Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a tumor cell line of the mouse anterior pituitary (AtT-20/D16-16) consisting of a homogeneous population of corticotrophs, corticotropin-releasing factor (CRF) activates adenylate cyclase and cAMP-dependent protein kinase. In addition, CRF induces a rise in cytosolic calcium levels in AtT-20/D16-16 cells and stimulates adrenocorticotropin hormone release. To determine whether activation of cAMP-dependent protein kinase is essential for CRF to stimulate calcium mobilization and trigger adrenocorticotropin hormone release, an inhibitor of cAMP-dependent protein kinase was inserted into AtT-20/D16-16 cells using a liposome technique. In control cells, CRF, forskolin (a direct activator of adenylate cyclase) and potassium increased cytosolic calcium levels. Insertion of the protein kinase inhibitor into AtT-20/D16-16 cells greatly attenuated CRF and forskolin-stimulated calcium mobilization although it did not alter the rise in cytosolic calcium induced by potassium. Treatment of the cells with liposomes lacking protein kinase inhibitor (but containing an equivalent amount of bovine serum albumin) had no effect upon the calcium mobilization elicited by any of the agents tested. These results reveal an essential role for cAMP-dependent protein kinase in mediating CRF-stimulated calcium mobilization and suggest that its activation may be an essential molecular event for CRF to evoke adrenocorticotropin hormone secretion.
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PMID:Molecular mechanisms of corticotropin-releasing factor stimulation of calcium mobilization and adrenocorticotropin release from anterior pituitary tumor cells. 303 99

Twelve hybridoma cell lines producing MAbs against morphine were established by using morphine hemisuccinate-conjugated bovine serum albumin as an immunogen. The MAbs belonged to the IgG1 subclass with kappa- or lambda-chains. The association constants of the antibodies ranged from 4.6 x 10(8) to 4.7 x 10(10) (M-1). These antibodies revealed slightly different cross-reactivities with various agonistic opiates and antagonists. In general, the antibodies were strongly cross-reactive with the opiate agonists, codeine, ethylmorphine, dihydromorphine and dihydrocodeine, while their cross-reactivities with norcodeine and the opiate antagonists, naloxone and naltrexone, were weak. The cross-reactivities with dihydromorphinone, dihydrocodeinone, naloxone, naltrexone, dextromethorphan and homatropine varied from clone to clone. Interestingly, certain MAbs displayed weak but significant cross-reactivities with the synthetic opiate, meperidine. However, none of the antibodies was cross-reactive with the opioid peptides, beta-endorphin, Met-enkephalin, and D-Ala2-D-Leu5-enkephalinamide. Radioimmunoassay for morphine using one of the antibodies (MOR 131.5.13) was shown to be sufficiently sensitive (IC50 = 0.1 nM) for the purposes of forensic analysis of morphine. This set of monoclonal anti-opiate antibodies is assumed to be suitable for analyzing the structure-function relationship in the hapten-antibody interaction, since the antibodies revealed similar but not identical cross-reactivities with various morphine related compounds.
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PMID:Production and characterization of high-affinity monoclonal antibodies against morphine. 321 Nov 62

The material presented here summarizes the bulk of the presently available immunologic data bearing upon the in vivo relationship between brown adipose tissue and the immune system. The experiments were carried out in rats adipectomized (by surgical excision of the interscapular brown adipose tissue at birth), thymectomized (by neonatal removal of the thymus), adipectomized and thymectomized, and corresponding sham-operated controls. The following immune phenomena were studied: antibody production to soluble and corpuscular antigens; Arthus and delayed hypersensitivity skin reactions to bovine serum albumin; rejection of allogeneic skin and thyroid grafts; lymph node enlargement in a host-versus-graft reaction; experimental allergic encephalomyelitis and thyroiditis; immune response in normal animals treated with extracts from brown adipose tissue; allergic encephalomyelitis in thymoadipectomized animals; plaque-forming cell response and hemagglutinating antibody titers in animals injected with met-enkephalin and leu-enkephalin; and survival rate of adipectomized mice inoculated with Sarcoma-I cells. The results indicated that the cell-mediated immune reactions were potentiated in adipectomized rats. Antibody production was not significantly changed by neonatal adipectomy. Adipectomized mice, inoculated with Sa-I tumor cells, survived longer than controls, thus indicating that adipectomy made possible the recognition of discrete histocompatible differences between Sa-I cells and A/JAX mice. Adipectomy increased the ability of rats to develop autoimmune diseases. Saline extracts from brown adipose tissue of newborn rats suppressed hypersensitivity skin reactions in normal adult rats. Thymoadipectomized rats showed an almost normal ability to develop allergic encephalomyelitis, a finding that suggested that the potentiating influence of adipectomy on encephalomyelitis was neutralized by thymectomy. It appears that brown adipose tissue functions as a natural antagonist of the thymus. Enkephalins were found to be more effective immunosuppressors in adipectomized than in normal animals. The last finding establishes a functional link between brown adipose tissue and neuropeptides. It seems that the potentiation of immune response in adipectomized animals is effected by altered release of yet unidentified mediators and modulators. The evidence indicates that brown adipose tissue, in which neurohumoral activity occurs, may be an important component of an integrated immunoneuroendocrine system.
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PMID:Brown adipose tissue. Its in vivo immunology and involvement in neuroimmunomodulation. 330 Apr 71

