Home Primary Antibodies Sp7/Osterix Antibody [J12J9]

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Sp7/Osterix Antibody [J12J9]

Catalog No.: F1545

    Application: Reactivity:
    • F1545-wb
      Lane 1: Saos-2

    Usage Information

    Dilution
    1:1000
    1:30
    1:1000
    Application
    WB, IP, IHC
    Reactivity
    Mouse, Rat, Human
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    45 kDa 45 kDa, 47 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.

    Datasheet & SDS

    Biological Description

    Specificity
    Sp7/Osterix Antibody [J12J9] detects endogenous levels of total Sp7/Osterix protein.
    Clone
    J12J9
    Synonym(s)
    OSX; SP7; Transcription factor Sp7; Zinc finger protein osterix
    Background
    Sp7, also known as Osterix (Osx), is a zinc-finger transcription factor of the Sp/KLF family that functions as a master regulator of osteoblast differentiation downstream of Runx2, essential for bone formation in vertebrates and primarily expressed in osteoblasts, osteocytes, and chondrocytes. Sp7 contains a proline-rich N-terminal transactivation domain and a C-terminal DNA-binding domain with three C2H2-type zinc finger motifs highly homologous to Sp1/Sp3/Sp4, though amino acid variations in the zinc finger reduce affinity for canonical GC-boxes and enable interaction with AT-rich motifs via protein-protein contacts. Sp7 promotes mesenchymal progenitor commitment to mature osteoblasts by inducing genes like Col1a1, Bglap (osteocalcin), Ibsp (bone sialoprotein), Sparc (osteonectin), and Alp while suppressing chondrogenesis; it acts primarily as a co-activator in complexes with Dlx family homeodomain factors (e.g., Dlx5) that bind AT-rich homeodomain-response elements in osteoblast enhancers, driving synergistic transcriptional activation via the Sp7 N-terminus. This non-canonical mechanism supports osteocyte maturation, lacuno-canalicular network formation, bone matrix mineralization, and adult bone homeostasis through pathways like BMP, Wnt/β-catenin, and MAPK signaling. Mutations in SP7 cause osteogenesis imperfecta and osteoporosis by disrupting osteoblast differentiation and bone mass maintenance.
    References
    • https://pubmed.ncbi.nlm.nih.gov/35628456/
    • https://pubmed.ncbi.nlm.nih.gov/27134141/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
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