β2アドレナリン受容体、β2アドレナリンレセプター

関: adrenergic beta-2 receptor、beta-2 adrenoceptor、beta-2 receptor、beta2 adrenergic receptor、beta2 adrenoceptor、beta2 receptor

WordNet

to remain unmolested, undisturbed, or uninterrupted -- used only in infinitive form; "let her be"
work in a specific place, with a specific subject, or in a specific function; "He is a herpetologist"; "She is our resident philosopher" (同)follow
have life, be alive; "Our great leader is no more"; "My grandfather lived until the end of war" (同)live
be identical to; be someone or something; "The president of the company is John Smith"; "This is my house"
happen, occur, take place; "I lost my wallet; this was during the visit to my parents house"; "There were two hundred people at his funeral"; "There was a lot of noise in the kitchen"
have the quality of being; (copula, used with an adjective or a predicate noun); "John is rich"; "This is not a good answer"
occupy a certain position or area; be somewhere; "Where is my umbrella?" "The toolshed is in the back"; "What is behind this behavior?"
spend or use time; "I may be an hour"
stake on the outcome of an issue; "I bet $100 on that new horse"; "She played all her money on the dark horse" (同)wager, play
the act of gambling; "he did it on a bet" (同)wager
maintain with or as if with a bet; "I bet she will be there!" (同)wager
second in order of importance; "the candidate, considered a beta male, was perceived to be unable to lead his party to victory"
the 2nd letter of the Greek alphabet
preliminary or testing stage of a software or hardware product; "a beta version"; "beta software"
a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
drug that has the effects of epinephrine (同)adrenergic_drug
relating to epinephrine (its release or action) (同)sympathomimetic

PrepTutorEJDIC

《連結語として補語を伴なって…『である』,…だ,…です / 《位置・場所を表す語句を伴って》(…に)『ある』,いる(occupy a place or situation) / 〈物事が〉『存在する』,ある(exist);〈生物が〉生存する,生きている(live) / 行われる,起こる,発生する(take place, occur) / 存続する,そのままでいる(remain as before) / 《『be to』 do》 / …する予定である,…することになっている / …すべきだ / 《受動態の不定詞を伴って》…できる / 《命令》…するのだ / 《条件節に》…する意図がある / 《『if…were to』 do》…するとしたなら / 《『be』 do『ing』》《進行形》 / 《進行中の動作》…している,しつつある / 《近い未来》…しようとしている,するつもり / 《動作の反復》(いつも)…している / 《『be』+『他動詞の過去分詞』》《受動態》…される,されている / 《『be』+『自動詞の過去分詞』》《完了形》…した[状態にある]
『かけ』・(…との)かけ《+『with』+『名』》 / かけた物(金) / かけの対象 / 〈金・物〉'を'『かける』 / (かけ事・ゲームなどで)〈人〉‘と'『かけをする』《+『名』〈人〉+『on』+『名』》 / (…に)『かける』《+『on』(『against』)+『名』(one's do『ing』)》
ベータ(ギリシア語アルファベットの第2文字;B,β;英語のB,b に遭当)
=sense organ / 受信装置

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/11/28 09:07:51」(JST)

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[Wiki en表示]

The beta-2 adrenergic receptor (β₂ adrenoreceptor), also known as ADRB2, is a beta-adrenergic receptor, and also denotes the human gene encoding it.^[3]

Gene

The ADRB2 gene is intronless. Different polymorphic forms, point mutations, and/or downregulation of this gene are associated with nocturnal asthma, obesity and type 2 diabetes.^[4]

Structure

The 3D crystallographic structure (see figure and links to the right) of the β₂-adrenergic receptor has been determined^[5]^[1]^[2] by making a fusion protein with lysozyme to increase the hydrophillic surface area of the protein for crystal contacts.

