Product: TGF beta 1 Mouse monoclonal Antibody
Catalog: BF8012
Description: Mouse monoclonal antibody to TGF beta 1
Application: WB IHC
Reactivity: Human, Mouse, Rat
Mol.Wt.: 33kDa; 44kD(Calculated).
Uniprot: P01137

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Monoclonal [AFfirm8012(AFB19416)]
TGF beta1 antibody detects endogenous levels of total TGF beta1.
Mouse IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Cartilage-inducing factor; CED; Differentiation inhibiting factor; DPD1; LAP; Latency-associated peptide; Prepro transforming growth factor beta 1; TGF beta 1; TGF beta; TGF beta 1 protein; TGF-beta 1 protein; TGF-beta-1; TGF-beta-5; TGF-beta1; TGFB; Tgfb-1; tgfb1; TGFB1_HUMAN; TGFbeta; TGFbeta1; Transforming Growth Factor b1; Transforming Growth Factor beta 1; Transforming growth factor beta 1a; transforming growth factor beta-1; transforming growth factor, beta 1; Transforming Growth Factor-ß1;



A synthesized peptide derived from human TGF beta1.


Highly expressed in bone (PubMed:11746498, PubMed:17827158). Abundantly expressed in articular cartilage and chondrocytes and is increased in osteoarthritis (OA) (PubMed:11746498, PubMed:17827158). Colocalizes with ASPN in chondrocytes within OA lesions of articular cartilage (PubMed:17827158).


PTMs - P01137 As Substrate

Site PTM Type Enzyme
K42 Sumoylation
K42 Ubiquitination
K56 Ubiquitination
N82 N-Glycosylation
K106 Ubiquitination
K163 Ubiquitination
K291 Ubiquitination
K309 Ubiquitination
Y317 Phosphorylation

Research Backgrounds


Transforming growth factor beta-1 proprotein: Precursor of the Latency-associated peptide (LAP) and Transforming growth factor beta-1 (TGF-beta-1) chains, which constitute the regulatory and active subunit of TGF-beta-1, respectively.

Required to maintain the Transforming growth factor beta-1 (TGF-beta-1) chain in a latent state during storage in extracellular matrix. Associates non-covalently with TGF-beta-1 and regulates its activation via interaction with 'milieu molecules', such as LTBP1, LRRC32/GARP and LRRC33/NRROS, that control activation of TGF-beta-1. Interaction with LRRC33/NRROS regulates activation of TGF-beta-1 in macrophages and microglia (Probable). Interaction with LRRC32/GARP controls activation of TGF-beta-1 on the surface of activated regulatory T-cells (Tregs). Interaction with integrins (ITGAV:ITGB6 or ITGAV:ITGB8) results in distortion of the Latency-associated peptide chain and subsequent release of the active TGF-beta-1.

Transforming growth factor beta-1: Multifunctional protein that regulates the growth and differentiation of various cell types and is involved in various processes, such as normal development, immune function, microglia function and responses to neurodegeneration (By similarity). Activation into mature form follows different steps: following cleavage of the proprotein in the Golgi apparatus, Latency-associated peptide (LAP) and Transforming growth factor beta-1 (TGF-beta-1) chains remain non-covalently linked rendering TGF-beta-1 inactive during storage in extracellular matrix. At the same time, LAP chain interacts with 'milieu molecules', such as LTBP1, LRRC32/GARP and LRRC33/NRROS that control activation of TGF-beta-1 and maintain it in a latent state during storage in extracellular milieus. TGF-beta-1 is released from LAP by integrins (ITGAV:ITGB6 or ITGAV:ITGB8): integrin-binding to LAP stabilizes an alternative conformation of the LAP bowtie tail and results in distortion of the LAP chain and subsequent release of the active TGF-beta-1. Once activated following release of LAP, TGF-beta-1 acts by binding to TGF-beta receptors (TGFBR1 and TGFBR2), which transduce signal. While expressed by many cells types, TGF-beta-1 only has a very localized range of action within cell environment thanks to fine regulation of its activation by Latency-associated peptide chain (LAP) and 'milieu molecules' (By similarity). Plays an important role in bone remodeling: acts as a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts (By similarity). Can promote either T-helper 17 cells (Th17) or regulatory T-cells (Treg) lineage differentiation in a concentration-dependent manner (By similarity). At high concentrations, leads to FOXP3-mediated suppression of RORC and down-regulation of IL-17 expression, favoring Treg cell development (By similarity). At low concentrations in concert with IL-6 and IL-21, leads to expression of the IL-17 and IL-23 receptors, favoring differentiation to Th17 cells (By similarity). Stimulates sustained production of collagen through the activation of CREB3L1 by regulated intramembrane proteolysis (RIP). Mediates SMAD2/3 activation by inducing its phosphorylation and subsequent translocation to the nucleus. Can induce epithelial-to-mesenchymal transition (EMT) and cell migration in various cell types.


Transforming growth factor beta-1 proprotein: The precursor proprotein is cleaved in the Golgi apparatus by FURIN to form Transforming growth factor beta-1 (TGF-beta-1) and Latency-associated peptide (LAP) chains, which remain non-covalently linked, rendering TGF-beta-1 inactive.

N-glycosylated. Deglycosylation leads to activation of Transforming growth factor beta-1 (TGF-beta-1); mechanisms triggering deglycosylation-driven activation of TGF-beta-1 are however unclear.

Subcellular Location:

Secreted>Extracellular space>Extracellular matrix.


Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Highly expressed in bone. Abundantly expressed in articular cartilage and chondrocytes and is increased in osteoarthritis (OA). Colocalizes with ASPN in chondrocytes within OA lesions of articular cartilage.

