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)

gamma MSH, a putative hormone in the N-terminal region of the ACTH/beta-endorphin (beta-EP) precursor protein, was studied by RIA with an antiserum against gamma 3MSH in ACTH-producing mouse pituitary tumor cells, AtT-20/D16v. Serial dilution of the culture medium or the cell extract gave parallel lines to the standard curve in the RIA for gamma MSH. Rat median eminence extracts enhanced the release of gamma MSH-like immunoreactivity (gamma MSH-LI) concomitant with ACTH-like immunoreactivity (ACTH-LI) and beta-EP-like immunoreactivity (beta-EP-LI). Dexamethasone suppressed the release of gamma MSH-LI as well as ACTH-LI and beta-EP-LI. Gel exclusion chromatography of the culture medium and the cell extract has revealed that gamma MSH-LI consists of two peaks; one eluted near the elution position of beta-lipotropin and the other near the elution position of beta-EP. There was no peak corresponding to the elution position of synthetic gamma 3MSH. However, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) has demonstrated that gamma MSH-LI migrated at five positions with molecular weights of 31K, 21-23K, 16-17K, 13-14K, and 3.8K, respectively. The 31K gamma MSH coincided with the migration position of 31K ACTH of 31K beta-EP, and 21-23K gamma MSH coincided with the position of 21-23K ACTH on SDS-PAGE. The 16-17K gamma MSH coincided with the mouse 16K fragment (reported by Eipper and Mains) of ACTH-beta-lipotropin precursor protein in the migration in SDS-PAGE and in immunoreactivity to anti-gamma MSH antiserum. [3H]Glucosamine was incorporated into 16K, 13K, and 3.8K gamma MSH. These results suggest that AtT-20/D16v cells produce gamma MSH-LIs with molecular weights of 31K, 21-23K, 16-17K, 13-14K, and 3.8K, and they are secreted concomitantly with ACTH-LI and beta-EP-LI.
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PMID:Characterization of gamma-melanotropin-like immunoreactivity and its secretion in an adrenocorticotropin-producing mouse pituitary tumor cell line. 628 79

beta-Endorphin, a pituitary morphino-mimetic peptide, was identified in a culture medium derived from a human corticotropic adenoma. Secretion products from cultured human cells derived from a small-cell carcinoma of the lung were shown to contain a high molecular weight precursor analagous to pro-opiocortin: this molecule is a polypeptide of the order of 28,000 daltons the enzymatic processing of which leads to the coordinated and simultaneous release of different peptide fragments: ACTH, beta- and gamma-lipotropins, beta-endorphin, fragment 16 K and gamma 3-MSH. All these peptides have been identified in human plasma, and pituitary and non-pituitary tumor extracts. Their plasma concentrations vary in a parallel manner, beta-endorphin and a peptide very similar to beta-MSH have been detected in human hypothalamus.
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PMID:[ACTH, beta-endorphin, lipotropins, and other pro-opiocortin-derived peptides: a new family of hormones (author's transl)]. 628 90

A pituitary tumor from a patient with severe Cushing's disease and marked hyperprolactinemia was extensively studied by immunohistochemical techniques. Tissues from two separate areas of the adenoma were found to contain similar cell proportions of PRL as well as ACTH and related peptides (beta-lipotropin, beta-endorphin, and alpha MSH). The tumor was composed of approximately 70% immunoreactive PRL cells and 5% ACTH-containing cells. Double immunostaining revealed that PRL or ACTH and related peptides were found in two distinct populations of tumor cells. These results document for the first time inappropriate synthesis and secretion of an unusual combination of pituitary hormones from a mixed pituitary adenoma.
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PMID:Concurrent production of adrenocorticotropin and prolactin from two distinct cell lines in a single pituitary adenoma: a detailed immunohistochemical analysis. 628 57