Mechanism

This receptor is directly associated with one of its ultimate effectors, the class C L-type calcium channel Ca_V1.2. This receptor-channel complex is coupled to the G_s G protein, which activates adenylyl cyclase, catalysing the formation of cyclic adenosine monophosphate (cAMP) which then activates protein kinase A, and the counterbalancing phosphatase PP2A. The assembly of the signaling complex provides a mechanism that ensures specific and rapid signaling. A two-state biophysical and molecular model has been proposed to account for the pH and REDOX sensitivity of this and other GPCRs.^[6]

Beta-2 Adrenergic Receptors have also been found to couple with G_i, possibly providing a mechanism by which response to ligand is highly localized within cells. In contrast, Beta-1 Adrenergic Receptors are coupled only to G_s, and stimulation of these results in a more diffuse cellular response.^[7] This appears to be mediated by cAMP induced PKA phosphorylation of the receptor.^[8]

Function

Actions of the β₂ receptor include:

Muscular system

Tissue/Effect		Function
Smooth muscle relaxation in:	uterus
	GI tract (decreases motility)	Delay digestion during fight-or-flight response
	detrusor urinae muscle of bladder wall^[9] This effect is stronger than the alpha-1 receptor effect of contraction.	Delay need of micturition
	seminal tract^[10]
	bronchi^[11]	Facilitate respiration (agonists can be useful in treating asthma)
blood vessels dilates smaller coronary arteries^[12] dilates hepatic artery dilates arteries to skeletal muscle	Increase perfusion of organs	needed during fight-or-flight
striated muscle	Tremor^[10] (via PKA mediated facilitation of presynaptic Ca2+ influx leading to acetylcholine release)
	Increased mass and contraction speed^[10]	fight-or-flight
	glycogenolysis^[10]	provide glucose fuel

Circulatory system

Heart muscle contraction
Increase cardiac output (minor degree compared to β₁).
- Increase heart rate ^[11] in sinoatrial node (SA node) (chronotropic effect).
- Increase atrial cardiac muscle contractility. (inotropic effect).
- Increases contractility and automaticity^[11] of ventricular cardiac muscle.
Dilate hepatic artery.
Dilate arteries to skeletal muscle.

Eye

In the normal eye, beta-2 stimulation by salbutamol increases intraocular pressure via net:

Increase in production of aqueous humour by the ciliary process,
Subsequent increased pressure-dependent uveoscleral outflow of humour, despite reduced drainage of humour via the Canal of Schlemm.

In glaucoma, drainage is reduced ( open-angle glaucoma) or blocked completely (closed-angle glaucoma). In such cases, beta-2 stimulation with its consequent increase in humour production is highly contra-indicated, and conversely, a topical beta-2 antagonist such as timolol may be employed.

Digestive system

Glycogenolysis and gluconeogenesis in liver.^[11]
Glycogenolysis and lactate release in skeletal muscle.^[11]
Contract sphincters of GI tract.
Insulin secretion from pancreas.^[11]^[13]
Thickened secretions from salivary glands.^[11]

Other

Inhibit histamine-release from mast cells.
Increase protein content of secretions from lacrimal glands.
Increase renin secretion from kidney.
Receptor also present in cerebellum.
Bronchiole dilation (targeted while treating asthma attacks)
Involved in brain - immune - communication ^[14]

Agonists

Main article: Beta₂-adrenergic agonist

spasmolytics in asthma and COPD
- salbutamol (albuterol in USA)
- bitolterol mesylate
- isoproterenol
- levosalbutamol (levalbuteral in USA)
- metaproterenol
- formoterol
- salmeterol
- terbutaline
- clenbuterol
ritodrine (tocolytic)

Antagonists

(Beta blockers)

butoxamine*^[10]
First generation (non-selective) β-blockers

* denotes selective agonists to the receptor.

