Home / Products / Polyclonal antibody /

GDF-6 Polyclonal Antibody

Product code: YP-Ab-16066
Promotional price:

Product introduction

Reactive species
Human;Mouse;Rat
Applications
WB;ELISA
Antibody type
Polyclonal Antibody
Gene Name
GDF6
Protein name
Growth/differentiation factor 6
Dalton(DA)
50kD
Immunogen
The antiserum was produced against synthesized peptide derived from the Internal region of human GDF6. AA range:311-360
Specificity
GDF-6 Polyclonal Antibody detects endogenous levels of GDF-6 protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
Western Blot: 1/500 - 1/2000. ELISA: 1/10000. Not yet tested in other applications.
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration
1 mg/ml
Stockpile
-20°C/1 year
Other name
GDF6; GDF16; Growth/differentiation factor 6; GDF-6; Growth/differentiation factor 16
Background
This gene encodes a secreted ligand of the TGF-beta (transforming growth factor-beta) superfamily of proteins. Ligands of this family bind various TGF-beta receptors leading to recruitment and activation of SMAD family transcription factors that regulate gene expression. The encoded preproprotein is proteolytically processed to generate each subunit of the disulfide-linked homodimer. This protein is required for normal formation of some bones and joints in the limbs, skull, and axial skeleton. Mutations in this gene are associated with Klippel-Feil syndrome, microphthalmia, and Leber congenital amaurosis. [provided by RefSeq, Sep 2016],
Function
disease:A chromosomal aberration involving GDF6 is associated with Klippel-Feil syndrome (KFS) [MIM:118100]. Paracentric inv(8)(q22;2q23.3).,disease:Defects in GDF6 are associated with Klippel-Feil syndrome (KFS) [MIM:118100]. Klippel-Feil syndrome is a complex skeletal disorder characterized by congenital fusion of vertebrae within the anterior/cervical spine. Vertebral fusion appears to be caused by a failure in the normal segmentation of vertebrae during the early weeks of fetal development and defective somitogenesis has been postulated as a mitigating factor. However, the etiology of KFS is still unknown and no definitive disease-causing genes have yet been identified. Although most cases are sporadic, both autosomal dominant and autosomal recessive inheritance have been reported.,function:Required for normal formation of bones and joints in the limbs, skull, and axial skeleton. Pla

Open

Product Details

Customer data and reviews (0)

Fold content

Citation

Fold content

Experimental scheme

Fold content
>