scholarly journals Delineation of the distribution of beta-adrenergic receptor subtypes in canine myocardium.

1988 ◽  
Vol 63 (1) ◽  
pp. 117-125 ◽  
Author(s):  
S S Murphree ◽  
J E Saffitz
1989 ◽  
Vol 25 (7) ◽  
pp. A197 ◽  
Author(s):  
Nedra Lexow ◽  
Roman Artymyshyn ◽  
Manual Cassanova ◽  
Andrew Winokur ◽  
Joel Kleinman ◽  
...  

1987 ◽  
Vol 43 ◽  
pp. 268
Author(s):  
Takashi Taniguchi ◽  
Shun Shimohama ◽  
Motohatsu Fujiwara ◽  
Masakuni Kameyama

1986 ◽  
Vol 8 (2) ◽  
pp. 349-356 ◽  
Author(s):  
Joel S. Karliner ◽  
Michael Stevens ◽  
Mark Grattan ◽  
Wanda Woloszyn ◽  
Norman Honbo ◽  
...  

1989 ◽  
Vol 142 (4) ◽  
pp. 1099-1101 ◽  
Author(s):  
Shun Kondo ◽  
Jamshid Latifpour ◽  
Takashi Morita ◽  
Robert M. Weiss

1989 ◽  
Vol 260 (1) ◽  
pp. 53-59 ◽  
Author(s):  
M T Nakada ◽  
K M Haskell ◽  
D J Ecker ◽  
J M Stadel ◽  
S T Crooke

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.


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