|Application ||WB, IHC-P, FC, E|
|Other Accession||Q01728, P70414, P48765|
|Calculated MW||108547 Da|
|Antigen Region||296-325 aa|
|Other Names||Sodium/calcium exchanger 1, Na(+)/Ca(2+)-exchange protein 1, Solute carrier family 8 member 1, SLC8A1, CNC, NCX1|
|Target/Specificity||This SLC8A1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 296-325 amino acids from the Central region of human SLC8A1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||SLC8A1 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Mediates the exchange of one Ca(2+) ion against three to four Na(+) ions across the cell membrane, and thereby contributes to the regulation of cytoplasmic Ca(2+) levels and Ca(2+)- dependent cellular processes (PubMed:1374913, PubMed:11241183, PubMed:1476165). Contributes to Ca(2+) transport during excitation-contraction coupling in muscle. In a first phase, voltage-gated channels mediate the rapid increase of cytoplasmic Ca(2+) levels due to release of Ca(2+) stores from the endoplasmic reticulum. SLC8A1 mediates the export of Ca(2+) from the cell during the next phase, so that cytoplasmic Ca(2+) levels rapidly return to baseline. Required for normal embryonic heart development and the onset of heart contractions.|
|Cellular Location||Cell membrane; Multi- pass membrane protein|
|Tissue Location||Detected primarily in heart and at lower levels in brain (PubMed:1374913). Expressed in cardiac sarcolemma, brain, kidney, liver, pancreas, skeletal muscle, placenta and lung (PubMed:1476165).|
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Provided below are standard protocols that you may find useful for product applications.
In cardiac myocytes, Ca(2+) concentrations alternate between high levels during contraction and low levels during relaxation. The increase in Ca(2+) centration during contraction is primarily due to release of Ca(2+) from intracellular stores. However, some Ca(2+) also enters the cell through the sarcolemma (plasma membrane). During relaxation, Ca(2+) is sequestered within the intracellular stores. To prevent overloading of intracellular stores, the Ca(2+) that entered across the sarcolemma must be extruded from the cell. The Na(+)-Ca(2+) exchanger is the primary mechanism by which the Ca(2+) is extruded from the cell during relaxation. In the heart, the exchanger may play a key role in digitalis action. The exchanger is the dominant mechanism in returning the cardiac myocyte to its resting state following excitation.
Palty,R., et.al., Proc. Natl. Acad. Sci. U.S.A. 107 (1), 436-441 (2010) Kepp,K., et.al., BMC Med. Genet. 11, 15 (2010)
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