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SLC8A1 Antibody (Center) Blocking Peptide

Synthetic peptide

     
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Product Information
Primary Accession P32418
Clone Names 90723124
Peptide ID 90723124
Additional Information
Gene ID 6546
Other Names Sodium/calcium exchanger 1, Na(+)/Ca(2+)-exchange protein 1, Solute carrier family 8 member 1, SLC8A1, CNC, NCX1
Target/Specificity The synthetic peptide sequence used to generate the antibody AP8939c was selected from the Center region of human SLC8A1. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
Format Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
PrecautionsThis product is for research use only. Not for use in diagnostic or therapeutic procedures.
Protein Information
Name SLC8A1
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).
Research Areas
Citations (0)

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Background

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.

References

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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$ 80.00
Cat# BP8939c
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