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

The effect of GRF adenylate cyclase activation was studied in normal human, bovine and rat pituitary tissues. Human GRF (hGRF) activates adenylate cyclase in normal human pituitary membrane preparations in a concentration dependent manner (ED5 0 = 10(-11) M). In bovine pituitary cells hGRF stimulates GH secretion into the medium (ED5 0 = 7 X 10(-12) M) and activates adenylate cyclase (ED5 0 = 10(-11) M). In normal rat pituitary cells in monolayer culture, rat GRF (rGRF) stimulates adenylate cyclase (ED5 0 = 3 X 10(-11) M). In normal human pituitary membrane preparations and in normal rat pituitary cells in culture, somatostatin inhibits GRF-stimulated adenylate cyclase in a non-competitive manner, while it does not affect basal (i.e. non-stimulated) adenylate cyclase levels. VIP, a peptide which is structurally homologous to hGRF and rGRF is a weak GRF-agonist and activates adenylate cyclase in human and rat pituitary preparations at concentrations greater than 10 nM.
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PMID:GRF is a highly potent activator of adenylate cyclase in the normal human, bovine and rat pituitary: interaction with somatostatin. 285 17

GH3 cells were used to study the effect of rat growth hormone-releasing factor on adenylate cyclase activity and its interaction with somatostatin. Rat GRF stimulates adenylate cyclase activity (ED5 0 = 6 X 10(-8) M) and somatostatin-14 inhibits this GRF-stimulated activity in a non-competitive manner without affecting the basal enzyme levels. Inhibition by somatostatin-14 is observed at concentrations as low as 10(-11) M and the half-maximal effect is obtained with 10(-8) M. Somatostatin-28 is more potent than SS-14 and has an ED5 0 of 3 X 10(-11) M. VIP is more active than rat GRF in stimulating adenylate cyclase activation. We conclude that in GH3 cells rat GRF behaves as a partial VIP agonist by interacting with VIP-preferring receptors and its effects are inhibited by somatostatin.
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PMID:Somatostatin inhibits growth hormone-releasing factor-stimulated adenylate cyclase activity in GH, cells. 285 18

The tissue distribution of somatostatin (SST) immunoreactivity was studied in the nasal and forebrain region in the chick embryo. On embryonic day (ED) 3, SST-immunoreactive (ir) cells were first detected in the cells migrating from the olfactory placode. Then, at ED3.5, SST-ir cells and -ir fibers appeared in the olfactory epithelium and olfactory nerve bundles. At ED6-8, one component of the SST-ir fibers was found to separate from the olfactory nerve and it entered the parenchyma of the medial forebrain surface. These SST-ir fibers extended dorsocaudally toward the preseptal area. During this same period, a few SST-ir cells were observed in the medial forebrain adjacent to the SST-ir fibers. SST immunoreactivity in the nasal and forebrain areas was most striking at ED5-8 but a reduction of SST immunoreactivity in the nasal and forebrain areas occurred at ED11 and it virtually disappeared by the day of hatching. These results indicate that the expression of SST in the nasal and forebrain regions is transient in the chick embryo. Since the SST-ir cells did not co-express luteinizing hormone-releasing hormone (LHRH), it, thus, appears that these SST-r cells belong to a different cell population from LHRH neurons that are also found in the olfactory-forebrain axis during embryonic development [23]. However, a close relationship exists between SST-ir cells and -ir neuronal fibers and LHRH neurons. This may play a role in development of LHRH neurons.
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PMID:Transient expression of somatostatin immunoreactivity in the olfactory-forebrain region in the chick embryo. 784 15