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Co-overexpression of AtNHX1 and SOS1 (show SOS1 Proteins) could significantly reduce yield loss caused by the combined stresses of heat and salt, confirming the hypothesis that stacked overexpression of two genes could substantially improve tolerance against multiple stresses.
Tonoplast-localized NHX1 and NHX2 proteins are essential for active K+ uptake at the tonoplast, for turgor regulation, and for stomatal function.
Overexpression of AtNHX1 gene not only improved salt tolerance but also drought tolerance in transgenic groundnut.
NHX1 and NHX2 mediate K+/H+ exchange to accumulate K+ in the vacuole. NHX1 and NHX2 function together to control cell expansion in vegetative tissues and male reproductive organs and are required for normal flower development.
Studies shoe that the rutin content of the roots, stems and leaves of AtNHX1 transgenic buckwheat increased than those of the control plants.
Use of the T-DNA insertional mutant of AtNHX1 (nhx1 plants) and DNA arrays to assess differences in transcriptional profiles and further characterize the roles of this protein.
the presence of a vacuolar calmodulin-like (show KRIT1 Proteins) protein acting on the vacuolar-localized AtNHX1 C terminus in a Ca(2 (show CA2 Proteins)+)- pH-dependent manner suggests the presence of signaling entities acting within the vacuole.
AtNHX1 has a role in calcium signaling, sulfur metabolism, cell structure and cell growth, as well as vesicular trafficking and protein processing.
To generate salt-tolerant turf and forage, tall fescue (Festuca arundinacea) was transformed with AtNHX1.
The results demonstrate that in renal cells, NHE1 is associated with several regulatory proteins including Hsp90 (show HSP90 Proteins), and that Hsp90 (show HSP90 Proteins) affects its function possibly through altered phosphorylation of the protein via the AKT (show AKT1 Proteins) kinase.
This study showed that extracellular acidification inhibits NBCn1 (show SLC4A7 Proteins) and NHE1 activity in VSMCs; NBCn1 (show SLC4A7 Proteins) is equivalently inhibited when pCO2 is raised or the bicarbonate level decreased. Lowering the sodium level inhibits NBCn1 (show SLC4A7 Proteins) and NHE1 markedly only below the typical physiological and pathophysiological range.
Cell volume homeostasis requiring Na+/H+ exchange signaled by JAK2 (show JAK2 Proteins) first becomes prominent during mouse embryonic development at the late one-cell stage.
Lack of Dicer (show DICER1 Proteins) leads to oxidative stress, cytosolic acidification, upregulated NHE1 expression and activity as well as swelling of CD4 (show CD4 Proteins)+ T cells, functions all reversed by miR (show MLXIP Proteins)-15b or miR (show MLXIP Proteins)-200b.
DJ-1 (show PARK7 Proteins) is a powerful regulator of reactive oxygen species production as well as NHE1 expression and activity in CD4 (show CD4 Proteins)(+) T cells.
Overexpressed NHE1 suppresses the expression of ABCA1 protein via increasing the calpain activity in RAW264.7 cells.
Inhibition of NHE1 by siRNA-NHE1 or with cariporide in CD4 (show CD4 Proteins)(+) T helper 9 (Th9) cells down-regulated IL-9 (show IL9 Proteins) and ATP production.
The current study concluded that NHE1 activity and pHi homeostasis are regulated by CoCl2 treatment in a time-dependent manner in astrocytes, and may be responsible for the changes in cell viability and injury observed under hypoxia-mimetic conditions induced by CoCl2 treatment.
During hypoxia, activation of ROCK enhances NHE1 activity and promotes pulmonary artery smooth muscle cell migration and proliferation.
Na/H exchanger is regulated in dendritic cells by Akt1 (show AKT1 Proteins).
This study evaluated the role for NHE-1 in diabetic cataract formation and retinal oxidative stress and apoptosis.
Results support the hypothesis that a blood-brain barrier Na/H exchanger, possibly NHE1 and/or NHE2, is stimulated during ischemia to participate in cerebral edema formation.
