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PECAM-1 / CD31 Antibody (clone JC/70A)
Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, IF |
|---|---|
| Primary Accession | P16284 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Clone Names | JC/70A |
| Calculated MW | 83kDa |
| Dilution | IHC-P (1:50) |
| Gene ID | 5175 |
|---|---|
| Other Names | Platelet endothelial cell adhesion molecule, PECAM-1, EndoCAM, GPIIA', PECA1, CD31, PECAM1 |
| Reconstitution & Storage | Stable for 24 months when stored at 2-8°C. |
| Precautions | PECAM-1 / CD31 Antibody (clone JC/70A) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | PECAM1 |
|---|---|
| Function | Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions (PubMed:19342684, PubMed:17580308). Tyr-690 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes (PubMed:19342684). Trans-homophilic interaction may play a role in endothelial cell-cell adhesion via cell junctions (PubMed:27958302). Heterophilic interaction with CD177 plays a role in transendothelial migration of neutrophils (PubMed:17580308). Homophilic ligation of PECAM1 prevents macrophage-mediated phagocytosis of neighboring viable leukocytes by transmitting a detachment signal (PubMed:12110892). Promotes macrophage-mediated phagocytosis of apoptotic leukocytes by tethering them to the phagocytic cells; PECAM1-mediated detachment signal appears to be disabled in apoptotic leukocytes (PubMed:12110892). Modulates bradykinin receptor BDKRB2 activation (PubMed:18672896). Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in endothelial cells (PubMed:18672896). Induces susceptibility to atherosclerosis (By similarity). |
| Cellular Location | Cell membrane; Single-pass type I membrane protein. Note=Cell surface expression on neutrophils is down-regulated upon fMLP or CXCL8/IL8- mediated stimulation. [Isoform Delta15]: Cell junction. Note=Localizes to the lateral border recycling compartment (LBRC) and recycles from the LBRC to the junction in resting endothelial cells |
| Tissue Location | Expressed on platelets and leukocytes and is primarily concentrated at the borders between endothelial cells (PubMed:18388311, PubMed:21464369). Expressed in human umbilical vein endothelial cells (HUVECs) (at protein level) (PubMed:19342684, PubMed:17580308). Expressed on neutrophils (at protein level) (PubMed:17580308). Isoform Long predominates in all tissues examined (PubMed:12433657). Isoform Delta12 is detected only in trachea (PubMed:12433657). Isoform Delta14-15 is only detected in lung (PubMed:12433657). Isoform Delta14 is detected in all tissues examined with the strongest expression in heart (PubMed:12433657). Isoform Delta15 is expressed in brain, testis, ovary, cell surface of platelets, human umbilical vein endothelial cells (HUVECs), Jurkat T- cell leukemia, human erythroleukemia (HEL) and U-937 histiocytic lymphoma cell lines (at protein level) (PubMed:12433657, PubMed:18388311). |
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Provided below are standard protocols that you may find useful for product applications.
Background
Induces susceptibility to atherosclerosis (By similarity). Cell adhesion molecule which is required for leukocyte transendothelial migration (TEM) under most inflammatory conditions. Tyr-690 plays a critical role in TEM and is required for efficient trafficking of PECAM1 to and from the lateral border recycling compartment (LBRC) and is also essential for the LBRC membrane to be targeted around migrating leukocytes. Prevents phagocyte ingestion of closely apposed viable cells by transmitting 'detachment' signals, and changes function on apoptosis, promoting tethering of dying cells to phagocytes (the encounter of a viable cell with a phagocyte via the homophilic interaction of PECAM1 on both cell surfaces leads to the viable cell's active repulsion from the phagocyte. During apoptosis, the inside-out signaling of PECAM1 is somehow disabled so that the apoptotic cell does not actively reject the phagocyte anymore. The lack of this repulsion signal together with the interaction of the eat-me signals and their respective receptors causes the attachment of the apoptotic cell to the phagocyte, thus triggering the process of engulfment). Isoform Delta15 is unable to protect against apoptosis. Modulates BDKRB2 activation. Regulates bradykinin- and hyperosmotic shock-induced ERK1/2 activation in human umbilical cord vein cells (HUVEC).
References
Simmons D.L.,et al.J. Exp. Med. 171:2147-2152(1990).
Stockinger H.,et al.J. Immunol. 145:3889-3897(1990).
Newman P.J.,et al.Science 247:1219-1222(1990).
Albelda S.M.,et al.J. Cell Biol. 114:1059-1068(1991).
Kirschbaum N.E.,et al.Blood 84:4028-4037(1994).
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