Also known as ADRB2 β-2 adrenergic receptor (β2-adrenergic receptors), β-adrenergic receptors, and the human gene is coding. An intron in the ADRB2 gene. (figure on the right, and see the link) of lysozyme is associated with inhibition nighttime asthma of this gene, obesity, type 2 diabetes.The 3D crystal structure polymorphism of different β2-adrenergic receptor, and point mutations, and / or I increase the size of the protein crystals contacts hydrophilic determined by the fusion protein.

One of the final effectors is related to the class CL-type calcium channel CaV1.2 direct this receptor. Is coupled to G, and activated protein G adenylyl cyclase catalyzes the formation cyclic adenosine monophosphate activated protein kinase (cAMP) this receptor-channel complex to neutralize the phosphatase PP2A. Assembly of signaling complexes, provides a mechanism to ensure the rapid transfer and concrete. Biophysics and two state model molecules have been proposed to account for the redox-sensitive and pH of GPCR this and other. β-2 adrenergic receptors are also found in pairs Wang and, if necessary, to provide a mechanism that is localized intracellularly very response of the ligand. In contrast, β-1 adrenergic receptor is associated with stimulation of these results to the diffusion cell responses and GS,. This seems to be done through the PKA-induced phosphorylation of cAMP receptor.

In the normal eye, β-2 stimulation salbutamol, an increase of intraocular pressure by the network cases an increase in the production of aqueous humor by the ciliary process
Reduced drainage of humor through Schlemm’s canal, but after raising the pressure according to the outflow outflow of humor. In glaucoma drainage completely or decreased (open-angle glaucoma) will be (angle-closure glaucoma) block. In such a case, it is possible to use a local β-2 agonists such as timolol, which is the back contraindicated strong β-2 stimulated by the increasing subsequent humor production.

So as to form a family of receptors that are expressed in many parts of the CNS and PNS in the differential nicotinic acetylcholine receptors (the nAChR). In response neurotransmitter acetylcholine of endogenous (acetylcholine), thereby contributing to a wide range of brain activity with neurodevelopmental and degeneration2 and cognitive function nAChR mother 1. The nAChR, is the target of some drugs, including nicotine
This is a wide range of drug abuse with therapeutic action potential of some, such as pain relief and improved cognition such. Whether it is a muscle and nerve cells, nAChR is an allosteric membrane protein that is assembled from five subunits according to the rules of a particular combination. was present at the end of the sensory organs, while in mammals and (B2-B4 and A2-A7) 9 homologous subunits, subunits a9 have been identified so far in the nervous system. Combination of popular pentamer of nAChR function is shown pharmacological properties and biophysical characteristic of the (box 1). However, the specificity with limited agonists and antagonists available, the contribution of five specific amount of nAChR particular, on the basis of the physical evidence, to evaluate is difficult it
Action. Here, the generation of mice lacking nAChR subunits one or more (Table 1) is a powerful experimental order to clarify the interface between the behavior and nicotine pharmacology and verify nAChR and functional subunits I will consider how to provide the typical approach. The first part of this assessment focuses on recent observations on the pharmacology and nAChR subunit composition of have Is obtained from the analysis of the knockout (KO) mice, nAChR provides a basis for analyzing the contribution of specific behavior. A New Perspective on the role of nicotine-induced electrophysiol and nicotine receptor function of endogenous

G-protein coupled receptors (GPCR), hormones and neurotransmitters, and is responsible for most of the cellular response to visual sense of taste, and smell. It is activated heteroaryl GTP binding protein agonist occupancy of the receptor (G protein) paradigm GPCR signaling. The activation of the stimulatory G protein-adrenergic receptor (β2 AR) GS, adenylyl cyclase, and has become a model system for signaling the long GPCR – β 2. Here, agonist occupancy mer β nucleotide release Gs and (2) AR presents the crystal structure of the ternary complex in the active state consisting of heteroaryl. The main interaction between β include amino and GS and propagation of structural changes in the nucleotide-binding pocket of the carboxy-terminal α-helix and GS (2) AR. end of the cytoplasm of the end of the cytoplasm and TM5 (TM6) transmembrane segment 6 of the α-helix extension, contains the movement AR 14 major structural changes in most of the β. Observation most amazing is the main displacement of Gαs relative to the GTP-ase domain, such as Ras of α-helix region. This crystal structure represents the view of high-resolution first of signaling through the GPCR.