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Recombinant Human Sclerostin (SOST), Biotinylated

ACP00588

Number
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High Purity LevelsPrecision and ReliabilityCustomization Options

Specifications


Cat.No ACP00588 Target NameSOST
FormLiquid or Lyophilized powderExpression SystemMammalian cell
Expression Range24-213aaMol Weight25.0 kDa
Protein LengthFull Length of Mature ProteinPurityGreater than 95% as determined by SDS-PAGE.
Storage Buffer5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0.

Immunogen Information


Target SpeciesHumanUniprot IDQ9BQB4
Background Information
  • Uniprot Id

    Q9BQB4

  • Target Species

    Human

  • Target Name

    SOST

  • Target Full Name

    Sclerostin

  • Target Function

    Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation.

  • Target Involvement

    Sclerosteosis 1 (SOST1); Van Buchem disease (VBCH); Craniodiaphyseal dysplasia autosomal dominant (CDD)

  • Target Subcellular Location

    Secreted, extracellular space, extracellular matrix.

  • Target Protein Families

    Sclerostin family

  • Target Tissue Specificity

    Widely expressed at low levels with highest levels in bone, cartilage, kidney, liver, bone marrow and primary osteoblasts differentiated for 21 days. Detected in the subendothelial layer of the aortic intima (at protein level).

  • Target Research Area

    Signal Transduction

  • Target Synonyms

    BEER; CDD; Cortical hyperostosis with syndactyly; Sclerosteosis; Sclerostin; Sost; SOST_HUMAN; SOST1; UNQ2976/PRO7455/PRO7476; VBCH

  • Target Background

    Sclerostin is a secreted glycoprotein with a C-terminal cysteine knot-like (CTCK) domain and sequence similarity to the DAN (differential screening-selected gene aberrative in neuroblastoma) family of bone morphogenetic protein (BMP) antagonists. Loss-of-function mutations in this gene are associated with an autosomal-recessive disorder, sclerosteosis, which causes progressive bone overgrowth. A deletion downstream of this gene, which causes reduced sclerostin expression, is associated with a milder form of the disorder called van Buchem disease.

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