Overview

  • Product name

    Anti-TGFBI antibody [EPR17990-13]
    See all TGFBI primary antibodies
  • Description

    Rabbit monoclonal [EPR17990-13] to TGFBI
  • Host species

    Rabbit
  • Tested applications

    Suitable for: WB, IPmore details
  • Species reactivity

    Reacts with: Mouse, Rat
  • Immunogen

    Recombinant fragment within Mouse TGFBI aa 500 to the C-terminus. The exact sequence is proprietary.
    Database link: P82198

  • Positive control

    • WB: Rat eyeball and liver lysates; Mouse eyeball and spleen lysates. IP: Mouse eyeball lysate.
  • General notes

    Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.

    This product is a recombinant rabbit monoclonal antibody.

Properties

Applications

Our Abpromise guarantee covers the use of ab187085 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB 1/1000. Detects a band of approximately 68 kDa (predicted molecular weight: 75 kDa).
IP 1/30.

Target

  • Function

    Binds 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 specificity

    Highly expressed in the corneal epithelium.
  • Involvement in disease

    Defects 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 similarities

    Contains 1 EMI domain.
    Contains 4 FAS1 domains.
  • Post-translational
    modifications

    Gamma-carboxyglutamate residues are formed by vitamin K dependent carboxylation. These residues are essential for the binding of calcium.
  • Cellular localization

    Secreted > extracellular space > extracellular matrix. May be associated both with microfibrils and with the cell surface.
  • Information by UniProt
  • Database links

  • Alternative names

    • RGD containing collagen associated protein antibody
    • AI181842 antibody
    • AI747162 antibody
    • Beta ig antibody
    • Beta ig h3 antibody
    • Beta ig-h3 antibody
    • BGH3_HUMAN antibody
    • Big h3 antibody
    • BIGH3 antibody
    • CDB1 antibody
    • CDG2 antibody
    • CDGG1 antibody
    • CSD antibody
    • CSD1 antibody
    • CSD2 antibody
    • CSD3 antibody
    • EBMD antibody
    • Kerato epithelin antibody
    • Kerato-epithelin antibody
    • LCD1 antibody
    • MGC150270 antibody
    • RGD CAP antibody
    • RGD-CAP antibody
    • RGD-containing collagen-associated protein antibody
    • TGFBI antibody
    • TGFBI transforming growth factor, beta induced, 68kDa antibody
    • Transforming growth factor beta induced protein ig h3 antibody
    • Transforming growth factor-beta-induced protein ig-h3 antibody
    see all

Images

  • All lanes : Anti-TGFBI antibody [EPR17990-13] (ab187085) at 1/1000 dilution

    Lane 1 : Rat eyeball lysate at 20 µg
    Lane 2 : Mouse eyeball lysate at 20 µg
    Lane 3 : Mouse spleen lysate at 10 µg
    Lane 4 : Rat liver lysate at 10 µg

    Secondary
    Lanes 1 & 3-4 : Goat Anti-Rabbit IgG H&L (HRP) (ab97051) at 1/100000 dilution
    Lane 2 : Goat Anti-Rabbit IgG H&L (HRP) (ab97051) at 1/20000 dilution

    Developed using the ECL technique.

    Predicted band size: 75 kDa
    Observed band size: 68 kDa
    why is the actual band size different from the predicted?



    Exposure time : Lane 1: 3 minutes; Lane 2: 1 second; Lanes 3 and 4: 3 minutes.

    Blocking/Dilution buffer: 5% NFDM/TBST.

    The molecular mass observed is consistent with what has been described in the literature (PMID: 19478074).

  • TGFBI was immunoprecipitated from 0.35 mg of mouse eyeball lysate with ab187085 at 1/30 dilution. Western blot was performed from the immunoprecipitate using ab187085 at 1/1000 dilution. VeriBlot for IP Detection Reagent (HRP) (ab131366), was used for detection at 1/1000 dilution.

    Lane 1: Mouse eyeball lysate 10 µg (Input). 

    Lane 2: ab187085 IP in mouse eyeball lysate (+). 

    Lane 3: Rabbit monoclonal IgG (ab172730) instead of ab187085 in mouse eyeball lysate (-).

    Blocking and dilution buffer and concentration: 5% NFDM/TBST.

    Exposure time: 1 second.

References

ab187085 has not yet been referenced specifically in any publications.

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