Anti-GDF 5 antibody - Aminoterminal end (ab38546)
- Product nameAnti-GDF 5 antibody - Aminoterminal endSee all GDF 5 primary antibodies ...
- DescriptionRabbit polyclonal to GDF 5 - Aminoterminal end
- SpecificityThis antibody is specific for GDF 5 (N term).
- Tested applicationsICC/IF, WB, ELISA more details
- Species reactivityReacts with: Mouse, Human
A KLH conjugated synthetic peptide (10-30 aa in length) at the N-term of first 50 aa of human GDF 5.
- Positive controlA549 cell lysate
- Storage instructionsStore at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze / thaw cycles.
- Storage bufferPreservative: 0.09% Sodium Azide
- Concentration information loading...
- PurityProtein G purified
- Purification notesThis antibody is purified through a protein G column and eluted out with both high and low pH buffers and neutralized immediately after elution then followed by dialysis against PBS.
- Clonality Polyclonal
- Research Areas
Our Abpromise guarantee covers the use of ab38546 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||WB: 1/100 - 1/500. Detects a band of approximately 55 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.
- Cellular localizationSecreted.
- BMP14 antibodyCartilage derived morphogenetic protein 1 antibodyCartilage-derived morphogenetic protein 1 antibody
- CDMP-1 antibodyCDMP1 antibodyGDF-5 antibodyGdf5 antibodyGDF5_HUMAN antibodyGrowth differentiation factor 5 antibodyGrowth/differentiation factor 5 antibodyLAP4 antibodyOS5 antibodyRadotermin antibodySYNS2 antibody
Anti-GDF 5 antibody - Aminoterminal end images
Anti-GDF 5 antibody - Aminoterminal end (ab38546) at 1/100 dilution + A549 cell lysate
Predicted band size : 55 kDa
Observed band size : 55 kDa
Additional bands at : 35 kDa. We are unsure as to the identity of these extra bands.
References for Anti-GDF 5 antibody - Aminoterminal end (ab38546)
ab38546 has not yet been referenced specifically in any publications.