Key Product Details

Species Reactivity

Validated:

Human

Cited:

Human

Applications

Validated:

Western Blot

Cited:

Western Blot

Label

Unconjugated

Antibody Source

Polyclonal Goat IgG

View all beta IG-H3 Antibodies »

Product Specifications

Immunogen

Mouse myeloma cell line NS0-derived recombinant human betaIG-H3
Gly24-His683
Accession # Q15582

Specificity

Detects human betaIG-H3 in direct ELISAs and Western blots. In direct ELISAs and Western blots, approximately 50% cross-reactivity with recombinant mouse betaIG-H3 is observed.

Clonality

Polyclonal

Host

Goat

Isotype

IgG

Scientific Data Images for Human betaIG-H3 Antibody

Detection of Human betaIG-H3 by Western Blot

Detection of Human betaIG-H3 by Western Blot

MLL1 knockdown attenuated the TGF beta1-induced expression of TGFBIp and ECM-associated genes. a Wild-type and GCD2-homozygous corneal fibroblasts were infected with MLL1 or control shRNA lentivirus. After puromycin selection, MLL1, H3K4me3, TGFBIp, and actin protein levels were analyzed by western blot. b-d Wild-type and GCD2-homozygous corneal fibroblasts were infected with MLL1 or control shRNA lentivirus. After puromycin selection, infected cells were stimulated with TGF beta1 (5 ng/ml) for 8 h, and mRNA and protein levels of TGFBIp were analyzed by RT-qPCR (b) and western blot (c). mRNA levels of ECM-associated genes were analyzed by RT-qPCR (d). Gene expression was normalized to that of GAPDH (internal control), and results are expressed as fold stimulation over control shRNA-infected wild-type control (mean ± standard error (SE); **P < 0.01 vs. control, n = 3) Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/26553048), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of betaIG-H3 by Western Blot

Detection of betaIG-H3 by Western Blot

Expression of transforming growth factor-beta-induced-gene protein (TGFBIp) in ten different normal corneal fibroblasts (NCF). A, B: western blots show evidence of differential expression of TGFBIp in cultured NCF-1 (37 year-old man), NCF-2 (62 year-old man), NCF-3 (20 year-old woman), NCF-4 (46 year-old man), NCF-5 (29 year-old man), NCF-6 (60 year-old man), NCF-7 (man with unknown-age), NCF-8 (woman with unknown-age), NCF-9 (69 year-old woman), NCF-10 (81 year-old man) from normal donor corneas. In the second experiment, NCF-4 was reloaded for a comparison of the two separate experiments. C, D: Relative density of TGFBIp expression of A and B, respectively. Relative density of NCF-4 was adjusted to 100% in both C and D for a comparison of the densities of normal corneal fibroblasts in two separate experiments. Blots containing 50 μg total protein from normal corneal fibroblasts were incubated with anti-TGFBIp antibody. TGFBIp expression was assayed using anti-TGFBIp polyclonal goat antibodies. beta-actin has been used as a control for equal loading. Numbers on the right correspond to the molecular weight markers in kilodaltons (kDa). Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/22815629), licensed under a CC-BY license. Not internally tested by R&D Systems.

Applications for Human betaIG-H3 Antibody

Application
Recommended Usage

Western Blot

0.1 µg/mL
Sample: Recombinant Human betaIG-H3 (Catalog # 3409-BG)

Formulation, Preparation, and Storage

Purification

Antigen Affinity-purified

Reconstitution

Reconstitute at 0.2 mg/mL in sterile PBS. For liquid material, refer to CoA for concentration.

Reconstitution Buffer Available:
Size / Price
Qty

Formulation

Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.

Shipping

Lyophilized product is shipped at ambient temperature. Liquid small pack size (-SP) is shipped with polar packs. Upon receipt, store immediately at the temperature recommended below.

Stability & Storage

Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 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: beta IG-H3

Beta IG-H3, also known as TGFBI and RGD-CAP, is a matricellular adaptor protein that is induced in most cell types in response to TGF-beta stimulation (1‑4). The human betaIG-H3 cDNA encodes a 683 amino acid (aa) precursor that includes a 23 aa signal sequence, one EMI domain, four FAS1 domains, and one RGD motif (1). Human betaIG-H3 shares 91% and 93% aa sequence identity with mouse and porcine betaIG-H3, respectively. betaIG-H3 is expressed as a 75 kDa protein with no post‑translational additions (5). Following secretion, cleavages at multiple positions near the C-terminal end liberate peptides with pro-apoptotic activity (5,6). Peptides that encompass the RGD motif contribute to the pro-apoptotic effects of TGF-beta (6). FAS1 domains contain YH motifs that are characterized by conserved Tyr and His residues (7). The YH motifs in each of the FAS1 domains enable betaIG-H3 binding to matrix Fibronectin, Collagen I, and Collagen VI (3, 8‑10) in addition to cell expressed Integrins alphaV beta3, alphaV beta5, and alpha3 beta1 (7, 8, 11, 12). The expression of betaIG-H3 is modulated at particular developmental stages in some cell types. It is upregulated in keratinocytes and immature dendritic cells but downregulated in osteoblasts (8, 11, 13). It promotes keratinocyte differentiation but blocks osteoblast differentiation (8,11). betaIG-H3 stimulates macrophage endocytosis and vascular endothelial cell proliferation and migration (12, 13). High glucose levels induce betaIG-H3 in renal proximal tubule cells which is predictive of diabetic nephropathy (3). Several point mutations (clustered in the fourth FAS1 domain) of betaIG-H3 are linked to different corneal dystrophies (14). betaIG-H3 is downregulated in many cancers (4, 15) and functions as a suppressor of tumorigenicity when overexpressed (2, 4, 15).

References

  1. Skonier, J. et al. (1992) DNA Cell Biol. 11:511.
  2. Skonier, J. et al. (1994) DNA Cell Biol. 13:571.
  3. Lee, S-H. et al. (2003) Kidney Int. 64:1012.
  4. Zhao, Y.L. et al. (2002) Oncogene 21:7471.
  5. Andersen, R.B. et al. (2004) Biochemistry 43:16374.
  6. Kim, J-E. et al. (2003) Oncogene 22:2045.
  7. Kim, J-E. et al. (2002) J. Biol. Chem. 277:46159.
  8. Thapa, N. et al. (2005) Bone 36:232.
  9. Hanssen, E. et al. (2003) J. Biol. Chem. 278:24334.
  10. Billings, P.C. et al. (2002) J. Biol. Chem. 277:28003.
  11. Oh, J-E. et al. (2005) J. Biol. Chem. 280:21629.
  12. Nam, J-O. et al. (2003) J. Biol. Chem. 278:25902.
  13. Cao, W, et al. (2006) Blood 107:2777. 
  14. Stewart, H.S. et al. (1999) Hum. Mutat. 14:126.
  15. Zhao, Y. et al. (2006) Mol. Carcinog. 45:84.

Long Name

TGF-beta Induced Gene H3

Alternate Names

beta IGH3, Kerato-epithelin, RGD-CAP, TGFBI, TGFBIP

Entrez Gene IDs

7045 (Human); 21810 (Mouse)

Gene Symbol

TGFBI

UniProt

Q15582

Additional beta IG-H3 Products

Product Documents for Human betaIG-H3 Antibody

Product Datasheets

Certificate of Analysis

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Product Specific Notices for Human betaIG-H3 Antibody

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