Anti-Mouse PLVAP (MECA-32) In Vivo Antibody - Low Endotoxin (ICH1264-1mg)

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

This product is the widely used rat anti-mouse PLVAP antibody, clone MECA-32 (rat IgG2a), produced in a low-endotoxin, carrier-free format for in-vivo and functional work. MECA-32 is one of the classic pan-endothelial reagents in vascular biology, originally raised as a marker of mouse endothelium and later shown to recognise plasmalemma vesicle-associated protein (PLVAP/PV-1). The rat IgG2a isotype and cross-reactivity with mouse endothelium make it well suited to studies in immunocompetent mouse models, where investigators want to label, track, or functionally interrogate the endothelial diaphragm apparatus rather than deplete a leukocyte subset. Validated applications include ELISA, flow cytometry, neutralization, and functional/blocking assays, so the same lot can support both readout and intervention arms of an experiment. Supplied at research-grade low endotoxin (typically under 1 EU/mg; ultra-low under 0.5 EU/mg) and available in bulk milligram-to-gram quantities, it is intended to minimise endotoxin-driven confounds in sensitive vascular, barrier, and inflammation models. All material is for research use only (RUO) and is not for diagnostic or therapeutic use. PLVAP (plasmalemma vesicle-associated protein, also called PV-1; UniProt Q91VC4) is a type II single-pass transmembrane glycoprotein that assembles into disulfide-linked homodimers on the endothelial cell surface. It is the structural building block of the stomatal and fenestral diaphragms that span caveolae, fenestrae, and transendothelial channels: roughly ten PLVAP dimers radiate like spokes across each 60-80 nm opening, forming a sieve-like grid that regulates the passage of solutes and cells. PLVAP is broadly expressed across fenestrated and continuous microvascular endothelium but is developmentally silenced in the CNS as the blood-brain barrier matures, making it a marker of barrier state. In pathology, PLVAP is re-induced in tumour neovasculature, including high-grade brain tumours, and contributes to microvascular permeability and leukocyte trafficking, positioning it as a marker and candidate target in angiogenesis and vascular-barrier research.