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)

Glucagon activated adenylate cyclase in a homogenate of a pheochromocytoma over the concentration range 1 times 10 minus 8M to 1 times 10 minus 6M. Several other hormones including adrenocorticotropin, thyrotropin, parathyroid hormone and histamine were without effect. The tumor glucagon receptor was characterized and found to be similar in several ways to the glucagon receptor previously reported in normal tissue such as liver and heart. One, the receptor specifically bound 125-I-glucagon. Two, solubilization of the pheochromocytoma abolished glucagon-activation of the adenylate cyclase. Three, glucagon-responsiveness of the adenylate cyclase was partially restored by the addition of phosphatidylserine to the incubations. One major difference was observed between the glucagon receptor in tumor tissue and that in liver and heart, namely, a marked lability in 125-I-glucagon binding and adenylate cyclase activity. Within four days, despite storage in liquid nitrogen, 75% of the binding activity and all of the adenylate cyclase activity in the solubilized preparation were lost. The factor(s) responsible for this lability remains unidentified.
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PMID:Characterization of the glucagon receptor in a pheochromocytoma. 16 16

Transitional epithelium lining rabbit urinary bladders was isolated and studied in vitro. The homogeneity of the isolated epithelium was demonstrated by light and electron microscopical monitoring as well as cell culture studies. Transitional epithelium responded to epinephrine and prostaglandin E1 (PGE1) in the presence of 2mM 1-methyl, 3-isobutylxanthine (MIX) with increases in intracellular levels of cyclic adenosine 3':5'-monophosphate (cyclic AMP). Corticotropin, aldosterone, insulin, parathyroid hormone and vasopressin were slightly but significantly stimulatory under similar conditions. Glucagon and oxytocin were not stimulatory at the concentrations tested. The effects of epinephrine and PGE1 were potentiated by 2mM MIX 20-fold or greater. The cells were slightly more sensitive to PGE1 then to epinephrine. The prostaglandin produced a noticeable response at about 10nM, while effects of epinephrine were discernible at 0.1muM. Maximal responses to both effectors were seen at about 10muM. The action of 10muM epinephrine, but not 10muM PGE1, was completely abolished by 0.1mM propranolol. Responses to combinations of epinephrine and PGE1 were additive. Cyclic AMP accumulated in the incubation medium of transitional epithelial cells exposed to epinephrine, PGE1, MIX, or combinations of the agonists. The appearance of cyclic AMP in the medium was slow compared to the rate of intracellular accumulation, but reached significant levels following prolonged stimulation.
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PMID:The effects of hormones on cyclic adenosine 3':5'-monophosphate accumulation in transitional epithelium of the urinary bladder. 17 60

Cholera toxin, through adenylate cyclase activation reproduced cyclic AMP-mediated effects of thyroid-stimulating hormone (TSH) in dog thyroid slices, i.e. protein iodination, [1-14C]glucose-oxidation and hormone secretion. Iodide and carbamylcholine decreased the cyclic AMP accumulation induced by cholera toxin as well as by TSH, which supports the hypothesis of an action of these agents beyond the steps of hormone-receptor and receptor-adenylate cyclase interaction. Cooling to 20 degrees C did not impair the TSH induced cyclic AMP accumulation in thyroid slices, but completely suppressed the cholera toxin effect. This observation has been extended to other hormones and target tissues, such as the parathyroid hormone (PTH) (kidney cortex), adrenocorticotropic hormone (ACTH) (adrenal cortex) and luteinizing hormone (LH) (ovary systems). As in thyroid, cooling dissociated the cholera toxin and hormonal effects on cyclic AMP accumulation. In homogenate, cooling decreased cyclic AMP generation in the presence of cholera toxin but at 20 degrees C and 16 degrees C a cholera toxin stimulation was still observed. These results bear strongly against the hypothesis that the glycoprotein hormones TSH and LH acetivate adenylate cyclase by a mechanism identical to cholera toxin.
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PMID:Dissociation by cooling of hormone and cholera toxin activation of adenylate cyclase in intact cells. 22 51

The diagnostic importance of monoclonal antibodies assays for peptide hormones in biological fluids and for histological peptide localization is rapidly increasing. In our laboratory a general protocol has been developed for immunization and fusion that has been proven very useful, with minor modifications, for generating monoclonal antibodies against insulin, calcitonin, adrenocorticotropin and parathyroid hormone. Our procedure offers the following advantages: 1) it requires a relatively low amount of antigen; 2) it takes only 16-20 days from the first immunization to the time of fusion; 3) it mostly generates IgG producing hybrids; 4) it involves few manipulations of the animals and no i.v. injections. The widely used methods utilized for peptide carrier conjugation, few guidelines for the choice of peptide fragments suitable as immunogens and some applications of antipeptide monoclonal antibodies will be briefly discussed.
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PMID:Production and characterization of murine monoclonal antibodies to polypeptide hormones and their fragments. 165 93