Chronic excess of glucocorticoids results in Cushing's syndrome in humans. A common cause of excess cortisol secretion is the presence of an adrenocorticotropin secreting pituitary tumor which stimulates the adrenal cortex to produce excess glucocorticoids. ACTH-secreting AtT-20 mouse pituitary cells transplanted subcutaneously in oestrogenized athymic nude mice form tumors rapidly. Six weeks after receiving the tumor transplants, the mice weighed 45% more than normal mice due to the increase in body fat. The tumor-bearing mice exhibit the familial "buffalo hump" appeaance due to the abnormal distribution of body fat. The adrenal glands of the tumor-bearing animals are enlarged due to hypertrophy of the zona fasciculata. The foamy looking fasciculata cells in normal mice were converted to dense, eosinophilic cells in the tumor-bearing mice. Transplantation of normal pituitary glands to athymic nude mice with or without oestrogen treatment did not produce these morphological changes. The experimental model described here may be useful for future studies of Cushing's syndrome.
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PMID:Transplantation of ACTH-secreting pituitary tumor cells in athymic nude mice. 629 Dec 29

The electrical and secretory activities of mouse pituitary tumor cells (AtT-20/D-16v), which contain and release the ACTH/beta-endorphin family of peptides, were studied by means of intracellular recordings and radioimmunoassays. Injection of depolarizing current pulses evoked action potentials in all cells and the majority (82%) displayed spontaneous action potential activity. Action potentials were found to be calcium-dependent. Barium increased membrane resistance, action potential amplitude and duration, and release of ACTH and beta-endorphin immunoactivity. Isoproterenol increased both action potential frequency and hormone secretion. Raising the external calcium concentration increased the frequency and amplitude of the action potentials and stimulated secretion of ACTH and beta-endorphin immunoactivity. Thus, stimulation of secretory activity in AtT-20 cells was closely correlated with increased electrical activity. However, a complete blockade of action potential activity had no effect on basal hormone secretion in these cells. These results suggest that the mechanisms underlying stimulated hormone secretion are different from those responsible for basal secretory activity. It is proposed that the increased influx of calcium due to the increased action potential frequency initiates the stimulated release of hormone from these cells.
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PMID:Correlation between electrical activity and ACTH/beta-endorphin secretion in mouse pituitary tumor cells. 629 40

The 41-residue synthetic ovine corticotropin-releasing factor (CRF; corticoliberin) has been shown to stimulate release of corticotropin (adrenocorticotropic hormone; ACTH) and beta-endorphin from AtT-20/D16-16 mouse pituitary tumor cells. Phospholipid methylation of phosphatidylethanolamine to phosphatidylcholine with S-adenosylmethionine as methyl donor has been suggested as a possible membrane transduction mechanism for some receptor-induced events. CRF increased phospholipid methylation in pituitary tumor cells at concentrations that also stimulated immunoreactive ACTH secretion, and both processes increased linearly and in parallel with time. The methionine sulfoxide derivative of CRF was less potent than CRF was in stimulating both phospholipid methylation and hormone secretion, and the COOH-terminal free acid analogue of CRF had no effect on either process. CRF-induced increases in phospholipid methylation and ACTH secretion were reduced when cells were treated with the phospholipid methyltransferase inhibitors 3-deazaadenosine and L-homocysteine thiolactone. These CRF-stimulated effects were also blocked by the glucocorticoid dexamethasone. It is suggested that phospholipid methylation may be a CRF receptor-mediated event associated with ACTH release in pituitary tumor cells.
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PMID:Corticotropin-releasing factor stimulates phospholipid methylation and corticotropin secretion in mouse pituitary tumor cells. 629 95

Pre-exposure of mouse anterior pituitary tumor cells (A+T-20/D16-16) to (-) isoproterenol reduces the ability of this beta-adrenergic agonist to restimulate cyclic AMP synthesis or adrenocorticotropin hormone (ACTH) release from these cells. This beta-adrenergic receptor desensitization is time and dose-dependent, recoverable and specific for beta-receptors. Longer pretreatment times are required to decrease beta-receptor density than to induce receptor desensitization. This initial beta-receptor refractoriness involves an uncoupling of the receptor from adenylate cyclase since (-) isoproterenol treatment does not alter forskolin-activated cyclic AMP formation or ACTH release. In addition to diminishing beta-receptor responsiveness, (-) isoproterenol treatment induces a prolonged elevation of basal ACTH release. This finding indicates that the intracellular events leading to ACTH secretion may also be altered during the desensitization process.
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PMID:Desensitization of beta 2-adrenergic receptors and adrenocorticotropin release. 629 84

