We report the molecular cloning of a beta 3-adrenergic receptor [beta 3-AR] cDNA from human brown adipose tissue. The cDNA-encoded protein is identical to the previously cloned beta 3-AR but with 6 additional amino acids at the C-terminus. The C-terminus is shared by the beta 3 receptors expressed in human neuroblastoma cells [SK-N-MC] [Mol. Pharmacol. 42 (1992) 964-970]. Furthermore, using a polymerase chain reaction strategy we have cloned and sequenced the beta 3-AR introns. Sequence analysis demonstrates that the human beta 3-AR gene comprises at least 3 exons and 2 introns and that the most abundant beta 3-AR transcripts encode a protein with an exon 3-derived C-terminus. Interestingly, although a similar organization has been found in rodent genes, the rat beta 3-AR transcripts encode a receptor with an exon 2-derived C-terminus.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0014-5793(93)81377-c | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Stereochemical influence of 4'-methyl substitutions on truncated 4'-thioadenosine derivatives: Impact on A adenosine receptor binding and antagonism.
Bioorg Chem
December 2024
Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, South Korea; Future Medicine Co., Ltd, 54 Changup-ro, Sujeong-gu, Seongnam, Gyeonggi-do 13449, Republic of Korea. Electronic address:
Herein, we investigated the stereochemical effects of 4'-methyl substitution on A adenosine receptor (AAR) ligands by synthesizing and evaluating a series of truncated 4'-thioadenosine derivatives featuring 4'-α-methyl, 4'-β-methyl, and 4',4'-dimethyl substitutions. We successfully synthesized these derivatives, using the stereoselective addition of an organometallic reagent, KSAc-mediated sulfur cyclization, and Vorbrüggen condensation. Binding assays demonstrated that the 4'-β-methyl substitution conferred the highest affinity for AAR, with compound 1 h exhibiting a K = 3.
View Article and Find Full Text PDFSacubitril/Valsartan Combination Partially Improves Cardiac Systolic, but Not Diastolic, Function through β-AR Responsiveness in a Rat Model of Type 2 Diabetes.
Int J Mol Sci
October 2024
Department of Pharmacology, Faculty of Pharmacy, Ankara University, Ankara 06560, Türkiye.
Cardiovascular complications are the major cause of diabetes mellitus-related morbidity and mortality. Increased renin-angiotensin-aldosterone system activity and decreased β-adrenergic receptor (β-AR) responsiveness contribute to diabetic cardiac dysfunction. We evaluated the effect of sacubitril/valsartan (neprilysin inhibitor plus angiotensin receptor antagonist combination) and valsartan treatments on the diabetic cardiac function through β-AR responsiveness and on protein expression of diastolic components.
View Article and Find Full Text PDFβAR-mTOR-lipin1 pathway mediates PKA-RIIβ deficiency-induced adipose browning.
Theranostics
September 2024
Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University, Beijing, China.
Enhancing white adipose tissue (WAT) browning combats obesity. The RIIβ subunit of cAMP-dependent protein kinase (PKA) is primarily expressed in the brain and adipose tissue. Deletion of the hypothalamic RIIβ gene centrally induces WAT browning, yet the peripheral mechanisms mediating this process remain unexplored.
View Article and Find Full Text PDFPhysiological and metabolic functions of the β-adrenergic receptor and an approach to therapeutic achievements.
J Physiol Biochem
November 2024
Creighton University Health Sciences Center, Omaha, NE, 68178, USA.
A specific type of beta-adrenergic receptor was discovered in the decade of 1980s and subsequently recognized as a new type of beta-adrenergic receptor, called beta-adrenoceptor (β-AR). β-AR expresses in different tissues, including adipose tissue, gall bladder, stomach, small intestine, cardiac myocytes, urinary bladder, and brain. Structurally, β-AR is very similar to β- and β-AR and belongs to a G-protein coupled receptor that uses cAMP as an intracellular second messenger.
View Article and Find Full Text PDFDynamic phenotypic shifts and M2 receptor downregulation in bladder smooth muscle cells induced by mirabegron.
Front Pharmacol
July 2024
Department of Urology, LMU University Hospital, LMU Munich, Munich, Germany.
Introduction: Mirabegron is available for treatment of overactive bladder (OAB). However, mechanisms underlying symptom improvements and long-term effects on bladder smooth muscle cells are uncertain. Contractility and growth of bladder smooth muscle contribute to OAB, and depend on smooth muscle phenotypes, and on muscarinic receptor expression.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!