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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 and GSK-3, which act on a Ser cluster in the same NHE3 C-terminal domain that binds ezrin
CaMKII 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 family member associating with NHE3 and the accompanying NHE3 complexes.
Our results support the scientific premise and physiological relevance that NHE3 in the proximal tubules plays an essential role in maintaining basal blood pressure homeostasis, and genetic deletion of NHE3 selectively in the proximal tubules of the kidney lowers blood pressure by increasing the pressure natriuretic response.
NHERF2 and NHERF3 have overlapping roles in NHE3 stimulation by LPA and inhibition by elevated Ca(2+) and cGMP.
Intestinal NHE3 gene expression is regulated by changes in its DNA methylation.
The data indicate that SLC9A3 has a vital role in acrosomal formation during spermatogenesis.
Renal NHE3 is required to maintain blood pressure and steady-state plasma sodium levels when dietary sodium chloride intake is modified.
no gender difference in expression
NHERF1 mediates ANG II-induced activation of renal NHE3, which requires coordination between IRBIT and the NHERF1 PDZ1 domain in binding and transporting NHE3
This study suggested an important role for NHE3 in generating the H(+) gradient that drives DMT1-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 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 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-induced hypertension.
Inflammation-induced loss of PDZK1 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 mediates the movement of NHE3 to the microvillus in intestinal epithelial cells.
Cyclic GMP kinase II (cGKII) inhibits NHE3 by altering its trafficking and phosphorylating NHE3 at three required sites
Both NHE3 and NHE8 likely play a role in neonatal acidification.
NHE3 partially associates with lipid rafts in the brush border membrane.
The gut microbiome plays a prominent role in the pathogenesis of colitis in NHE3 knockout mice, and, reciprocally, NHE3 also plays a critical role in shaping the gut microbiota.
Hepatocyte nuclear factor 4alpha directly regulates NHE3 promoter activity and its basal expression in the intestine.
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 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, 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.
Data demonstrate a role for Per1 in the transcriptional regulation of NHE3 and SGLT1 in the kidney.
Results demonstrate decreased transport activity in three SNPs of NHE3 and provide mechanistic insight into how these SNPs impact NHE3 function.
NHE3 may play a role in the pathogenesis of human cholesterol gallstone disease
Study identifies RSK2 as a new kinase that regulates NHE3 activity by direct phosphorylation.
the three NHE3 SNPs are unlikely to play a major role in the pathogenesis of SIDS in Caucasian infants;further genetic investigations in different ethnicities are required to determine whether variations in NHE3 are associated with an increased SIDS risk
C. difficile inhibits NHE3 in vivo, which creates an altered environment favored by C. difficile.
PKC-eta associates with NHE3 and gamma tubulin to promote the cell polarity during migration.
Human NHE3, but not non-primates NHE3s, is ubiquitinated by Nedd4-2.
NHE3 can act as a direction sensor for cells and that NHE3 phosphorylation in persistent directional cell migration does not involve PI3K/Akt during electrotaxis.
We propose that ouabain can simultaneously regulate renal tubule basolateral Na(+)-K(+)-ATPase 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