CYSLTR1 Antibody (Center) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q9Y271 |
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Clone Names | 100525128 |
Gene ID | 10800 |
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Other Names | Cysteinyl leukotriene receptor 1, CysLTR1, Cysteinyl leukotriene D4 receptor, LTD4 receptor, G-protein coupled receptor HG55, HMTMF81, CYSLTR1, CYSLT1 |
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 | CYSLTR1 |
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Synonyms | CYSLT1 |
Function | Receptor for cysteinyl leukotrienes mediating bronchoconstriction of individuals with and without asthma. Stimulation by LTD4 results in the contraction and proliferation of smooth muscle, edema, eosinophil migration and damage to the mucus layer in the lung. This response is mediated via a G-protein that activates a phosphatidylinositol-calcium second messenger system. The rank order of affinities for the leukotrienes is LTD4 >> LTE4 = LTC4 >> LTB4. |
Cellular Location | Cell membrane; Multi-pass membrane protein. |
Tissue Location | Widely expressed, with highest levels in spleen and peripheral blood leukocytes. Lower expression in several tissues, such as lung (mostly in smooth muscle bundles and alveolar macrophages), placenta, small intestine, pancreas, colon and heart |
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Provided below are standard protocols that you may find useful for product applications.
Background
The cysteinyl leukotrienes LTC4, LTD4, and LTE4 areimportant mediators of human bronchial asthma. Pharmacologicstudies have determined that cysteinyl leukotrienes activate atleast 2 receptors, the protein encoded by this gene and CYSLTR2.This encoded receptor is a member of the superfamily of Gprotein-coupled receptors. Activation of this receptor by LTD4results in contraction and proliferation of smooth muscle, oedema,eosinophil migration and damage to the mucus layer in the lung.
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)Boulay, M.E., et al. Prostaglandins Leukot. Essent. Fatty Acids 83(1):15-22(2010)Schuurhof, A., et al. Pediatr. Pulmonol. 45(6):608-613(2010)Hasegawa, S., et al. Platelets 21(4):253-259(2010)Sokolowska, M., et al. BMC Immunol. 10, 63 (2009) :
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