Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1:1000 |
1:10-1:50 |
1:10-1:50 |
Not tested in other applications.
Calculated MW
Predict Reactivity
Rat, Bovine(>80% identity)
Form
Liquid
Buffer
PBS
Preservative
0.09% Sodium azide
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
Batch dependent (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
KLH conjugated synthetic peptide between 296-325 amino acids from the Central region of human SLC8A1.
Purification
Protein A purified, followed by peptide affinity purification.
Conjugation
Unconjugated
RRID
AB_11172722
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
solute carrier family 8 member A1 , NCX1
Cellular Localization
Cell membrane
Background
In cardiac myocytes, Ca(2+) concentrations alternate between high levels during contraction and low levels during relaxation. The increase in Ca(2+) concentration 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.[supplied by OMIM, Apr 2004]
Database
Research Area