Interactions

Beta-2 adrenergic receptor has been shown to interact with Delta Opioid receptor,^[15] Sodium-hydrogen antiporter 3 regulator 1,^[16]^[17]^[18] AKAP12^[19]^[20] and Grb2.^[21]

References

^ ^a ^b PDB 2RH1; Cherezov V, Rosenbaum DM, Hanson MA, Rasmussen SG, Thian FS, Kobilka TS, Choi HJ, Kuhn P, Weis WI, Kobilka BK, Stevens RC (2007). "High-resolution crystal structure of an engineered human β₂-adrenergic G protein-coupled receptor". Science 318 (5854): 1258–65. doi:10.1126/science.1150577. PMC 2583103. PMID 17962520. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2583103/.
^ ^a ^b Rosenbaum DM, Cherezov V, Hanson MA, Rasmussen SG, Thian FS, Kobilka TS, Choi HJ, Yao XJ, Weis WI, Stevens RC, Kobilka BK (2007). "GPCR engineering yields high-resolution structural insights into β₂-adrenergic receptor function". Science 318 (5854): 1266–73. doi:10.1126/science.1150609. PMID 17962519.
^ "Entrez Gene: ADRB1 adrenergic, beta-1-, receptor". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=153.
^ "Entrez Gene: ADRB2 adrenergic, beta-2-, receptor, surface". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=154.
^ Rasmussen SG, Choi HJ, Rosenbaum DM, Kobilka TS, Thian FS, Edwards PC, Burghammer M, Ratnala VR, Sanishvili R, Fischetti RF, Schertler GF, Weis WI, Kobilka BK (2007). "Crystal structure of the human β₂-adrenergic G-protein-coupled receptor". Nature 450 (7168): 383–7. Bibcode 2007Natur.450..383R. doi:10.1038/nature06325. PMID 17952055.
^ Rubenstein LA, Zauhar RJ, Lanzara RG (2006). "Molecular dynamics of a biophysical model for β₂-adrenergic and G protein-coupled receptor activation". J. Mol. Graph. Model. 25 (4): 396–409. doi:10.1016/j.jmgm.2006.02.008. PMID 16574446.
^ Chen-Izu Y, Xiao RP, Izu LT, Cheng H, Kuschel M, Spurgeon H, Lakatta EG (November 2000). "G(i)-dependent localization of beta(2)-adrenergic receptor signaling to L-type Ca(2+) channels". Biophys. J. 79 (5): 2547–56. Bibcode 2000BpJ....79.2547C. doi:10.1016/S0006-3495(00)76495-2. PMC 1301137. PMID 11053129. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1301137/.
^ Zamah AM, Delahunty M, Luttrell LM, Lefkowitz RJ (August 2002). "Protein kinase A-mediated phosphorylation of the beta 2-adrenergic receptor regulates its coupling to Gs and Gi. Demonstration in a reconstituted system". J. Biol. Chem. 277 (34): 31249–56. doi:10.1074/jbc.M202753200. PMID 12063255.
^ von Heyden B, Riemer RK, Nunes L, Brock GB, Lue TF, Tanagho EA (1995). "Response of guinea pig smooth and striated urethral sphincter to cromakalim, prazosin, nifedipine, nitroprusside, and electrical stimulation". Neurourol. Urodyn. 14 (2): 153–68. doi:10.1002/nau.1930140208. PMID 7540086.
^ ^a ^b ^c ^d ^e Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4. Page 163
^ ^a ^b ^c ^d ^e ^f ^g Fitzpatrick, David; Purves, Dale; Augustine, George (2004). "Table 20:2". Neuroscience (Third ed.). Sunderland, Mass: Sinauer. ISBN 0-87893-725-0.
^ Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4. Page 270
