| First Author | Nakada MT | Year | 1989 |
| Journal | Biochem J | Volume | 260 |
| Issue | 1 | Pages | 53-9 |
| PubMed ID | 2549959 | Mgi Jnum | J:30048 |
| Mgi Id | MGI:77570 | Doi | 10.1042/bj2600053 |
| Citation | Nakada MT, et al. (1989) Genetic regulation of beta 2-adrenergic receptors in 3T3-L1 fibroblasts. Biochem J 260(1):53-9 |
| abstractText | The beta 2-adrenergic receptor from mouse 3T3-L1 cells is up-regulated through genetic mechanisms by glucocorticoids and butyrate. To study the genetic regulation of these receptors, we sequenced a 5 kb region of genomic DNA from 3T3-L1 cells, containing the beta-adrenergic receptor gene and approx. 1.5 kb of both 5' and 3' flanking sequences. The sequence contained one copy of an 8 bp consensus sequence which can confer phorbol ester-responsiveness to genes. Phorbol esters attenuated the up-regulation of beta 2-adrenergic receptors by glucocorticoids but not by butyrate. This effect was probably due to a phorbol ester-induced decrease in glucocorticoid receptor number. Using methylation-sensitive restriction enzymes, we examined the methylation of a CG-rich region occurring 5' to the gene and did not detect any changes in methylation of this region upon dexamethasone or butyrate treatment. A total of 16 putative glucocorticoid response elements were found which may mediate the glucocorticoid-induced increase in beta 2-adrenergic receptors. A comparison of the regulatory sequences of the two beta-adrenergic receptor subtypes from human and mouse confirms the observed physiological controls of receptor subtype expression and offers an explanation as to why the subtypes differ in genetic regulation. |
