共查询到20条相似文献,搜索用时 31 毫秒
1.
Anna Siniscalchi Donata Rodi Stefania Gessi Franca Campi Pier A. Borea 《Neurochemistry international》1999,34(6):517-522
The effects of brain ischemia on the maximum binding capacity (Bmax) and affinity (Kd) of A1 receptors were studied in the rat cerebral cortex, with an in vitro approach. The results were correlated with changes in 3H-adenosine release, studied under identical experimental conditions. Fifteen minutes of in vitro ‘ischemia’ (hypoxic, glucose-free medium) induced a significant increase in both Bmax (2398±132 fmol/mg protein, 151% of the control, P<0.05) and in Kd (2.43±0.12 nM, 161% of the control, P<0.01). At the same time, an increase in tritium efflux from [3H]-adenosine labeled cerebral cortex slices to 324% of the control was observed. A trend toward normalization was evident 5–15 min after ‘reoxygenation’ (restoring normal medium), but the binding parameters were still altered after 60 min (Bmax 2110±82 fmol/mg protein, Kd 2.26±0.14 nM, P<0.01 vs the corresponding control) as was adenosine release (196% of the control). These findings suggest that the increased availability of adenosine and its receptors may be a defense mechanism against ischemic injury, while the reduced affinity of A1 receptors, possibly due to desensitization, may be a sign of ischemia-induced cellular damage. 相似文献
2.
Navolotskaya EV Kovalitskaya YA Zolotarev YA Kudryashova NY Goncharenko EN Kolobov AA Kampe-Nemm EA Malkova NV Yurovsky VV Lipkin VM 《Peptides》2003,24(12):1941-1946
β-Endorphin-like peptide immunorphin (SLTCLVKGFY), a selective agonist of nonopioid β-endorphin receptor, was labeled with tritium to specific activity of 24 Ci/mmol. It was used for the detection and characterization of nonopioid β-endorphin receptors on rat adrenal cortex membranes (Kd=31.6±0.2 nM, Bmax=37.4±2.2 pmol/mg protein). Immunorphin at concentrations of 10−9 to 10−6 M was found to inhibit the adenylate cyclase activity in adrenal cortex membranes, while intramuscular injection of immunorphin at doses of 10–100 μg/kg was found to reduce the secretion of 11-oxycorticosteroids from the adrenals to the bloodstream. 相似文献
3.
Jacques Puiroux Anne Pedelaborde Barry G. Loughton 《Insect biochemistry and molecular biology》1992,22(8):859-865
The binding of [3H]proctolin to oviduct membranes has been analyzed to investigate the nature of proctolin binding sites in the oviduct. Proctolin binding was found to be time dependent, proportional to concentration of membrane protein, saturable, specific and reversible. Two apparent proctolin binding sites were recognized. The first had a Kd of 400 ± 82 nM and a Bmax of 23.7 ± 6.7 pmol/mg protein. The second had a Kd of 2.4 ± 0.2 μM and a Bmax of 96.3 ± 16.7 pmo/mg protein.
Binding was specific in thatcompetition experiments with a wide range of peptides showed that only Arg-Tyr-Leu-Pro-Ala was an effective competitor at μM concentrations. All other peptides examined weekly reduced proctolin binding at concentrations above 50 μM. Certain peptides were found to potentiate [3]pproctolin binding at low μM concentrations (1–10 μM) and to inhibit proctolin binding at higher concentrations. The significance of these findings is discussed. 相似文献
4.
Glucagon-like peptide-1 (7–36)amide (GLP-1 (7–36)amide) represents a physiologically important incretin in mammals including man. Receptors for GLP-1 (7–36)amide have been described in RINm5F cells. We have solubilized active GLP-1 (7–36)amide receptors from RINm5F cell membranes utilizing the detergents octyl-β-glucoside and CHAPS; Triton X-100 and Lubrol PX were ineffective. Binding of radiolabeled GLP-1(7–36)amide to the solubilized receptor was inhibited conentration-dependently by addition of unlabeled peptide. Scatchard analysis of binding data revealed a single class of binding sites with Ka= 0.26 ± 0.03 nM and Bmax= 65.4 ± 21.24 fmol/mg of protein for the membrane-bound receptor and Ka= 22.54 ± 4.42 μM and Bmax= 3.9 ± 0.79 pmol/mg of protein for the solubilized receptor. The binding of the radiolabel to the solubilized receptor was dependent both on the concentrations of mono- and divalent cations and the protein/detergent ratio in the incubation buffer. The membrane bound receptor is sensitive to guanine-nucleotides, however neither GTP-γ-S nor GDP-β-S affected binding or labeled peptide to solubilized receptor. These data indicate that the solubilized receptor may have lost association with its G-protein. In conclusion, the here presented protocol allows solubilization of the GLP-1(7–36)amide receptor in a functional state and opens up the possibility for further molecular characterization of the receptor protein. 相似文献
5.