^ Trovik TS, Vaartun A, Jorde R, Sager G (1995). "Dysfunction in the beta 2-adrenergic signal pathway in patients with insulin dependent diabetes mellitus (IDDM) and unawareness of hypoglycaemia". Eur. J. Clin. Pharmacol. 48 (5): 327–32. doi:10.1007/BF00194946. PMID 8641318.
^ Elenkov, I. J., R. L. Wilder, et al. (2000). "The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system.". Pharmacol Rev 52 (4): 595–638. PMID 11121511.
^ McVey, M; Ramsay D, Kellett E, Rees S, Wilson S, Pope A J, Milligan G (Apr. 2001). "Monitoring receptor oligomerization using time-resolved fluorescence resonance energy transfer and bioluminescence resonance energy transfer. The human delta -opioid receptor displays constitutive oligomerization at the cell surface, which is not regulated by receptor occupancy". J. Biol. Chem. (United States) 276 (17): 14092–9. doi:10.1074/jbc.M008902200. ISSN 0021-9258. PMID 11278447.
^ Karthikeyan, Subramanian; Leung Teli, Ladias John A A (May. 2002). "Structural determinants of the Na+/H+ exchanger regulatory factor interaction with the beta 2 adrenergic and platelet-derived growth factor receptors". J. Biol. Chem. (United States) 277 (21): 18973–8. doi:10.1074/jbc.M201507200. ISSN 0021-9258. PMID 11882663.
^ Hall, R A; Ostedgaard L S, Premont R T, Blitzer J T, Rahman N, Welsh M J, Lefkowitz R J (Jul. 1998). "A C-terminal motif found in the beta2-adrenergic receptor, P2Y1 receptor and cystic fibrosis transmembrane conductance regulator determines binding to the Na+/H+ exchanger regulatory factor family of PDZ proteins". Proc. Natl. Acad. Sci. U.S.A. (UNITED STATES) 95 (15): 8496–501. Bibcode 1998PNAS...95.8496H. doi:10.1073/pnas.95.15.8496. ISSN 0027-8424. PMC 21104. PMID 9671706. //www.ncbi.nlm.nih.gov/pmc/articles/PMC21104/.
^ Hall, R A; Premont R T, Chow C W, Blitzer J T, Pitcher J A, Claing A, Stoffel R H, Barak L S, Shenolikar S, Weinman E J, Grinstein S, Lefkowitz R J (Apr. 1998). "The beta2-adrenergic receptor interacts with the Na+/H+-exchanger regulatory factor to control Na+/H+ exchange". Nature (ENGLAND) 392 (6676): 626–30. Bibcode 1998Natur.392..626H. doi:10.1038/33458. ISSN 0028-0836. PMID 9560162.
^ Fan, G; Shumay E, Wang H, Malbon C C (Jun. 2001). "The scaffold protein gravin (cAMP-dependent protein kinase-anchoring protein 250) binds the beta 2-adrenergic receptor via the receptor cytoplasmic Arg-329 to Leu-413 domain and provides a mobile scaffold during desensitization". J. Biol. Chem. (United States) 276 (26): 24005–14. doi:10.1074/jbc.M011199200. ISSN 0021-9258. PMID 11309381.
^ Shih, M; Lin F, Scott J D, Wang H Y, Malbon C C (Jan. 1999). "Dynamic complexes of beta2-adrenergic receptors with protein kinases and phosphatases and the role of gravin". J. Biol. Chem. (UNITED STATES) 274 (3): 1588–95. doi:10.1074/jbc.274.3.1588. ISSN 0021-9258. PMID 9880537.
^ Karoor, V; Wang L, Wang H Y, Malbon C C (Dec. 1998). "Insulin stimulates sequestration of beta-adrenergic receptors and enhanced association of beta-adrenergic receptors with Grb2 via tyrosine 350". J. Biol. Chem. (UNITED STATES) 273 (49): 33035–41. doi:10.1074/jbc.273.49.33035. ISSN 0021-9258. PMID 9830057.

