PLSCR4 Antibody (Center) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q9NRQ2 |
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Clone Names | 100406224 |
Gene ID | 57088 |
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Other Names | Phospholipid scramblase 4, PL scramblase 4, Ca(2+)-dependent phospholipid scramblase 4, Cell growth-inhibiting gene 43 protein, TRA1, PLSCR4 |
Target/Specificity | The synthetic peptide sequence used to generate the antibody AP13974c was selected from the Center region of PLSCR4. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | PLSCR4 |
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Function | May mediate accelerated ATP-independent bidirectional transbilayer migration of phospholipids upon binding calcium ions that results in a loss of phospholipid asymmetry in the plasma membrane. May play a central role in the initiation of fibrin clot formation, in the activation of mast cells and in the recognition of apoptotic and injured cells by the reticuloendothelial system. |
Cellular Location | Membrane; Single-pass type II membrane protein |
Tissue Location | Expressed in heart, brain, placenta, lung, liver, kidney, pancreas, spleen, thymus, prostate, testis, uterus, small intestine and colon. Not detected in peripheral blood lymphocytes |
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Provided below are standard protocols that you may find useful for product applications.
Background
PLSCR4 may mediate accelerated ATP-independent bidirectional transbilayer migration of phospholipids upon binding calcium ions that results in a loss of phospholipid asymmetry in the plasma membrane. May play a central role in the initiation of fibrin clot formation, in the activation of mast cells and in the recognition of apoptotic and injured cells by the reticuloendothelial system.
References
Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :Sahu, S.K., et al. Biochim. Biophys. Acta 1790(10):1274-1281(2009)Py, B., et al. PLoS ONE 4 (3), E5006 (2009) :Shibata, H., et al. J. Biol. Chem. 283(15):9623-9632(2008)Wiedmer, T., et al. Biochim. Biophys. Acta 1467(1):244-253(2000)
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