TGF-beta 2 Antibody Summary
TGF‑ beta 1.2 but will cross-react with other TGF-beta variants with at least 100-fold lower sensitivity. It will also neutralize the biological activity of TGF-beta 1.2, at a 50 fold higher IgG concentration.
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of Human TGF‑ beta 2 by Western Blot. Western blot shows lysates of human heart tissue and human breast cancer tissue. PVDF membrane was probed with 0.25 µg/mL of Goat Anti-TGF‑ beta 2 Polyclonal Antibody (Catalog # AB-112-NA) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017). A specific band was detected for TGF‑ beta 2 at approximately 70 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.
Detection of Human TGF‑ beta 2 by Simple WesternTM.
Simple Western lane view shows lysates of human heart tissue and human breast cancer tissue, loaded at 0.2 mg/mL. A specific band was detected for TGF‑ beta 2 at approximately 63 kDa (as indicated) using 2.5 µg/mL of Goat
Anti-TGF‑ beta 2 Polyclonal Antibody
(Catalog # AB-112-NA) followed by 1:50 dilution of HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF109). This experiment was conducted under reducing conditions and using the
12-230 kDa separation system.
TGF‑ beta 2 Inhibition of IL‑4-dependent Cell Proliferation and Neutralization by TGF‑ beta 2 Antibody.
Porcine TGF‑ beta 2 (Catalog # 102-B2) inhibits Recombinant Mouse IL‑4 (Catalog # 404-ML) induced proliferation in the HT‑2 mouse T cell line in a dose-dependent manner (orange line). Inhibition of Recombinant Mouse IL‑4 (7.5 ng/mL) activity elicited by Porcine TGF‑ beta 2 (1 ng/mL) is neutralized (green line) by increasing concentrations of Sheep Anti-TGF‑ beta 2 Polyclonal Antibody (Catalog # AB-112-NA). The ND50 is typically
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: TGF-beta 2
TGF-beta 2 (transforming growth factor beta 2) is one of three closely related mammalian members of the large TGF-beta superfamily that share a characteristic cysteine knot structure (1-7). TGF-beta 1, -2 and -3 are highly pleiotropic cytokines proposed to act as cellular switches that regulate processes such as immune function, proliferation and epithelial-mesenchymal transition (1-4). Each TGF-beta isoform has some non-redundant functions; for TGF-beta 2, mice with targeted deletion show defects in development of cardiac, lung, craniofacial, limb, eye, ear and urogenital systems (2). Human TGF-beta 2 cDNA encodes a 414 amino acid (aa) precursor that contains a 19 aa signal peptide and a 395 aa proprotein (8). A furin-like convertase processes the proprotein to generate an N-terminal 232 aa latency-associated peptide (LAP) and a C-terminal 112 aa mature TGF- beta 2 (8, 9). Disulfide-linked homodimers of LAP and TGF-beta 2 remain non-covalently associated after secretion, forming the small latent TGF-beta 1 complex (8-10). Covalent linkage of LAP to one of three latent TGF-beta binding proteins (LTBPs) creates a large latent complex that may interact with the extracellular matrix (9, 10). TGF-beta is activated from latency by pathways that include actions of the protease plasmin, matrix metalloproteases, thrombospondin 1 and a subset of integrins (10). Mature human TGF-beta 2 shows 100% aa identity with porcine, canine, equine and bovine TGF-beta 2, and 97% aa identity with mouse and rat TGF-beta 2. It demonstrates cross-species activity (1). TGF-beta 2 signaling begins with binding to a complex of the accessory receptor betaglycan (also known as TGF-beta RIII) and a type II ser/thr kinase receptor termed TGF-beta RII. This receptor then phosphorylates and activates another ser/thr kinase receptor, TGF-beta RI (also called activin receptor-like kinase (ALK) -5), or alternatively, ALK-1. The whole complex phosphorylates and activates Smad proteins that regulate transcription (3, 11, 12). Use of other signaling pathways that are Smad-independent allows for disparate actions observed in response to TGF-beta in different contexts (11).
- Sporn, M.B. (2006) Cytokine Growth Factor Rev. 17:3.
- Dunker, N. and K. Krieglstein, 2000, Eur. J. Biochem. 267:6982.
- Wahl, S.M. (2006) Immunol. Rev. 213:213.
- Chang, H. et al. (2002) Endocr. Rev. 23:787.
- Lin, J.S. et al. (2006) Reproduction 132:179.
- Hinck, A.P. et al. (1996) Biochemistry 35:8517.
- Mittl, P.R.E. et al. (1996) Protein Sci. 5:1261.
- deMartin, R. et al. (1987) EMBO J. 6:3673.1.
- Miyazono, K. et al. (1988) J. Biol. Chem. 263:6407.
- Oklu, R. and R. Hesketh (2000) Biochem. J. 352:601.
- de Caestecker, M. et al. (2004) Cytokine Growth Factor Rev. 15:1.
- Zuniga, J.E. et al. (2005) J. Mol. Biol. 354:1052.
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