The activity of the muscarinic cholinergic system (acetylcholine, ACh; acetylcholinesterase, AChE; choline acetyltransferase, ChAT; muscarinic acetylcholine receptors) was studied in the carp brain. The ACh content (13.9 ± 1.1 nmol/g wet tissue) was estimated by gas chromatography after microwave irradiation focused to the head. The AChE and ChAT activities were 153 ± 13 nmol/min/mg protein and 817 ± 50 pmol/min/mg protein, respectively. The characteristics of [3H](−)quinuclidinyl benzilate ([3H](−)QNB) and [3H]pirenzepine ([3H]PZ) binding were also studied in brain membranes. Their specific binding was linearly dependent on the protein content and they appeared to bind with high affinity to a single, saturable binding site. A dissociation constant (Kd) of 47 ± 6.3 pM and a maximum number of binding sites (Bmax) of 627 ± 65 fmol/mg protein were obtained for [3H](−)QNB, with a Kd value of 3.85 ± 0.67 nM and a Bmax value of 95.3 ± 6.25 fmol/mg protein for [3H]PZ binding. The [3H]PZ binding amounted to only 15% of the [3H](−)QNB-labeled sites, as estimated from the ratio of the Bmax values of [3H](−)QNB and [3H]PZ, suggesting a low density of M1 subtype. Atropine sulfate, atropine methylnitrate and PZ inhibited the binding of both radioligands with Hill slopes (nH) close to unity. The nH value of AF-DX 116 was close to 1 against [3H](−)QNB binding, while it was 0.75 against [3H]PZ binding. The displacement curves of oxotremorine and carbachol were shallow for the binding of both radioligands. The rank order of potency of muscarinic ligands against [3H](−)QNB binding (Ki nM) was atropine sulfate (0.55) > atropine methylnitrate (1.61) > PZ (61.19) > oxotremorine (156.3) > AF-DX 116 (307) > carbachol (1301), while in the case of [3H]PZ binding it was atropine sulfate (0.24) > atropine methylnitrate (0.34) > PZ (10.38) > AF-DX 116 (55.87) > oxotremorine (62.79) > carbachol (1696). The results indicate the presence of a well-developed muscarinic cholinergic system with predominantly M2 receptors in the carp brain. 相似文献
6.
The binding of the Ca2+-channel blocker d-cis-[3H]diltiazem to guinea pig skeletal muscle microsomes is temperature-dependent. At 2°C the KD is 39 nM and Bmax is 11 pmol/mg protein. The binding is fully reversible (K−1 = 0.02 min−1). The binding sites discriminate between the diastereoisomers 1- and d-cis-diltiazem, recognize verapamil, gallopamil and tiapamil, and are sensitive to La3+-inhibition. At 30°C the KD is 37 nM and the Bmax is 2.9 pmol/mg protein. D-cis-diltiazem-labelling is regulated by the 1,4-dihydropyridine Ca2+-channel blockers and a novel Ca2+-channel activator in a temperature-dependent manner. At 30°C an enhancement of d-cis-diltiazem binding by the channel blockers is observed. This is attributed to a Bmax increase. EC50-values for enhancement and the maximal enhancement differ for the individual 1,4-dihydropyridines. At 2°C 1,4-dihydropyridines inhibit d-cis-[3H]diltiazem binding. This is attributed to a Bmax decrease. We have directly labelled one of the drug receptor sites within the Ca2+-channel which can allosterically interact with the 1,4-dihydropyridine binding sites. 相似文献
7.
