Mouse SHH (Hedgehog Homolog, Sonic) ELISA Kit

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935106861
info@markelab.com
name
Mouse SHH (Hedgehog Homolog, Sonic) ELISA Kit
category
ELISA Kits
provider
FineTest
reference
EM1360
tested applications
ELISA

Documents del producto

Instrucciones
Descargar
Data sheet

Product specifications

Category
ELISA Kits
Reactivity
Mouse
Detection Method
Colorimetric
Assay Data
4 hours
Assay Type
Sandwich ELISA, Double Antibody
Test Range
15.625-1000pg/ml
Sensitivity
9.375pg/ml
Size 1
96T
Tested Applications
ELISA
Sample Type
Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples
Availability
Shipped within 10-14 working days.
Storage
2-8 °C for 12 months
UniProt ID
Q62226
Alias
Sonic hedgehog protein, SHH, HHG-1, Shh unprocessed N-terminal signaling and C-terminal autoprocessing domains, ShhNC, Sonic hedgehog protein N-product, ShhN, Shh N-terminal processed signaling domains, ShhNp, SHH
Background
Elisa kits for SHH
Status
RUO

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FNab07847

SHH antibody

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.

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