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)

Treatment of isolated rat adipocytes with adrenocorticotropin (ACTH) caused a 1.5-fold increase in phospholipid methyltransferase activity within 5 min. This effect of ACTH was concentration-dependent with maximal activation at 2 milliunits/ml ACTH, and was reproduced by dibutyryl cyclic AMP. ACTH (2 milliunits/ml) caused an increase in the Vmax value of phospholipid methyltransferase without changing the Km for S-adenosyl-L-methionine. Insulin caused a concentration-dependent inhibition of both control and ACTH-stimulated phospholipid methyltransferase. Half-maximal inhibition by insulin was demonstrated with 5 microunits/ml insulin in control cells and with 25 microunits/ml insulin in ACTH-stimulated cells. The rapid and sensitive activation of adipocyte phospholipid methyltransferase by ACTH and inhibition by insulin are consistent with a role for this pathway in the hormonal response of the adipocyte.
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PMID:Adrenocorticotropic stimulation and insulin inhibition of adipocyte phospholipid methylation. 298 71

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