TGF beta 3/TGFB3 Protein, Human (HEK293)

TGF-β3 (transforming growth factor-β3) is a member of a TGF­-beta superfamily subgroup that performs many cellular functions. TGF-β3 has a role in embryogenesis and cell differentiation. TGF-β3 also plays a critical role in palatogenesis, the wound healing process. TGF-β3 is capable of binding directly to the type II receptor (TβRII)^[1][2]. TGF beta 3/TGFB3 Protein, Human (HEK293) is produced in HEK293 cells, and consists of 112 amino acids (A301-S412).

Three TGF-β isoforms have been found in mammals: TGF-β1, 2, and 3, which are structurally and functionally similar. TGF-β3 is important in embryonic development, scarless repair of injury in the embryo, adult wound healing and tissue homeostasis. It has an important role in regulating cell migration, angiogenesis, epithelial-mesenchymal transition, apoptosis, modulation of immune function, extracellular matrix (ECM) production and the regulation of ECM remodelling; biological processes that are often required for tumour growth and maintenance^[1][2].
As with all members of the family, TGF-β3 is highly conserved across species, with mouse, rat and human TGF-β3 demonstrating >97% sequence homology.
TGF-β3 is released from LAP by integrins: integrin-binding results in distortion of the LAP chain and subsequent release of the active TGF-β3. TGF-β3 is capable of binding directly to the type II receptor (TβRII). TGF-β3 expression increases in fetal wound healing and reduces fibronectin and collagen I and III deposition, and also improves the architecture of the neodermis. Fibroblasts are key cells in the wound healing process. In addition, TGF-β3 may actually play a protective role against tumourigenesis in a range of tissues including the skin, breast, oral and gastric mucosa. TGF-β3 is a more potent inhibitor of DNA synthesis in human keratinocytes compared to TGF-β1 and TGF-β2. TGF-β3 mRNA is expressed in lymphocytes such as CD4⁺ T cells, CD8⁺ T cells, γδT cells, and B cells. TGF-β3 has the potential to regulate systemic autoimmune diseases by inhibiting B cells. Moreover, during palatogenesis, TGF-β3 is supposed to transduce signals via both canonical Smad-dependent and non-canonical Smad-independent signaling. In human B cells, TGF-β3 induces phosphorylation of Smad1/5 along with Smad2 and Smad3^[1][2][3].
TGF-β3 is involved in cell differentiation, embryogenesis and development. TGF-β3 is crucial in tissue regeneration and scarless tissue repair. TGF-β3 is also involved in palatogenesis, chondrogenesis, and pulmonary development. Furthermore, TGF-β3 plays a role in cancer and immune diseases^[1][2][3].

Recombinant TGF-β3 (0.01-10 ng/mL) induces fibronectin expression in leiomyoma cells and directly stimulates leiomyoma cell proliferation^[4].
Recombinant TGF-β3 (0.5 ng/mL) promotes mRNA expression, and increased protein levels of osteocalcin (OCN) and type I collagen (COL I) in mouse pulpal mesenchymal cells. TGF-β3 also induces the expression of dentin sialophosphoprotein and dentin matrix protein 1^[5].
Recombinant TGF-β3 (0.005-3 ng/mL) adds to rat Sertoli cells cultured in vitro on Matrigel-coated bicameral units perturbed the inter-Sertoli tight junction (TJ) permeability barrier dose-dependently. Moreover, the presence of TGF-β3 also inhibits the transient and/or basal expression of several TJ-associated proteins, which include occludin, zonula occludens-1, and claudin-11 when inter-Sertoli TJs are being assembled in vitro^[8].

Recombinant TGF-β3 (1 μg/kg; i.p; once every week) decelerates the progress of radiation-induced pulmonary fibrosis and hindered the recruitment of fibrocytes to lung in radiation-induced mouse pulmonary fibrosis^[6].
Recombinant TGF-β3 (local infiltration (0.5 μg, 1.0 μg, 2.5 μg, and 50 μg) or intravenous application (500 μg/kg); for 7 days) treatment accelerates gastric ulcer healing in rats^[7].

1.The ED₅₀ is <0.2 ng/mL as measured in a cell proliferation assay using mouse HT-2 cells.
2.Measured by its ability to inhibit the IL-4-dependent proliferation of TF-1 mouse T cells. The ED₅₀ for this effect is 10-80 pg/mL.
3.Measured by its ability to inhibit the IL-4-dependent proliferation of TF-1 human erythroleukemic cells. The ED₅₀ for this effect is 10-80 pg/mL.

Human

HEK293

Tag Free

P10600-1 (A301-S412)

7043  [NCBI]

Full Length of Mature TGFB3

ALDTNYCFRNLEENCCVRPLYIDFRQDLGWKWVHEPKGYFANFCSGPCPYLRSADTTHSTVLGLYNTLNPEASASPCCVPQDLEPLTILYYVGRTPKVEQLSNMVVKSCKCS

Approximately 12-14 kDa, based on SDS-PAGE under reducing conditions.

≥ 95%, as determined by reducing SDS-PAGE.

Lyophilized powder

1.Lyophilized from a 0.22 μm filtered solution of 4 mM HCl.
2.Lyophilized from a 0.22 μm filtered solution of 50 mM Glycine-HCl, 150 mM NaCl, pH 2.5.
Please refer to the lot-specific COA for specific buffer information.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Mahmoudi Rad M, et al. Expression of TGF-β3 in isolated fibroblasts from foreskin. Rep Biochem Mol Biol. 2015 Apr;3(2):76-81.  [Content Brief]

  [2]. Laverty HG, et al. TGF-beta3 and cancer: a review. Cytokine Growth Factor Rev. 2009 Aug;20(4):305-17.  [Content Brief]

  [3]. Toshihiko Komai, et al. Reevaluation of Pluripotent Cytokine TGF-β3 in Immunity. Int J Mol Sci. 2018 Aug 1;19(8):2261.  [Content Brief]

  [4]. A Arici, et al. Transforming growth factor-beta3 is expressed at high levels in leiomyoma where it stimulates fibronectin expression and cell proliferation. Fertil Steril. 2000 May;73(5):1006-11.  [Content Brief]

  [5]. Muhetaer Huojia, et al. TGF-beta3 induces ectopic mineralization in fetal mouse dental pulp during tooth germ development. Dev Growth Differ. 2005 Apr;47(3):141-52.  [Content Brief]

  [6]. Long Xu, et al. Transforming growth factor β3 attenuates the development of radiation-induced pulmonary fibrosis in mice by decreasing fibrocyte recruitment and regulating IFN-γ/IL-4 balance. Immunol Lett. 2014 Nov;162(1 Pt A):27-33.  [Content Brief]

  [7]. S Coerper, et al. Recombinant human transforming growth factor beta 3 accelerates gastric ulcer healing in rats. Scand J Gastroenterol. 1997 Oct;32(10):985-90.  [Content Brief]

  [8]. W Y Lui, et al. Transforming growth factor-beta3 perturbs the inter-Sertoli tight junction permeability barrier in vitro possibly mediated via its effects on occludin, zonula occludens-1, and claudin-11. Endocrinology. 2001 May;142(5):1865-77.  [Content Brief]