anti-Solute Carrier Family 8 (Sodium/calcium Exchanger), Member 3 (SLC8A3) Antibodies

Human Solute Carrier Family 8 (Sodium/calcium Exchanger), Member 3 (SLC8A3) interaction partners

1. These results...suggest that cells can use a dynamic Ca(2+) signaling toolkit in which the NCX3 sub-cellular localization changes in synchrony with the cell cycle

2. Structure-Dynamic Coupling Through Ca(2+)-Binding Regulatory Domains of Mammalian NCX Isoform/Splice Variants

3. stimulation of NCX3 by PKA occurred through residue S524. This effect may well participate in the fight-or-flight response in skeletal muscle and the long-term potentiation in hippocampus.

4. In the discovery phase, 60 loci not previously associated with rheumatoid arthritis risk showed evidence for association and were tested for replication in the validation cohort. A total of 12 loci were replicated at the nominal level. When combining the discovery and validation cohorts, an intronic SNP in SLC8A3 was found to be associated with ACPA-positive rheumatoid arthritis at a genome-wide level of significance.

5. Ayloid beta mediates calpain cleavage of NCX3 in Alzheimer's disease brain.

6. NCX1 and NCX3 -represent two promising druggable targets for setting on new strategies in stroke therapy.

7. NCX isoforms (NCX2, NCX3) contribute to mitochondrial Na(+)/Ca(2+) exchange in human DAergic neurons and may act downstream of PINK1 in the prevention of neurodegeneration by m[Ca(2+)] accumulation.

8. the large cytosolic loop of NCX1, NCX2, and NCX3 is involved in acquisition of immunosuppressive drug specificity

9. Functional studies, as well as mRNA and protein expression analyses, revealed that NCX1 and NCX3, but not NCX2, were divergently modulated during OPC differentiation into oligodendrocyte.

10. human macrophages and monocytes express NCX1 and NCX3 that operate in a bidirectional manner to restore [Ca(2+)](i) to generate Ca(2+) signals and to induce TNF-alpha production.

11. calcium signaling mediated by NCX3 has a crucial role in oligodendrocyte maturation and myelin formation.

12. Human platelets express K(+) -independent Na(+) /Ca(2+) exchangers NCX1.3, NCX3.2 and NCX3.4.

13. Data suggest that NCX-mediated Ca(2+) fluxes normally exist in human ASM (potentially contributing to rapid Ca(2+) fluxes), and contribute to enhanced [Ca(2+)](i) regulation in airway inflammation.

14. Results demonstrate a selective regulation of NCX1, NCX2 and NCX3 isoforms in Alzheimer's disease cortex, specifically in terminals containing amyloid-beta.

15. The gene promoter of the human isoform of this protein is controlled by cAMP and calcium.

16. This review examines the regulatory features and expression pattern of the SLC8A3 gene which suggest that NCX3 activity could be crucial in neuronal functions such as memory formation and sensory processing.

17. Studies show that both alternatively spliced variants can be translated into protein.

18. The downregulation of the regulator of Ca2+ homeostasis NCX3 by Ca2+-regulated DREAM is a striking example of the autoregulatory property of the Ca2+ signal in neurons.

19. plasma membrane Na+/Ca2+ exchangers have inhibitory interactions with the 14-3-3 proteins

Mouse (Murine) Solute Carrier Family 8 (Sodium/calcium Exchanger), Member 3 (SLC8A3) interaction partners

1. NCX2 and NCX3 protein and mRNA levels are relatively reduced in hippocampal CA1 of APP23 and APP-KI mice. Likewise, NCX2(+/-) or NCX3(+/-) mice exhibited impaired hippocampal LTP and memory-related behaviors. Moreover, relative to controls, calcium/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation significantly decreased in NCX2(+/-) mouse hippocampus but increased in hippocampus of NCX3(+/-) mice.

2. This study demonstrate that knocking-out NCX3 impairs oligodendrocyte response and worsens clinical symptoms in EAE without altering the immune T-cell population.

3. Demonstrate that NCX3 genetic deletion protects against ziram-induced neurotoxicity and suggest NCX3 and its downstream molecular pathways as key factors involved in ziram toxicity.

4. NCX3 regulates mitochondrial calcium handling from the outer mitochondrial membrane through an AKAP121-anchored signaling complex.

5. Function and regulation of the Na+-Ca2+ exchanger NCX3 splice variants in brain and skeletal muscle.

6. the use of genetic-modified mice for NCX1, NCX2, and NCX3 represents a fruitful strategy to characterize the physiological role exerted by NCX in CNS

7. Functional studies, as well as mRNA and protein expression analyses, revealed that NCX1 and NCX3, but not NCX2, were divergently modulated during OPC differentiation into oligodendrocyte.

8. the solution structure of NCX3 calcium binding domain 2B

9. calcium signaling mediated by NCX3 has a crucial role in oligodendrocyte maturation and myelin formation.

10. Results show that glucocorticoid treatment blunts LPS-induced increase in [Ca(2+)](i) in dendritic cells by increasing expression and activity of Na(+)/Ca(2+) exchanger NCX3.

11. The deletion of the NCX3 gene has detrimental consequences on basal synaptic transmission, long term potentiation regulation, spatial learning, and memory performance.

12. These results showed significant expression of NCX1 and NCX3 in ameloblasts, indicating their involvement in the directional Ca(2+) extrusion pathway from cells to the enamel mineralizing front

13. NCX3 plays an important role in vivo in the control of Ca(2+) concentrations in the skeletal muscle fibers and at the neuromuscular junction

14. three NCX variants are expressed in mouse osteoclasts and play an important role for Ca(2+) transport and regulation during osteoclastic bone resorption

15. NCX3 was found to serve as a major contributor of Ca++ translocation out of osteoblasts into calcifying bone matrix. NCX1 had little to no involvement.

16. Data suggest that the electrostatic switch in CBD1 and the associated conformational change are necessary for Na+/Ca2+ exchanger activation.