High impact information on Avpi1

• Finally, we were able to identify CREB as a nuclear protein that bound to the VIT32 CRE in gel mobility shift assays [1].
• The increase in gene expression was abolished by H89 and by actinomycin D, suggesting that cAMP stimulates VIT32 mRNA expression by a PKA-mediated increase in gene transcription [1].
• Furthermore, DDAVP-stimulated VIT32 promoter-reporter activity was inhibited by H89 and by a dominant negative CREB construct [1].
• AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5'-flanking region of the VIT32 gene [1].
• In summary, DDAVP stimulates transcription of VIT32 via a CRE within the proximal promoter region of the VIT32 gene [1].

Biological context of Avpi1

• Elevation of cAMP with forskolin and IBMX increased VIT32 gene expression with a peak effect at 2 h [1].
• An approximately 1.5-kb fragment of the 5'-flanking region of VIT32 was cloned and was able to confer cAMP-stimulated reporter gene activity when transfected into M-1 and H441 cells [1].

Anatomical context of Avpi1

• VIT32, a vasopressin-induced transcript, inhibits Na(+) transport when coexpressed with the epithelial sodium channel in Xenopus laevis oocytes (EMBO J 21: 5109-5117, 2002) [1].
• To understand the mechanism of VIT32 gene regulation, we examined the effect of DDAVP and cAMP stimulation on VIT32 expression in M-1 mouse collecting duct cells and in H441 human airway epithelial cells [1].

Associations of Avpi1 with chemical compounds

• By deletion analysis and site-directed mutagenesis, a cAMP response element (CRE) was identified within the proximal promoter region that was sufficient to account for the increase in VIT32 gene expression seen with DDAVP and elevation of cAMP [1].

Other interactions of Avpi1

• Effects of nonapeptide antagonists on oxytocin- and arginine-vasopressin-induced analgesia in mice [2].

References