External links

"β₂-adrenoceptor". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. http://www.iuphar-db.org/GPCR/ReceptorDisplayForward?receptorID=2189.

UpToDate Contents

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1. β-2アドレナリン受容体機能不全および喘息の多型性 beta 2 adrenergic receptor dysfunction and polymorphism in asthma
2. 喘息の遺伝学 genetics of asthma
3. 昇圧剤および強心剤の使用 use of vasopressors and inotropes
4. 喘息におけるβ刺激剤：急性期投与および予防的使用 beta agonists in asthma acute administration and prophylactic use
5. 喘息におけるβ刺激剤：長期使用に関する議論 beta agonists in asthma controversy regarding chronic use

English Journal

A β1/2 adrenergic receptor-sensitive intracellular signaling pathway modulates CCL2 production in cultured spinal astrocytes.

Morioka N, Abe H, Araki R, Matsumoto N, Zhang FF, Nakamura Y, Hisaoka-Nakashima K, Nakata Y.Author information Department of Pharmacology, Hiroshima University Graduate School of Biomedical and Health Sciences, Minami-ku, Hiroshima, Japan.AbstractThe phosphorylation of c-jun N-terminal kinase (JNK) and the subsequent production of C-C chemokine CCL2 (monocyte chemoattractant protein; MCP-1) in spinal astrocytes contribute to the initiation of neurological disorders including chronic pain. Astrocytes express neurotransmitter receptors which could be targeted to ameliorate neurological disorders. In the current study, the involvement of the β-adrenergic system in the regulation of JNK activity and CCL2 production after stimulation with tumor necrosis factor (TNF)-α, one of many initiators of neuroinflammation, was elucidated. Treatment of cultured spinal astrocytes with isoproterenol (a β-adrenergic receptor agonist; 1 µM) reduced both TNF-α-induced JNK1 phosphorylation, as observed by Western blotting, and the subsequent increase of both CCL2 mRNA expression and CCL2 production, which were measured by real time-PCR and ELISA, respectively. The effects of isoproterenol were completely blocked by pretreatment with either propranolol (a β-adrenoceptor antagonist) or H89 (a protein kinase A [PKA] inhibitor). The current study revealed that the regulation of glycogen synthase kinase-3β (GSK-3β) activity is a crucial factor in the inhibitory action of isoproterenol. The TNF-α-induced JNK1 phosphorylation was significantly blocked by treatment with GSK-3β inhibitors (either LiCl or TWS119), and stimulation of β-adrenergic receptors induced the inhibition of GSK-3β through the phosphorylation of Ser(9) . Moreover, treatment with isoproterenol markedly suppressed the TNF-α-induced increase of CCL2 mRNA expression and CCL2 production through a β-adrenergic receptor-PKA pathway mediated by GSK-3β regulation. Thus, activation of β1/2 adrenergic receptors expressed in spinal astrocytes could be a novel method of moderating neurological disorders with endogenous catecholamines or selective agonists.
Journal of cellular physiology.J Cell Physiol.2014 Mar;229(3):323-32. doi: 10.1002/jcp.24452.
The phosphorylation of c-jun N-terminal kinase (JNK) and the subsequent production of C-C chemokine CCL2 (monocyte chemoattractant protein; MCP-1) in spinal astrocytes contribute to the initiation of neurological disorders including chronic pain. Astrocytes express neurotransmitter receptors which c
PMID 24037783

Adrenergic and glucocorticoid modulation of the sterile inflammatory response.

