Product nameAnti-GDF1 antibody [EPR5815]
See all GDF1 primary antibodies
DescriptionRabbit monoclonal [EPR5815] to GDF1
Tested applicationsSuitable for: WB, IPmore details
Unsuitable for: Flow Cyt,ICC or IHC-P
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide corresponding to residues in Human GDF1 protein (P27539).
- U87-MG and Human fetal brain lysates.
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Dissociation constant (KD)KD = 8.40 x 10 -11 M Learn more about KD
Storage bufferpH: 7.20
Preservative: 0.01% Sodium azide
Constituents: 9% PBS, 40% Glycerol, 0.05% BSA, 50% Tissue culture supernatant
Concentration information loading...
PurityTissue culture supernatant
Our Abpromise guarantee covers the use of ab124706 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Predicted molecular weight: 39 kDa.|
|IP||1/10 - 1/100.|
FunctionMay mediate cell differentiation events during embryonic development.
Tissue specificityExpressed in the brain.
Involvement in diseaseDefects in GDF1 are a cause of conotruncal heart malformations (CTHM) [MIM:217095]. A group of congenital heart defects involving the outflow tracts. Examples include truncus arteriosus communis, double-outlet right ventricle and transposition of great arteries. Truncus arteriosus communis is characterized by a single outflow tract instead of a separate aorta and pulmonary artery. In transposition of the great arteries, the aorta arises from the right ventricle and the pulmonary artery from the left ventricle. In double outlet of the right ventricle, both the pulmonary artery and aorta arise from the right ventricle.
Defects in GDF1 are the cause of transposition of the great arteries dextro-looped type 3 (DTGA3) [MIM:613854]. A congenital heart defect consisting of complete inversion of the great vessels, so that the aorta incorrectly arises from the right ventricle and the pulmonary artery incorrectly arises from the left ventricle. This creates completely separate pulmonary and systemic circulatory systems, an arrangement that is incompatible with life. The presence or absence of associated cardiac anomalies defines the clinical presentation and surgical management of patients with transposition of the great arteries.
Defects in GDF1 are a cause of tetralogy of Fallot (TOF) [MIM:187500]. A congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. In this condition, blood from both ventricles (oxygen-rich and oxygen-poor) is pumped into the body often causing cyanosis.
Sequence similaritiesBelongs to the TGF-beta family.
- Information by UniProt
- DORV antibody
- DTGA3 antibody
- Embryonic growth/differentiation factor 1 antibody
All lanes : Anti-GDF1 antibody [EPR5815] (ab124706) at 1/1000 dilution
Lane 1 : U87-MG cell lysate
Lane 2 : Human fetal brain lysates cell lysate
Lysates/proteins at 10 µg per lane.
Predicted band size: 39 kDa
Equilibrium disassociation constant (KD)
Learn more about KD
Click here to learn more about KD
This product has been referenced in:
- Ginkel C et al. Ablation of neuronal ceramide synthase 1 in mice decreases ganglioside levels and expression of myelin-associated glycoprotein in oligodendrocytes. J Biol Chem 287:41888-902 (2012). WB ; Mouse . Read more (PubMed: 23074226) »