Self recently described a substrate system for alkaline phosphatase (AP)-dependent ELISAs which markedly increased sensitivity, compared to using p-nitrophenyl phosphate. This increase is achieved by having AP, the primary enzyme, produce an activator for a secondary enzyme-substrate system, within which marked amplification occurs. We adapted this technique to study antibodies to casein, bovine serum albumin, ovalbumin, and cardiolipin in the sera of patients with systemic lupus erythematosus (SLE) and normal individuals. The new substrate system yielded titres 30-50-fold higher than those with p-nitrophenyl phosphate (Sigma 104, p-NPP). In addition, when used in a solid-phase C1q binding assay we were able to use a 1 : 100,000 dilution of AP-conjugated anti-human IgG with the amplified substrate, compared to the 1 : 1000 dilution needed with p-NPP. This system is extremely valuable because of its flexibility. It can either be very sparing of limited samples, or if the added sensitivity is not needed, 100-fold less AP conjugate may be used. Thus rare or expensive conjugates can be significantly conserved.
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PMID:A substrate amplification system for enzyme-linked immunoassays. Demonstration of its general applicability to ELISA systems for detecting antibodies and immune complexes. 349 82

Body, thymus, and spleen weights, and cellular makeup of lymphoid tissues of rat were not affected to a great extent by intraperitoneal injections of met-enkephalin, leu-enkephalin, or naloxone. However, enkephalins induced a diminution of peripheral blood leukocytes and lymphocytes. In addition, met-enkephalin depleted the population of T4 helper/inducer lymphocytes. On the other hand, there was an increase of blood leukocytes and lymphocytes in naloxone-treated animals. Arthus and delayed skin hypersensitivity reactions to bovine serum albumin and old tuberculin were sharply reduced in enkephalin-treated rats. Rejection of allogenic thyroid graft implanted under the renal capsule was considerably delayed by repeated injections of enkephalins. Mesenteric mast cell degranulation in rats sensitized to ovalbumin and injected with a shocking dose of antigen was less pronounced after treatment with enkephalins. These results show that enkephalins, in dosage levels of 5 mg/kg b.w., exert a suppressive influence on cell-mediated immune reactions. Other experiments from our laboratory, reported in a companion paper in this volume, suggest that much lower doses may have opposite (immunoenhancing) effects.
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PMID:Enkephalins and immunity. II: In vivo modulation of cell-mediated immunity. 349 23

A perifusion system was developed to investigate the control of alpha-melanocyte-stimulating hormone (alpha-MSH) release from rat brain. Hypothalamic slices were perifused with Krebs-Ringer bicarbonate (KRB) medium supplemented with glucose, bacitracin and bovine serum albumin. Fractions were set apart every 3 min and alpha-MSH levels were measured by means of a specific and sensitive radioimmunoassay method. Hypothalamic tissue in normal KRB medium released alpha-MSH at a constant rate corresponding to 0.1% of the total hypothalamic content per 3 min. The basal release was not altered by Ca2+ omission in the medium or addition of the sodium channel blocker tetrodotoxin (TTX). Depolarizing agents such as potassium (50 mM) and veratridine (50 microM), which is known to increase Na+ conductance, significantly stimulated alpha-MSH release in a Ca2+-dependent manner. When Na+-channels were blocked by TTX (0.5 microM) the stimulatory effect of veratridine was completely abolished whereas the K+-evoked release was unaffected. These findings suggest that: voltage-dependent sodium channels are present on alpha-MSH hypothalamic neurons; depolarization by K+ induces a marked stimulation of alpha-MSH release; K+- and veratridine-evoke releases are calcium-dependent. Altogether, these data provide evidence for a neurotransmitter or neuromodulator role for alpha-MSH in rat hypothalamus.
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PMID:alpha-Melanocyte-stimulating hormone (alpha-MSH) release from perifused rat hypothalamic slices. 360 76

The polypeptide hormones insulin, glucagon, thyrotropin (TSH), pregnant mare serum gonadotropin (PMSG) and adrenocorticotropin (ACTH) stimulated the growth of the Tetrahymena, and the non-hormone polypeptides (bovine serum albumin (BSA), protamine) had a similar effect. Re-exposure after 24 h accounted for a greater growth stimulation than pre-exposure alone in cultures treated with TSH and PMSG, and re-exposure after 7 days had such effect in all polypeptide-treated cultures. It follows that the non-hormone polypeptides had a similar imprinting potential to the polypeptide hormone. The non-hormone polypeptides were also able to cross-imprint for one another, i.e. pre-exposure to one enhanced the binding capacity of the cells for the other on re-exposure, and vice versa. A single treatment with a polypeptide hormone or a non-hormone polypeptide did in itself stimulate the growth of the Tetrahymena for as long as 1 week.
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PMID:Chemical reception mechanisms at a low level of phylogeny. Influence of polypeptide hormones and non-hormone polypeptides on the growth of Tetrahymena. 392 47

