Human Transforming Growth Factor Beta 3 (TGFB3) ELISA Kit
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Description
Human Transforming Growth Factor Beta 3 (TGFB3) ELISA Kit is an ELISA Kit for the in vitro quantitative measurement of Human Transforming Growth Factor beta 3 (TGFb3) concentrations in serum, plasma, tissue homogenates, cell culture supernatants and other biological fluids. This assay has high sensitivity and excellent specificity for detection of Transforming Growth Factor Beta 3 (TGFb3)
Documents del producto
Product specifications
| Category | ELISA Kits |
| Immunogen Target | Transforming Growth Factor Beta 3 (TGFB3) |
| Reactivity | Human |
| Detection Method | Colorimetric |
| Assay Data | Quantitative |
| Assay Type | Sandwich |
| Test Range | 15.6 pg/ml - 1000 pg/ml |
| Sensitivity | < 5.7 pg/ml |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Size 1 | 96 tests |
| Size 2 | 5 × 96 tests |
| Size 3 | 10 × 96 tests |
| Form | Lyophilized |
| Tested Applications | ELISA |
| Sample Type | Serum, plasma, tissue homogenates, cell culture supernatants and other biological fluids. |
| Availability | Shipped within 5-7 working days. The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request. |
| Storage | Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual. |
| Dry Ice | No |
| Alias | ARVD,ARVD1,LDS5,RNHF,TGF-beta3,Latency-associated peptide LAP,Transforming growth factor beta-3 |
| Background | Elisa kits for TGFB3 |
| Status | RUO |
| Note | Validity: The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request. This product is for research use only. The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments. Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein. |
Descripción
TGFB3 is another member of the TGF-β family that is predominantly involved in embryonic development, tissue remodeling, and wound healing. TGFB3 regulates processes such as epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) deposition, and immune suppression. It is highly expressed during palatogenesis, craniofacial development, and lung morphogenesis, where it plays an essential role in cell signaling and tissue architecture. TGFB3 facilitates proper scar formation and tissue repair by modulating fibroblast activation and ECM production while reducing excessive fibrosis. In cancer, TGFB3 contributes to tumor progression by inducing EMT and promoting metastatic dissemination. Mutations or dysregulation of TGFB3 are associated with cleft palate, cardiovascular abnormalities, and fibrotic diseases. Knockout models reveal impaired wound healing, disrupted tissue morphogenesis, and craniofacial defects, highlighting TGFB3’s role in tissue development, regeneration, and fibrotic regulation.
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TGFB3 antibody
This gene encodes a secreted ligand of the TGF-beta (transforming growth factor-beta) superfamily of proteins. Ligands of this family bind various TGF-beta receptors leading to recruitment and activation of SMAD family transcription factors that regulate gene expression. The encoded preproprotein is proteolytically processed to generate a latency-associated peptide (LAP) and a mature peptide, and is found in either a latent form composed of a mature peptide homodimer, a LAP homodimer, and a latent TGF-beta binding protein, or in an active form consisting solely of the mature peptide homodimer. The mature peptide may also form heterodimers with other TGF-beta family members. This protein is involved in embryogenesis and cell differentiation, and may play a role in wound healing. Mutations in this gene are a cause of aortic aneurysms and dissections, as well as familial arrhythmogenic right ventricular dysplasia 1.
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