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)

The effects of Vibrio cholerae enterotoxin on steroidogenesis and on formation of adenosine 3':5'-cyclic phosphate (cyclic AMP) in two adrenal tumor cell lines were compared. Steroidogenesis was half-maximal at concentrations of 1 ng of cholera toxin/ml in the mutant OS-3 cells and 3 ng of cholera toxin/ml in the parent Y-1 cells. At the end of an 8-hr incubation, toxin-induced formation of cyclic AMP in the mutant cell line was reduced by 90%. A molar ratio of GM1 ganglioside (galactosyl-N-acetylgalactosaminyl [sialosyl] lactosyl ceramide; GGnSLC) to cholera toxin of 3:1 caused half-maximal inhibition of steroidogenesis in both cell lines. When equine antiserum to choleragenoid was added to adrenal cells 15 min after cholera toxin, there was marked inhibition of cyclic AMP formation and of steroidogenesis. Pretreatment of Y-1 cells with adrenocorticotropin rendered them unresponsive to hormonal induction of cyclic AMP formation, but these cells had an unimpaired response to cholera toxin. These studies, utilizing two adrenal cell lines, suggest important differences between the mode of action of cholera toxin and that of adrenocorticotropin in cultured adrenal tumor cells.
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PMID:Mode of action of Vibrio cholerae enterotoxin in cultured adrenal tumor cells. 17 80

Gangliosides inhibit 125I-labeled thyrotropin binding to the thyrotropin receptors on bovine thyroid plasma membranes, on guinea pig retro-orbital tissue plasma membranes, and on human adipocyte membranes. This inhibition by gangliosides is critically altered by the number and location of the sialic acid residues within the ganglioside structure, the efficacy of inhibition having the following order: GD1b greater than GT1 greater than GM1 greater than GM2 = GM3 greater than GD1a. The inhibition results from the interaction of thyrotropin and gangliosides, rather than the interaction of membrane and gangliosides. Fluorescence studies show that the inhibition is associated with a distinct conformational change of the thyrotropin molecule and that the progression from a "noninhibitory conformation" to an "inhibitory conformation" parallels exactly the order of effectiveness in inhibiting 125I-labeled thyrotropin binding. The ganglioside inhibition of 125I-labeled thyrotropin binding appears to be hormonally specific in that it is not affected by albumin, glucagon, insulin, prolactin, follicle-stimulating hormone, growth hormone, or corticotropin. The possibility that a ganglioside or ganglioside-like structure is a component of the thyrotropin receptor is suggested by the finding that gangliosides more complex than N-acetylneuraminylgalactosylglucosylceramide are present in bovine thyroid membranes in much higher quantities than have been previously found in extraneural tissue. The finding that the B component of cholera toxin, which also interacts with gangliosides, has a peptide sequence in common with the beta subunit of thyrotropin, suggests that thyrotropin and cholera toxin may be analogous in their mode of action on the membrane.
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PMID:Thyrotropin-ganglioside interactions and their relationship to the structure and function of thyrotropin receptors. 17 57

Human beta-endorphin adopts a partial helical conformation in aqueous solutions of cerebroside sulfate, ganglioside GM1, phosphatidylserine, and phosphatidic acid, but not of cerebroside and phosphatidylcholine, as evidenced by circular dichroic spectra. Addition of Ca2+ to the peptide in cerebroside sulfate solution can break up the helix; at 10 mM Ca2+ the peptide (12 microM) essentially exists in an unordered form. For comparison, sheep beta-lipotropin in acidic cerebroside sulfate solution (pH less than 4) also has a partial helical conformation of the complex between human beta-endorphin and lipids may be related to the opiatelike function of this peptide hormone.
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PMID:beta-Endorphin: formation of alpha-helix in lipid solutions. 22 73

Reconstitution of 3- to 4-week-old BALB/c nude (nu/nu) mice with 10(7) syngeneic splenocytes, 48 h before intracerebral inoculation with a temperature-sensitive (ts) mutant of VSV (tsG31 KS5), provided protection from the fatal consequences of clinical disease in 80-90% of the infected animals. Reconstitution of animals with 10(7) splenocytes, first depleted of natural killer (NK) cells with anti-asialo GM1 and complement, also afforded protection against the infectious disease. Depletion of T-lymphocytes with anti-thy-1.2 antibody and complement, however, provided little protection with approximately 40% of the animals succumbing to the virus infection within 30 days post-infection. A single intracerebroventricular injection with 14 pM of beta-endorphin, 24 h prior to viral infection, led to an increased fatality of mice previously reconstituted with T-lymphocytes but not in animals receiving only syngeneic NK cells. The increased fatality caused by the neuropeptide was antagonized by naloxone but not beta-endorphin-(1-27). Separation of splenocyte cell populations by buoyant density centrifugation demonstrated that small race lymphocytes, and not the large granular lymphocytes, were responsible for protection of nude mice from the central nervous system infection with ts-VSV. The beta-endorphin-responsive immune cells were shown to be a minor fraction of the small race T-lymphocyte population that bear the asialo-GM1 marker.
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PMID:An immune cell population that responds to beta-endorphin and is responsible for protecting nude mice from the fatal consequences of a virus infection of the central nervous system. 165 24

