Human Mer Antibody

Detection of Human Mer by Western Blot.

Western blot shows lysates of U937 human histiocytic lymphoma cell line and PANC-1 human pancreatic carcinoma cell line. PVDF membrane was probed with 1 µg/mL of Goat Anti-Human Mer Antigen Affinity-purified Polyclonal Antibody (Catalog # AF891) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017). A specific band was detected for Mer at approximately 170-230 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

Western Blot Shows Human Mer Specificity by Using Knockout Cell Line.

Western blot shows lysates of HepG2 human hepatocellular carcinoma parental cell line and Mer knockout HepG2 cell line (KO). PVDF membrane was probed with 1 µg/mL of Goat Anti-Human Mer Antigen Affinity-purified Polyclonal Antibody (Catalog # AF891) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017). A specific band was detected for Mer at approximately 175 kDa (as indicated) in the parental HepG2 cell line, but is not detectable in knockout HepG2 cell line. GAPDH (Catalog # AF5718) is shown as a loading control. This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

Detection of Human Mer by Western Blot

Implication of both MERTK and TYRO3 receptors in PROS1-induced Src and VEC phosphorylation. (A,B) represent Western blot analysis (A) and subsequent quantification (B) of VEC phosphorylation on Tyr685, c-Src phosphorylation on Tyr416 or MLC phosphorylation. (B) Integrated intensity for the target proteins was divided by that for actin, and all conditions were normalized to their corresponding untreated controls. Analysis was performed with the Fiji software. (C) Proposed mechanism through which PROS1 interferes with EC permeability. PROS1 activates its tyrosine kinase receptors MERTK and TYRO3, leading to the phosphorylation of c- Src on Tyr416 and PAK-1 on Ser144 which in turn phosphorylate, respectively, VEC at Tyr685 and Ser665, two specific sites involved in the cleavage and internalization of VEC, respectively. The PROS1/MERTK-TYRO3/c-Src-Tyr416/VEC-Tyr685 pathway activates the cleavage of VEC extracellular domain, which destabilizes cell–cell junctions. The PROS1/MERTK-TYRO3/ PAK-1-Ser144/VEC-Ser665 pathway activates VEC internalization thus preventing VEC recognition between two adjacent endothelial cells. The Rho/ROCK/MLC pathway involved in the regulation of endothelial permeability is also activated by human PROS1. * p < 0.05; *** p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://www.mdpi.com/1467-3045/46/4/205), licensed under a CC-BY license. Not internally tested by R&D Systems.