NHE isoform switching and KChIP2 (show KCNIP2 Proteins) upregulation takes place in aging porcine atria.
NHE-1 inhibitor cariporide attenuates skeletal muscle infarction when administered before ischemia or reperfusion.
The suppression of NHE1 in esophageal squamous cell carcinoma (ESCC) may enhance malignant potential by mediating PI3K (show PIK3CA Proteins)-AKT (show AKT1 Proteins) signaling and epithelial-mesenchymal transition via Notch (show NOTCH1 Proteins) signaling, and may be related to a poor prognosis in patients with ESCC.
Genetic disruption of the intracellular pH-regulating proteins Na+/H+ exchanger 1 (SLC9A1) and carbonic anhydrase 9 (show CA9 Proteins) reduces the proliferation of colon cancer cells.
NHE1 mutation is associated with metastatic potential and epithelial-mesenchymal transition of triple-negative breast cancer.
The expression pattern of sNHE suggested that this protein may be involved in the regulation of sperm motility, and aberration of its expression in sperm may contribute to the pathogenesis of asthenozoospermia.
Data show for the first time that PRLR (show PRLR Proteins) activation stimulates breast cancer cell invasiveness via the activation of NHE1. Data propose that PRL (show PRL Proteins)-induced NHE1 activation and the resulting NHE1-dependent invasiveness may contribute to the metastatic behavior of human breast cancer cells.
These data provides the first insight into the signalling molecules that form the NHE1 interactome in triple-negative breast cancer cells.
NHE1 is a plasma membrane transporter that uses the energy of the chemical gradient created by the Na+/K+ ATPase (show ATP1A1 Proteins) to couple the transport of one extracellular sodium for one intracellular proton. NHE1 functional domains, functional features, protein interactions, role in cell migration, and inhibitors are reviewed. A model of its role in pH control in tumor cells is described. Review.
The transcription factor Zeb1 binds to the Na+/H+ exchanger 1 promoter, suggesting that Zeb1 directly controls Na+/H+ transcription.
NHE1 function plays an important role in glioma-microglia interactions, enhancing glioma proliferation and invasion by stimulating microglial release of soluble factors.
results demonstrate that early stop codon polymorphisms have significant and deleterious effects on the activity of the SLC9A1 protein product. The 735-NHE1 mutant, without the last 80 amino acids, had more minor defects
In vitro phosphorylation of NHE1 C-terminal fusion proteins determined that ERK (show MAPK1 Proteins)-dependent phosphorylation of the cytoplasmic region was not dependent on Ser (show SIGLEC1 Proteins)(703); however, phosphorylation by p90(rsk (show RPS6KA1 Proteins)) required Ser (show SIGLEC1 Proteins)(703).
This gene encodes a Na+/H+ antiporter that is a member of the solute carrier family 9. The encoded protein is a plasma membrane transporter that is expressed in the kidney and intestine. This protein plays a central role in regulating pH homeostasis, cell migration and cell volume. This protein may also be involved in tumor growth.
, Na(+)/H(+) exchanger 1
, Na+/H+ antiporter
, Na+/H+, amiloride sensitive
, slow-wave epilepsy
, sodium/hydrogen exchanger 1
, solute carrier family 9 member 1
, solute carrier family 9, member 1
, sodium proton exchanger
, solute carrier family 9 (sodium/hydrogen exchanger), isoform 1 (antiporter, Na+/H+, amiloride sensitive)
, solute carrier family 9 (sodium/hydrogen exchanger), member 1 (antiporter, Na+/H+, amiloride sensitive)
, Solute carrier family 9 member 1
, NA(+)-H+ exchanger protein
, Na-Li countertransporter
, Solute carrier family 9 (sodium/hydrogen exchanger 1), antiporter, Na+/H+, (amiloride sensitive)
, solute carrier family 9 (sodium/hydrogen exchanger), member 1
, Na+/H+ exchanger
, pH regulatory protein (Na(+) /H(+) exchanger)