Hazem A. Hassan Hansen M. Hsiung Xing-Yue Zhang Dennis P. Smith David L. Smiley Mark L. Heiman 《Peptides》1995,16(8):1469-1473
To study structure-activity relationships of growth hormone-releasing hormone (GHRH), a competitive binding assay was developed using cloned porcine adenopituitary GHRH receptors expressed in human kidney 293 cells. Specific binding of [His1,125I-Tyr10,Nle27]hGHRH(1–32)-NH2 increased linearly with protein concentration (10–45 μg protein/tube). Binding reached equilibrium after 90 min at 30°C and remained constant for at least 240 min. Binding was reversible to one class of high-affinity sites (Kd = 1.04 ± 0.19 nM, Bmax = 3.9 ± 0.53 pmol/mg protein). Binding was selective with a rank order of affinity (IC50) for porcine GHRH (2.8 ± 0.51 nM), rat GHRH (3.1 ± 0.69 nM), [N-Ac-Tyr1,
-Arg2]hGHRH(3–29)-NH2 (3.9 ± 0.58 nM), and [
-Thr7]GHRH(1–29)-NH2 (189.7 ± 14.3 nM), consistent with their binding to a GHRH receptor. Nonhydrolyzable guanine nucleotides inhibited binding. These data describe a selective and reliable method for a competitive GHRH binding assay that for the first time utilizes rapid filtration to terminate the binding assay. 相似文献
8.
Dihydropyridine-sensitive Ca2+ channels and the relationship between binding of dihydropyridine derivatives and depolarization-induced Ca2+ uptake have been studied in aneurally cultured human muscle. Analysis of the equilibrium binding of the 1,4-dihydropyridine derivative (+)-PN200-110 revealed a single high-affinity binding site with a Kd of 0.15±0.05 nM and a Bmax of 87±12 fmol/mg protein. Inhibition of (+)-[3H]PN200-110 binding by nitrendipine revealed a Ki of 0.8 nM for the nitrendipine-receptor complex. Depolarization of cultured human muscle achieved by elevating the K+ concentration increased the uptake 45Ca2+ which was inhibited by nitrendipine with an IC50 of 1.1 nM. This study demonstrates that aneurally cultured human muscle has dihydropyridine-sensitive voltage-dependent Ca2+ channels which are functional when the fibers are depolarized. 相似文献
9.
We demonstrate binding of [125I][Nle13-po]motilin to homogenates of cat gastric and small intestinal, but not to colonic smooth muscle tissue. The density was (Bmax in fmol/mg protein): 0 (fundus); 12 ± 2 (corpus); 22 ± 3 (antrum); 55 ± 12 (duodenum); 44 ± 10 (jejunum); 17 ± 1 (ileum); 0 (colon). A significant (p < 0.05) difference was found between the dissociation constant for motilin in the stomach (pKd = 8.84 ± 0.06) and in the small intestine (pKd = 8.58 ± 0.08). The motilides erythromycin-A (EM-A), EM-523, and EM-A N-oxide displaced labeled [Nle13-po]motilin bound to cat duodenal receptor with potencies (pKd) of 5.47 ± 0.23, 7.60 ± 0.24, and < 4.3, respectively. Studies with [Leu13-po]motilin fragments showed that the N-terminus of motilin interacts with the receptor. In the tissue bath, duodenal strips mounted in the longitudinal direction responded to motilin, EM-523, and EM-A (pEC50: 8.29 ± 0.08; 7.12 ± 0.12; 5.99 ± 0.15). The compounds had a comparable intrinsic activity (83 ± 3%; 80 ± 5%; 82 ± 5% of the response to ACh), which was unaffected by atropine, TTX, hexamethonium, and zacopride but reduced by verapamil and calcium-free medium. Cat stomach and small intestine possess smooth muscle motilin receptors, which have comparable properties as those found in man and in rabbit. 相似文献
10.