Monoclonal antibodies were produced following immunization of mice with either [Leu5]enkephalin-bovine serum albumin or [Met5]enkephalin-keyhold limpet hemocyanin conjugates. Two monoclonal antibodies coded NOC1 and NOC2, respectively, were derived. These monoclonal antibodies did not discriminate between Leu- and Met-enkephalin in either radioimmunoassay or immunocytochemistry. NOC1 was characterized in detail. In radioimmunoassay NOC1 displayed about 40% crossreactivity with C-terminal extended Met-enkephalin hexapeptides and 7% with the extended heptapeptide (-Arg-Phe-OH), but did not recognize other endogenous peptides. In immunocytochemistry the NOC1 and NOC2 recognized all well-established "enkephalin immunoreactive sites," but they did not bind to areas known to contain beta-endorphin or high levels of pro-enkephalin. NOC1 was shown to be a suitable tool to demonstrate enkephalin immunoreactive sites by radioimmunocytochemistry utilizing both internally and externally labeled monoclonal antibodies.
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PMID:Characterization and immunocytochemical application of monoclonal antibodies against enkephalins. 608 44

Synthetic bovine parathyroid hormone containing the 1-34 NH2 terminal amino acids [bPTH-(1-34)] is capable of inhibiting stimulated uterine contraction. The purpose of the present investigation is to determine whether the inhibitory action of bPTH-(1-34) is a direct action of the hormone fragment. The effect of different synthetic preparations of bPTH-(1-34), salmon calcitonin, corticotropin-inhibiting peptide and bovine serum albumin on oxytocin-stimulated uterine contraction was determined. In addition, the effects of atropine, propranolol, phentolamine, pyrilamine, cimetidine and the prostaglandin synthetase inhibitor indomethacin on the inhibitory action of bPTH-(1-34) on uterine contraction was determined. Both synthetic preparations of bPTH-(1-34) inhibited oxytocin-initiated contractions similarly. Salmon calcitonin, corticotropin-inhibiting peptide, and bovine serum albumin did not alter oxytocin-stimulated uterine contractions. The salmon calcitonin also did not alter the ability of bPTH-(1-34) to exert its inhibitory effect on uterine contraction. Cholinergic, alpha and beta adrenergic, histaminergic (H1 and H2) and prostaglandin synthetase inhibitors did not alter the action of bPTH-(1-34). These results suggest that the action of bPTH-(1-34) is 1) not due to the presence of a contaminant in the synthetic hormone preparation and 2) that the effect could be due to a direct action effect of the hormone fragment on uterine tissue.
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PMID:Direct effect of parathyroid hormone on rat uterine contraction. 608 71

A radioimmunoassay was established for the measurement of androst-4-en-17 beta-ol-3,11-dione (11-oxotestosterone). Highly specific antiserum was raised in rabbits using androst-4-en-17 beta-ol-3,11-dione-3-bovine serum albumin conjugate as antigen. Cross reactivity with all steroids measured was less than 4%. [1,2-3H2]androst-4-en-17 beta-ol-3,11-dione was synthesized from [1,2-3H2]pregn-4-ene-17 alpha, 21-diol-3,11,20-trione in a two step reaction with [1,2-3H2]androst-4-ene-3,11,17-trione as intermediate. Purification of plasma androst-4-en-17 beta-ol-3,11-dione was performed by thin-layer chromatography. The intra- and interassay variation was 7.6% and 8.9%, respectively. Furthermore, the radioimmunological procedure was checked against the measurement of androst-4-en-17 beta-ol-3,11-dione in human plasma by gas chromatography/mass spectrometry. Mean plasma levels of androst-4-en-17 beta-ol-3,11-dione at 8 a.m. in healthy young subjects were 2.04 +/- 0.63 nmol/l (means +/- SD) in males and 2.18 +/- 0.89 nmol/l in females. In both groups there was a marked decrease during the night (p less than 0.01), becoming 0.96 +/- 0.33 and 0.96 +/- 0.40 nmol/l, respectively, at 11 p.m. Administration of human chorionic gonadotropin on 3 consecutive days did not influence the plasma concentrations of androst-4-en-17 beta-ol-3,11-dione, whereas both corticotropin (from 2.35 +/- 1.12 to 1.65 +/- 0.76 nmol/l; p less than 0.02) and dexamethasone (from 2.40 +/- 1.75 to 0.40 +/- 0.16 nmol/l; p less than 0.01) caused a significant decrease of androst-4-en-17 beta-ol-3,11-dione.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The measurement of androst-4-en-17 beta-ol-3,11-dione (11-oxotestosterone) by radioimmunoassay in human plasma. 609 May 77


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