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GDF6 Antibody

     
  • 1 - GDF6 Antibody ASC10726
    Western blot analysis of GDF6 in SK-N-SH lysate with GDF6 antibody at (A) 0.5 and (B) 1 µg/mL.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession Q6KF10
Other Accession NP_001001557, 48475062
Reactivity Human, Mouse, Rat
Host Rabbit
Clonality Polyclonal
Isotype IgG
Calculated MW 50662 Da
Concentration (mg/ml) 1 mg/mL
Conjugate Unconjugated
Application Notes GDF6 antibody can be used for detection of GDF6 by Western blot at 0.5 to 1 µg/mL.
Additional Information
Gene ID 392255
Other Names Growth/differentiation factor 6, GDF-6, Bone morphogenetic protein 13, BMP-13, Growth/differentiation factor 16, GDF6, BMP13, GDF16
Target/Specificity GDF6;
Reconstitution & Storage GDF6 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
PrecautionsGDF6 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name GDF6
Synonyms BMP13, GDF16
Function Growth factor that controls proliferation and cellular differentiation in the retina and bone formation. Plays a key role in regulating apoptosis during retinal development. Establishes dorsal- ventral positional information in the retina and controls the formation of the retinotectal map (PubMed:23307924). Required for normal formation of bones and joints in the limbs, skull, digits and axial skeleton. Plays a key role in establishing boundaries between skeletal elements during development. Regulation of GDF6 expression seems to be a mechanism for evolving species-specific changes in skeletal structures. Seems to positively regulate differentiation of chondrogenic tissue through the growth factor receptors subunits BMPR1A, BMPR1B, BMPR2 and ACVR2A, leading to the activation of SMAD1- SMAD5-SMAD8 complex. The regulation of chondrogenic differentiation is inhibited by NOG (PubMed:26643732). Also involved in the induction of adipogenesis from mesenchymal stem cells. This mechanism acts through the growth factor receptors subunits BMPR1A, BMPR2 and ACVR2A and the activation of SMAD1-SMAD5-SMAD8 complex and MAPK14/p38 (By similarity).
Cellular Location Secreted.
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

GDF6 Antibody: Growth differentiation factors (GDFs) are members of the transforming growth factor (TGF) superfamily that is involved in embryonic development and adult tissue homeostasis. Both GDF6 and GDF7 are closely related to GDF5 which has been shown to induce activation of plasminogen activator, thereby inducing angiogenesis. It is predominantly expressed in long bones during fetal embryonic development and is involved in bone formation. In Xenopus, GDF6 is expressed at the edge of the neural plate and within the anterior neural plate including the eye fields. GDF6 is required for normal formation of some bones and joints in the limbs, skull, and axial skeleton. It may regulate patterning of the ectoderm by interacting with bone morphogenetic proteins (BMPs), and control eye development. Mutations in this gene result in colobomata, which are congenital abnormalities in ocular development, and in Klippel-Feil syndrome (KFS), a congenital disorder of spinal segmentation.

REFERENCES

Massague J. 1990. The transforming growth factor-beta family. Ann. Rev. Cell Biol.6:597-641.
McPherron AC, Lawler AM, and Lee SJ. Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature1997; 387:83-90.
Hanel ML and Hensey C. Eye and neural defects associated with loss of GDF6. BMC Dev. Biol.2006; 6:43.
Settle SH Jr., Rountree RB, Sinha A, et al. Multiple joint and skeletal patterning defects caused by single and double mutations in the mouse Gdf6 and Gdf5 genes. Dev. Biol.2003; 254:116-130.

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