BD-PT5653

GDF-6 Rabbit Polyclonal Antibody

GDF6; GDF16; Growth/differentiation factor 6; GDF-6; Growth/differentiation factor 16

常规抗体

GDF6

Growth/differentiation factor 6

WB

Human,Mouse,Rat

1 mg/ml

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% New type preservative N.

392255

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=392255

Q6KF10

http://www.uniprot.org/uniprotkb/Q6KF10/entry

242316

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=242316

P43028

http://www.uniprot.org/uniprot/P43028

252834

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=252834

Q6HA10

http://www.uniprot.org/uniprot/Q6HA10

The antiserum was produced against synthesized peptide derived from the Internal region of human GDF6. AA range:311-360

GDF-6 Polyclonal Antibody detects endogenous levels of GDF-6 protein.

WB 1:500 - 1:2000. ELISA: 1:10000. Not yet tested in other applications.

50kD

-20°C/1 year

Polyclonal, Rabbit,IgG

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],

Hindbrain,Testis,

Secreted .

TGF-beta;

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. Play a key role in establishing boundaries between skeletal elements during development.,similarity:Belongs to the TGF-beta family.,subunit:Homodimer; disulfide-linked.,

现货

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.