Subunit Structure:

Homodimer; disulfide-linked. Interacts with the serine proteases, HTRA1 and HTRA3: the interaction with either inhibits TGFB1-mediated signaling. The HTRA protease activity is required for this inhibition (By similarity). May interact with THSD4; this interaction may lead to sequestration by FBN1 microfibril assembly and attenuation of TGFB signaling (By similarity). Interacts with CD109, DPT and ASPN. Latency-associated peptide: Homodimer; disulfide-linked. Latency-associated peptide: Interacts with Transforming growth factor beta-1 (TGF-beta-1) chain; interaction is non-covalent and maintains (TGF-beta-1) in a latent state; each Latency-associated peptide (LAP) monomer interacts with TGF-beta-1 in the other monomer. Latency-associated peptide: Interacts with LTBP1; leading to regulate activation of TGF-beta-1. Latency-associated peptide: Interacts with LRRC32/GARP; leading to regulate activation of TGF-beta-1 on the surface of activated regulatory T-cells (Tregs). Interacts with LRRC33/NRROS; leading to regulate activation of TGF-beta-1 in macrophages and microglia (Probable). Latency-associated peptide: Interacts (via cell attachment site) with integrins ITGAV and ITGB6 (ITGAV:ITGB6), leading to release of the active TGF-beta-1. Latency-associated peptide: Interacts with NREP; the interaction results in a decrease in TGFB1 autoinduction (By similarity). Latency-associated peptide: Interacts with HSP90AB1; inhibits latent TGFB1 activation. Transforming growth factor beta-1: Homodimer; disulfide-linked. Transforming growth factor beta-1: Interacts with TGF-beta receptors (TGFBR1 and TGFBR2), leading to signal transduction.


The 'straitjacket' and 'arm' domains encircle the Transforming growth factor beta-1 (TGF-beta-1) monomers and are fastened together by strong bonding between Lys-56 and Tyr-103/Tyr-104.

The cell attachment site motif mediates binding to integrins (ITGAV:ITGB6 or ITGAV:ITGB8) (PubMed:28117447). The motif locates to a long loop in the arm domain called the bowtie tail (PubMed:28117447). Integrin-binding stabilizes an alternative conformation of the bowtie tail (PubMed:28117447). Activation by integrin requires force application by the actin cytoskeleton, which is resisted by the 'milieu molecules' (such as LTBP1, LRRC32/GARP and/or LRRC33/NRROS), resulting in distortion of the prodomain and release of the active TGF-beta-1 (PubMed:28117447).

Belongs to the TGF-beta family.


1). Yuan L et al. Airway epithelial ITGB4 deficiency induces airway remodeling in a mouse model. The Journal of allergy and clinical immunology 2022 Oct 13;S0091-6749(22)01342-2. (PubMed: 36243221) [IF=14.2]

2). Ding L et al. Chrysin ameliorates synovitis and fibrosis of osteoarthritic fibroblast-like synoviocytes in rats through PERK/TXNIP/NLRP3 signaling. Frontiers in Pharmacology 2023 Mar 20;14:1170243. (PubMed: 37021049) [IF=5.6]

3). Zou XZ et al. The alcohol extracts of Sceptridium ternatum (Thunb.) Lyon exert anti-pulmonary fibrosis effect through targeting SETDB1/STAT3/p-STAT3 signaling. Journal of Ethnopharmacology 2023 Apr 27; (PubMed: 37120058) [IF=5.4]

4). Liu F et al. ZIC2 promotes colorectal cancer growth and metastasis through the TGF-β signaling pathway. Experimental Cell Research 2022 Apr 4;415(2):113118. (PubMed: 35390314) [IF=3.7]

5). Li D et al. Kainic acid induced hyperexcitability in thalamic reticular nucleus that initiates an inflammatory response through the HMGB1/TLR4 pathway. NEUROTOXICOLOGY 2023 Jan 18;95:94-106. (PubMed: 36669621) [IF=3.4]

6). Li Z et al. Single-Cell RNA-Sequencing Reveals the Cellular and Genetic Heterogeneity of Skin Scar to Verify the Therapeutic Effects and Mechanism of Action of Dispel-Scar Ointment in Hypertrophic Scar Inhibition. Evidence-based Complementary and Alternative Medicine 2022 Jun 8;2022:7331164. (PubMed: 35722137)

Application: IF/ICC    Species: Rat    Sample: skin tissues

Figure 9 (a) Immunofluorescence staining of TGF-β1 and Smad4 in skin tissues. TGF-β1 (red), Smad4 (green), and DAPI (blue). Bar = 100 μm. (b) Immunofluorescence staining of Col1a1 and MMP9 in skin tissues. Col1a1 (red), MMP9 (green), and DAPI (blue). Bar = 100 μm. (c) Quantitative analysis of TGF-β1-positive and Smad4-positive area density; n = 5 for each group. (d) Quantitative analysis of Col1a1- and MMP9-positive area density; n = 5 for each group. Significant differences between different groups or any other groups vs the model group are expressed as ∗=P < 0.05, ∗∗=P < 0.01, and ∗∗∗=P < 0.001, while significant differences between any other group and the control group are expressed as # = P < 0.05, ## = P < 0.01, and ### = P < 0.001.

Application: WB    Species: Rat    Sample:

Figure 10 (a) Expression levels of TGF-β1, pSmad3, pSmad4, Col1a1, and MMP2 proteins were evaluated via (b) western blotting. β-actin levels served as a control (n = 3/group). Significant differences among different groups are indicated as ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, vs model group or with any other group; #P < 0.05, ##P < 0.01, and ###P < 0.01 vs control group.

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