AtT-20 cells comprise a mouse anterior pituitary tumor cell line that synthesizes and secretes adrenocorticotropin hormone (ACTH). beta-Adrenergic receptors were characterized on AtT-20 cells using receptor binding methodology and the ability of beta-receptor agonists to stimulate intracellular cyclic adenosine 3':5'-monophosphate (cAMP) formation and the release of ACTH immunoreactivity. The density of beta-receptors on membrane preparations of these cells is 64 fmol/mg of protein and their affinity constant (KD value) for tritiated dihydroalprenolol is 11 nM. The binding of [3H] dihydroalprenolol to AtT-20 cells is stereoselectively inhibited by propranolol and isoproterenol but is not affected by phentolamine. The beta-receptors on these cells appear to be of the beta 2-receptor subtype since a selective beta 2-receptor agonist, salmefamol, can inhibit [3H]dihydroalprenolol binding, whereas practolol, a beta 1-receptor blocker, is ineffective. (-)-Isoproterenol stimulates cAMP formation in AtT-20 cells and this effect is blocked by dl-propranolol. Both l-epinephrine and l-norepinephrine induce dose-dependent increases in cAMP formation with the former agonist being more potent. Salmefamol also stimulates cAMP formation in these cells. The secretion of ACTH from AtT-20 cells is induced by (-)-isoproterenol as well as by other adrenergic agonists. The isoproterenol effect on ACTH release is stereoselective, calcium dependent, and blocked by dl-propranolol but not by phentolamine or practolol.
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PMID:Activation of beta 2-adrenergic receptors on mouse anterior pituitary tumor cells increases cyclic adenosine 3':5'-monophosphate synthesis and adrenocorticotropin release. 630 Mar 55

A cytosolic peptide activator (Mr approximately equal to 2,200) of cholesterol side-chain cleavage in the adrenal cortex has been isolated from normal corticotropin-treated rats and from rats implanted with the MtT/F4 corticotropin-secreting pituitary tumor. The isolation techniques were those common to peptide hormone purification, including tissue extraction into a highly acidic medium, gel filtration, and reverse-phase HPLC. The amino acid composition has been determined on acid hydrolysates. The activity of this adrenal peptide is acutely increased in hypophysectomized animals treated with corticotropin, and this increase is blocked by cycloheximide. The addition of activator peptide to adrenal mitochondrial preparations results in a rapid stimulation of pregnenolone formation that is dependent on activator concentration and a source of NADPH. In the absence of NADPH, addition of activator peptide to adrenal mitochondria increases the rate of cholesterol association with side-chain cleavage cytochrome P-450. The peptide therefore exhibits properties that are believed to characterize the hypothetical corticotropin-dependent labile activator of adrenal steroidogenesis.
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PMID:Cholesterol side-chain cleavage in the rat adrenal cortex: isolation of a cycloheximide-sensitive activator peptide. 630 Aug 76

Using HeLa whole cell extracts, we have demonstrated that transcription in vitro of the cloned human and bovine corticotropin/beta-lipotropin precursor genes is initiated accurately and efficiently. DNA sequences required for promoter function have been assessed by using a series of 5'-deletion mutants of a fusion gene that contains the 5'-flanking sequence and capping site of the human corticotropin/beta-lipotropin precursor gene and the structural sequence of the herpes simplex virus thymidine kinase gene. The results obtained have shown that the region between 22 base pairs and 35 base pairs upstream from the capping site is essential for the correct and efficient transcriptional initiation in vitro. Thus, the 'TATA box' present in this region seems to be the main promoter element for transcription of the human corticotropin/beta-lipotropin precursor gene in the HeLa cell-free system. We have also developed a transcription system in vitro from the corticotropin-producing mouse pituitary tumor cell line AtT-20 in culture. Deletion mapping of the fusion gene promoter has indicated that the 'TATA box' region is required for the accurate and efficient transcriptional initiation in this system as well. Characteristic of this system is that the deletion of the sequence lying between 53 base pairs and 59 base pairs upstream from the capping site increases the transcriptional efficiency. Because this effect is observed in the AtT-20 cell-free system, but hardly in the HeLa cell-free system, it seems reasonable to assume that the interaction of this upstream sequence with some factor(s) in the AtT-20 cell extract is responsible for the modulation of transcription of the human corticotropin/beta-lipotropin precursor gene.
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PMID:Sequence requirement for transcription in vitro of the human corticotropin/beta-lipotropin precursor gene. 630 52


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