A multifunctional polypeptide which regulates cellular growth, differentiation, extracellular matrix deposition, immunosuppression, embryogenesis, repair of tissue and regulation of hematopoiesis.
Immunosuppressive effects of this family of proteins promotes tumor progression and diminishes responses to therapy.
61% of patients with colorectal cancer stage III with MSI also have TGF-beta RII mutation.
It is associated with a poor prognosis in advanced stage endometrial carcinoma.
TGF-β blocks the conversion of dermal fibroblasts into fat cells; with fewer fat cells underneath to provide support, the skin becomes saggy and wrinkled.
Immunosuppressive effects of this family of proteins promotes tumor progression and diminishes responses to therapy.
The cytokine transforming growth factor beta (TGF-β) is essential for Treg cells to differentiate from naïve CD4+ cells and is important in maintaining Treg cell homeostasis.
The TGF-ß pathway inhibits erythropoiesis, and binds the ligands, promoting the formation of red blood cells.
61% of patients with colorectal cancer stage III with MSI also have TGF-beta RII mutation.
Superfamily plays significant role in embryogenesis and regulates, cell proliferation, differentiation and apoptosis.
A cytokine that regulates tissue homeostasis.
Superfamily consists of TGFb, activin, and bone morphogenetic protein subfamilies.
TGFb signaling depends on the cellular content and tissue micro environment
its dysregulation is involved in several disease, including cancer.
In normal tissues it can inhibit proliferation of epithelial cells and promote differentiation, reflecting its tumor suppressor activity.
It can play and oncogenic roll by promoting cancer cell proliferation, cancer cell renewal, epithelial-to-mesenchymal transition, invasion, tumor progression, metastatic spread, and immune escape.
High levels of TGF beta confers poor prognosis, associated with early recurrence after surgery, resistance to chemo or immunotherapy and shorter survival.
Mutations in TGFBR types 1 and 2 found in association with presentations similar to Marfan’s syndrome, with familial thoracic aortic aneurysm and dissection or rupture.
Mutations in TGFBR types 1 and 2 associated with hypertelorism, bifid uvula, cleft palate or both, arterial tortuosity, vascular aneurysms and dissections (Loeys-Dietz syndrome).
Skin aging is caused in part by TGF-β, which reduces the subcutaneous fat that gives skin a pleasant appearance and texture.