A1 adenosine receptors in coated vesicles have been characterized by radioligand binding and photoaffinity labelling. Saturation experiments with the antagonist 8-cyclopentyl-1,3-[3H]dipropyl-xanthine ([3H]DPCPX) gave a Kd value of 0.7 nM and a Bmax value of 82 ± 13 fmol/mg protein. For the highly A1-selective agonist 2-chloro-N6-[3H]cyclopentyladenosine ([3H]CCPA) a Kd value of 1.7 nM and a Bmax value of 72 ± 29 fmol/mg protein was estimated. Competition of agonists for [3H]DPCPX binding gave a pharmacological profile with R-N6-phenylisopropyladenosine (R-PIA) > CCPA > S-PIA > 5′-N-ethylcarboxamido-adenosine (NECA), which is identical to brain membranes. The competition curves were best fitted according to a two-site model, suggesting the existence of two affinity states. GTP shifted the competition curve for CCPA to the right and only one affinity state similar to the low affinity state in the absence of GTP was detected. The photoreactive agonist 2-azido-N6-125I-p-hydroxyphenylisopropyladenosine ([125I]AHPIA) specifically labelled a single protein with an apparent molecular weight of 35,000 in coated vesicles, which is identical to A1 receptors labelled in brain membranes. Therefore, coated vesicles contain A1 adenosine receptors with similar binding characteristics as membrane-bound receptors, including GTP-sensitive high-affinity agonist binding. Photoaffinity labelling data suggest that A1 receptors in these vesicles are not a processed receptor form. These results confirm that A1 receptors in coated vesicles are coupled to a G-protein, and it appears that the A1 receptor systems in coated vesicles and in plasma membranes are identical. 相似文献
11.
The binding kinetics of the specific dopamine D2 antagonist [3H]raclopride to dopamine D2 receptors in rat neostriatum were studied. The pseudo-first-order rate constants of [3H]raclopride binding with these membranes revealed a hyperbolic dependence upon the antagonist concentration, indicating that the reaction had at least two consecutive and kinetically distinguished steps. The first step was fast binding equilibrium, characterized by the dissociation constant KA = 12 ± 2 nM. The following step corresponded to a slow isomerization of the receptor-antagonist complex, characterized by the isomerization equilibrium constant Ki = 0.11. The dissociation constant Kd = 1.3 nM, calculated from these kinetic data, was similar to Kd = 2.4 nM, determined from equilibrium binding isotherm for the radioligand. Implications of the complex reaction mechanism on dopamine D2 receptor assay by [3H]raclopride were discussed. 相似文献
12.
High affinity Ins(1,4,5)P3-binding sites of permeabilized hepatocytes are probably the ligand recognition sites of the receptors that mediate the effects of Ins91,4,5)P3 on intracellular Ca2+ mobilization. We have now solubilized these sites from rat liver membranes in the zwitterionic detergent, CHAPS, and shown that the solubilized bind Ins(1,4,5)P3 with an affinity (Kd = 7.26 ± 0.52 nM, Hill coefficient H = 1.05 ± 0.06) similar to that of the sites in native membranes (Kd = 6.02 ± 0.02). ATP and a range of inositol phosphates (Ins(2,4,5)P3 Ins(4,5)P2, and inositol 1,4,5-trisphosphorothioate) also bound with similar affinities to the native and solubilized sites. Solubilization of the liver InsP3 receptor will allow its further characterization, purification, and comparison of its properties with those of InsP3 receptors already purified from cerebellum and smooth muscle. 相似文献
13.
Two functional isoforms (1) and + (3) of the Na,K-ATPase catalytic subunit coexist in canine cardiac myocytes [J. Biol. Chem. (1987) 262, 8941-8943]. The in vitro turnover rates of ATP hydrolysis have been determined in sarcolemma preparations by comparing [3H]ouabain-binding and Na,K-ATPase activity at various doses of ouabain (0.3–300 nM). The correlation between the occupancy of the ouabain-binding sites and the degree of Na,K-ATPase inhibition was not linear. The results showed that the form of low-affinity for ouabain (Kd = 300–700 nM) exhibited a lower turnover rate (88 ± 10 vs. 147 ± 15 molecules of ATP hydrolyzed per second per ouabain-binding site) than the high affinity form (Kd = 1–8 nM). Thus our results indicate this specific isoform kinetic difference could contribute to differences in the cardiac cellular function. 相似文献
14.
Vasoactive intestinal polypeptide (VIP) containing nerves are present in close proximity to epithelial, endocrine, and vascular smooth muscle cells. The pineal gland, known also as a “neuroendocrine transducer organ” contains a high content of VIP which prompted us to characterize the binding sites for VIP in this organ. [Tyr10−125I]VIP was bound selectively and specifically to pineal membrane preparations in a time-dependent fashion. Scatchard analysis demonstrated a single class of high affinity binding sites with a dissociation constant (Kd) value of 5.7 ± 0.52 nmol/1 and a receptor density (Bmax) value of 440 ± 35 fmol/mg protein. A Hill Plot with a slope of 1.013 indicated the absence of cooperativity. Covalent crosslinking with [Tyr10−125I]VIP followed by SDS electrophoresis and autoradiography, revealed that the VIP binding protein exhibited a molecular weight of 51.8 ± 0.5 kDa. The precise function of pineal VIP binding protein remains to be delineated. 相似文献
15.