Neuroendocrine differentiation in prostatic neoplasms has in the past been considered extremely uncommon. The histologic neuroendocrine patterns reported previously vary from small cell to carcinoidlike to mixed adenocarcinoma--small cell or carcinoid. The majority of the tumors reported are of the mixed variety. We reviewed 2648 autopsies, revealing 69 prostatic carcinomas, eight with neuroendocrine differentiation (five mixed adenocarcinoma--small-cell carcinoma, two "pure" small cell, and one "pure" carcinoidlike). The mean patient age was 69.5 years. One patient presented with markedly elevated serum corticotropin and another was severely hypercalcemic with elevated serum parathyroid hormone level. Three neoplasms were incidental autopsy findings. The mean survival time, after diagnosis, was 19 months for the other patients. Three of the cases were examined ultrastructurally and showed cytoplasmic processes containing membrane-bound granules in the neuroendocrine component. The areas with neuroendocrine differentiation were positive for markers as follows: neuron-specific enolase, seven of eight; prostate-specific antigen (PSA), none of eight; chromogranin A, seven of eight; synaptophysin, four of eight; and calcitonin, four of eight. Those neoplasms mixed with an adenocarcinoma component showed well-defined PSA positivity in the glandular elements. This study suggests that neuroendocrine differentiation in prostatic neoplasms may be more common than previously thought. Often, the areas with neuroendocrine differentiation are considered to represent poorly differentiated adenocarcinoma. It is important to recognize neuroendocrine components in prostatic carcinomas owing to prognostic and potential therapeutic implications.
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PMID:Neuroendocrine differentiation in prostatic carcinomas. A retrospective autopsy study. 246 64

Current understanding of the phenomenon of ectopic hormone production is largely based on a histopathological and immunocytochemical analysis of peptide hormone secreting tumours arising in non-endocrine tissues. Recent advances in the study of gene regulation show that the tissue-specific expression of genes is a highly sophisticated process and is unlikely to be disturbed by a spontaneous event such as point mutation in DNA. Study of several genes for frequently found ectopic hormones, i.e. prop-opiomelanocortin, vasopressin/neurophysin II, gastrin-releasing peptide, parathyroid hormone-related peptide, calcitonin gene-related peptide and beta-chorionic gonadotropin, suggests they are transcribed as they would be in their natural cell of origin. It is argued therefore that these data are compatible with the concept that the tumour cell of origin was capable of expressing these peptides, if only in a minor or transient manner. In one example, the ectopic ACTH syndrome, it is also necessary to explain the non-suppression of this gene's expression by elevated levels of glucocorticoids. Recent work suggests that this may result from physically present, but biologically inactive glucocorticoid receptors, a phenomenon that has occasionally been noted in hormonally inactive tumour tissue and cell lines.
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PMID:Ectopic hormone production. 247 14

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

The effects of a vegetarian low-protein, low-phosphorus diet supplemented with essential amino acids and ketoanalogues, on the serum beta-endorphin, growth hormone, parathyroid hormone, thyroid hormones (T3 and T4), pituitary TSH and total cortisol were studied in 12 male chronic uremics. beta-Endorphin decreased, as well as growth hormone. Parathyroid hormone and T3 improved significantly, reaching almost normal values. It is hypothesized that the correction of the beta-endorphin excess may account in part for the improvement of some endocrinological and metabolic effects exerted by this dietary treatment. The possible pathophysiological mechanisms which could explain the antiendorphinic action of this treatment in uremic patients are discussed, as well as the possible beneficial endocrine and metabolic effects exerted by the fall in circulating beta-endorphin.
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PMID:Effects of a low-phosphorus, low-nitrogen diet supplemented with essential amino acids and ketoanalogues on serum beta-endorphin in chronic renal failure. 253 Apr 57

A bioactive biotin-containing derivative of the synthetic bovine parathyroid hormone analog [Nle8,Nle18,Tyr34]bovine parathyroid hormone-(1-34) (bPTH-(1-34] amide was prepared by reacting the peptide with N-biotinyl-epsilon-aminocaproic acid N-hydroxysuccinimide ester. The derivative was incubated with particulate renal plasma membranes or with detergent [3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate) extracts of renal cortical membranes, and two membrane components were identified. Labeling of these components was competitively inhibited by underivatized bPTH-(1-34) or bPTH-(3-34) but not by insulin, adrenocorticotropin, or oxidized rat PTH-(1-34). PTH-binding components that were immobilized on nitrocellulose could be detected by incubating the membrane with biotinyl-bPTH-(1-34). Binding components of apparent molecular mass 68, 70, and 150 kDa were specifically labeled in plasma membranes derived from canine, human, and porcine renal cortex, rat liver, and human fibroblasts. The 68-kDa binding protein was found to be consistently more acidic than the 70-kDa binding protein in human, porcine, and canine renal membranes analyzed by two-dimensional electrophoresis. The 68-70-kDa receptor doublet could be specifically isolated by streptavidin-agarose chromatography of solubilized membrane extracts that had first been incubated with biotinyl-BPTH-(1-34). Biotinyl-bPTH-(1-34) should be useful as a tool for further characterization and purification of the PTH receptor.
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PMID:Characterization of soluble and particulate parathyroid hormone receptors using a biotinylated bioactive hormone analog. 282 99

The present study was aimed at investigating the relationship between "chronic constitutional tetany" (spasmophilia) and headache. Several adult patients presenting with neuromuscular hyperexcitability, anxiety, dysautonomia, and oculofrontal headache were subjected to a series of ion and hormone blood tests, and the results were compared with those in control subjects. Calcium and parathyroid hormone levels were significantly decreased, and phosphorus and beta-endorphin-like immunoreactivity were significantly increased. A subgroup of the patients had all four abnormalities. In most cases the family history was positive for headache. Sleep disturbances and personal histories of periodic syndrome in infancy were recorded. It is concluded that a correlation may exist between the symptoms assessed and an impairment of some ion and hormone levels. There are several traits in common with "common migraine", and our patients may form a subgroup of that group. A possible linkage between headache/tetany and the periodic and hyperventilation syndromes is discussed. The increased beta-endorphin-like immunoreactivity is putatively a reactive phenomenon.
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PMID:Calcium deficiency and supraorbital headache: a clinical study of adult subjects. 294 51


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