Transforming Growth Factor-Beta 1 (TGFβ1) (Rat)
- SKU:
- BE69208
- Bulk Pricing:
-
- Buy 5 - 20 and get 5% off
- Buy 21 - 30 and get 10% off
- Buy 31 - 50 and get 15% off
- Buy 51 or more – call for best pricing
The cookie settings on this website are set to 'allow all cookies' to give you the very best experience. Please click Accept Cookies to continue to use the site.
Sandwich enzyme-linked immune-sorbent assay (ELISA) for the determination of TGFβ1 concentrations in serum, body fluids, tissue homogenate or cell culture supernates from rat. For research use only, not for use in diagnostic procedures.<br><br>
Transforming growth factor beta 1 or TGFβ1 is a polypeptide member of the transforming growth factor beta superfamily of cytokines. In humans, TGFβ1 is encoded by the TGFβ1 gene. This gene contains 7 exons and very large introns, maps to 19q13.1-q13.3. TGFβ1 acts synergistically with TGFA in inducing transformation. It also acts as a negative autocrine growth factor. The TGFβ1 is directly involved in the pathogenesis of bone marrow reticulin fibrosis in hairy cell leukemia. The expression of TGFβ1 in the early stages of DMD may be critical in initiating muscle fibrosis and suggested that antifibrosis treatment might slow progression of the disease, increasing the utility of gene therapy.
Sandwich enzyme-linked immune-sorbent assay (ELISA) for the determination of TGFβ1 concentrations in serum, body fluids, tissue homogenate or cell culture supernates from rat. For research use only, not for use in diagnostic procedures.<br><br>
Transforming growth factor beta 1 or TGFβ1 is a polypeptide member of the transforming growth factor beta superfamily of cytokines. In humans, TGFβ1 is encoded by the TGFβ1 gene. This gene contains 7 exons and very large introns, maps to 19q13.1-q13.3. TGFβ1 acts synergistically with TGFA in inducing transformation. It also acts as a negative autocrine growth factor. The TGFβ1 is directly involved in the pathogenesis of bone marrow reticulin fibrosis in hairy cell leukemia. The expression of TGFβ1 in the early stages of DMD may be critical in initiating muscle fibrosis and suggested that antifibrosis treatment might slow progression of the disease, increasing the utility of gene therapy.