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)

A structure-function study of alpha-melanotropin has shown that this tridecapeptide consists of two message sequences, (-Glu)-His-Phe-Arg-Trp- and -Gly-Lys-Pro-Val-NH2, and a potentiator sequence, Ac.Ser-Tyr-Ser-Met-(Glu-), when acting on its melanophore receptors. The key elements of the message, -Phe-Arg- and -Lys-Pro-, do not correspond exactly to those responsible for eliciting the effect in other tissues. It appears that alpha-MSH contains more information than would be necessary to interact with only one complementary receptor site; therefore, the topography of the hormone exposed to the binding site may be different on contact with the receptors of different target cells. To further investigate this aspect, new methods for the isolation and characterization of functional receptors must be developed. We are investigating the use of chemically well-defined, biologically active, covalent hormone-macromolecule complexes for this purpose. Another approach utilizes model receptors with a recognition pattern similar to that of the biological receptor, as described in this communication for certain highly specific antibodies.
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PMID:Mechanism of alpha-melanotropin action. 20 1

The purpose of this investigation was to elucidate the biological significance of lysine11 and of the tripeptide sequence =Lys-Pro-Val-NH2 for the biological activity of alpha-melanocyte-stimulating hormone. To this end the in vitro melanotropic activities of twenty-four synthetic peptides related to the hormone were determined. Extension or reduction of the length of the lysine11 side chain results in a marked decrease of the melanotropic potency of the respective analogue. The C-terminal tripeptide (11--13), the tetrapeptide (10--13), and the pentapeptide (9--13) were found to be hormonally active in the same order of magnitude as the central hexapeptide (5--10). The following conclusion was drawn: alpha-MSH possesses (in contrast to ACTH) two message sequences (active sites), (i)-Glu-His-Phe-Arg-Trp-, and (ii)-Gly-Lys-Pro-Val-NH2 which are capable of independently triggering the hormone receptor responsible for melanin dispersion. Thus, despite the close structural similarity of the two hormones, alpha-MSH and ACTH appear to react with their respective target cell receptors by quite different chemical mechanisms, implying different receptor structures.
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PMID:Hormone-receptor interactions. The message sequence of alpha-melanotropin: demonstration of two active sites. 21 33

An accurate, highly reproducible and sensitive bioassay for melanocyte-stimulating hormone (MSH) using the skin of Anolis carolinensis in vitro is described. The time taken for green Anolis skin fragments to change to a specific, visually assessed, green-brown color is dose-related, and this forms the basis of the new assay. The method is simple to perform, and 1 person may assay 20 samples in a day using the dorsal skin from a single adult lizard. The mean dose-response ranges between 48 X 10(-12) and 375 X 12(-12) M (38 to 625 pg/ml). Using the assay, alpha-MSH, beta-MSH, ACTH (4-10), and ACTH (1-10) were equipotent on a molar basis. For repeated bioassay of rat pituitary extracts, the dose-response curves were highly significant, and only 1 of the 9 pituitary dose-response curves deviated significantly from the slope of the standard alpha-MSH curve. The index of precision, lambda, for the 9 pituitary bioassays ranged between 0.037 and 0.081, while the mean 95% fiducial limits were -6.6 and 7.1% on either side of the estimated potency. The new rate method is compared with an earlier quantal method which also uses the isolated skin of Anolis carolinensis. The quantal method does not have dose-response characteristics and is therefore less accurate and reproducible than the new method; the coefficient of variation for repeated bioassay of the same pituitary extracts ranged from between 12 to 20% for the quantal method and between 2.9 to 5.7% for the new rate method.
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PMID:Sensitive new in vitro bioassay for melanocyte-stimulating activity using the skin of Anolis carolinensis. 21 84

The cerebral uptake of subcutaneously injected [3H]2-deoxy-D-glucose (2DG) in 16 brain regions was examined following 30 noncontingent random footshocks or the acute injection of saline, ACTH1-24 (0.5 microgram/g), ACTH/MSH4-10 (0.25 microgram/g), [D-Phe7]ACTH4-10 (0.25 microgram/g), [Met4SO2,D-Lys8,Phe9]ACTH4-9 (0.01 microgram/g), ALPHA-MSH (0.5 microgram/g), corticosterone (2.5 microgram/g) or lysine vasopressin (0.05 microgram/g). Footshock selectively decreased 2DG uptake in parietal cortex and brain stem, and increased that in the hypothalamus. Whole brain 2DG uptake was decreased by injection of saline or most of the hormones relative to uninjected animals, but this effect was probably peripheral since plasma glucose content was increased by the injections. The only regionally specific effect of the hormones was an increased 2DG uptake in olfactory bulb by saline, ACTH/MSH4-10 And corticosterone relative to uninjected animals. Since alpha-MSH had been reported previously to decrease blood flow (measured by antipyrene uptake) in all brain regions except occipital cortex [5,6], we directly compared antipyrene uptake with 2DG uptake in the same animals using a double-isotope procedure. The results revealed an increase in 2DG uptake relative to antipyrene in cortical regions relative to subcortical regions, contradicting earlier assumptions [19].
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PMID:Mouse brain deoxyglucose uptake after footshock, ACTH analogs, alpha-MSH, corticosterone or lysine vasopressin. 21 66

Intracerebroventricular injection of antiserum to alpha--MSH induces a weak reduction of passive avoidance latencies after administration prior to retention testing. Administration of antiserum to ACTH 1--24 induces a more marked effect in this respect, whereas injection of a combination of these antisera results in the strongest reduction of passive avoidance retention. No effect of this treatment is observed when these antisera are injected immediately after the learning trial. In active avoidance behavior a facilitation of extinction of the response is observed after intracerebroventricular administration of the antisera prior to each extinction session. This effect is comparable with the one observed in passive avoidance behavior. From these data it is suggested that ACTH and alpha-MSH play an important role in processes related to the retrieval of information stored in the brain.
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PMID:Involvement of ACTH and MSH in active and passive avoidance behavior. 21 76

