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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 correlate to inhibition of both alpha1A- and alpha1B-adrenergic receptors.
5 raint previously described for the wild-type alpha(1b)-adrenergic receptor.
6 he switch mutant compared with the wild-type alpha(1b)-adrenergic receptor.
7 ecombinant M(3) muscarinic acetylcholine and alpha(1B) -adrenergic receptors.
8 inine substitutions in the DRY motifs of the alpha(1B) adrenergic receptor (alpha(1B)-AR) and angiote
9 ) within the dominant P2 promoter of the rat alpha(1b) adrenergic receptor (alpha(1b)AR) gene is reco
10 patocytes or tranfected HepG2 cells with the alpha(1B)-adrenergic receptor (alpha(1B)AR) agonist phen
11 2-base pair promoter fragment from the mouse alpha(1B)-adrenergic receptor (alpha(1B)AR) gene was exa
12 sponsible for this activity, the role of the alpha(1B)-adrenergic receptor (alpha(1B)AR) in this proc
13                   In contrast, activation of alpha1B-adrenergic receptors (alpha1B-ARs) induced trans
14 ection of NF1/L, NF1/Red1, or NF1/X with the alpha1B adrenergic receptor (alpha1BAR) gene middle (P2)
15  Progress toward elucidating the function of alpha1B-adrenergic receptors (alpha1BARs) in the central
16                                    Since the alpha1B adrenergic receptor and dopamine receptor type 1
17 ]prazosin dissociation from the alpha1A- and alpha1B-adrenergic receptors and noncompetitively inhibi
18                    The affinity of selective alpha(1b)-adrenergic receptor antagonists for the switch
19 ial-targeted overexpression of the wild-type alpha1B adrenergic receptor (AR) (Tg alpha43), we studie
20              We previously demonstrated that alpha1B-adrenergic receptor (AR) gene transcription, mRN
21 pecific overexpression of the wild-type (WT) alpha1B-adrenergic receptor (AR) using the murine alpha-
22 both the alpha1a-adrenergic receptor and the alpha1b-adrenergic receptor (AR), that account almost en
23 vated G protein-coupled receptors, including alpha(1B)-adrenergic receptors (ARs), resulting in desen
24 wn previously to antagonize noncompetitively alpha(1B)-adrenergic receptors (ARs).
25           Overall, this study identified the alpha1B adrenergic receptor as a pharmacologic target in
26 tonation of the homologous amino acid in the alpha(1B) adrenergic receptor (Asp(142)) may be involved
27 o activation of rhodopsin (Glu(134)) and the alpha(1B) adrenergic receptor (Asp(142)).
28                    The analogous residues in alpha1b-adrenergic receptors, aspartic acid 125 and lysi
29  type A receptor, dopamine D1A receptor, and alpha1b adrenergic receptor) bound betaarrestin2 with hi
30                    Upon agonist stimulation, alpha1B-adrenergic receptors couple to Gq proteins, calc
31    We investigated the role of this motif in alpha1B-adrenergic receptor function and regulation.
32 and CP1 bind to the major P2 promoter of the alpha1B adrenergic receptor gene to generate footprint I
33 specific regulation of the expression of the alpha1B adrenergic receptor gene.
34 e roles of the carboxyl-terminal tail of the alpha(1B)-adrenergic receptor in its expression, functio
35                                        Y348A alpha1B-adrenergic receptors in which this sequence was
36 tivation, (ii) provide further evidence that alpha1B-adrenergic receptor internalization can be separ
37 cific regions and individual residues of the alpha(1B)-adrenergic receptor involved in internalizatio
38                                The expressed alpha1b-adrenergic receptor mutant demonstrated a 6-fold
39 ere obtained for a lysine to a glutamic acid alpha1b-adrenergic receptor mutation.
40                        Taken together, these alpha1b-adrenergic receptor mutations suggest a molecula
41 were also observed for two aspartic acid 125 alpha1b-adrenergic receptor mutations, consistent with t
42 icular traffic were investigated by studying alpha1B-adrenergic receptor-Rab protein interactions, us
43 of radioligand binding sites for two mutated alpha1B-adrenergic receptors reported previously was inv
44                                         This alpha1b-adrenergic receptor salt bridge constraint is th
45               N54-alpha(s) failed to inhibit alpha(1B)-adrenergic receptor stimulation of inositol 1,
46 tors resulted in increased expression of the alpha(1B)-adrenergic receptor subtype, proneural basic h
47 K/K331D) was no different from the wild-type alpha(1b)-adrenergic receptor, suggesting that both rece
48  beta2 but not in cells transfected with the alpha1B-adrenergic receptor, suggesting that the PLC bet
49 vates both alpha(s) and alpha(q) or with the alpha(1B)-adrenergic receptor that activates only alpha(
50                                         When alpha1B-adrenergic receptors that had been mutated at pr
51 an important role for Tyr348 in coupling the alpha1B-adrenergic receptor to G protein and subsequent
52 Data suggest that protein kinase C modulates alpha1B-adrenergic receptor transfer to late endosomes a
53 f VMN neurons that respond to stimulation of alpha(1b)-adrenergic receptors, which is expected in tur