Human TGFBI protein fragment (ab86989)
- Product nameHuman TGFBI protein fragmentSee all TGFBI proteins and peptides ...
- SourceE. coli
- Amino Acid Sequence
- SequenceMGTVMDVLKG DNRFSMLVAA IQSAGLTETL NREGVYTVFA PTNEAFRALP PRERSRLLGD AKELANILKY HIGDEILVSG GIGALVRLKS LQGDKLEVSL KNNVVSVNKE PVAEPDIMAT NGVVHVITNV LQPPANRPQE RGDELADSAL EIFKQASAFS RASQRSVRLA PVYQKLLERM KH
- Amino acids0 to 0
Our Abpromise guarantee covers the use of ab86989 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
- Purity> 95
% by SDS-PAGE.
ab86989 is purified using conventional chromatography techniques.
- Additional NotesEndotoxin Level: < 1.0 EU per 1 µg of protein (determined by LAL method).
- Concentration information loading...
Preparation and Storage
- Stability and Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Constituents: 20% Glycerol, 20mM Tris HCl, 1mM EDTA, 0.1mM PMSF, pH 8.0
- RGD containing collagen associated protein
- Beta ig
- Beta ig h3
- Beta ig-h3
- Big h3
- Kerato epithelin
- RGD CAP
- RGD-containing collagen-associated protein
- TGFBI transforming growth factor, beta induced, 68kDa
- Transforming growth factor beta induced protein ig h3
- Transforming growth factor-beta-induced protein ig-h3
- 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.
Human TGFBI protein fragment images
15% SDS-PAGE showing ab86989 at approximately 19.9kDa (3µg).
Note: Real molecular weight on SDS-PAGE is shifted up compared to predicted molecular weight.
References for Human TGFBI protein fragment (ab86989)
ab86989 has not yet been referenced specifically in any publications.