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| Product Name | LEGEND MAX™ Human LAP ELISA Kit with Pre-coated Plates |
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| Description | As an important regulator of TGF-β activity, Latency-Associated Peptide (LAP) is secreted as a complex with TGF-β. LAP and TGF-β1 are synthesized as a single propeptide precursor of 390 amino acids with an N-terminal signal peptide of 29 amino acids, a 249 amino acids pro-region (LAP), and a 112 amino acids C-terminal region (TGF-β1). Both LAP and TGF-β1 exist as homodimers in circulation, but the disulfide linked homodimers of LAP and TGF-β1 remain non-covalently associated, forming the small latent TGF-β1 complex (SLC, 100 kD). The large latent TGF- β1 complex (LLC, 235 – 260 kD) contains a third component, the latent TGF- β binding protein (LTBP), which is linked to LAP by a single disulfide bond. LTBP does not confer latency but is for efficient secretion of the complex to extracellular sites. Previously, LAP was presumed to function only as a sequestering agent for TGF-β1. However, recent studies showed that LAP has in vitro or in vivo functions independent of TGF-β1. LAP can induce epithelial cell migration and promote chemotaxis of monocytes and block inflammation. In vivo, LAP enhances hepatocyte regeneration and reduces fibrosis. LAP is also a surface marker of activated regulatory T cells. LEGEND MAX™ Human LAP ELISA kit is a Sandwich Enzyme-Linked Immunosorbent Assay (ELISA) with 96-well strip plates that are pre-coated with a capture antibody specific for LAP. This Human LAP kit is specifically designed for use with cell culture supernatant, serum, plasma or other biological samples. This kit is analytically validated with ready-to-use reagents. |
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| Size | 5 Pre-coated Plates |
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| Concentration | ELISA |
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| Applications | n/a |
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| Other Names | Latency Associated Peptide (LAP), CED, DPD1, TGFb, TGFbeta, TGF beta, LAP Precoated ELISA Kit |
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| Gene, Accession, CAS # | Gene ID: 7040 |
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| Catalog # | 436808 |
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| Order / More Info | LEGEND MAX™ Human LAP ELISA Kit with Pre-coated Plates from BIOLEGEND |
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| Product Specific References | n/a |
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