Target：GDF-6

Fields：Cytokine-cytokine receptor interaction;TGF-beta signaling pathway;Hippo signaling pathway

Gene Name：GDF6

Protein Name：Growth/differentiation factor 6

Human Gene Id：392255

Human Swiss Prot No：Q6KF10

Mouse Gene Id：242316

Mouse Swiss Prot No：P43028

Rat Gene Id：252834

Rat Swiss Prot No：Q6HA10

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.

Formulation：Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Source：Polyclonal, Rabbit,IgG

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

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

Concentration：1 mg/ml

Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)

Other Name：GDF6;GDF16;Growth/differentiation factor 6;GDF-6;Growth/differentiation factor 16

Observed Band(KD)：50kD

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

Subcellular Location：Secreted .

Expression： Hindbrain,Testis,