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 saponin fraction was isolated from Momordica charantia seeds by delipidation, saline extraction, ammonium sulfate precipitation, and extraction of the resulting supernatant with n-butanol. Thin-layer chromatography, in the upper phase of the n-butanol--ethyl acetate--water (4:1:5, by volume) system on plastic sheets coated with silica gel 60 F254, revealed the presence of a single spot after spraying with 10% sulfuric acid. The lack of contamination of the saponin preparation with proteins was judged by the absence of protein bands in sodium dodecyl sulfate--polyacrylamide gel electrophoresis, agarose electrophoresis and agarose diffusion, and by the absence of an absorption maximum around 278 nm. The saponin acted as a noncompetitive inhibitor of corticotropin, glucagon, and epinephrine in lipolysis in isolated rat adipocytes, and it also antagonized dibutyryl cAMP induced lipolysis. The antilipolytic activity was resistant to heat, trypsin, chymotrypsin, pronase, and glutathione, in keeping with the chemical nature of saponin. Incorporation of [3-3H]glucose into lipid was inhibited. Adipocyte viability and ATP content were not affected by the saponin, suggesting that its inhibitory effects on lipolysis and lipogenesis were not due to an adverse effect on cell viability.
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PMID:A steryl glycoside fraction from Momordica charantia seeds with an inhibitory action on lipid metabolism in vitro. 302 Nov 85

We have shown that two unrelated prostaglandin antagonists block both thyrotropin (TSH) and prostaglandins E (PGE(1), PGE(2)) stimulation of thyroidal adenyl cyclase activation and cyclic 3',5'-adenosine monophosphate (cAMP) formation, suggesting that prostaglandins play an important role in regulating thyroid function. To further explore this postulate, we measured prostaglandin content by radioimmunoassay in homogeneous bovine thyroid cell preparations in the presence and absence of TSH. Antibodies to albumin-conjugated PGE(1) and PGF(2alpha) showed specificity for prostaglandins E and F, respectively, but reacted, albeit far less effectively, with heterologous prostaglandins. A double antibody system was used to separate free from antibody-bound PGE(1)-(3)H and PGF(2alpha)-(3)H. Thyroid cells were extracted with ethanol/ethyl acetate and the various prostaglandins separated on silicic acid columns. Recoveries of added PGE(1)-(3)H and PGF(2alpha)-(3)H through the extraction and separation procedures ranged from 50-80%. The sensitivity of the method was 10-50 pg. Basal thyroid cell content of PGE(1) and PGF(2alpha) "equivalents" varied between cell preparations (range = 2-6 ng/0.2 ml cell suspension) but, in each instance, remained constant during 5-30-min incubations at 37 degrees C. TSH, 10-100 mU/ml, increased the levels of cell PGE(1) and PGF(2alpha) "equivalents" 30-80% above basal during 5-15-min incubations. The stimulatory effect was specific for TSH, no increase in PGE(1) or PGF(2alpha) "equivalent" levels being seen with luteinizing hormone (LH), human growth hormone (HGH), adrenocorticotropic hormone (ACTH), or glucagon. These data support the thesis that prostaglandins may mediate TSH effects on thyroid.
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PMID:Thyrotropin increases prostaglandin levels in isolated thyroid cells. 462 70

The effect of colchicine was studied on the rapid, reversible darkening of frog skin under the influence of melanocyte-stimulating hormone (MSH). Darkening is due to dispersion of melanin granules in melanocytes and is thought to be accompanied by a gel-to-sol cytoplasmic transformation. After subsequent washing, the skin lightens, with aggregation of melanin granules and cytoplasmic gelation. Preincubation of skin with colchicine had the following effects: 1. Darkening induced by MSH was increased in comparison to control skins, and on removal of MSH, lightening was inhibited. Inhibition was a function of both concentration (1 x 10(-5) to 9 x 10(-5)M) and exposure time (2 to 30 minutes). Once established, inhibition was maintained throughout the remainder of the experiment. 2. The same effects were noted (a) when darkening was effected by agents other than MSH (ATP) 0.9 x 10(-3)M; caffeine, 5.2 x 10(-3)M; ethyl acetate, 0.8 x 10(-2)M), and (b) when lightening was effected by addition of chemical agents (melatonin, 4.3 x 10(-10)M; hydrocortisone, 1 x 10(-3)M; norepinephrine, 1 x 10(-3)M), instead of by washing. 3. Colchicine alone produced a gradual, irreversible, dosage-dependent darkening over several hours. This darkening was inhibited by melatonin, 4.3 x 10(-10)M. The melanocyte model is used to construct a general theory of colchicine action on living cells, an action resulting in decreased protoplasmic viscosity. In this formulation colchicine lowers the potential limit of protoplasmic gelation, and does it rapidly, reversibly, in low concentration, in a dosage-dependent manner, and without killing the cell. The theory allows interpretation of "synergism" and "antagonism" to colchicine by other substances. It suggests a tentative approach to the understanding of colchicine action in acute gouty arthritis, where interference with ameboid activities of polymorphonuclear leukocytes is one possible aspect of the anti-inflammatory effect of colchicine. Finally, the colchicine-treated melanocyte is viewed as a good, live physical model that can be used to elucidate some fundamental biological properties.
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PMID:ON THE ACTION OF COLCHICINE, THE MELANOCYTE MODEL. 1431 40

Bioassay-guided fractionation of Curcuma longa by solvent partitioning and purification with octadecylsilane open column chromatography yielded a partial purification. The active 80% methanol chromatographic fraction from the ethyl acetate layer [partial purification from C. longa (PPC)] was used to investigate the alpha-melanocyte-stimulating hormone (alpha-MSH)-stimulated melanogenesis signal pathway in B16F10 cells. In cells stimulated alpha-MSH, PPC inhibited cellular melanin contents, tyrosinase activity and expression of melanogenesis-related proteins including microphthalmia-associated transcription factor (MITF), tyrosinase and tyrosinase-related proteins (TRP). Melanogenesis-regulating signalling such as mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/Akt was activated by PPC in alpha-MSH-stimulated B16F10 cells. The suppressive activity of PPC on alpha-MSH-induced melanogenesis was abrogated by selective inhibition of MEK/ERK (PD98059) and PI3K (LY294002). MEK/ERK or Akt activation by PPC may contribute to reduced melanin synthesis via MITF and its downstream signal pathway including tyrosinase and TRPs in alpha-MSH-induced melanogenesis.
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PMID:Partially purified Curcuma longa inhibits alpha-melanocyte-stimulating hormone-stimulated melanogenesis through extracellular signal-regulated kinase or Akt activation-mediated signalling in B16F10 cells. 1946 2