|Tested species reactivity||Human, Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Synthetic peptide conjugated to KLH derived from within residues 1 - 100 of Human Sonic Hedgehog.|
|Purification||Antigen affinity chromatography|
|Storage buffer||PBS, pH 7.4, with 1% BSA|
|Contains||0.02% sodium azide|
|Storage Conditions||Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Tested Applications||Dilution *|
|ELISA (ELISA)||0.5 µg/ml|
|Immunocytochemistry (ICC)||5 µg/ml|
|Immunofluorescence (IF)||5 µg/ml|
|Western Blot (WB)||1 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
Not suitable for use with Immunohistochemistry - Free Floating.
This antibody is predicted to react with rat, chicken, cow, human, Xenopus laevis, zebrafish and many species based on sequence homology.
Sonic Hedgehog, which is expressed only during embryogenesis, is instrumental in patterning the early embryo. It has been implicated as the key inductive signal in patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites. Of three human proteins showing sequence and functional similarity to the Sonic Hedgehog protein of Drosophila, this protein is the most similar. The protein is made as a precursor that is autocatalytically cleaved; the N-terminal portion is soluble and contains the signalling activity while the C-terminal portion is involved in precursor processing. More importantly, the C-terminal product covalently attaches a cholesterol moiety to the N-terminal product, restricting the N-terminal product to the cell surface and preventing it from freely diffusing throughout the developing embryo. Defects in this protein or in its signalling pathway are a cause of holoprosencephaly (HPE), a disorder in which the developing forebrain fails to correctly separate into right and left hemispheres. HPE is manifested by facial deformities. In addition, it is thought that mutations in this gene or in its signalling pathway may be responsible for VACTERL syndrome, which is characterized by vertebral defects, anal atresia, tracheoesophageal fistula with esophageal atresia, radial and renal dysplasia, cardiac anomalies, and limb abnormalities.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.