| transforming growth factor beta | Factor synthesised in a wide variety of tissues including platelets, placenta, and both normal and transformed cell lines. It acts synergistically with tgf-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. Tgf-beta also has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. There are at least three forms of tgf-beta: tgf-beta1, tgf-beta2, and tgf-beta1.2. The latter is a heterodimer made up of both tgf-beta1 and tgf-beta2. (12 Dec 1998) |
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| endothelium-derived growth factor synthase | <enzyme> Converts l-arginine to a smooth muscle relaxing factor and stimulates the formation of cyclic-GMP Registry number: EC 1.5.1.- Synonym: edrf synthase (26 Jun 1999) |
| epidermal growth factor | <growth factor> A mitogenic polypeptide initially isolated from male mouse submaxillary gland. The name refers to the early bioassay, but epidermal growth factor is active on a variety of cell types, especially but not exclusively epithelial. Human equivalent originally named urogastrone owing to its hormone activity. Acronym: EGF (18 Nov 1997) |
| epidermal growth factor-urogastrone | <chemical> Single chain, nonhelical, acidic polypeptides of about 52 amino acids found in most mammals. Epidermal growth factor and urogastrone are not identical but seem to share biological acivities. They promote growth of, and cell proliferation in, certain tissues, especially epidermal structures and inhibit acid secretion by the stomach. They have been used to treat gastrointestinal ulcers. Chemical name: Epidermal growth factor (12 Dec 1998) |
| keratinocyte growth factor | <growth factor> A growth factor structurally related to fibroblast growth factor. (18 Nov 1997) |
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
| amino acid receptor | <biochemistry> Ligand gated ion channels with specific receptors for amino acid transmitters. An extended protein superfamily that also includes subunits of the nicotinic acetylcholine receptor. (18 Nov 1997) |
| AMPA receptor | <cell biology> Glutamate operated ion channel. See: excitatory amino acid receptor channels. (05 Feb 1998) |
| ANP receptor | <molecular biology> Family of 3 receptors for atrial natriuretic peptide. ANP A and ANP B have intracellular guanylate cyclase and protein kinase like domains. ANP C, shares the extracellular ligand binding and transmembrane domains, but lacks the functional intracellular domains and is not thought to be involved in signal transduction. (18 Nov 1997) |
| asialoglycoprotein receptor | A surface receptor found in hepatocytes that binds galactose-terminal glycoproteins; thus, this receptor removes those proteins from circulation and they are in turn acted upon by hepatocyte lysosomes. (05 Mar 2000) |
| auditory receptor cells | Columnar cell's in the epithelium of the organ of Corti, having hairs (stereocilia) on their apical ends. See: Corti's cells. (05 Mar 2000) |
| beta-adrenergic receptor blocking agent | A class of drugs that compete with beta-adrenergic agonists for available receptor sites; some compete for both b1 and b2 receptors (e.g., propranolol) while others are primarily either b1 (e.g., metoprolol) or b2 blockers; used in the treatment of a variety of cardiovascular diseases where beta-adrenergic blockade is desirable. Synonym: beta-adrenergic receptor blocking agent, beta-adrenoreceptor antagonist, beta-blocker. (05 Mar 2000) |
| beta-adrenergic receptor kinase | <enzyme> Cyclic-AMP protein kinase which specifically phosphorylates the agonist-occupied form of beta-adrenergic receptor Registry number: EC 2.7.1.- Synonym: beta-ar kinase, beta-adrenergic receptor kinase 1, g-protein-coupled receptor kinase 2, grk2 (kinase), beta-adrenergic receptor kinase 2, beta-ar kinase 2 (26 Jun 1999) |
| cAMP receptor protein | catabolite (gene) activator protein |
| GABA receptor | <physiology> Ligand gated chloride ion channel forming receptor opened by gamma aminobutyric acid. Two distinct types: A and B. A receptor: One of a family of neurotransmitter receptors with fast intrinsic ion channels that includes the glycine receptor and the nicotinic acetylcholine receptor. Distinct from another major receptor family, the muscarininc acetylcholine receptor and rhodopsin, with no intrinsic ion channel. The A receptor is specifically blocked by bicuculline. It consists of two pairs of protein chains forming an A2B2 complex, the A chains bind benzodiazepine and the B chains bind GABA. The 4 subunits are thought to form a tight group with the chloride channel in the middle. There is considerable similarity between the amino acid sequences of the receptor subunits and those of the nicotinic acetylcholine receptor suggesting that both receptors are derived from some evolutionary ancestor. See: amino acid receptor superfamily. B receptor: Brain receptor (80 kD) for the inhibitory neurotransmitter gamma amino butyric acid. Differs from the A receptor both in agonist specificity (baclofen is a specific agonist) and its effects on cells. It modulates intracellular calcium levels through a Go mediated effect on N type calcium channels and also lowers intracellular cAMP levels by an effect on adenylyl cyclase, thereby reducing the secretion of catecholamines. (05 Jan 1998) |