|TGF-beta 1 in Human PBMCs. TGF-beta 1 was detected in immersion fixed human peripheral blood mononuclear cells (PBMCs) using Goat Anti-Human LAP TGF-beta 1 Polyclonal Antibody (Catalog # AB-246-NA) at 10 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Goat IgG Secondary Antibody (yellow; Catalog # NL001) and counterstained with DAPI (blue).View our protocol for Fluorescent ICC Staining of Non-adherent Cells.|
|LAP (TGF-beta 1) in Human Prostate Cancer Tissue. LAP (TGF-beta 1) was detected in immersion fixed paraffin-embedded sections of human prostate cancer tissue using Goat Anti-Human LAP (TGF-beta 1) Antigen Affinity-purified Polyclonal Antibody (Catalog # AF-246-NA) at 10 µg/mL overnight at 4 °C. Tissue was stained using the Anti-Goat HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS008) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm in epithelial cells. View our protocol for Chromogenic IHC Staining of Paraffin-embedded Tissue Sections.|
|LAP TGF‑ beta 1 Inhibition of TGF‑ beta 1 Activity and Neutralization by Human LAP TGF‑ beta 1 Antibody. Recombinant Human LAP TGF‑ beta 1 (Catalog # 246-LP) inhibits Recombinant Human TGF‑ beta 1 (Catalog # 240‑B) growth inhibition activity in the HT‑2 mouse T cell line in a dose-dependent manner (orange line). Inhibition of Recombinant Human TGF‑ beta 1 (0.25 ng/mL) activity elicited by Recombinant Human LAP TGF‑ beta 1 (125 ng/mL) is neutralized (green line) by increasing concentrations of Goat Anti-Human LAP TGF‑ beta 1 Polyclonal Antibody (Catalog # AB-246-NA). The ND50 is typically 15‑30 µg/mL.|
TGF- beta 1 (transforming growth factor beta 1) and the closely related TGF-beta 2 and -beta 3 are members of the large TGF-beta superfamily. TGF- beta proteins are highly pleiotropic cytokines that regulate processes such as immune function, proliferation and epithelial-mesenchymal transition (1‑3). Human TGF-beta 1 cDNA encodes a 390 amino acid (aa) precursor that contains a 29 aa signal peptide and a 361 aa proprotein (4). A furin-like convertase processes the proprotein within the trans-Golgi to generate an N-terminal 249 aa (aa 30-278) latency-associated peptide (LAP) and a C-terminal 112 aa (aa 279-390) mature TGF- beta 1 (4‑6). Disulfide-linked homodimers of LAP and TGF-beta 1 remain non-covalently associated after secretion, forming the small latent TGF-beta 1 complex (4‑8). Purified LAP is also capable of associating with active TGF-beta with high affinity, and can neutralize TGF-beta activity (9). Covalent linkage of LAP to one of three latent TGF-beta binding proteins (LTBPs) creates a large latent complex that may interact with the extracellular matrix (5‑7). TGF-beta activation from latency is controlled both spatially and temporally, by multiple pathways that include actions of proteases such as plasmin and MMP9, and/or by thrombospondin 1 or selected integrins (5, 8). The LAP portion of human TGF-beta 1 shares 91%, 92%, 85%, 86% and 88% aa identity with porcine, canine, mouse, rat and equine TGF-beta 1 LAP, respectively, while mature human TGF-beta 1 portion shares 100% aa identity with porcine, canine and bovine TGF-beta 1, and 99% aa identity with mouse, rat and equine TGF-beta 1. Although different isoforms of TGF-beta are naturally associated with their own distinct LAPs, the TGF-beta 1 LAP is capable of complexing with, and inactivating, all other human TGF-beta isoforms and those of most other species (9). Mutations within the LAP are associated with Camurati-Engelmann disease, a rare sclerosing bone dysplasia characterized by inappropriate presence of active TGF-beta 1 (10).
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