Mouse Anti-TGFBI Recombinant Antibody (CBYJT-2785) (CBMAB-T2008-YJ)

Mouse

Human

CBYJT-2785

IgG

ELISA, WB

Recombinant protein corresponding to aa502-636 from human TGFBI expressed in E. coli

Human

IgG

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

PBS, pH 7.4, 10% Glycerol

0.02% Sodium Azide

Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

aa 502-636

TGFBI Gene(Protein Coding) Transforming Growth Factor Beta Induced

TGFBI is an RGD-containing protein that binds to type I, II and IV collagens. The RGD motif is found in many extracellular matrix proteins modulating cell adhesion and serves as a ligand recognition sequence for several integrins. TGFBI plays a role in cell-collagen interactions and may be involved in endochondrial bone formation in cartilage. TGFBI is induced by transforming growth factor-beta and acts to inhibit cell adhesion. Mutations in TGFBI are associated with multiple types of corneal dystrophy.

Transforming Growth Factor Beta Induced; Transforming Growth Factor, Beta-Induced, 68kD; RGD-Containing Collagen-Associated Protein; Kerato-Epithelin; Beta Ig-H3; RGD-CAP; BIGH3; Transforming Growth Factor-Beta-Induced Protein Ig-H3; Transforming Growth Factor, Beta-Induced, 68kDa; Transforming Growth Factor Beta-Induced 68kDa; Betaig-H3

Plays a role in cell adhesion (PubMed:8024701).
May play a role in cell-collagen interactions (By similarity).

Biological Process angiogenesisSource:UniProtKB1 Publication
Biological Process cell adhesionSource:GO_Central1 Publication
Biological Process cell population proliferationSource:ProtInc1 Publication
Biological Process chondrocyte differentiationSource:Ensembl
Biological Process extracellular matrix organizationSource:GO_Central1 Publication
Biological Process localizationSource:DisProt1 Publication
Biological Process negative regulation of cell adhesionSource:ProtInc1 Publication
Biological Process response to stimulusSource:UniProtKB-KW
Biological Process visual perceptionSource:ProtInc1 Publication

Secreted
Secreted, extracellular space, extracellular matrix
May be associated both with microfibrils and with the cell surface (PubMed:8077289).

Corneal dystrophy, epithelial basement membrane (EBMD):
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.
Corneal dystrophy, Groenouw type 1 (CDGG1):
A rare form of stromal corneal dystrophy characterized by multiple small deposits in the superficial central corneal stroma, and progressive visual impairment.
Corneal dystrophy, lattice type 1 (CDL1):
A form of lattice corneal dystrophy, a class of inherited stromal amyloidoses characterized by pathognomonic branching lattice figures in the cornea. CDL1 is characterized by progressive visual impairment, and the presence of delicate, double-contoured, interdigitating, elongated deposits that form a reticular pattern in the corneal stroma. Systemic amyloidosis is absent. Recurrent corneal ulceration sometimes occurs.
Corneal dystrophy, Thiel-Behnke type (CDTB):
A bilateral disorder of the cornea characterized by progressive honeycomb-like, subepithelial corneal opacities with recurrent erosions.
Corneal dystrophy, Reis-Bucklers type (CDRB):
A bilateral disorder of the cornea characterized by intermittent attacks of ocular irritation, recurrent painful corneal erosions starting in childhood, corneal opacities in a geographic pattern at the level of the Bowman layer, and a progressive decrease of visual acuity. The lesions are primarily in Bowman membrane with secondary involvement of the epithelium and superficial part of the stroma. Bowman membrane is almost completely replaced by pathologic materials including disoriented collagen fibrils.
Corneal dystrophy, lattice type 3A (CDL3A):
A form of lattice corneal dystrophy, a class of inherited stromal amyloidoses characterized by pathognomonic branching lattice figures in the cornea. CDL3A is characterized by decreased visual acuity, and the presence of thick, ropy branching lattice lines and accumulations of amyloid deposits in the corneal stroma. Systemic amyloidosis is absent. 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.
Corneal dystrophy, Avellino type (CDA):
A corneal disease resulting in reduced visual acuity and characterized by gray, crumb-like granular deposits in the anterior third of the stroma in each corneal button. Fusiform amyloid deposits, histochemically and morphologically identical to those of lattice corneal dystrophy, are found in the deeper stroma. Additional features include recurrent corneal erosions, and glare and decreased night vision.

Gamma-carboxylation is controversial. Gamma-carboxyglutamated; gamma-carboxyglutamate residues are formed by vitamin K dependent carboxylation; these residues may be required for binding to calcium (PubMed:18450759).
According to a more recent report, does not contain vitamin K-dependent gamma-carboxyglutamate residues (PubMed:26273833).
The EMI domain contains 2 expected intradomain disulfide bridges (Cys-49-Cys85 and Cys-84-Cys-97) and one unusual interdomain disulfide bridge to the second FAS1 domain (Cys-74-Cys-339). This arrangement violates the predicted disulfide bridge pattern of an EMI domain.