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)

By potentiometric equilibrium measurements and the computer evaluation of experimental data, the protonation equilibrium constants of four fragments of corticotropin (ACTH), ACTH1-32. ACTH1-28, ACTH1-14 and ACTH1-4, were determined and assigned to the corresponding functional groups. From the dependence of the protonation constants on the length of the peptide chain, it was established which functional groups participate in the formation of intramolecular hydrogen-bonds in aqueous solutions at various pH. These results indicated a pH-dependent conformation of the molecule.
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PMID:Coordination-chemistry study of polypeptides. III. protonation-deprotonation equilibrium study of synthetic alphaH -corticotropin1-32. Data on the pH-dependent conformation of corticotropin. 2 5

Proton magnetic resonance studies of [Met5]-enkephalin (lipotropin 61-65) in aqueous solution indicate a conformational preference for the pentapeptide backbone. The structural differences between [Met5]-enkephalin and other, more flexible peptides have been investigated using paramagnetic probe techniques. An outline structure for beta-endorphin (lipotropin 61-91) in aqueous solution is obtained from binding studies using Gd(III) as a relaxation probe.
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PMID:Proton magnetic resonance studies on [methionine]-enkephalin and beta-endorphin in aqueous solution. 53 45

To assess the effect of extracellular hydrogen ion concentration (PH+) on aldosterone secretion, studies in which other known modulators could be controlled were performed on 13 patients undergoing hemodialysis. High (35 mM) or low (14-17 mM) dialysate bicarbonate concentrations were utilized on separate days to either decrease or increase PH+, while plasma potassium concentrations (PK) were held at constant levels and changes in plasma renin activity (PRA) were minimized by avoiding changes in body weight. Changes in PH+ were associated with concordant changes in plasma aldosterone concentration (Pa) in both high- and low-bicarbonate studies. When these changes in Pa in high- and low-bicarbonate studies were analyzed together as a function of corresponding changes in PH+, a significant correlation could be demonstrated (r = 0.659, P less than 0.001). There was no correlation between changes in Pa and changes in PK, plasma sodium, plasma adrenocorticotropic hormone (ACTH), or PRA. Using the same methods to control PH+ and other variables during hemodialysis, the effects of altered PH+ on ACTH-stimulated aldosterone and cortisol secretion were evaluated in studies on six patients who received incremental infusions of ACTH after pretreatment with dexamethasone. In these studies, there was no demonstrable effect of PH+ on Pa or plasma cortisol concentration. We conclude that physiological changes in PH+ have a weak modulating effect on basal aldosterone secretion that may not be evident in the presence of other acutely applied stimuli.
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PMID:Modulation of plasma aldosterone by physiological changes in hydrogen ion concentration. 131 33

The effect of excitatory amino acid receptor antagonists, (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5, 10-imine hydrogen maleate ((+)-MK-801), (+/-)-3-(2-carboxy-piperazin-4-yl)-propyl-1-phosphonic acid (CPP), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (+/-)-2-amino-4-phosphonobutanoic acid (AP-4), on penile erection and yawning induced by subcutaneous apomorphine (80 micrograms/kg), intracerebroventricular (i.c.v.) oxytocin (30 ng) and adrenocorticotropin (ACTH)-(1-24) (10 micrograms) was studied in male rats. Intraperitoneal (0.1-0.4 mg/kg) and i.c.v. (10-50 micrograms) (+)-MK-801 prevented dose dependently the penile erection and yawning induced by the three drugs. The (+)-MK-801 effect coincided with the appearance of head weaving, body rolling, hyperlocomotion and ataxia. Haloperidol (0.5 mg/kg i.p.) antagonized the prevention by (+)-MK-801 of oxytocin responses. Penile erection but not yawning was also prevented by high, but not low doses of CPP and CNQX, which impaired motor performance, AP-4 was ineffective at all doses tested. The above compounds were ineffective when injected into the paraventricular nucleus of the hypothalamus, the brain area where apomorphine and oxytocin act to induce penile erection and yawning. The results suggest that excitatory amino acid transmission is not involved in the expression of penile erection and yawning induced by the above compounds.
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PMID:Effect of excitatory amino acid receptor antagonists on apomorphine-, oxytocin- and ACTH-induced penile erection and yawning in male rats. 135 47

