anti-TGFB1 Antibody from antibodies-online

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anti-TGFB1 Antibody

Description

Product Characteristics: TGF-beta-1 is a multifunctional cytokine that belongs to a superfamily of structurally related regulatory proteins, including three mammalian TGF-beta isoforms (TGF-beta-1, -beta-2, and -beta-3), activin/inhibins and bone morphogenetic proteins. The most abundant isoform, TGF-beta-1, is a 25kDa homodimer composed of two 12.5 kDa subunits joined by disulfide bonds. TGF-beta-1 is a highly conserved molecule, the amino acid sequence between human and mouse differs by only one residue. Although originally defined by its ability to cause anchorage independent cell growth and changes in cell morphology of rat fibroblasts, subsequent research has revealed that TGF-beta is actually a major growth inhibitor for most cell types. It is produced by a wide variety of cell and tissue types during all stages of cell differentiation. TGF-beta-1 sources include platelets, bone and soft tissues, such as placenta and kidneys.
Synonyms: Camurati Engelmann disease antibody, CED antibody, Diaphyseal dysplasia 1 progressive antibody, DPD1 antibody, LAP antibody, Latency-associated peptide antibody, TGF beta 1 antibody
Target Information: This gene encodes a member of the transforming growth factor beta (TGFB) family of cytokines, which are multifunctional peptides that regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types. Many cells have TGFB receptors, and the protein positively and negatively regulates many other growth factors. The secreted protein is cleaved into a latency-associated peptide (LAP) and a mature TGFB1 peptide, and is found in either a latent form composed of a TGFB1 homodimer, a LAP homodimer, and a latent TGFB1-binding protein, or in an active form composed of a TGFB1 homodimer. The mature peptide may also form heterodimers with other TGFB family members. This gene is frequently upregulated in tumor cells, and mutations in this gene result in Camurati-Engelmann disease.[provided by RefSeq, Oct 2009]