G protein-coupled receptor regulation

Krupnick, J. G. and Benovic, J. L., The role of receptor kinases and arrestins in G-protein-coupled receptor regulation, Annu. Rev. Pharmacol. Toxicol., 38, 289-319, 1998. 

Ferguson, S. S., Barak, L. S., Zhang, J., and Caron, M. G. (1996) G-protein-coupled receptor regulation role of G-protein-coupled receptor kinases and arrestins. Can. J. Physiol. Pharmacol. 74, 1095-1110. 

Krupnick JG, Benovic JL (1998) The role of receptor kinases and arrestins in G protein-coupled receptor regulation. Annu Rev Pharmacol Toxicol 38 289-319 Lefkowitz RJ (1998) G protein-coupled receptors. III. New roles for receptor kinases and beta-arrestins in receptor signaling and desensitization. J Biol Chem 273(30) 18677-18680 Lefkowitz RJ (2004) Historical review a brief history and personal retrospective of seven-trans-membrane receptors. Trends Pharmacol Sci 25(8) 413—422 Liang BT, Jacobson KA (1998) A physiological role of the adenosine A3 receptor sustained car-dioprotection. Proc Natl Acad Sci USA 95(12) 6995-6999 Lohse MJ (1993) Molecular mechanisms of membrane receptor desensitization. Biochim Biophys Acta 1179(2) 171-188... 

Scholze T, Moskvina E, Mayer M et al (2002) Sympathoexcitation by bradykinin involves Ca2+-independent protein kinase C. J Neurosci 22 5823-32 Schwartz EJ, Blackmer T, Gerachshenko T et al (2007) Presynaptic G-protein-coupled receptors regulate synaptic cleft glutamate via transient vesicle fusion. J Neurosci 27 5857-68 Searl TJ, Silinsky EM (1998) Increases in acetylcholine release produced by phorbol esters are not mediated by protein kinase C at motor nerve endings. J Pharmacol Exp Ther 285 247-51 Seino S, Shibasaki T (2005) PKA-dependent and PKA-independent pathways for cAMP-regulated exocytosis. Physiol Rev 85 1303 12... 

Cotecchia S et al (2004) Structural determinants involved in the activation and regulation of G protein-coupled receptors lessons from the ai -adrenergic receptor sub-types. Biol Cell 96 327-333... 

The family of apelin peptides is derived from a single gene, activate a single G-protein-coupled receptor and are substrates for the angiotensin converting enzyme-2 (ACE2). Apelins regulate cardiovascular function and fluid homeostasis. The apelin receptor also functions as a co-receptor for infection of CD4-positive cells by human immunodeficiency vims ( HIV). 

Apelin receptors activate several signalling pathways including coupling through inhibitory G-proteins (G ) and Ras-independent activation of extracellular-regulated kinases (ERKs) via protein kinase C (PKC). The apelin receptor is one of number of G-protein-coupled receptors that can act as an alternative coreceptor for entry into cells of HIV and simian immunodeficiency vims (SIV) strains in human U87 cells expressing CD4 in vitro. Apelin peptides blocks entry of HIV but display different potencies, with apelin-36 being more effective than shorter sequences [3]. 

Neuromedin U is a neuropeptide which is widely distributed in the gut and central nervous system. Peripheral activities of neuromedin U include stimulation of smooth muscle, increase in blood pressure, alteration of ion transport in the gut, control of local blood flow and regulation of adrenocortical function. The actions of neuromedin U are mediated by G-protein coupled receptors (NMU1, NMU2) which are coupled tO Gq/11. 

Pituitary Adenylyl Cyclase-activating Polypeptide (PACAP) is a 38-amino acid peptide (PACAP-38), which is widely expressed in the central nervous system. PACAP is most abundant in the hypothalamus. It is also found in the gastrointestinal tract, the adrenal gland and in testis. Its central nervous system functions are ill-defined. In the periphery, PACAP has been shown to stimulate catecholamine secretion from the adrenal medulla and to regulate secretion from the pancreas. Three G-protein coupled receptors have been shown to respond to PACAP, PAQ (PACAP type I) specifically binds PACAP, VPACi and VPAC2 also bind vasoactive intestinal peptide (VDP). Activation of PACAP receptors results in a Gs-mediated activation of adenylyl cyclase. 

Somatostatin acts on various organs, tissues and cells as neurotransmitter, paracrine/autocrine and endocrine regulator on cell secretion, smooth muscle contractility, nutrient absorption, cell growth and neurotransmission [1]. Some of its mainly inhibitory effects are listed in Table 1. Somatostatin mediates its function via a family of heptahelical G-protein-coupled receptors termed... 

A sequence stretch 300 base pairs upstream of the transcriptional start site suffices for most of the transcriptional regulation of the IL-6 gene (Fig. 1). Within this sequence stretch several transcription factors find their specific recognition sites. In 5 to 3 direction, AP-1, CREB, C/EBP 3/NF-IL6, SP-1 and NF-kB can bind to the promoter followed by TATA and its TATA binding protein TBP. Most enhancer factors become active in response to one or several different stimuli and the active factors can trigger transcription individually or in concert. For example, AP-1 is active upon cellular stress, or upon stimuli that tell cells to proliferate CREB becomes also active if cells experience growth signals, but also upon elevation of intracellular levels of cyclic adenosine monophosphate (cAMP), which occurs upon stimulation if so called hormone-activated G protein-coupled receptors. 

Thyrotropin (TSH) regulates the production and secretion of thyroid hormones as well as thyroid epithelial cell growth via the TSH receptor. The TSH receptor belongs to the family of G protein-coupled receptors. It is composed of 764 amino acids. The receptor contains a long hydrophilic region orientated towards the exterior of the cell (ectodomain), 7 hydrophobic transmembrane domains and a short cytoplasmic region. 

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