The selective antagonist radioligand [3H]2-propylthioadenosine-5′-adenylic acid (1,1-dichloro-1-phosphonomethyl-1-phosphonyl) anhydride ([3H]PSB-0413) was prepared by catalytic hydrogenation of its propargyl precursor with a high specific radioactivity of 74 Ci/mmol. In preliminary saturation binding studies, [3H]PSB-0413 showed high affinity for platelet P2Y12 receptors with a KD value of 4.57 nM. Human platelets had a high density of P2Y12 receptors exhibiting a Bmax value of 7.66 pmol/mg of protein. 相似文献
16.
The effect of agonists on VIP receptor regulation has been investigated in mononuclear human blood leucocytes. VIP receptor number and affinity, as well as VIP-stimulated cyclic AMP accumulation were measured after pretreatment with VIP, PHM-27 or secretin. Pretreatment for 30 min with 0.1 μM VIP caused 28% (S.E.M. = 15) reduction in specific binding, and 52% (S.E.M. = 12) reduction in cyclic AMP accumulation, while 3 h of pretreatment caused 59% (S.E.M. = 10) and 68% (S.E.M. = 12) reduction. Only VIP concentrations at the nanomolar level and higher were shown to have any effect. Bmax of the high-affinity receptor was reduced by 66% (S.E.M. = 8) after 30 min, and 95% (S.E.M. = 3) after 3 h of exposure to 0.1 μM VIP. No significant change was observed in receptor affinity, in Bmax of the low-affinity receptor, in ED50, or in ED100 of VIP-stimulated cyclic AMP accumulation. Pretreatment with PHM-27 (0.1 μM, 3 h) caused 24% reduction in [125I]VIP binding and 25% reduction in cyclic AMP accumulation, while no effect was detected after pretreatment with secretin (0.1 μM, 3 h). 相似文献
17.
The transport of [3H]adenosine at 22°C was investigated in guinea pig cerebral cortical synaptosomes using an inhibitor-stop filtration method. Under these conditions adenosine was not significantly metabolized during the incubation period used to determine the initial rates of adenosine transport. The dose response curves for the inhibition of adenosine transport by nitrobenzylthioinosine (NBMPR), dilazep and dipyridamole were biphasic—approx. 50–60% of the transport activity was inhibited with IC50 values of 0.7, 1 and 9 nM respectively, but the remaining activity was insensitive to concentrations as high as 1 μ M. Adenosine influx by both components was saturable (Km values of 17 ± 3 and 68 ± 8 μ M; Vmax values of 2.8 ± 0.3 and 6.1 ± 0.4 pmol/mg protein per s for NBMPR-sensitive and -insensitive components, respectively), and inhibited by other nucleosides and benzodiazepines. The two transport components also differed in their sensitivity to inhibition by other nucleosides and benzodiazepines indicating that the NBMPR-sensitive component of nucleoside transport in guinea pig synaptosomes exhibits a higher affinity than the NBMPR-insensitive component. However, both components have a broad specificity. Inhibition of adenosine transport by NBMPR was associated with high affinity binding of NBMPR to the synaptosomes (Kd 88 ± 6 pM). Binding of NBMPR to these sites was blocked by dilazep and dipyridamole with K1 values similar to those measured for inhibiting NBMPR-sensitive adenosine influx. These results, together with previous findings using NBMPR and dipyridamole as ligand probes, suggest that there are two components of nucleoside transport in mammalian cerebral cortical synaptosomes that differ in their sensitivity to inhibition by NBMPR and other transport inhibitors. 相似文献
18.
