Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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.
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).
our results suggest that activation of NHE1 induces hypertrophy through the activation of NFAT3 (show NFATC4 Proteins)/Gata4 (show GATA4 Proteins) and OPN (show SPP1 Proteins) expression
NHE1 function is necessary for maintaining mammary branched architecture.
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.
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
the accumulation of reactive oxygen species (ROS (show ROS1 Proteins)) in cells expressing JAK2V617F compromises the NHE-1/Bcl-xL (show BCL2L1 Proteins) deamidation pathway by repressing NHE-1 upregulation in response to DNA damage. hematopoietic stem cells (HSCs), FOXO3A (show FOXO3 Proteins) is largely localized within the nuclei despite the presence of JAK2V617F mutation, suggesting that JAK2 (show JAK2 Proteins)-FOXO (show FOXO3 Proteins) signaling has a different effect on progenitors compared with stem cells.
Findings suggest that Na(+)/H(+) exchanger1 (NHE1) could be a target for anti-invasion/metastasis therapy.
These data identify a molecular mechanism for pH-sensitive PI(4,5)P2 binding regulating NHE1 activity and suggest that the evolutionarily conserved cluster of four histidines in the proximal cytoplasmic domain of NHE1 may constitute a proton modifier site.
Results indicate that Nav 1.7 promotes GC progression through MACC1 (show MACC1 Proteins)-mediated upregulation of NHE1.
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)