- Catalogue N°
- 650.010.096 - 1 x 96 (pre-coated)
650.010.192 - 2 x 96 (pre-coated)
- Assay Range
- 31.25 pg/ml - 2000 pg/ml
- 9 pg/ml
- Target species
- Recognizes both natural and recombinant human TGF-β1
- Sample Type
- Serum, Plasma, Cell culture supernatant
- Sample Size
- 100 µl
- Cross Reaction
- Cross reactivity with sheep and pig TGF-β1
- Kit Content
- Diaclone ELISA Kits include pre-coated strip plates, biotinylated secondary antibody, standards, controls (where applicable), buffers, streptavidin-HRP, TMB, stop reagents and a detailed procedure.
Transforming growth factor-b (TGF-b) belongs to a family of dimeric 25 kDa polypeptides that are ubiquitously distributed in tissues and synthesized by many different cells. Three isoforms of transforming Growth Factor-b (TGF-beta1, beta-2 and beta-3) exist in mammals. They play critical roles in growth regulation and development. Each isoform is encoded by a unique gene on different chromosomes. All three of these growth factors are secreted by most cell types, generally in a latent form, requiring activation before they can exert biological activity. The TGF-betas possess three major activities: they inhibit proliferation of most cells, but can stimulate the growth of some mesechymal cells; they exert immunosuppressive effects and they enhance the formation of extracellular matrix. Two types of membrane receptors possessing kinase activity are involved in signal transduction. The TGF-betas are involved in wound repair processes and in starting inflammatory reaction and then in the resolution through chemotactic attraction of inflammatory cells and fibroblast.
TGF-b1 is the first recognized transforming growth factor, its subunits of each 12.5 kDa are bound via disulphide bridges. TGF-b1 is inhibitive to T- and B cell proliferation as well as to maturation and activation of macrophages. It furthermore inhibits activity of natural killer cells and lymphokine activated killer cells and blocks production of cytokines.
Measurement of TGF-b1 in blood has been advocated for diagnosis of various diseases. TGF-b1 has been shown to be an organizer of responses to neurodegeneration.
In this context, it turned out to be interesting in monitoring Alzheimer’s disease, Down’s syndrome, AIDS and Parkinson’s disease. Serum and cerebrospinal fluid levels of Multiple Sclerosis patients were shown to be of great value to monitor remission and acute phases. TGF-b1 is thought to play an important role in bone metabolism, it is considered a putative regulator of osteoclastic-osteoblastic interaction, thus it can be regarded as a marker for osteoporosis. TGF-b1 is involved in the pathogenesis of glomerular diseases such as diabetic nephropathy and glomerulosclerosis. TGF-b1 has been described to be functionally connected to major immune system abnormalities as in autoimmunity (SLE). Serum levels have been shown to correlate with disease activity in autoimmune hepatitis. Elevated serum levels of TGF-b1 are determined in Chronic fatigue syndrome patients and in Guillain-Baire syndrome patients. An inverse correlation with disease activity was described for TGF-b1 levels in Kawasaki disease and patients with IgA deficiency.
TGF-b1 has been confirmed to promote fibrotic processes, thus it is implicated in the myelofibrosis with myeloid metaplasia. Increased serum levels of TGF-b1 in patients affected by thrombotic thromocytopenic purpura implicate its function on bone marrow haematopoiesis. Determination of circulating TGF-b1 turned out to reflect the various stages in solid tumors as has been shown for cervical cancer, elevations were furthermore found in prostatic cancer, bladder cancer, and liver cancer.
Decreased levels of TGF-b1 in the serum of sepsis and acute stroke patients may reflect the changing immunological-inflammatory status of these patients. Decreased TGF-b1 serum levels were described for patients with acute Plasmodium falciparum malaria.
Version 6 - 07.19
For research use only
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