Cox SS1, Speaker KJ1, Beninson LA1, Craig WC1, Paton MM1, Fleshner M2.Author information 1Department of Integrative Physiology, University of Colorado, Boulder, United States.2Department of Integrative Physiology, University of Colorado, Boulder, United States; Center for Neuroscience, University of Colorado, Boulder, United States. Electronic address: fleshner@colorado.edu.AbstractExposure to an intense, acute stressor, in the absence of a pathogen, alters immune function. Exposure to a single bout of inescapable tail shock increases plasma and tissue concentrations of cytokines, chemokines, and the danger associated molecular pattern (DAMP) Hsp72. Although previous studies have demonstrated that adrenergic receptor (ADR) and glucocorticoid receptor (GCR)-mediated pathways alter pathogen or microbial associated molecular pattern (MAMP)-evoked levels of cytokines, chemokines, and Hsp72, far fewer studies have tested the role of these receptors across multiple inflammatory proteins or tissues to elucidate the differences in magnitude of stress-evoked sterile inflammatory responses. The goals of the current study were to (1) compare the sterile inflammatory response in the circulation, liver, spleen, and subcutaneous (SQ) adipose tissue by measuring cytokine, chemokine, and DAMP (Hsp72) responses; and (2) to test the role of alpha-1 (α1), beta-1 (β1), beta-2 (β2), and beta-3 (β3) ADRs, as well as GCRs in signaling the sterile inflammatory response. The data presented indicate plasma and SQ adipose are significantly more stress responsive than the liver and spleen. Further, administration of ADR and GCR-specific antagonists revealed both similarities and differences in the signaling mechanisms of the sterile inflammatory response in the tissues studied. Finally, given the selective increase in the chemokine monocyte chemotactic protein-1 (MCP-1) in SQ tissue, it may be that SQ adipose is an important site of leukocyte migration, possibly in preparation for infection as a consequence of wounding. The current study helps further our understanding of the tissue-specific differences of the stress-induced sterile inflammatory response.
Brain, behavior, and immunity.Brain Behav Immun.2014 Feb;36:183-92. doi: 10.1016/j.bbi.2013.11.018. Epub 2013 Dec 7.
Exposure to an intense, acute stressor, in the absence of a pathogen, alters immune function. Exposure to a single bout of inescapable tail shock increases plasma and tissue concentrations of cytokines, chemokines, and the danger associated molecular pattern (DAMP) Hsp72. Although previous studies h
PMID 24321216

The role of monocytes in angiogenesis and atherosclerosis.

Jaipersad AS1, Lip GY1, Silverman S2, Shantsila E3.Author information 1University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom.2Department of Vascular Surgery, City Hospital, Birmingham, United Kingdom.3University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom. Electronic address: e.shantsila@bham.ac.uk.AbstractNew vessel formation inside the arterial wall and atherosclerotic plaques plays a critical role in pathogenesis of heart attacks and strokes. The 2 known mechanisms resulting in the formation of new vessels within the plaque are local ischemia and inflammation. Blood monocytes play an important role in both processes. First, they express receptors for vascular endothelial growth factor and some of them may serve as circulating ancestors of endothelial cells. Second, monocytes are associated with inflammation by synthesis of inflammatory molecules following their activation (e.g., after stimulation of Toll-like receptors). Neovascularization is a reparative response to ischemia, and includes 3 processes: angiogenesis, arteriogenesis, and vasculogenesis. Angiogenesis, the formation of new capillary vessels is known to occur in response to a hypoxic environment. The interaction between leukocytes and vascular wall via overexpression of various molecules facilitates the migration of inflammatory cells into the plaque microenvironment. Monocytes are intimately involved in tissue damage and repair and an imbalance of these processes may have detrimental consequences for plaque development and stability. Importantly, monocytes are comprised of distinct subsets with different cell surface markers and functional characteristics and this heterogeneity may be relevant to angiogenic processes in atherosclerosis. The aim of this review article is to present an overview of the available evidence supporting a role for monocytes in angiogenesis and atherosclerosis.
Journal of the American College of Cardiology.J Am Coll Cardiol.2014 Jan 7;63(1):1-11. doi: 10.1016/j.jacc.2013.09.019. Epub 2013 Oct 16.
New vessel formation inside the arterial wall and atherosclerotic plaques plays a critical role in pathogenesis of heart attacks and strokes. The 2 known mechanisms resulting in the formation of new vessels within the plaque are local ischemia and inflammation. Blood monocytes play an important role
PMID 24140662

Japanese Journal

β(2)-Adrenergic and M(2)-muscarinic receptors decrease basal t-tubular L-type Ca2+ channel activity and suppress ventricular contractility in heart failure

