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)

Electrical stimulation of rat posterior lobes in vitro inhibited bioactive corticotropin (ACTH) release from the intermediate lobe and promoted the release of corticotropin-releasing factor(s) (CRF). Both effects were calcium dependent. Released posterior lobe CRF was inactivated by thioglycolate, and the CRF activity could be accounted for by vasopressin. Results suggest strongly that vasopressin is the predominant CRF released from neurohypophysial axons, and that intermediate lobe ACTH release is submitted to an inhibitory control.
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PMID:Release of corticotropin and corticotropin-releasing factors from rat posterior pituitary in vitro. 624 58

Effects of corticotropin-releasing hormone (CRH) on the superoxide anion (O2-) production in macrophages (M phi s) were investigated. CRH by itself failed to induce the O2- production of rabbit peritoneal M phi s elicited with thioglycollate medium. However, M phi s preincubated with CRH showed significant enhancement of O2- production following stimulation with a chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP), at CRH concentrations from 10(-10) to 10(-7) M. Maximal enhancement of O2- production was obtained with 10 min preincubation with CRH for FMLP stimulation. CRH had no effect on O2- production when stimulated with phorbol 12-myristate 13-acetate. Neither corticotropin nor beta-endorphin augmented the O2- production induced with FMLP. These results indicate that CRH has priming effects on FMLP-induced O2- production of rabbit peritoneal M phi s, although the underlying mechanism remains to be clarified.
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PMID:Corticotropin-releasing hormone enhances the superoxide anion production of rabbit peritoneal macrophages stimulated with N-formyl-methionyl-leucyl-phenylalanine. 810 31

Previous studies from our laboratory have characterized a naloxone-insensitive beta-endorphin (beta-End) receptor on the human pro-monocytic cell line U937. Since monocytes are macrophage precursors, we sought to identify and characterize this site on fully differentiated effector macrophages. Mice (ICR females, 6-8 wk old) were injected (i.p.) with 1 mL of thioglycollate to induce an inflammatory response. Elicited cells were harvested 3 d later by lavage. Macrophages were enriched by adherence and analyzed via radioreceptor assay (with [125I] beta-End, 2,000 Ci mmol-1) as either intact cells or membrane preparations. Scatchard analysis revealed a single saturable binding site for beta-End (Kd = 9.75 +/- 2.6 x 10(-9) M; 8218 +/- 2360 sites/cell). Competition studies showed that other opiate receptor ligands including naloxone, DAMGO, U69593, or 2,5 DPDP-enkephalin were ineffective at displacing [125I] beta-End when compared to unlabeled beta-End. Analysis of competition studies utilizing fragments and analogs of beta-End revealed that beta-End (6-31) and beta-End (1-5, 16-31) were equipotent, and N-acetylated beta-End was less potent, than beta-end (1-31) in displacing [125I] beta-End binding. In contrast, beta-End (1-27) and beta-End (28-31) were ineffective. In summary, we have identified a naloxone-resistant beta-End binding site on murine peritoneal macrophages that is similar to one we have previously characterized on U937 cells and cultured murine splenocytes.
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PMID:Characterization of a naloxone-insensitive beta-endorphin receptor on murine peritoneal macrophages. 904 61

The effects of single injections of 2-deoxyglucose or 2-mercaptoacetate on the expression of mRNA of neuropeptide Y, pro-opiomelanocortin, and melanin-concentrating hormone in rat hypothalamus were studied by in situ hybridization in order to elucidate the role of these neuropeptides in the mechanisms of alimentary behavior caused by decreased levels of available fatty acids and glucose. The levels of neuropeptide Y mRNA in arcuate nuclei neurons are significantly increased under conditions of glucose deficiency, while the synthesis of melanin-concentrating hormone in the lateral hypothalamic neurons is increased in fatty acid deficiency. These data indicate that glyco- and lipodeprivation are different metabolic signals activating various neuropeptide systems responsible for alimentary behavior.
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PMID:Effects of blockers of carbohydrate and lipid metabolism on expression of mRNA of some hypothalamic neuropeptides. 1117 38