Description

  • Product name

    Recombinant human Noggin protein
    See all Noggin proteins and peptides
  • Biological activity

    Measured by ability of ab198773 to inhibit BMP-4-induced alkaline phosphatase production by C2C12 mouse myoblast cells. The ED50 is <20 ng/ml in the presence of 30 ng/ml of Human BMP-4

  • Purity

    > 70 % SDS-PAGE.

  • Endotoxin level

    < 1.000 Eu/µg
  • Expression system

    Freestyle 293-F cells
  • Accession

  • Protein length

    Full length protein
  • Animal free

    No
  • Nature

    Recombinant
    • Species

      Human
    • Sequence

      QHYLHIRPAPSDNLPLVDLIEHPDPIFDPKEKDLNETLLRSLLGGHYDPG FMATSPPEDRPGGGGGAAGGAEDLAELDQLLRQRPSGAMPSEIKGLEFSE GLAQGKKQRLSKKLRRKLQMWLWSQTFCPVLYAWNDLGSRFWPRYVKVGS CFSKRSCSVPEGMVCKPSKSVHLTVLRWRCQRRGGQRCGWIPIQYPIISE CKCSC
    • Predicted molecular weight

      28 kDa
    • Amino acids

      28 to 232
    • Additional sequence information

      Mature disulfide-linked homodimer without signal peptide. NM_005450.

Specifications

Our Abpromise guarantee covers the use of ab198773 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications

    Functional Studies

    SDS-PAGE

  • Form

    Lyophilised
  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped at 4°C. Store at -20°C or -80°C. Avoid freeze / thaw cycle.

    pH: 8.00
    Constituents: 0.61% Tris, 6.96% Sodium chloride, 0.02% Potassium chloride, 0.1% BSA

    Lyophilized from a 0.2 µm filtered solution

    This product is an active protein and may elicit a biological response in vivo, handle with caution.

  • Reconstitution
    Reconstitute in sterile water with 0.1% BSA to a final concentration of 0.1 mg/ml. Final formulation will be 50 mM Tris, pH 8.0, 1.2 M NaCl, 2.7 mM KCl, 0.1% BSA. This solution can then be diluted into other buffers. To maximize product collection from vial surface, vortex briefly and then spin down to recollect the liquid. Store reconstituted protein in aliquots at -20°C to -80°C for up to 6 months. Avoid freeze/thaw cycles.

General Info

  • Alternative names

    • Nog
    • NOGG_HUMAN
    • Noggin
    • SYM 1
    • SYM1
    • Symphalangism 1 (proximal)
    • Synostoses (multiple) syndrome 1
    • SYNS 1
    • SYNS1
    see all
  • Function

    Essential for cartilage morphogenesis and joint formation. Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite.
  • Involvement in disease

    Defects in NOG are a cause of symphalangism proximal syndrome (SYM1) [MIM:185800]. SYM1 is characterized by the hereditary absence of the proximal interphalangeal (PIP) joints (Cushing symphalangism). Severity of PIP joint involvement diminishes towards the radial side. Distal interphalangeal joints are less frequently involved and metacarpophalangeal joints are rarely affected whereas carpal bone malformation and fusion are common. In the lower extremities, tarsal bone coalition is common. Conducive hearing loss is seen and is due to fusion of the stapes to the petrous part of the temporal bone.
    Defects in NOG are the cause of multiple synostoses syndrome type 1 (SYNS1) [MIM:186500]; also known as synostoses, multiple, with brachydactyly/symphalangism-brachydactyly syndrome. SYNS1 is characterized by tubular-shaped (hemicylindrical) nose with lack of alar flare, otosclerotic deafness, and multiple progressive joint fusions commencing in the hand. The joint fusions are progressive, commencing in the fifth proximal interphalangeal joint in early childhood (or at birth in some individuals) and progressing in an ulnar-to-radial and proximal-to-distal direction. With increasing age, ankylosis of other joints, including the cervical vertebrae, hips, and humeroradial joints, develop.
    Defects in NOG are the cause of tarsal-carpal coalition syndrome (TCC) [MIM:186570]. TCC is an autosomal dominant disorder characterized by fusion of the carpals, tarsals and phalanges, short first metacarpals causing brachydactyly, and humeroradial fusion. TCC is allelic to SYM1, and different mutations in NOG can result in either TCC or SYM1 in different families.
    Defects in NOG are a cause of stapes ankylosis with broad thumb and toes (SABTS) [MIM:184460]; also known as Teunissen-Cremers syndrome. SABTS is a congenital autosomal dominant disorder that includes hyperopia, a hemicylindrical nose, broad thumbs, great toes, and other minor skeletal anomalies but lacked carpal and tarsal fusion and symphalangism.
    Defects in NOG are the cause of brachydactyly type B2 (BDB2) [MIM:611377]. BDB2 is a subtype of brachydactyly characterized by hypoplasia/aplasia of distal phalanges in combination with distal symphalangism, fusion of carpal/tarsal bones, and partial cutaneous syndactyly.
  • Sequence similarities

    Belongs to the noggin family.
  • Cellular localization

    Secreted.
  • Information by UniProt

Images

  • 4-20% SDS-PAGE analysis of ab198773 with Coomassie staining.

    Lane 1: 3 µg ab198773
    Lane 2: Protein marker

  • Functional analysis of ab198773.

References

ab198773 has not yet been referenced specifically in any publications.

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