MTOR-regulated phosphorylation of electrogenic sodium bicarbonate cotransporter 1, NBCe1, at S255-257 regulates NBCe1 functional expression in mouse cortical astrocyte
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive HF
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Astrocyte Of The Cerebral Cortex
SUBMITTER: 
Jana Zecha
LAB HEAD: Bernhard Kuster
PROVIDER: PXD014034 | Pride | 2019-07-15
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 02941_BE3_P033643_B00_A00_R1.raw | Raw | |||
| 02941_BF3_P033644_B00_A00_R1.raw | Raw | |||
| 02941_BG3_P033645_B00_A00_R1.raw | Raw | |||
| 02941_BH3_P033646_B00_A00_R1.raw | Raw | |||
| 02982_GA4_P034211_B00_A00_R1.raw | Raw |
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David C Whitcomb, G Bard Ermentrout, Pancreas 2004 29:e30-40; PubMedID:15257112
Abstract:
OBJECTIVE:
To develop a simple, physiologically based mathematical model of pancreatic duct cell secretion using experimentally derived parameters that generates pancreatic fluid bicarbonate concentrations of >140 mM after CFTR activation.
METHODS:
A new mathematical model was developed simulating a duct cell within a proximal pancreatic duct and included a sodium-2-bicarbonate cotransporter (NBC) and sodium-potassium pump (NaK pump) on a chloride-impermeable basolateral membrane, CFTR on the luminal membrane with 0.2 to 1 bicarbonate to chloride permeability ratio. Chloride-bicarbonate antiporters (Cl/HCO3 AP) were added or subtracted from the basolateral (APb) and luminal (APl) membranes. The model was integrated over time using XPPAUT.
RESULTS:
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CONCLUSIONS:
A simple CFTR-dependent duct cell model can explain active, high-volume, high-concentration bicarbonate secretion in pancreatic juice that reproduces the experimental findings. This model may also provide insight into why CFTR mutations that predominantly affect bicarbonate permeability predispose to pancreatic dysfunction in humans.
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