EUROPEAN JOURNAL OF PHARMACOLOGY 724, 122-131, 2014-02-05
NAID 120005440173

4) 幼少期の高アンドロゲン環境とインスリン抵抗性からみたPCOSの病因および管理に関する検討(シンポジウム3:生殖「多嚢胞性卵巣症候群(PCOS)の病因・病態と管理」,第65回日本産科婦人科学会・学術講演会)

日本産科婦人科學會雜誌 65(12), 2721-2736, 2013-12-01
NAID 110009685697

総説 : 自律神経と末梢前庭器 : 末梢前庭系における分子生物学的考察

Equilibrium research 71(3), 200-206, 2012-06-01
NAID 10030781927

Related Pictures

★リンクテーブル★

リンク元	「beta-2 receptor」「beta-2 adrenoceptor」「adrenergic beta-2 receptor」「β2アドレナリンレセプター」
関連記事	「adrenergics」「adrenergic」「beta」「be」「adrenergic receptor」

「beta-2 receptor」

Adrenoceptor beta 2, surface
	; Crystallographic structure of the β2-adrenergic receptor depicted as a green cartoon and the bound partial inverse agonist carazolol ligand as spheres (carbon atom = grey, oxygen = red, nitrogen = blue). The phospholipid bilayer is depicted as blue spheres (phosphate head groups) and yellow lines (lipid sidechains).
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1GQ4, 2R4R, 2R4S, 2RH1, 3D4S, 3KJ6, 3NY8, 3NY9, 3NYA, 3P0G, 3PDS, 3SN6, 4GBR
Identifiers
Symbols	ADRB2; ADRB2R; ADRBR; B2AR; BAR; BETA2AR
External IDs	OMIM: 109690 MGI: 87938 HomoloGene: 30948 IUPHAR: β2-adrenoceptor ChEMBL: 210 GeneCards: ADRB2 Gene
Gene Ontology
Molecular function	• beta2-adrenergic receptor activity; • protein binding; • drug binding; • adenylate cyclase binding; • potassium channel regulator activity; • dopamine binding; • ionotropic glutamate receptor binding; • protein homodimerization activity; • epinephrine binding; • norepinephrine binding;
Cellular component	• nucleus; • lysosome; • endosome; • plasma membrane; • integral to plasma membrane; • caveola; • apical plasma membrane; • axon; • neuronal cell body membrane; • sarcolemma; • dendritic spine; • receptor complex;
Biological process	• diet induced thermogenesis; • vasodilation by norepinephrine-epinephrine involved in regulation of systemic arterial blood pressure; • desensitization of G-protein coupled receptor protein signaling pathway by arrestin; • diaphragm contraction; • positive regulation of the force of heart contraction by epinephrine; • receptor-mediated endocytosis; • cell surface receptor signaling pathway; • activation of transmembrane receptor protein tyrosine kinase activity; • adenylate cyclase-modulating G-protein coupled receptor signaling pathway; • adenylate cyclase-activating G-protein coupled receptor signaling pathway; • activation of adenylate cyclase activity; • positive regulation of cell proliferation; • endosome to lysosome transport; • response to cold; • positive regulation of sodium ion transport; • negative regulation of ossification; • positive regulation of bone mineralization; • positive regulation of protein ubiquitination; • heat generation; • synaptic transmission, glutamatergic; • negative regulation of urine volume; • negative regulation of multicellular organism growth; • wound healing; • positive regulation of apoptotic process; • positive regulation of potassium ion transport; • positive regulation of MAPK cascade; • bone resorption; • positive regulation of vasodilation; • positive regulation of transcription from RNA polymerase II promoter; • negative regulation of smooth muscle contraction; • positive regulation of skeletal muscle tissue growth; • negative regulation of inflammatory response; • brown fat cell differentiation; • regulation of sensory perception of pain; • regulation of excitatory postsynaptic membrane potential;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
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