|Other Names||Sonic hedgehog protein, SHH, HHG-1, Sonic hedgehog protein N-product, Sonic hedgehog protein C-product, SHH|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Intercellular signal essential for a variety of patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior- posterior axis of the developing limb bud. Displays both floor plate- and motor neuron-inducing activity. The threshold concentration of N-product required for motor neuron induction is 5-fold lower than that required for floor plate induction. Activates the transcription of target genes by interacting with its receptor PTCH1 to prevent normal inhibition by PTCH1 on the constitutive signaling activity of SMO (By similarity).|
|Cellular Location||Sonic hedgehog protein C-product: Secreted, extracellular space. Note=The C-terminal peptide diffuses from the cell.|
|Tissue Location||Expressed in fetal intestine, liver, lung, and kidney. Not expressed in adult tissues|
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This gene encodes a protein that is instrumental inpatterning the early embryo. It has been implicated as the keyinductive signal in patterning of the ventral neural tube, theanterior-posterior limb axis, and the ventral somites. Of threehuman proteins showing sequence and functional similarity to thesonic hedgehog protein of Drosophila, this protein is the mostsimilar. The protein is made as a precursor that isautocatalytically cleaved; the N-terminal portion is soluble andcontains the signalling activity while the C-terminal portion isinvolved in precursor processing. More importantly, the C-terminalproduct covalently attaches a cholesterol moiety to the N-terminalproduct, restricting the N-terminal product to the cell surface andpreventing it from freely diffusing throughout the developingembryo. Defects in this protein or in its signalling pathway are acause of holoprosencephaly (HPE), a disorder in which thedeveloping forebrain fails to correctly separate into right andleft hemispheres. HPE is manifested by facial deformities. It isalso thought that mutations in this gene or in its signallingpathway may be responsible for VACTERL syndrome, which ischaracterized by vertebral defects, anal atresia, tracheoesophagealfistula with esophageal atresia, radial and renal dysplasia,cardiac anomalies, and limb abnormalities. Additionally, mutationsin a long range enhancer located approximately 1 megabase upstreamof this gene disrupt limb patterning and can result in preaxialpolydactyly.
Maloverjan, A., et al. J. Biol. Chem. 285(39):30079-30090(2010)Li, F., et al. Arterioscler. Thromb. Vasc. Biol. 30(9):1787-1794(2010)Lesiak, A., et al. Pol. Merkur. Lekarski 29(170):141-143(2010)Choi, S.S., et al. Hepatology 52(1):278-290(2010)Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :
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