C20H30N4O8, M(r) = 454.48, monoclinic, P2(1), a = 13.411 (2), b = 12.592 (2), c = 14.710 (1) A, beta = 104.30 (1) degrees, V = 2407 (6) A3, Z = 4, Dx = 1.254 Mg m-3, lambda (Cu K alpha) = 1.5418 A, mu = 0.783 mm-1, F(000) = 968, room temperature, final R = 0.086, wR = 0.080 for 4055 observed reflections. The title compound is a model for the intermediate formed in the deamidation reaction of porcine adrenocorticotropin hormone. The structure presents a pseudo-translational symmetry and was solved by using a modified version of the SIR88 package. In the refinement, few stereochemical restraints were needed to handle the static disorder shown by the C-terminal fragment of one molecule in the asymmetric unit. The conformation of the two independent molecules is almost identical and is a II' beta-bend, stabilized by an intramolecular hydrogen bond. In the crystal, screw-related molecules are linked by hydrogen bonds. The two molecules in the independent unit are related by the translation vector u = 0.4962 (2)a + 0.7310 (2)b + 0.5075 (2)c.
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PMID:Solid-state conformations of aminosuccinyl peptides: structure of tert-butyloxycarbonyl-L-prolyl-L-aminosuccinyl-glycyl-L-alanine methyl ester (Boc-L-Pro-L-Asu-Gly-L-Ala-OMe). A case of pseudo-translational symmetry. 138 44

The oxidative burst of rainbow trout (Oncorhynchus mykiss) phagocytes was previously found to be differentially modulated by adrenocorticotropic hormone (ACTH) and the catecholamine receptor agonists phenylephrine and isoproterenol. From data obtained using both luminol-enhanced chemiluminescence (LECL) and ferricytochrome C (cyt C) reduction to measure oxidative burst kinetics, we postulated that the observed modulation was mediated by affects on enzymes responsible for the production and metabolism of superoxide anion. Using exogenous superoxide dismutase (SOD) and catalase as scavengers, nitroprusside to poison endogenous SOD, and an assay for hydrogen peroxide, we have tested our postulates by exploiting the differences with which various reactive oxygen intermediates influence LECL and cyt C reduction. The ability of ACTH to potentiate both assays of the oxidative burst appears due to its enhancing influence on the production of superoxide. Phenylephrine, an alpha-adrenergic receptor agonist, appears to enhance the activity of endogenous SOD, whereas isoproterenol, a beta-adrenergic receptor agonist, may suppress SOD activity. This work reveals how components of the natural immune system may be regulated by products of the neuroendocrine system. Also, lymphocyte-derived ACTH may provide a novel pathway for lymphoid regulation of inflammation.
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PMID:Modulation of the oxidative burst in trout myeloid cells by adrenocorticotropic hormone and catecholamines: mechanisms of action. 165 72

Conjugate of horseradish peroxidase and wheat germ agglutinin (HRP-WGA conjugate) was injected into the midbrain central gray (MCG) of three adult rats. Frontal sections of the diencephalon were first treated with diaminobenzidine and hydrogen peroxide to detect the retrogradely transported conjugate. They were then stained immunohistochemically to detect pro-opiomelanocortin (POMC)-derived peptides (ACTH, beta-endorphin and alpha-MSH). The coexistence of the three POMC-derived peptides was confirmed by the immunohistochemistry of three consecutive sections stained with antiserum specific to each peptide. Some of the neuronal perikarya distributed in and around the arcuate nucleus were positive to the immunohistochemical stain for POMC-derived peptides, and, concomitantly, were labeled with HRP-WGA conjugate, which indicated that they projected to the MCG. They were mostly concentrated in the rostral three-fifths of the arcuate nucleus. The finding that some of the POMC neurons in the arcuate nucleus project to the midbrain central gray deserves interest, because the central gray is involved in analgesia induced by opioid peptides.
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PMID:Projection of pro-opiomelanocortin neurons from the rat arcuate nucleus to the midbrain central gray as demonstrated by double staining with retrograde labeling and immunohistochemistry. 245 87

