Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the transcriptional regulation of the vasopressin gene in vitro, 3 kb of the 5' regulatory region of the rat vasopressin gene was isolated and subcloned, along with a series of various deletion mutants, into vectors containing the luciferase reporter gene. After transfecting these genes transiently into the human choriocarcinoma cell line JEG-3 along with a glucocorticoid receptor (GR) expression vector, transcriptional activity was quantitated using the luciferase assay. Forskolin, 8-bromo-cAMP, and protein kinase A catalytic subunit expression all markedly increased transcription from the 3-kb promoter. Analyses with deletion mutants of the promoter showed that two cAMP-responsive element (CRE)-like sequences (-227 to -220 bp and -123 to -116 bp) contribute to this positive regulation. Expression of KCREB, a dominant negative mutant of the cAMP-responsive element binding protein (CREB), suggested the involvement of CREB. Transfection of the activator protein 2 (AP2) DNA consensus sequence partially blocked transcription. Dexamethasone suppressed forskolin-stimulated expression. The negative effect of glucocorticoid was GR dependent and may be mediated by a mechanism not involving GR binding to DNA because it was independent of the putative glucocorticoid-responsive element previously reported in the vasopressin promoter (-622 to -608 bp) and was preserved in the shorter promoter constructs in which no glucocorticoid-responsive element-like sequence was found. Our data suggest that several trans-acting factors including CREB, AP2, and GR are likely to be involved in vasopressin gene transcription and that the positive and negative regulation of vasopressin gene transcription is complex.
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PMID:Positive and negative regulation of the rat vasopressin gene promoter. 938 10

Human pregnancy serum and placenta have the ability to degrade uterotonic peptide oxytocin (OT). Placental leucine aminopeptidase (P-LAP), which is also called cystine aminopeptidase, is the only membrane aminopeptidase known to functionally degrade OT as oxytocinase (OTase). P-LAP/OTase hydrolyzes several peptides other than OT including vasopressin and angiotensin III. P-LAP/OTase predicted from cDNA sequence is a type II integral membrane protein, which is converted to a soluble form existing in maternal serum by metalloproteases, possibly ADAM (a disintegrin and metalloproteinase) members. P-LAP/OTase activity increases with normal gestation, while decreases in the patients with preterm delivery and severe preeclampsia. In placenta, P-LAP/OTase is predominantly expressed in differentiated trophoblasts, syncytiotrophoblasts. Activator protein-2 (AP-2) and Ikaros transcription factors play significant roles in exerting high promoter activity of P-LAP/OTase in the trophoblastic cells. Moreover, P-LAP/OTase is transcriptionally regulated in a trophoblast-differentiation-dependent fashion via up-regulation of AP-2, putatively AP-2alpha. P-LAP/OTase may be involved in maintaining pregnancy homeostasis via metabolizing peptides such as OT and vasopressin.
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PMID:Gene regulation and physiological function of placental leucine aminopeptidase/oxytocinase during pregnancy. 1589 23

Abstract Vasopressin and oxytocin genes are expressed in mutually exclusive sets of magnocellular neurons in the hypothalamus. Cell specificity and regulation are probably controlled by extra- and intracellular signals acting on one or the other gene. In order to identify factors that regulate peptide expression, we have used primary dissociated cultures derived from 14-day old foetal rats. Vasopressin expression was monitored by combined immunocytochemistry and in situ hybridization. Treatment of cultures with forskolin and/or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), both of which result in elevated intracellular cyclic AMP levels, increased the numbers of vasopressin-expressing cells up to 10-fold. The specific Vasopressin messenger ribonucleic acid accumulation was verified quantitatively by ribonuclease protection assays. Forskolin and IBMX did not change the levels of the general neuronal markers, neuron-specific enolase and synaptophysin, suggesting that the effect of these drugs was specific for vasopressin-expressing cells. The drugs were not mitogenic for magnocellular neurons. Furthermore, their effect was not mediated trans-synaptically, as the drugs were also effective in cultures grown in low Ca(2+)/high Mg(2+) medium, as well as in cultures treated with either tetanus toxin or tetrodotoxin. The presence of putative response elements for the transcription factor AP-2 in the 5'promoter regions of all vasopressin genes sequenced so far may provide the molecular basis of the observed cyclic AMP effect. No such elements are present in the genes for oxytocin, the messenger ribonucleic acid levels of which were not measurably affected by forskolin and IBMX in our cultures.
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PMID:Vasopressin Expression in Cultured Neurons is Stimulated by Cyclic AMP. 1921 30