Key features and details
- Rabbit polyclonal to GDF 5
- Suitable for: ICC/IF, IHC-P, WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-GDF 5 antibody
See all GDF 5 primary antibodies
DescriptionRabbit polyclonal to GDF 5
Tested applicationsSuitable for: ICC/IF, IHC-P, WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat, Rabbit, Horse, Chicken, Dog, Baboon
Synthetic peptide corresponding to Human GDF 5 aa 350-450 conjugated to keyhole limpet haemocyanin.
(Peptide available as
- This antibody gave a positive signal when tested against recombinant GDF 5 protein. This antibody gave a positive result in IHC in the following FFPE tissue: Human normal pancreas.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Batches of this product that have a concentration < 1mg/ml may have BSA added as a stabilising agent. If you would like information about the formulation of a specific lot, please contact our scientific support team who will be happy to help.
Concentration information loading...
PurityImmunogen affinity purified
Immunizing Peptide (Blocking)
Our Abpromise guarantee covers the use of ab93855 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use a concentration of 1 µg/ml.|
|IHC-P||Use a concentration of 5 µg/ml.|
|WB||Use a concentration of 1 µg/ml. Detects a band of approximately 13 kDa (predicted molecular weight: 55 kDa).|
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.
- Information by UniProt
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ICC/IF image of ab93855 stained HepG2 cells. The cells were 4% PFA fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab93855, 1µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
This antibody was tested against recombinant full length protein. Human GDF5 is a homodimer consisting of two 117 residue polypeptide chains.
IHC image of GDF 5 staining in Human normal pancreas formalin fixed paraffin embedded tissue section, performed on a Leica BondTM system using the standard protocol F. The section was pre-treated using heat mediated antigen retrieval with sodium citrate buffer (pH6, epitope retrieval solution 1) for 20 mins. The section was then incubated with ab93855, 5µg/ml, for 15 mins at room temperature and detected using an HRP conjugated compact polymer system. DAB was used as the chromogen. The section was then counterstained with haematoxylin and mounted with DPX.
For other IHC staining systems (automated and non-automated) customers should optimize variable parameters such as antigen retrieval conditions, primary antibody concentration and antibody incubation times.
ab93855 has been referenced in 6 publications.
- Li Y et al. Growth/differentiation 5 promotes the differentiation of retinal stem cells into neurons via Atoh8. J Cell Physiol 234:21307-21315 (2019). PubMed: 31066042
- Jia Z et al. CDMP1 overexpression mediates inflammatory cytokine-induced apoptosis via inhibiting the Wnt/ß-Catenin pathway in rat dorsal root ganglia neurons. Int J Mol Med 42:1247-1256 (2018). PubMed: 29901085
- Zeng J et al. Co-culture of ?broblast-like synoviocytes with umbilical cord-mesenchymal stem cells inhibits expression of pro-in?ammatory proteins, induces apoptosis and promotes chondrogenesis. Mol Med Rep 14:3887-93 (2016). PubMed: 27599675
- Qu X et al. MiR-132-3p Regulates the Osteogenic Differentiation of Thoracic Ligamentum Flavum Cells by Inhibiting Multiple Osteogenesis-Related Genes. Int J Mol Sci 17:N/A (2016). WB ; Human . PubMed: 27556448
- Liu W et al. Inhibition of microRNA-34a prevents IL-1ß-induced extracellular matrix degradation in nucleus pulposus by increasing GDF5 expression. Exp Biol Med (Maywood) 241:1924-1932 (2016). PubMed: 27385596
- Osório C et al. Growth differentiation factor 5 is a key physiological regulator of dendrite growth during development. Development 140:4751-62 (2013). ICC/IF ; Mouse . PubMed: 24173804