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1 including the m5 muscarinic receptor and the alpha1B adrenergic receptor.
2 te allosteric modulation of the alpha1A- and alpha1B-adrenergic receptors.
3 lls transfected with mutant versus wild-type alpha1b-adrenergic receptors.
4 raint previously described for the wild-type alpha(1b)-adrenergic receptor.
5 he switch mutant compared with the wild-type alpha(1b)-adrenergic receptor.
6 ecombinant M(3) muscarinic acetylcholine and alpha(1B) -adrenergic receptors.
7 inine substitutions in the DRY motifs of the alpha(1B) adrenergic receptor (alpha(1B)-AR) and angiote
8 ) within the dominant P2 promoter of the rat alpha(1b) adrenergic receptor (alpha(1b)AR) gene is reco
9 patocytes or tranfected HepG2 cells with the alpha(1B)-adrenergic receptor (alpha(1B)AR) agonist phen
10 2-base pair promoter fragment from the mouse alpha(1B)-adrenergic receptor (alpha(1B)AR) gene was exa
11 sponsible for this activity, the role of the alpha(1B)-adrenergic receptor (alpha(1B)AR) in this proc
13 ection of NF1/L, NF1/Red1, or NF1/X with the alpha1B adrenergic receptor (alpha1BAR) gene middle (P2)
14 Progress toward elucidating the function of alpha1B-adrenergic receptors (alpha1BARs) in the central
16 ]prazosin dissociation from the alpha1A- and alpha1B-adrenergic receptors and noncompetitively inhibi
18 ial-targeted overexpression of the wild-type alpha1B adrenergic receptor (AR) (Tg alpha43), we studie
20 pecific overexpression of the wild-type (WT) alpha1B-adrenergic receptor (AR) using the murine alpha-
21 both the alpha1a-adrenergic receptor and the alpha1b-adrenergic receptor (AR), that account almost en
22 vated G protein-coupled receptors, including alpha(1B)-adrenergic receptors (ARs), resulting in desen
24 tonation of the homologous amino acid in the alpha(1B) adrenergic receptor (Asp(142)) may be involved
27 type A receptor, dopamine D1A receptor, and alpha1b adrenergic receptor) bound betaarrestin2 with hi
30 and CP1 bind to the major P2 promoter of the alpha1B adrenergic receptor gene to generate footprint I
32 e roles of the carboxyl-terminal tail of the alpha(1B)-adrenergic receptor in its expression, functio
34 tivation, (ii) provide further evidence that alpha1B-adrenergic receptor internalization can be separ
35 cific regions and individual residues of the alpha(1B)-adrenergic receptor involved in internalizatio
39 were also observed for two aspartic acid 125 alpha1b-adrenergic receptor mutations, consistent with t
40 icular traffic were investigated by studying alpha1B-adrenergic receptor-Rab protein interactions, us
41 of radioligand binding sites for two mutated alpha1B-adrenergic receptors reported previously was inv
44 tors resulted in increased expression of the alpha(1B)-adrenergic receptor subtype, proneural basic h
45 K/K331D) was no different from the wild-type alpha(1b)-adrenergic receptor, suggesting that both rece
46 beta2 but not in cells transfected with the alpha1B-adrenergic receptor, suggesting that the PLC bet
47 vates both alpha(s) and alpha(q) or with the alpha(1B)-adrenergic receptor that activates only alpha(
49 an important role for Tyr348 in coupling the alpha1B-adrenergic receptor to G protein and subsequent
50 Data suggest that protein kinase C modulates alpha1B-adrenergic receptor transfer to late endosomes a
51 f VMN neurons that respond to stimulation of alpha(1b)-adrenergic receptors, which is expected in tur
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