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)

We have characterized the specific binding of human beta-endorphin (1-31) to novel binding sites which are formed in human plasma or serum in the presence of heparin. The formation of the binding sites is temperature-dependent and does not occur in the presence of other anticoagulants, such as sodium-EDTA, sodium-oxalate, or sodium-citrate. The specific binding of 125I-beta H-endorphin to heparin-induced binding sites in human plasma is saturable and reversible. It is not inhibited by morphine or naloxone or by various opioid peptides which share their NH2-terminal opioid-active sequence with beta H-endorphin. In contrast, binding is inhibited by the COOH-terminal beta H-endorphin fragment Gly-Glu indicating that binding is to nonopioid sites. Electroimmunoprecipitation techniques revealed that these binding sites are identical with S protein/vitronectin or derivatives thereof. S protein is a plasma alpha 1-glycoprotein involved in attachment and spreading of cells and also in blood coagulation and complement activation. It is possible that the interaction of beta-endorphin with S protein is of physiological significance.
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PMID:Characterization and identification of heparin-induced nonopioid-binding sites for beta-endorphin in human plasma. 282 69

Epidemiological information on calcium oxalate urolithiasis is reviewed and interpreted according to a proposed stress-related mechanism. This mechanism involves hypothalamo-hypophyseal secretion firstly of vasopressin which acts directly to produce hypertonic urine and secondly of adrenocorticotropin which acts via a secondary hyperparathyroid mechanism to raise serum calcium levels.
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PMID:Stress as a principal cause of calcium oxalate urolithiasis. 302 44

The factors regulating Ca2+ transport by isolated sarcoplasmic reticulum (SR) vesicles have been studied using the fluorescent indicator Fluo-3 to monitor extravesicular free [Ca2+]. ATP, in the presence of 5 mM oxalate, which clamps intravesicular [Ca2+] at approximately 10 microM, induced a rapid decline in Fluo-3 fluorescence to reach a limiting steady state level. This corresponds to a residual medium [Ca2+] of 100 to 200 nM, and has been defined as [Ca2+]lim, whilst thermodynamic considerations predict a level of less than 1 nM. This value is similar to that measured in intact muscle with Ca2+ fluophores, where it is presumed that sarcoplasmic free [Ca2+] is a balance between pump and leaks. Fluorescence of Fluo-3 at [Ca2+]lim was decreased 70% to 80% by histidine, imidazole and cysteine. The K0.5 value for histidine was 3 mM, suggesting that residual [Ca2+]lim fluorescence is due to Zn2+. The level of Zn2+ in preparations of SR vesicles, measured by atomic absorption, was 0.47+/-0.04 nmol/mg, corresponding to 0.1 mol per mol Ca-ATPase. This is in agreement with findings of Papp et al. (Arch. Biochem. Biophys., 243 (1985) 254-263). Histidine, 20 mM, included in the buffer, gave a corrected value for [Ca2+]lim of 49+/-1.8 nM, which is still higher than predicted on thermodynamic grounds. A possible 'pump/leak' mechanism was tested by the effects of varying active Ca2+ transport 1 to 2 orders with temperature and pH. [Ca2+]lim remained relatively constant under these conditions. Alternate substrates acetyl phosphate and p-NPP gave similar [Ca2+]lim levels even though the latter substrate supported transport 500-fold slower than with ATP. In fact, [Ca2+]lim was lower with 10 mM p-NPP than with 5 mM ATP. The magnitude of passive efflux from Ca-oxalate loaded SR during the steady state of [Ca2+]lim was estimated by the unidirectional flux of 45Ca2+, and directly, following depletion of ATP, by measuring release of 40Ca2+, and was 0.02% of Vmax. Constant infusion of CaCl2 at [Ca2+]lim resulted in a new steady state, in which active transport into SR vesicles balances the infusion rate. Varying infusion rates allows determination of [Ca2+]-dependence of transport in the absence of chelating agents. Parameters of non-linear regression were Vmax=853 nmol/min per mg, K0.5(Ca)=279 nM, and nH(Ca)=1.89. Since conditions employed in this study are similar to those in the sarcoplasm of relaxed muscle, it is suggested that histidine, added to media in studies of intracellular Ca2+ transients, and in the relaxed state, will minimise contribution of Zn2+ to fluophore fluorescence, since it occurs at levels predicted in this study to cause significant overestimation of cytoplasmic free [Ca2+] in the relaxed state. Similar precautions may apply to non-muscle cells as well. This study also suggests that [Ca2+]lim in the resting state is a characteristic feature of Ca2+ pump function, rather than a balance between active transport and passive leakage pathways.
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PMID:Regulation of Ca2+ transport by sarcoplasmic reticulum Ca2+-ATPase at limiting [Ca2+]. 1020 10

The antinociceptive effects of the enantiomorphs of mexiletine (2-(2, 6-dimethylphenoxy)-1-methylethylamine monohydrochloride) and its main metabolite ((+/-)2-(2-hydroxymethyl-6-methylphenoxy)-1-methylethylamine oxalate: KOE2259) were studied in streptozotocin-induced diabetic mice using the tail-pinch and tail-flick test. Both (+)mexiletine and (-)mexiletine, at doses of 10 and 30 mg given i.p., produced dose-dependent inhibition of the tail-pinch response in diabetic, but not non-diabetic mice. On the other hand, KOE2259 had no significant effect on the tail-pinch response in both non-diabetic and diabetic mice. (+/-) Mexiletine given po also produced marked inhibition of the tail-pinch and tail-flick responses in both non-diabetic and diabetic mice. However, lidocaine, given either i.p. or po, had no significant effect on the tail-pinch response in both non-diabetic and diabetic mice. Intraperitoneal administration of mexiletine (30 mg/kg) significantly increased the serum beta-endorphin level in diabetic mice, but not in non-diabetic mice. These results indicate that both enantiomorphs of mexiletine produced an antinociceptive effect in diabetic mice. Furthermore, it is possible that the activation of the endogenous beta-endorphinergic system may be, at least in part, involved in the antinociceptive effect of mexiletine.
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PMID:[Antinociceptive effects of the enantiomorphs and its main metabolite in streptozotocin-induced diabetic mice]. 1089 18