Abcam’s anti-CD31 antibody is used in the analysis of susceptibility to atherosclerosis. The antibody is expressed in leukocytes and platelets.
- Product Name - Anti-CD31 antibody
- Description - Rabbit polyclonal to CD31
- Host Species - Rabbit
- Specificity - Customer feedback shows that certain batch-to-batch variation may exist with regard to mouse cross-reactivity. Abcam suggests ab124432 as an alternative antibody for mouse samples.
- Tested Applications - It is best suited for WB, IHC-FoFr, ICC/IF, IHC-P, and IHC-Fr.
- Species Reactivity - Reacts with pig, mouse, and human.
- Immunogen - Synthetic peptide within Mouse CD31 aa 700 to the C-terminus (C terminal). The precise sequence is proprietary.
- Positive Control - IHC-Fr: Human fetal heart tissue. WB: Human vascular endothelial cell lysate; Jurkat whole cell lysate (ab7899). IHC-P: Human tonsil tissue; xenograft tissue, mouse skin
Abcam’s Abpromise guarantee covers the usage of ab28364 in the tested applications listed in the table below. Recommended starting dilutions have been mentioned; the end-user should determine the ideal concentrations/dilutions.
||1/50. Heat-mediated antigen retrieval should be performed before starting with IHC staining protocol.
||1/20. PubMed: 17316380.
||Should be used at an assay dependent concentration.
The anti-CD31 antibody promotes susceptibility to atherosclerosis (by similarity). It is a cell adhesion molecule, which is needed for transendothelial migration (TEM) of leukocytes under the majority of the inflammatory conditions.
Tyr-690 has an important role to play in TEM and is needed for efficient trafficking of PECAM1 both to and from the lateral border recycling compartment, or LBRC. In addition, it is vital for the LBRC membrane to be targeted around the migrating leukocytes.
By transmitting “detachment” signals, the antibody prevents phagocyte ingestion of closely apposed viable cells and alters the function on apoptosis. This causes the dying cells to tether to phagocytes.
When a viable cell encounters a phagocyte through PECAM1’s homophilic interaction on the surfaces of both cells, it causes the viable cell to actively repel the phagocyte. At the time of apoptosis, PECAM1’s inside-out signaling is slightly disabled so that the phagocyte is no longer actively rejected by the apoptotic cell. The absence of this repulsion signal along with the interaction of the eat-me signals and their corresponding receptors causes the apoptotic cell to attach to the phagocyte, thereby stimulating the process of engulfment.
Isoform Delta15 is not capable of protecting against apoptosis. It modulates BDKRB2 activation and controls the activation of bradykinin- and hyperosmotic shock-induced ERK1/2 in human umbilical cord vein cells, or HUVEC for short.
The antibody is expressed in leukocytes and platelets, and is mainly concentrated at the boundaries between endothelial cells.
Isoform Long prevails in all the examined tissues. Isoform Delta12 and Delta14-15 are detected only in the trachea and lung, respectively. Isoform Delta14 is identified in all the examined tissues with the most intense expression in the heart.
Isoform Delta15 is expressed in the cell surface of platelets, ovary, testis, brain, HUVECs, human erythroleukemia (HEL), Jurkat T-cell leukemia, and U937 histiocytic lymphoma cell lines (at protein level).