid X receptor binding. A single element confers T-3 and COUP-TF1 regulation of CaMKIV expression.
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