Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pancreatic polypeptide with some hormonal properties has been purified from chicken and turkey pancreas using acid-ethanol extraction, gel filtration and anion-exchange chromatography. The material has been crystallised. The crystals are monoclinic with space group C2. Preliminary isomorphous replacement experiments have so far provided a single-site derivative with Hg(NO3)2. A low-resolution electron density map phased with this derivative using anomalous scattering considered together with Patterson function calculations suggest that the molecules are partly helical and are arranged as a compact dimer about the crystallographic two-fold axis. The structure and association of these molecules are compared with those of insulin and glucagon, pancreatic protein and polypeptide hormones respectively, which have been studied in great detail.
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PMID:Purification, crystallisation and preliminary X-ray studies on avian pancreatic polypeptide. 91 91

Vasoactive intestinal peptide (VIP) has been shown to stimulate adenylate cyclase activity in plasma membranes isolated from canine renal cortex, outer and inner medulla in vitro. Though related hormones such as glucagon also stimulate adenylate cyclase in these membrane preparations, it is likely that VIP interacts with specific VIP receptors since the VIP receptor antagonist, (4Cl-D-Phe6, Leu17)-VIP, is capable of reducing the response to VIP, but not that to glucagon. Also binding of 125I-VIP to cortical renal plasma membranes shows competition by unlabelled VIP, but not by glucagon. Strain 1 (and clone CL(8)1b cells derived from the established cultured dog kidney cell line, MDCK, have been shown also to respond selectively to VIP by an increase in adenylate cyclase activity and cyclic AMP accumulation in intact cells. A physiological correlate of VIP activation of adenylate cyclase has been sought by addition of VIP to reconstituted epithelial monolayers of strain 1 MDCK cells clamped in Ussing chambers. VIP addition to the basal-lateral cell aspects generates an inward short-circuit current that is sensitive to replacement of medium Cl- by NO3-, and to inhibition by the Cl- channel blocker, 3-nitro-2(3-phenylpropylamino)-benzoic acid, consistent with VIP stimulation of transepithelial Cl- secretion.
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PMID:Vasoactive intestinal peptide control of renal adenylate cyclase: in vitro studies of canine renal membranes and cultured canine renal epithelial (MDCK) cells. 254 73

Addition of lipopolysaccharide plus interferon gamma, tumour necrosis factor alpha and interleukin 1 beta to cultured hepatocytes resulted in the induction of inducible nitric oxide synthase (iNOS) activity as measured by NO3(-)+NO2- formation, the conversion of L-[U-14C]arginine into citrulline and Western blotting of the iNOS protein. The inclusion of 1 microM glucagon during the induction period significantly decreased the effect of the cytokines on iNOS activity, the major effect being at the level of the total amount of protein, rather than alterations in substrate supply or covalent modification of the existing protein. In contrast, 1 microM insulin was without effect. The effect of glucagon was mediated via cAMP and could be mimicked by the presence of either dibutyryl cAMP or forskolin to activate adenylate cyclase directly. It was rapid in onset and long-lived, a 30 min pretreatment period protecting the cells from the induction of NO synthesis over the next 21 h in the presence of cytokines. Addition of glucagon at any time point up to 9 h after treatment of the cells with lipopolysaccharide plus the cytokines resulted in a significant inhibition of iNOS activity, glucagon being most potent when added during the first 3 h.
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PMID:Inhibition of cytokine-induced inducible nitric oxide synthase expression by glucagon and cAMP in cultured hepatocytes. 933 67

Culturing hepatocytes with a combination of tumor necrosis factor alpha, interferon gamma, and interleukin 1 beta plus lipopolysaccharide resulted in an induction of nitric oxide synthase and concomitant inhibition of both hepatic gluconeogenesis and glycogenolysis. The inhibition of gluconeogenesis was evident both under basal conditions and in cells stimulated acutely with glucagon. The stimulation of glycogen mobilization by glucagon was largely prevented by the presence of the cytokines. Chronic 24-h treatment of the cells with glucagon attenuated the cytokine response on both glucose output and NO formation in the dexamethasone-treated cells. This effect was antagonized by insulin. Inclusion of 1 mM NG-nitro-L-arginine methyl ester or 0.5 mM NG-monomethyl-L-arginine in the incubation abolished the increase in NO2- plus NO3- induced by the cytokine mixture and partially reversed the inhibitory effects on glucose mobilization in the presence of either insulin or glucagon, confirming the involvement of NO. In contrast the NO synthase inhibitors had little effect on either gluconeogenesis or glycogenolysis in the presence of dexamethasone alone, indicating that NO is only partially responsible for the inhibitory action of the cytokines, and the extent of its involvement depends upon the influence of other hormonal factors on the pathways. The antioxidant trolox also suppressed the inhibition of glucose release by the cytokines under conditions where nitric oxide synthase inhibitors were ineffective, suggesting that both reactive oxygen intermediates and NO may act as mediators, the relative importance of each depending upon the metabolic status of the cell.
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PMID:The importance of nitric oxide in the cytokine-induced inhibition of glucose formation by cultured hepatocytes incubated with insulin, dexamethasone, and glucagon. 943 95