It was admitted that human beta-MSH was responsible for the hyper-pigmentation observed in some syndromes associated with ACTH hypersecretion. beta-LPH was a pituitary polypeptide, containing the entire sequence of beta-MSH in its fragment 37-58, and the physiological role of which remained unknown. alpha-MSH and CLIP (Corticotrophin-like Intermediary Peptide) were thought to be specific of certain species possessing a distinct pituitary pars intermedia. Recent data give new insight upon some of these conceptions. beta-MSH seems not to exist in man; it is almost established now that plasma "Immunoreactive beta-MSH" (IR-beta-MSH) is in fact beta- and/or gamma-LPH. In chronic renal failure plasma IR-beta-MSH is elevated because of a decreased plasma disappearance rate, whereas ACTH is normal. Good evidence suggests that both LPH and ACTH are synthesized in the same pituitary cell within a common polypeptidic precursor. Endogenous peptides with morphinomimetic activity (Endorphins) have been isolated from brain and hypophysis; they are all made up of different fractions of beta-LPH-C-terminal fragment 61-91; It is likely that they represent a new class of brain neurotransmitters involved in some functions of the central nervous system, structural similarities suggest that beta-LPH may be the biosynthetic precursor of Endorphins, however such a hypothesis remains to be clearly demonstrated.
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PMID:[Recent data on the group of melanotropic and lipotropic pituitary hormones (MSH-LPH) and on the brain morphinomimetic peptides (endorphins)]. 21 12

The number of dendrites and the total length of dendrites in the epidermal melanocytes positive for the dopa reaction were shown to increase when newborn mice were injected with alpha-MSH or DBc-AMP. Moreover, both indices of the degree of dendritogenesis increased when skin explants of newborn mice were cultured in medium containing alpha-MSH or DBc-AMP. Electron-microscopic observation showed that the number of melanosomes was also increased by alpha-MSH treatment. Many mature melanosomes were observed in the dendrites of the epidermal melanocytes of alpha-MSH-injected mice. Highly dendritic melanocytes seem to be the cells stimulated by MSH to form melanosomes and translocate them to dendrites. Dendritogenesis stimulated by the hormone was suppressed by actinomycin D or cycloheximide, suggesting that the dendritogenesis in the epidermal melanocytes requires de novo transcription and translation.
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PMID:Stimulation of dendritogenesis in the epidermal melanocytes of newborn mice by melanocyte-stimulating hormone. 21 54

Hypophysectomy increases both periosteal resorption and endosteal apposition along the femur diaphysis in rat. Administration of alpha-MSH decreased the periosteal resorption but had no effect on the endosteal apposition. ACTH had only minor effects on the endosteum. Thus, alpha-MSH and ACTH, in the doses used, have different effects on cortical bone in rat. The effect of alpha-MSH on cortical bone could be an effect of the hormone alone or by its stimulation of other factors.
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PMID:Influence of alpha-MSH and ACTH on cortical bone remodelling in hypophysectomized rats. 21 12

The effects of K+-enhanced and Ca++-free media on alpha-MSH and adrenocorticotropic hormone (ACTH) release from superfused neurointermediate lobe (NIL) were studied in the same experiments. High K+ caused reversible and repeatable inhibition of alpha-MSH release and stimulation of ACTH release, Removal of Ca++ impaired the effect of K+, irreversibly for alpha-MSH and reversibly for ACTH. The existence of both melanotrophic and corticotrophic cells within the intermediate lobe (IL) of rat hypophysis could account for the different effects of ionic modifications on in vitro alpha-MSH and ACTH release.
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PMID:Different effects of K+ and Ca++ on alpha-MSH and ACTH release from superfused neurointermediate lobe of the rat hypophysis. 22 May 51

We propose than an alarm mechanism is operative in animals, designed to regulate neuromuscular irritability by regulating [Ca2+]. Epinephrine or corticotropin (ACTH), injected intramuscularly into animals, causes a hypercitricemia, resulting in decreased [Ca2+]. This increases muscular excitability to facilitate escape. To avoid over reaction, [Cl-] is shifted into the plasma without a concomitant shift of Na+, thus generating an acidosis and an increase in ionization of Ca. Plasma pH, pCO2, total CO2, and [K+] decrease, and [Mg2+] increases. The acidosis, decrease in K+, and increase in [Mg2+] serve to counteract the effect of the decrease in [Ca2+], to protect against tetany. In the rabbit the hypercitricemia observed upon ACTH administration is accompained by a severe hypocalcemia and drop in blood pressure, resluting in tetanic convulsions. This seems to indicate calcitonin release, independent of the hypercitricemia. Thyroidectomized rabbits show only mild hypocalcemia when given ACTH, but develop a severe acidosis and typical grand mal epileptiform seizures. Administration of ACTH and then calcitonin to the goat, an animal resistant to the effects of ACTH alone, simulates the effect observed in the rabbit with respect to changes in blood components and blood pressure. Changes in the blood in the goat and rabbit resemble those in humans before an epileptic seizure. alpha-Melanotropin, containing a portion of the ACTH sequence, reacts in a manner similar to ACTH but more rapidly.
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PMID:Clinical biochemistry of epilepsy. II. Observations on two types of epileptiform convulsions induced in rabbits with corticotropin. 22 Nov 37


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