Overview

  • Product nameAnti-GDF 5 antibody
    See all GDF 5 primary antibodies
  • Description
    Rabbit polyclonal to GDF 5
  • Tested applicationsSuitable for: ELISA, IHC-Pmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Sheep, Horse, Dog, Pig
  • Immunogen

    Synthetic peptide:

    APDLGQRPQGTRPG

    conjugated to KLH, corresponding to amino acids 28-41 of Human GDF 5 (NP_000548.1).

  • Positive control
    • Human Skin tissue.

Properties

Associated products

Applications

Our Abpromise guarantee covers the use of ab115678 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
ELISA 1/1 - 1/1000.
IHC-P Use a concentration of 10 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.

Target

  • FunctionCould be involved in bone and cartilage formation. Chondrogenic signaling is mediated by the high-affinity receptor BMPR1B.
  • Tissue specificityPredominantly expressed in long bones during embryonic development.
  • Involvement in diseaseDefects in GDF5 are the cause of acromesomelic chondrodysplasia Grebe type (AMDG) [MIM:200700]. Acromesomelic chondrodysplasias are rare hereditary skeletal disorders characterized by short stature, very short limbs, and hand/foot malformations. The severity of limb abnormalities increases from proximal to distal with profoundly affected hands and feet showing brachydactyly and/or rudimentary fingers (knob-like fingers). AMDG is an autosomal recessive form characterized by normal axial skeletons and missing or fused skeletal elements within the hands and feet.
    Defects in GDF5 are the cause of acromesomelic chondrodysplasia Hunter-Thompson type (AMDH) [MIM:201250]. AMDH is an autosomal recessive form of dwarfism. Patients have limb abnormalities, with the middle and distal segments being most affected and the lower limbs more affected than the upper. AMDH is characterized by normal axial skeletons and missing or fused skeletal elements within the hands and feet.
    Defects in GDF5 are the cause of brachydactyly type C (BDC) [MIM:113100]. BDC is an autosomal dominant disorder characterized by an abnormal shortness of the fingers and toes.
    Defects in GDF5 are the cause of Du Pan syndrome (DPS) [MIM:228900]; also known as fibular hypoplasia and complex brachydactyly. Du Pan syndrome is a rare autosomal recessive condition characterized by absence of the fibulae and severe acromesomelic limb shortening with small, non-functional toes. Although milder, the phenotype resembles the autosomal recessive Hunter-Thompson [MIM:201250] and Grebe types [MIM:200700] of acromesomelic chondrodysplasia.
    Defects in GDF5 are a cause of symphalangism proximal syndrome (SYM1) [MIM:185800]. SYM1 is characterized by the hereditary absence of the proximal interphalangeal (PIP) joints (Cushing symphalangism). Severity of PIP joint involvement diminishes towards the radial side. Distal interphalangeal joints are less frequently involved and metacarpophalangeal joints are rarely affected whereas carpal bone malformation and fusion are common. In the lower extremities, tarsal bone coalition is common. Conducive hearing loss is seen and is due to fusion of the stapes to the petrous part of the temporal bone.
    Defects in GDF5 are the cause of multiple synostoses syndrome type 2 (SYNS2) [MIM:610017]. Multiple synostoses syndrome is an autosomal dominant condition characterized by progressive joint fusions of the fingers, wrists, ankles and cervical spine, characteristic facies and progressive conductive deafness.
    Defects in GDF5 are a cause of brachydactyly type A2 (BDA2) [MIM:112600]. Brachydactylies (BDs) are a group of inherited malformations characterized by shortening of the digits due to abnormal development of the phalanges and/or the metacarpals. They have been classified on an anatomic and genetic basis into five groups, A to E, including three subgroups (A1 to A3) that usually manifest as autosomal dominant traits.
    Genetic variations in GDF5 are associated with susceptibility to osteoarthritis type 5 (OS5) [MIM:612400]. Osteoarthritis is a degenerative disease of the joints characterized by degradation of the hyaline articular cartilage and remodeling of the subchondral bone with sclerosis. Clinical symptoms include pain and joint stiffness often leading to significant disability and joint replacement.
    Defects in GDF5 may be a cause of brachydactyly type A1 (BDA1) [MIM:112500]. Brachydactylies (BDs) are a group of inherited malformations characterized by shortening of the digits due to abnormal development of the phalanges and/or the metacarpals. They have been classified on an anatomic and genetic basis into five groups, A to E, including three subgroups (A1 to A3) that usually manifest as autosomal dominant traits.
  • Sequence similaritiesBelongs to the TGF-beta family.
  • Cellular localizationSecreted.
  • Information by UniProt
  • Database links
  • Alternative names
    • BMP14 antibody
    • Cartilage derived morphogenetic protein 1 antibody
    • Cartilage-derived morphogenetic protein 1 antibody
    • CDMP-1 antibody
    • CDMP1 antibody
    • GDF-5 antibody
    • Gdf5 antibody
    • GDF5_HUMAN antibody
    • Growth differentiation factor 5 antibody
    • Growth/differentiation factor 5 antibody
    • LAP4 antibody
    • OS5 antibody
    • Radotermin antibody
    • SYNS2 antibody
    see all

Anti-GDF 5 antibody images

  • ab115678, at 10µg/ml, staining GDF5 in Formalin-fixed, Paraffin-embedded Human Skin tissue by Immunohistochemistry.

References for Anti-GDF 5 antibody (ab115678)

ab115678 has not yet been referenced specifically in any publications.

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