Effect of α-Methyldopa on α-Noradrenergic Receptor Binding Sites in the Mouse Brain

Pharmacology ◽  
1984 ◽  
Vol 28 (3) ◽  
pp. 130-138 ◽  
Author(s):  
M. Oide
Keyword(s):  
Mouse Brain ◽  
Receptor Binding ◽  
Binding Sites

scholarly journals Localization of the insulin receptor binding sites for the SH2 domain proteins p85, Syp, and GAP.

1994 ◽  
Vol 269 (44) ◽  
pp. 27186-27192
Author(s):  
P A Staubs ◽  
D R Reichart ◽  
A R Saltiel ◽  
K L Milarski ◽  
H Maegawa ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Receptor Binding ◽  
Binding Sites ◽  
Sh2 Domain ◽  
Insulin Receptor Binding

scholarly journals Androgen and glucocorticoid receptor direct distinct transcriptional programs by receptor-specific and shared DNA binding sites

2021 ◽  
Vol 49 (7) ◽  
pp. 3856-3875
Author(s):  
Marina Kulik ◽  
Melissa Bothe ◽  
Gözde Kibar ◽  
Alisa Fuchs ◽  
Stefanie Schöne ◽  
...  
Keyword(s):  
Gene Regulation ◽  
Transcription Factor ◽  
Dna Binding ◽  
Receptor Binding ◽  
Binding Sites ◽  
Specific Gene ◽  
Functional Diversification ◽  
Enhancer Activity ◽  
Sequence Composition

Abstract The glucocorticoid (GR) and androgen (AR) receptors execute unique functions in vivo, yet have nearly identical DNA binding specificities. To identify mechanisms that facilitate functional diversification among these transcription factor paralogs, we studied them in an equivalent cellular context. Analysis of chromatin and sequence suggest that divergent binding, and corresponding gene regulation, are driven by different abilities of AR and GR to interact with relatively inaccessible chromatin. Divergent genomic binding patterns can also be the result of subtle differences in DNA binding preference between AR and GR. Furthermore, the sequence composition of large regions (>10 kb) surrounding selectively occupied binding sites differs significantly, indicating a role for the sequence environment in guiding AR and GR to distinct binding sites. The comparison of binding sites that are shared shows that the specificity paradox can also be resolved by differences in the events that occur downstream of receptor binding. Specifically, shared binding sites display receptor-specific enhancer activity, cofactor recruitment and changes in histone modifications. Genomic deletion of shared binding sites demonstrates their contribution to directing receptor-specific gene regulation. Together, these data suggest that differences in genomic occupancy as well as divergence in the events that occur downstream of receptor binding direct functional diversification among transcription factor paralogs.

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