|Reactivity||Human, Mouse, Rat|
|Calculated MW||100523 Da|
|Homology||Human, mouse - identical.|
|Other Names||Sodium/calcium exchanger 2, Na(+)/Ca(2+)-exchange protein 2, Solute carrier family 8 member 2, Slc8a2, Ncx2|
|Related products for control experiments||Control peptide antigen (supplied with the antibody free of charge).|
|Target/Specificity||Peptide (C)RVGDAQGMFEPDGG, corresponding to amino acid residues 486-499 of rat NCX-2 (Accession P48768). 3rd intracellular loop.|
|Peptide Confirmation||Confirmed by mass-spectrography and amino acid analysis.|
|Format||Affinity purified antibody, lyophilized powder|
|Reconstitution||50 µl or 0.2 ml deionized water, depending on the sample size.|
|Antibody Concentration After Reconstitution||0.8 mg/ml.|
|Buffer After Reconstitution||Phosphate buffered saline (PBS), pH 7.4, 1% BSA, 0.05% NaN3.|
|Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Storage After Reconstitution||The reconstituted solution can be stored at 4ºC for up to 2 weeks. For longer periods, small aliquots should be stored at -20ºC or below. Avoid multiple freezing and thawing. The further dilutions should be made using a carrier protein such as BSA (1%). Centrifuge all antibody preparations before use (10000 × g 5 min).|
|Control Antigen Storage Before Reconstitution||Lyophilized powder can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C.|
|Control Antigen Reconstitution||100 µl DDW.|
|Control Antigen Storage After Reconstitution||-20ºC.|
|Preadsorption Control||1 µg peptide per 1 µg antibody.|
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Provided below are standard protocols that you may find useful for product applications.
Ca2+ has proven to be a universal signaling molecule in excitable and non-excitable cells. However, being that its intracellular concentration is 1000 time lower than the extracellular milieu, it is important for the cell to keep this ratio for proper function. NCX, a Na+/Ca2+ exchanger is responsible for most of the efflux of Ca2+ out from the cell1-3. The NCX transporter is a member of the SLC8 family of solute carriers which in turn belong to the CaCA superfamily1,4,5. NCX-1 is one of three Na+/Ca2+ exchangers (NCX-1, NCX-2, NCX-3) leading to one Ca2+ movement across the plasma membrane in exchange of three Na+ influx. However, the transporter can reverse the direction of the transport if the concentrations of Na+ and Ca2+ change6. The transporter has nine transmembrane domains and intracellular N- and C-terminals. Between tansmembrane domains 5 and 6, the presence of an extra-long intracellular loop, termed the f loop is responsible for regulating the activity of NCX-1 via several different mechanisms like ion binding, phosphorylation, etc. The f loop also has sites which undergo alternative splicing7. Of the three NCX-1 expressed in mammalian cells, NCX-1 is the most widely expressed. Its expression is detected in the heart, brain, and kidney. NCX-1 undergoes alternative splicing in a tissue dependent manner. The first splice region does not change the overall structure of the protein but rather enables the expression of the gene specific to the tissues which require the expression of the gene. The second splicing site leads to a number of proteins varying in length. NCX-2 expression is much more limited; it is expressed only in neurons. NCX-3 is expressed in skeletal muscle and in some regions of the brain and undergoes alternative splicing in a similar fashion to that of NCX-11,8. Due to its central role in modulating Ca2+ levels in the cell, NCX exchangers are involved in various pathophysiological diseases/disorders such as hypoxia, aging, alzheimer’s7, to name a few.
References 1. Lytton, J. (2007) Biochem. J. 406, 365. 2. Lee, S.H. et al. (2002) J. Neurosci. 22, 6891. 3. Wanaverbecq, N. et al. (2003) J. Physiol. 550, 83. 4. Schwarz, E. and Benzer, S. (1997) Proc. Natl. Acad. Sci. U.S.A. 94, 10249. 5. Cai, X. and Lytton, J. (2004) Mol. Biol. Evol. 21, 1692. 6. Kimura, J. et al. (2009) Biol. Pharm. Bull. 32, 325. 7. Annunziato, L. et al. (2004) Pharmacol. Rev. 56, 633. 8. Papa, M. et al. (2003) J. Comp. Neurol. 461, 31.
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