Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various peptide immunoreactivities in the respiratory system have been reported, indicating complex physiological mechanisms. There is only little information on the upper respiratory system of man. The present study was carried out to demonstrate regulatory peptides in the nasal mucosa, larynx (vocal cords and ventricular folds) and soft palate of man using highly efficient immunocytochemical methods. In addition, some peptide immunoreactivities were measured by use of radioimmunoassay (RIA). Using indirect immunofluorescence and immunogold-silver staining (IGSS) with silver acetate autometallography, a series of peptides could be detected, including vasoactive intestinal polypeptide (VIP), peptide histidine methionine (PHM), galanin, calcitonin gene-related peptide (CGRP), substance P, neuropeptide tyrosine (NPY), C-flanking peptide of NPY (CPON) and somatostatin. In addition, antibodies to protein gene-product (PGP) 9.5, neuron-specific enolase (NSE), S-100, PHE-5 and neurofilament proteins gave positive reactions in tissue sections. Using RIA, CGRP, substance P, and neurokinin A were measured. Our results demonstrate a complex network of regulatory peptide-containing nerve fibers and the possible existence of endocrine cells regulating various functions of the upper respiratory system, which need to be further investigated.
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PMID:Regulatory peptides and general neuroendocrine markers in human nasal mucosa, soft palate and larynx. 171 32

Large cell neuroendocrine (LCNE) carcinomas of the lung are a newly recognized, highly aggressive and frequently misdiagnosed entity. We report a case of stage I LCNE lung carcinoma initially misdiagnosed as large cell undifferentiated carcinoma or poorly differentiated adenocarcinoma. The tumor was very extensively necrotic and its neuroendocrine differentiation was only demonstrable with immunohistochemical staining with PHE-5 monoclonal antibody and with antisera against synaptophysin and calcitonin. ACTH, somatostatin and neurofilaments were not demonstrable. The clinical course was ominous and the patient died within 17 months. The reason for this rapid fatal outcome could be ascribed either to the neuroendocrine phenotype of the tumor, or to the extensive necrosis, or both.
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PMID:Large cell neuroendocrine carcinoma of the lung. 255 26

Radioligand binding and functional assays were employed to demonstrate the existence of somatostatin receptors in the murine neuroblastoma clone N1E-115. Saturation experiments with [125I][Tyr11]somatostatin-14 indicated the presence of a single class of binding sites in membranes prepared from N1E-115 cells (Kd = 83 pM; Bmax = 21,000 receptors/cell). Somatostatin-14, somatostatin-28 and L363586 (cyclo(N-Me-ALA-TYR-D-TRP-LYS-VAL-PHE] all displaced the 125I-ligand monophasically in N1E-115 cells (Ki values were 28, 82 and 34 pM, respectively), which contrasted with the binding heterogeneity apparent with L363586 in rat brain membranes. The binding of [125I][Tyr11]somatostatin-14 was reduced by GppNHp, indicating that N1E-115 somatostatin receptors interacted with guanine nucleotide binding protein(s). Somatostatin agonists decreased by 30-50% the levels of [3H]cyclic AMP induced in intact cells by forskolin, prostaglandin E1, or vasoactive intestinal polypeptide. The EC50 values for inhibition of the [3H]cyclic AMP response to PGE1 by L363586, somatostatin-14, and somatostatin-28 were 0.24, 0.63 and 1.0 nM, respectively. Pertussis toxin treatment of N1E-115 cells reduced both binding to the receptor and the functional response to somatostatin-14. These data suggest that a single class of somatostatin receptors in N1E-115 cells are linked to the inhibition of adenylate cyclase through a Gi protein.
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PMID:Biochemical evidence for somatostatin receptors in murine neuroblastoma clone N1E-115. 256 62

The possible occurrence of adrenergic and non-adrenergic vasoconstrictor mechanisms has been studied in human nasal mucosa biopsies. The tissue contractions (reflecting vascular tone variation) in response to exogenous noradrenaline (NA), neuropeptide Y (NPY) and somatostatin (SOM) were measured in vitro. Dose-dependent contraction of the nasal mucosa was observed for the three agents studied and the rank order of their vasoconstrictive potency was NA > SOM > NPY. On a molar basis NPY showed an 80% less potent vasoconstrictive activity than SOM. Pretreatment with the alpha-adrenoceptor antagonist phenoxybenzamine (10(-6) M) almost completely abolished the vasoconstrictive response to NA, whereas the effects of NPY and SOM remained intact. The responses to SOM were significantly reduced after pretreatment with high dose of the competitive SOM-antagonist analog cyclo(7-aminoheptanoyl-PHE-D-TRP-LYS-THR[BZL]). When SOM was administered simultaneously with NA, the contractile response was significantly reduced as compared to the effect of NA alone. In contrast, concomitant administration of NPY and NA potentiated the vasoconstrictive effect of NA. The present data suggest that both adrenergic and non-adrenergic vasoconstrictor mechanisms are present in the human nasal mucosa vascular bed. Furthermore, NPY and SOM may act as modulators of the NA-induced vasoconstrictive effects.
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PMID:Adrenergic and non-adrenergic vasoconstrictor mechanisms in the human nasal mucosa. 810 Jun 40