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)

Adrenocortical function and plasma growth hormone pattern were investigated in 15 patients with chronic obstructive lung disease, in a period of acute respiratory failure and again after recovery. During the acute period, secretion rate and plasma concentrations of cortisol were markedly enhanced; urinary excretion of cortisol metabolites was only slightly increased, suggesting an alteration of the catabolism of cortisol under these conditions; adrenocortical sensitivity to corticotropin and capacity of maximal adrenal secretion were normal. The increase of cortisol secretion was probably due to hypoxemia and/or hypercapnia acting through the hypothalamo-pituitary axis. During the chronic phase of respiratory insufficiency, adrenocortical secretion and responsiveness were within the normal range. Finally, respiratory failure did not stimulate the secretion of growth hormone.
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PMID:Adrenocortical and somatotrophic secretions in acute and chronic respiratory insufficiency. 114 86

Plasma opioid peptides, norepinephrine, atrial natriuretic factor (ANF) and blood pressure (BP) were assessed in 24 chronic obstructive pulmonary disease patients with acute respiratory failure. Hypoxemic-hypercapnic patients had high BP, beta-endorphin, Met-enkephalin and dynorphin B, whereas hypoxemic-normocapnic and hypoxemic-hypocapnic patients showed normal BP, high beta-endorphin, and normal Met-enkephalin and dynorphin B. Norepinephrine and ANF were high in all patients, particularly in hypoxemic-hypercapnic patients. Infusion with the opioid antagonist naloxone hydrochloride significantly increased systolic blood pressure (SBP) in hypoxemic-hypercapnic (182.0 +/- 3.2 versus 205.1 +/- 3.0 mmHg; P < 0.01), hypoxemic-normocapnic (149.3 +/- 1.8 versus 169.1 +/- 2.2 mmHg; P < 0.01) and hypoxemic-hypocapnic (147.3 +/- 1.3 versus 166.8 +/- 2.2 mmHg; P < 0.01) patients, norepinephrine in hypoxemic-hypercapnic patients (3583.2 +/- 371.8 versus 5371.3 +/- 260.0 fmol/ml; P < 0.01), and reduced ANF in hypoxemic-normocapnic (18.3 +/- 0.8 versus 11.9 +/- 1.0 fmol/ml; P < 0.05) and hypoxemic-hypocapnic (18.1 +/- 1.2 versus 12.1 +/- 2.1 fmol/ml; P < 0.05) patients. These results indicate that the endogenous opioid system attenuates SBP responses in acute respiratory failure by affecting norepinephrine or ANF release.
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PMID:Opioid peptides attenuate blood pressure increase in acute respiratory failure. 1131 34

Propeptide processing occurs in specific compartments of the secretory pathway, but how these processing-competent organelles are generated from their processing-incompetent precursor compartments is unknown. To dissect the process biochemically, we have developed a novel cell-free system reconstituting the production of processing-competent secretory granules in AtT-20 cells. Using donor membranes containing [(35)S]sulfate labeled pro-opiomelanocortin (POMC)(5) in the trans-Golgi, we can reconstitute cytosol- and ATP-dependent prohormone processing as well as incorporation of processed ACTH into immature secretory granules (ISGs). Under limiting cytosol conditions, both reactions are greatly stimulated by ADP-ribosylation factor 1 (ARF1) but not by the GDP-bound ARF1 T31N mutant. pH studies show that lumenal acidification, most likely due to ARF-mediated sorting of proton pumps and leaks during budding, confers processing competency to the resulting organelle. Surprisingly, comparison of onset of processing and ISG release reveals that they are distinct biochemical processes with different kinetics and separate cytosolic requirements. Moreover, ARF regulates the onset of prohormone processing but not ISG release. Our data suggest a two-step mechanism (onset of processing followed by ISG release) for the production of processing-competent organelles from the trans-Golgi and provide the first system with which these two steps may be individually dissected.
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PMID:Biogenesis of processing-competent secretory organelles in vitro. 1166 40

Bmi1 is a member of the polycomb repressive complex 1 and plays different roles during embryonic development, depending on the developmental context. Bmi1 over expression is observed in many types of cancer, including tumors of astroglial and neural origin. Although genetic depletion of Bmi1 has been described to result in tumor inhibitory effects partly through INK4A/Arf mediated senescence and apoptosis and also through INK4A/Arf independent effects, it has not been proven that Bmi1 can be causally involved in the formation of these tumors. To see whether this is the case, we developed two conditional Bmi1 transgenic models that were crossed with GFAP-Cre mice to activate transgenic expression in neural and glial lineages. We show here that these mice generate intermediate and anterior lobe pituitary tumors that are positive for ACTH and beta-endorphin. Combined transgenic expression of Bmi1 together with conditional loss of Rb resulted in pituitary tumors but was insufficient to induce medulloblastoma therefore indicating that the oncogenic function of Bmi1 depends on regulation of p16(INK4A)/Rb rather than on regulation of p19(ARF)/p53. Human pituitary adenomas show Bmi1 overexpression in over 50% of the cases, which indicates that Bmi1 could be causally involved in formation of these tumors similarly as in our mouse model.
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PMID:GFAP-Cre-mediated transgenic activation of Bmi1 results in pituitary tumors. 2257 28