This study examines whether treatment with GM1 ganglioside or the corticotropin (ACTH)(4-9) analogue ORG2766 can facilitate the behavioural recovery of adult rats with medial prefrontal cortex (mPFC) lesions, as animals are impaired in their food hoarding and spatial delayed alternation performance following mPFC lesions. No ameliorating effects of GM1 treatment on performance of these behaviours were observed. Although treatment with ORG2766 somewhat improved the hoarding performance of lesioned animals, the intermediate amount of pellets hoarded was not significantly different from that of either sham-operated or vehicle-treated lesioned rats. No effect of ORG2766 treatment was observed in the spatial delayed alternation test. Further, no changes were detected in the mesocortical dopamine innervation, presumed to be involved in the neural mechanism of behavioural sparing, in response to either treatment.
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PMID:Ineffectiveness of GM1 and ORG2766 on behavioural recovery after prefrontal cortical lesions in adult rats. 838 53

A single intracerebroventricular (i.c.v.) injection of 14 pmol of beta-endorphin into 6-7-week-old BALB/c (+/+) donor mice, 24 h prior to isolation of their T lymphocytes for use for reconstitution of athymic BALB/c (nu/nu) nude mice, altered the immuno-protective effect of adoptive transfer against an intracerebral (i.c.) infection with a temperature-sensitive mutant of vesicular stomatitis virus (tsG31 KS5 VSV). Simultaneous injection of beta-endorphin and naloxone into donor animals negated the opiate effects on splenic lymphocytes. T lymphocytes, isolated from beta-endorphin-treated donors, and then depleted with anti-asialo GM1 antiserum and complement failed to demonstrate the detrimental effects of beta-endorphin.
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PMID:Transferred T lymphocytes are compromised when the donor is pretreated with beta-endorphin. 850 9

The ultra-potent opioid analgesic, etorphine, elicits naloxone-reversible, dose-dependent inhibitory effects, i.e., shortening of the action potential duration (APD) of naive and chronic morphine-treated sensory dorsal root ganglion (DRG) neurons, even at low (pM-nM) concentrations. In contrast, morphine and most other opioid agonists elicit excitatory effects, i.e., APD prolongation, at these low opioid concentrations, require much higher (ca. 0.1-1 microM) concentrations to shorten the APD of naive neurons, and evoke only excitatory effects on chronic morphine-treated cells even at high > 1-10 microM concentrations. In addition to the potent agonist action of etorphine at mu-, delta- and kappa-inhibitory opioid receptors in vivo and on DRG neurons in culture, this opioid has also been shown to be a potent antagonist of excitatory mu-, delta- and kappa-receptor functions in naive and chronic morphine-treated DRG neurons. The present study demonstrates that the potent inhibitory APD-shortening effects of etorphine still occur in DRG neurons tested in the presence of a mixture of selective antagonists that blocks all mu-, delta- and kappa-opioid receptor-mediated functions, whereas addition of the epsilon (epsilon)-opioid-receptor antagonist, beta-endorphin(1-27) prevents these effects of etorphine. Furthermore, after markedly enhancing excitatory opioid receptor functions in DRG neurons by treatment with GM1 ganglioside or pertussis toxin, etorphine shows excitatory agonist action on non-mu-/delta-/kappa-opioid receptor functions in these sensory neurons, in contrast to its usual potent antagonist action on mu-, delta- and kappa-excitatory receptor functions in naive and even in chronic morphine-treated cells which become supersensitive to the excitatory effects of mu-, delta- and kappa-opioid agonists. This weak excitatory agonist action of etorphine on non-mu-/delta-/kappa-opioid receptor functions may account for the tolerance and dependence observed after chronic treatment with extremely high doses of etorphine in vivo.
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PMID:Etorphine elicits anomalous excitatory opioid effects on sensory neurons treated with GM1 ganglioside or pertussis toxin in contrast to its potent inhibitory effects on naive or chronic morphine-treated cells. 900 33