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The expression of NHE3 in the rumen of sheep and cattle and its role in sodium transport are reported.
Lysophosphatidic acid stimulation of NHE3 exocytosis includes a signaling pathway that regulates fixation of NHE3 to the microvillar cytoskeleton.
1) NHE3 basal activity is regulated by a signaling complex that is controlled by sequential effects of two kinases, Akt (show AKT1 ELISA Kits) and GSK-3 (show GSK3b ELISA Kits), which act on a Ser (show SIGLEC1 ELISA Kits) cluster in the same NHE3 C-terminal domain that binds ezrin (show EZR ELISA Kits)
CaMKII (show CAMK2G ELISA Kits) binding to and phosphorylation of the NHE3 C terminus are parts of the physiologic regulation of NHE3 that occurs in fibroblasts as well as in the brush border of an intestinal Na(+)-absorptive cell.
Regulation of NHE3 depends on the nature of the NHERF (show SLC9A3R1 ELISA Kits) family member associating with NHE3 and the accompanying NHE3 complexes.
NHERF1 (show SLC9A3R2 ELISA Kits) mediates ANG II (show AGT ELISA Kits)-induced activation of renal NHE3, which requires coordination between IRBIT (show AHCYL1 ELISA Kits) and the NHERF1 (show SLC9A3R2 ELISA Kits) PDZ1 domain in binding and transporting NHE3
This study suggested an important role for NHE3 in generating the H(+) gradient that drives DMT1 (show SLC11A2 ELISA Kits)-mediated iron uptake at the intestinal brush border.
The Slc9a3-deficient mice with impaired male excurrent ducts in this study provide proof for our clinical findings that some Taiwanese of CBAVD carry SLC9A3 deletion but without major CFTR (show CFTR ELISA Kits) mutations.
Data suggest that increased phosphorylation of Nhe3/Slc9a3 accompanies gallstone formation and leads to increased turnover of the exchanger, resulting in decreased concentrating function of the gallbladder epithelium.
hepcidin (show HAMP ELISA Kits) is one of the promising therapeutic agents for calcium malabsorption in beta-thalassemia. It mainly stimulates the transcellular calcium transport across the duodenal epithelium in an NHE3-dependent manner.
azilsartan (but not candesartan) improved salt sensitivity possibly by decreasing NHE3 expression via ubiquitin-proteasomal degradation.
NHE3 in proximal tubules of the kidney, along with NHE3 in intestines, is required for maintaining basal blood pressure as well as the full development of ANG II (show AGT ELISA Kits)-induced hypertension.
Inflammation-induced loss of PDZK1 (show PDZK1 ELISA Kits) expression may contribute to the NHE3 dysfunction observed in the inflamed intestine.
these findings indicate the importance of NHE3 in diabetic diarrhea and suggest LPA administration as a potential therapeutic strategy for management of diabetic diarrhea.
Myosin VI (show MYO6 ELISA Kits) mediates the movement of NHE3 to the microvillus in intestinal epithelial cells.
We demonstrate that NHE3-799C is a common variant of NHE3 that is enriched in Asian populations; however its presence seems to have limited clinical significance in humans and is not associated with compromised function or abnormal transport regulation.
This review focuses on novel findings of NHE3 in the intestine and the kidney as well as novel drug developments targeting NHE3. [review]
NHE3 binds to NHERF (show SLC9A3R1 ELISA Kits) proteins via both an internal Class II PBM and C-terminal Class I PBM, which interact. The former determines NHE3 stability in the PM, and the latter determines total expression and percent PM expression.
Expression of NHE3 and DRA was reduced with high tacrolimus levels and impaired renal function after intestinal transplantation.
Recessive mutations in NHE3, a downstream target of GC-C (show GUCY2C ELISA Kits), caused congenital sodium diarrhea and implied primary basal NHE3 malfunction as a predisposition for inflammatory bowel disease in a subset of patients.
CCH-mediated inhibition of NHE3 activity is not dependent on clathrin and involves lipid rafts and requires Cdc42 (show CDC42 ELISA Kits).
Data demonstrate a role for Per1 (show PER1 ELISA Kits) in the transcriptional regulation of NHE3 and SGLT1 (show SLC5A1 ELISA Kits) in the kidney.
Results demonstrate decreased transport activity in three SNPs of NHE3 and provide mechanistic insight into how these SNPs impact NHE3 function.
We propose that ouabain can simultaneously regulate renal tubule basolateral Na(+)-K(+)-ATPase (show ATP1A1 ELISA Kits) and apical NHE3, leading to inhibition of transepithelial Na(+) transport.
displays Na+/H+ exchanger transport activity\; mediates sodium ion transport across the renal proximal tubule
sodium proton exchanger
, sodium/hydrogen exchanger 3
, solute carrier family 9 (sodium/hydrogen exchanger), member 3
, sodium/hydrogen exchanger 3 (nhe3)
, Sodium/hydrogen exchanger 3
, Na(+)/H(+) exchanger 3
, Na+/H+ exchanger homolog
, solute carrier family 9 member 3
, Solute carrier family 9 (sodium/hydrogen exchanger 3), antiporter 3, Na+/H+ (amiloride insensitive)
, plasma membrane ion transport protein
, solute carrier family 9, member 3
, solute carrier family 9 (sodium/hydrogen exchanger)
, sodium/hydrogen exchanger