Jacques Abello Colette Roche Jean-Claude Cuber Christine Bernard Jacques Philippe Jean-Alain Chayvialle 《FEBS letters》1990,270(1-2):37-40
The mechanisms of cholinergic stimulation of gastrin cells were studied in the rat pancreatic cell line B6 RIN. Carbachol induced an increase in intracellular Ca2+ and stimulated gastrin release in a dose-dependent manner over the range 10−5-10−3 M. These effects were completely abolished by atropine, suggesting the implication of muscarinic cholinergic receptors. The binding properties of these receptors were investigated. [N-Methyl-3H]scopolamine ([3h]nms) binding on cell homogenates was time-dependent, saturable and consistent with a single high-affinity binding class (Kd = 39.5 pM, and Bmax = 7.9 fmol/mg DNA). Carbachol competitively inhibited [3H]NMS binding. The potency of inhibition of [3H]NMS binding by subtype selective antagonists was hexahydrodifenidol> pirenzepine> AF-DX 116. These results suggest the M3, muscarinic receptors may be involved in the carbachol-induced gastrin release from B6 RIN cells. 相似文献
19.
Bombesin (BBS)/gastrin-releasing peptide (GRP) binding sites were characterized and their distribution examined in the goldfish brain and pituitary by radioligand binding and autoradiography. Binding of 125I-[Tyr4]-BBS-14 to tissue sections was found to be saturable, reversible, time-dependent and displaceable by BBS/GRP-like peptides. Analysis of saturable equilibrium binding revealed a one-site model fit with a Kd of 0.665 ± 0.267 nM. This binding site displayed high affinity for members of the BBS subfamily of peptides, including GRP10 (Ki; 0.292 ± 0.038 nM) and GRP27 (Ki; 2.034 ± 1.597 nM), but showed no affinity for the BBS8–14 fragment. While an approximate 100-fold lower binding affinity was displayed by the binding site for neuromedin B (Ki; 61.5 ± 28.2 nM), litorin was highly effective in displacing radiolabeled BBS binding (Ki; 1.469 ± 0.427 nM). The localization of saturable and high affinity BBS/GRP binding sites in specific areas of the goldfish brain and pituitary generally revealed a similar anatomical distribution to BBS/GRP-like immunoreactive material reported previously by our laboratory. Quantitative densitometric analysis of radiolabeled BBS binding to brain nuclei and the pituitary revealed a moderate concentration of BBS/GRP binding sites in the hypothalamic feeding area, including the nucleus diffusus lobi inferioris, nucleus recessus lateralis, nucleus lateral tuberis, and nucleus anterior tuberis. Other brain nuclei known to influence the brain feeding center which contained a high density of BBS/GRP binding sites included nuclei of the dorsal and ventro-medial telencephalon, the preoptic hypothalamus, and the optic tectum. High densities of BBS/GRP binding sites were also localized in the dorsal cerebellum, and nucleus habenularis. In the pituitary, BBS/GRP binding sites were present in high concentration in the neurointermediate lobe, with a relatively lower density localized in the pars distalis. The present study further supports a role for BBS/GRP-like peptides in the regulation of feeding behavior and anterior pituitary hormone secretion in teleosts. 相似文献
20.
Amylin binding sites in a human hepatoblastoma cell line (HepG2) have been characterized in detail. 125I-Amylin (rat) bound to HepG2 cells with high affinity. Binding was reversible and selective, and dependent on time and temperature. Scatchard analysis revealed the presence of high (Kd = 0.11 ± 0.04 nM) and low (Kd = 1.3 ± 0.4 μM) affinity binding sites for 125I-amylin in HepG2 cells. The dissociation experiments also showed that 125I-amylin dissociated from high- and low-affinity sites. The association data, however, indicated the presence of only one binding site. Rat amylin was more potent than human amylin and rat calcitonin gene-related peptide (CGRP) in displacing 125I-amylin bound to HepG2 cells. Nonhomologous peptides did not displace 125I-amylin. Rat amylin was, however, less potent than rat CGRP in displacing 125I[Tyr0]CGRP from HepG2 cells. Pretreatment of HepG2 cells with rat amylin (10 nM) reduced the specific binding of 125I-amylin by 75%, whereas rat CGRP (10 nM) pretreatment had no effect on amylin binding. Calcitonin gene-related peptide, as well as rat and human amylin, stimulated the adenylate cyclase activity of HepG2 cell membrane preparation in a dose-dependent manner, with an order of potency of CGRP > rat amylin > human amylin. A CGRP antagonist, CGRP(8–37), significantly attenuated the stimulatory effect of both amylin and CGRP on adenylate cyclase activity. These investigations show that distinct receptors of amylin and CGRP are present in HepG2 cells and that amylin stimulates adenylate cyclase activity through CGRP receptors. This system could now be exploited for studying amylin receptors and amylin-mediated signal transduction. 相似文献