Key features and details
- Goat polyclonal to TGFBI
- Suitable for: WB, IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-TGFBI antibody
See all TGFBI primary antibodies
DescriptionGoat polyclonal to TGFBI
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat, Dog
Synthetic peptide from an internal region of Human TGFBI, conjugated to KLH
- Human Kidney, Renal Duct Human Kidney lysate
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C long term.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 99% Tris buffered saline, 0.5% BSA
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab122975 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.2 - 0.5 µg/ml. Predicted molecular weight: 75 kDa.|
|IHC-P||Use a concentration of 3.75 µg/ml.|
FunctionBinds to type I, II, and IV collagens. This adhesion protein may play an important role in cell-collagen interactions. In cartilage, may be involved in endochondral bone formation.
Tissue specificityHighly expressed in the corneal epithelium.
Involvement in diseaseDefects in TGFBI are the cause of epithelial basement membrane corneal dystrophy (EBMD) [MIM:121820]; also known as Cogan corneal dystrophy or map-dot-fingerprint type corneal dystrophy. EBMD is a bilateral anterior corneal dystrophy characterized by grayish epithelial fingerprint lines, geographic map-like lines, and dots (or microcysts) on slit-lamp examination. Pathologic studies show abnormal, redundant basement membrane and intraepithelial lacunae filled with cellular debris. Although this disorder usually is not considered to be inherited, families with autosomal dominant inheritance have been identified.
Defects in TGFBI are the cause of corneal dystrophy Groenouw type 1 (CDGG1) [MIM:121900]; also known as corneal dystrophy granular type. Inheritance is autosomal dominant. Corneal dystrophies show progressive opacification of the cornea leading to severe visual handicap.
Defects in TGFBI are the cause of corneal dystrophy lattice type 1 (CDL1) [MIM:122200]. Inheritance is autosomal dominant.
Defects in TGFBI are a cause of corneal dystrophy Thiel-Behnke type (CDTB) [MIM:602082]; also known as corneal dystrophy of Bowman layer type 2 (CDB2).
Defects in TGFBI are the cause of Reis-Buecklers corneal dystrophy (CDRB) [MIM:608470]; also known as corneal dystrophy of Bowman layer type 1 (CDB1).
Defects in TGFBI are the cause of lattice corneal dystrophy type 3A (CDL3A) [MIM:608471]. CDL3A clinically resembles to lattice corneal dystrophy type 3, but differs in that its age of onset is 70 to 90 years. It has an autosomal dominant inheritance pattern.
Defects in TGFBI are the cause of Avellino corneal dystrophy (ACD) [MIM:607541]. ACD could be considered a variant of granular dystrophy with a significant amyloidogenic tendency. Inheritance is autosomal dominant.
Sequence similaritiesContains 1 EMI domain.
Contains 4 FAS1 domains.
modificationsGamma-carboxyglutamate residues are formed by vitamin K dependent carboxylation. These residues are essential for the binding of calcium.
Cellular localizationSecreted > extracellular space > extracellular matrix. May be associated both with microfibrils and with the cell surface.
- Information by UniProt
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ab122975 has not yet been referenced specifically in any publications.