Opioid peptides have been shown to modulate the function of cells associated with host defense. Both opiate and nonopiate receptor mechanisms have been shown to mediate cell responses to these peptides. In this study we used a ferricytochrome C reduction microassay to measure superoxide (O2-) production by human polymorphonuclear leukocytes after stimulation with beta-endorphin (beta-END). beta-END was found to stimulate O2- release at concentrations from 10(-14) to 10(-8) M; the peak response occurred at 10(-12) M. A microassay based on the horseradish peroxidase-mediated oxidation of phenol red was used to demonstrate the production of hydrogen peroxide H2O2, by beta-END at 10(-12) M. The accumulation of H2O2 was reduced by the inhibitor, nitroprusside, and by the converting enzyme, catalase. The accumulation of O2- in response to the potent chemotactic peptide formyl-methionine-leucine-phenylalanine was studied and a distinctly different dose-response profile with a peak response at 10(-8) M was observed. Because beta-END can apparently bind to and activate cellular functions by nonopiate receptors, N-acetyl-beta-END was tested. At doses between 10(-14) and 10(-8) M, it failed to effect O2- accumulation. Moreover, (-)-naloxone 10(-12) M was shown to completely abolish the stimulatory effect of equimolar beta-END whereas (+)-naloxone was entirely ineffective. At 10(-8) M both stereoisomers also failed to inhibit formyl-methionine-leucine-phenylalanine 10(-8) M. Thus, at the picomolar concentration present in the human systemic circulation, beta-END activates oxygen metabolism by polymorphonuclear leukocytes through stereoselective, naloxone-sensitive opiate receptors.
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PMID:Beta-endorphin stimulates human polymorphonuclear leukocyte superoxide production via a stereoselective opiate receptor. 303 21

We examined the effect of chronic metabolic acidosis on adrenocortical hormone production by administering NH4Cl for 5 days to four normal subjects. Plasma aldosterone concentration, aldosterone secretion, and urinary excretion of aldosterone-18-glucuronide increased significantly, whereas there were no significant changes in the plasma concentrations of cortisol, corticosterone, or deoxycorticosterone, or in the urinary excretion of 17-hydroxycorticoids. By day 2, plasma renin activity (PRA) and concentration (PRC) were not significantly different from control, and the slope of the regression line relating plasma aldosterone concentration to PRA was significantly greater than the slope in the control period, i.e., the sensitivity of aldosterone secretion to renin stimulation was increased. By day 5, however, PRA and PRC were increased above control. Plasma potassium concentration did not change significantly. Thus chronic NH4Cl-induced acidosis induces a sustained stimulation of aldosterone secretion in the absence of a change in adrenocorticotropin-dependent adrenocortical hormone secretion. Factors other than an increase in renin secretion and plasma potassium concentration may be involved in at least the early phase of aldosterone stimulation, suggesting that plasma hydrogen ion concentration might be a separate regulator of aldosterone secretion.
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PMID:Adrenocortical hormone secretory response to chronic NH4Cl-induced metabolic acidosis. 310 28

The decay of the indole triplet of single tryptophan-containing proteins and model compounds can be readily determined at room temperature in solution by monitoring the triplet absorption or emission following an exciting laser pulse. The dioxygen triplet quenching constants, can be measured for all these molecules and compared to the analogous singlet values determined by fluorescence methods. The dioxygen triplet quenching constant (tkq) ranged from a high of 5.1.10(9) M-1.s-1 for the exposed indole of corticotropin to a low of 0.1.10(9) M-1.s-1 for the buried indole of asparaginase. The ratio of these values with their respective dioxygen singlet quenching constants (skq), tkq/skq, ranged from 0.3 to 0.6 for aqueous exposed polypeptide indoles. For globular proteins the tkq/skq value is observed to be 0.2 +/- 0.1. This lower value for protein indoles is not attributable to 'bulk' environmental or hydrogen bonding effects, since the magnitude of tkq/skq (= 0.5 +/- 0.1) for model indoles was independent of solvent dielectric constant, polarity, and proticity. Temperature-dependence studies were done to test whether tkq could be used to characterize the nature of the protein matrix. The activation energy (Ea) for tkq was found to be 11 +/- 2 kcal/mol for most proteins. This Ea was independent of whether the indole side-chain was solvent exposed or buried in the non-aqueous protein interior. Large Ea values were also obtained for model indoles, naphthalene and nalidixic acid, dissolved in water, whereas the same compounds dissolved in 95% ethanol exhibited much smaller Ea values. These data, in combination with the observation that the tkq of model indoles is insensitive to changes in solvent viscosity, indicate that dioxygen quenching at the triplet level can not be easily used to characterize the dynamics of proteins.
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PMID:Determination of the dioxygen quenching constant for protein and model indole triplets. 319 Nov 39


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