Browse our anti-Solute Carrier Family 9 (Sodium/hydrogen Exchanger), Member 8 (SLC9A8) Antibodies

Mouse (Murine) Solute Carrier Family 9 (Sodium/hydrogen Exchanger), Member 8 (SLC9A8) interaction partners

1. work has uncovered a crucial role of NHE8 in acrosome biogenesis and suggests that some forms of human globozoospermia might be caused by a loss of function of this Na(+)/H(+) exchanger.

2. NHE8 may be involved in the establishment of intestinal mucosal integrity by regulating the functions of goblet and Paneth cells.

3. NHE8 function is necessary for the survival of photoreceptor cells and NHE8 is important for RPE (show RPE Antibodies) cell polarity and function

4. The NHE8 protein is required in the RPE (show RPE Antibodies) to maintain correct regulation of endosomal volume and/or pH which is essential for the cellular integrity and subsequent function of RPE (show RPE Antibodies)

5. Suggest a novel role of NHE8 in male fertility through its effect on modifying luteinizing hormone receptor (show LHCGR Antibodies) function.

6. Both NHE3 and NHE8 likely play a role in neonatal acidification.

7. Altered ocular surface function and reduced epithelial DRA expression in NHE8-/- mice suggest that the role of NHE8 in ocular surface tissue involve in tear production and ocular epithelial protection.

8. NHE3 (show SLC9A3 Antibodies) is the predominant Na(+)/H(+) exchanger in adult mice. NHE8 may play a compensatory role in renal acidification and blood pressure regulation in NHE3 (show SLC9A3 Antibodies)(-/-) mice.

9. NHE8 is indirectly involved in gastric bicarbonate secretion and gastric mucosal protection

10. the role of NHE8 in the intestine involves both sodium absorption and bicarbonate secretion

Human Solute Carrier Family 9 (Sodium/hydrogen Exchanger), Member 8 (SLC9A8) interaction partners

1. work has uncovered a crucial role of NHE8 in acrosome biogenesis and suggests that some forms of human globozoospermia might be caused by a loss of function of this Na(+)/H(+) exchanger.

2. NHE8 is expressed in goblet cells, and the inflammatory cytokine TNF-alpha downregulates NHE8 expression by a transcriptional mechanism.

3. Exonic mutations in NHE8 cannot account for congenital sodium diarrhea.

4. This review defines NHE6-9 as organellar NHEs that are fairly dynamic, implying that they are subjected to intracellular trafficking and thus they continuously shuttle between organelles and the plasma membrane.

5. These data point to a role for the ion exchange activity of NHE8 being required to maintain endosome morphology.

6. EGF inhibits intestinal NHE8 gene expression by reducing its basal transcription.

7. No mutation was found in the coding regions and intron-exon boundaries of the genes for CA II (show CA2 Antibodies), CA IV (show CA4 Antibodies), CA XIV (show CA14 Antibodies), kNCB1, NHE3 (show SLC9A3 Antibodies), NHE8, NHRF1, NHRF2 and SLC26A6 (show SLC26A6 Antibodies) amplified from genomic DNA of family members with pRTA.

8. NHE8 is expressed along the gastrointestinal tract and NHE8 is a functional Na(+)/H(+) exchanger with kinetic characteristics that differ from other apically expressed NHE isoforms.

9. Tumor necrosis factor-alpha downregulates intestinal NHE8 expression by reducing basal promoter activity.