Calcium-activated calcium release channel phosphopeptides altered in abundance in response to dDAVP in rat IMCD suspensions* (See below for narrative)
*Peptides satisfied dual criteria: |Mean log2(dDAVP/Control)| > 0.342 and FDR < 0.005. The value 0.342 defines the 95% confidence interval for control:control comparisons.
§, Phosphorylated amino acid indicated by *; #, deamidated asparagine or glutamine; †, False Discovery Rate
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| Gene Symbol | UniProt no. | Residue(s) | Peptide§ | Mean log2(dDAVP/Vehicle) | SD log2(dDAVP/Vehicle) | FDR† |
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Vasopressin-mediated increase in intracellular calcium. Vasopressin, working through the V2 receptor, triggers aperiodic intracellular calcium spikes (https://esbl.nhlbi.nih.gov/ca_spikes_video/) that are believed to be involved in regulation of AQP2 trafficking and the concomitant increase in water permeability in the collecting duct [(Balasubramanian, 2008), (Pisitkun, 2008)] (Figure 0). Prior studies in nonrenal cells had previously shown that PKA enhances inositol trisphosphate (ITP)-stimulated calcium mobilization (Wojcikiewicz, 1998). Previously, in cultured mouse mpkCCD cells, we identified two sites of PKA-mediated phosphorylation in a calcium-sensitive calcium release channel, Itpr3 (Inositol 1,4,5-trisphosphate receptor type 3) at Ser934 and Ser1832 (Isobe, 2017) (https://hpcwebapps.cit.nih.gov/ESBL/PKANetwork/Ca_mobiliztion.html). In the present study, there were large increases in phosphorylation of both of these sites in response to dDAVP as well as basophilic sites in Itpr1, supporting the idea that vasopressin may increase intracellular calcium at least in part through phosphorylation-mediated effects on calcium-transport from the endoplasmic reticulum via Itpr1 and Itpr3.