Muscarinic acetylcholine receptor M2 is expressed in the heart and many other tissues. The gene encoding it is localized on human chromosome 7.
Immunogen
synthetic peptide corresponding to the third cytoplasmic loop of human muscarinic acetylcholine receptor M2, conjugated to KLH. The immunizing peptide has 100% homology with the mouse and rat gene.
Biochem/physiol Actions
Muscarinic acetylcholine receptor M2 plays an important role in regulating functions of the heart and processes like pain perception and cognition. It is regarded as a good model in G protein-coupled receptors (GPCR) pharmacological studies. This receptor has a function in airway remodeling and it enhances the proliferation of airway smooth muscle cells (ASM) which is induced by transforming growth factor-β (TGF-β).
Physical form
Solution in phosphate buffered saline, containing 0.1% sodium azide.
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Despite recent advances in crystallography and the availability of G-protein-coupled receptor (GPCR) structures, little is known about the mechanism of their activation process, as only the β2 adrenergic receptor (β2AR) and rhodopsin have been crystallized in fully active conformations. Here
Proceedings of the National Academy of Sciences of the United States of America, 110(27), 10982-10987 (2013-06-20)
G-protein-coupled receptors (GPCRs) mediate cellular responses to various hormones and neurotransmitters and are important targets for treating a wide spectrum of diseases. Although significant advances have been made in structural studies of GPCRs, details of their activation mechanism remain unclear.
P300 amplitude in childhood predicts substance use disorders by young adulthood. Trajectories of visual P300 amplitude show an association between low amplitude P300 and familial risk for alcohol dependence (AD). Variation in the cholinergic muscarinic receptor gene (CHRM2) has previously
American journal of respiratory cell and molecular biology, 49(1), 18-27 (2013-03-02)
Transforming growth factor-β₁ (TGF-β₁) is a central mediator in tissue remodeling processes, including fibrosis and airway smooth muscle (ASM) hyperplasia, as observed in asthma. The mechanisms underlying this response, however, remain unclear because TGF-β₁ exerts only weak mitogenic effects on
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