SHH Antibody, KO Validated | 18-208

SHH Antibody, KO Validated | 18-208 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: A synthetic peptide of human SHH

Research Area: Cancer, Cell Cycle, Neuroscience, Stem Cell

Tested Application: WB, IHC

Application: WB: 1:500 - 1:2000
IHC: 1:50 - 1:200

Specificiy: N/A

Positive Control 1: HeLa

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: Observed: 50kDa

Validation: Antibody is Knockout validated.

Isoform: N/A

Purification: Affinity purification

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.

Concentration: N/A

Storage Condition: Store at -20˚C. Avoid freeze / thaw cycles.

Alternate Name: SHH, HHG1, HLP3, HPE3, SMMCI, TPT, TPTPS, MCOPCB5

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: This gene encodes a protein that 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. It is also 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. Additionally, mutations in a long range enhancer located approximately 1 megabase upstream of this gene disrupt limb patterning and can result in preaxial polydactyly.