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)

The cell-specific expression of both the oxytocin (OT) and vasopressin (VP) genes in magnocellular neurons (MCNs) of the hypothalamus has been proposed to be under the control of cis-elements in an intergenic region downstream of the VP gene. We examined this hypothesis using transgenic mice containing mouse genomic DNA-derived constructs linked to chloramphenicol acetyltransferase (CAT) reporters. VP gene expression was studied using constructs containing 3.8 kbp of the 5' flanking region and all the exons and introns in the mouse VP gene, which was fused at the end of exon 3 to a CAT reporter. The two VP-transgene constructs differed by the lengths of their VP gene 3' flanking regions (2.1 versus 3.6 kbp). A similar construct for the oxytocin CAT transgene was used which contained the full-length (3.6 kbp) downstream intergenic region between the mouse genes. All three transgenic constructs produced cell-specific expression of the CAT-reporter in the magnocellular neurons as determined by CAT-immunoreactivity. Oxytocin transgene expression was restricted to OT cells in two founders, and the two VP transgenes to VP cells in five founders. Electron microscopic immunocytochemistry showed that the CAT fusion proteins produced from the OT- and VP-transgenes were efficiently trafficked through the regulated secretory pathways in their respective magnocellular neurons, packaged into large dense core vesicles, and transported to nerve terminals in the posterior pituitary.
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PMID:Cell-specific expression and subcellular localization of neurophysin-CAT-fusion proteins expressed from oxytocin and vasopressin gene promoter-driven constructs in transgenic mice. 1157 78

The neurohypophyseal nonapeptide Arg8 vasopressin (AVP) promotes differentiation of cultured L6 and L5 myogenic cell lines and mouse primary satellite cells. Here, we investigated the molecular mechanism involved in the induction of the myogenic program by AVP. In L6 cells, AVP treatment rapidly induces Myf-5, myogenin, and myocyte enhancer factor 2 (MEF2) mRNAs, without affecting the expression of known myogenic growth factors such as IGF-I, IGF-II, or their receptors. In the presence of cycloheximide, AVP up-regulates the expression of MEF2, but not of myogenin, indicating that the synthesis of a protein intermediate is not necessary for MEF2 induction. Notably, AVP treatment activates a calcium/calmodulin kinase signaling pathway that induces cytosolic compartmentalization of the histone deacetylase 4, a mechanism related to the transcriptional activation of MEF2. The activity of chloramphenicol acetyltransferase reporter constructs carrying the Myo184 and Myo84 fragments of the myogenin promoter is also induced by AVP. Mutation of the MEF2 site completely abolishes the response to AVP, whereas deletion of the E1 site present in pMyo84 does not impair this response. Together, these results show that AVP induces myogenic differentiation through the transcriptional activation of MEF2, a mechanism that is critical for myogenesis.
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PMID:AVP induces myogenesis through the transcriptional activation of the myocyte enhancer factor 2. 1204 25