Recombinant human Noggin protein (ab134390)
Key features and details
- Expression system: HEK 293 cells
- Purity: > 95% SDS-PAGE
- Active: Yes
- Suitable for: SDS-PAGE, HPLC, Functional Studies
Description
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Product name
Recombinant human Noggin protein
See all Noggin proteins and peptides -
Biological activity
Determined by its ability to inhibit 5.0 ng/ml of BMP4 induced alkaline phosphatase production by ATDC-5 chondrogenic cells. The expected ED50 for this effect is 2.0-3.0 ng/ml of Noggin.
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Purity
> 95 % SDS-PAGE.
Purity is greater than 95% by SDS-PAGE gel and HPLC analyses. -
Expression system
HEK 293 cells -
Accession
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Protein length
Full length protein -
Animal free
No -
Nature
Recombinant -
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Species
Human -
Sequence
QHYLHIRPAP SDNLPLVDLI EHPDPIFDPK EKDLNETLLR SLLGGHYDPG FMATSPPEDR PGGGGGAAGG AEDLAELDQL LRQRPSGAMP SEIKGLEFSE GLAQGKKQRL SKKLRRKLQM WLWSQTFCPV LYAWNDLGSR FWPRYVKVGS CFSKRSCSVP EGMVCKPSKS VHLTVLRWRC QRRGGQRCGW IPIQYPIISE CKCSC -
Predicted molecular weight
23 kDa -
Amino acids
28 to 232
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Associated products
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Related Products
Specifications
Our Abpromise guarantee covers the use of ab134390 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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Applications
SDS-PAGE
HPLC
Functional Studies
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Form
Lyophilized -
Concentration information loading...
Preparation and Storage
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Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
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ReconstitutionCentrifuge vial prior to opening. Reconstitute in water to 0.1-1.0 mg/ml. Do not vortex. Store at 2°C to 8°C for 1 week, or prepare for extended storage. If the product is required to be stored after reconstitution it must be prepared for extended storage. Follow reconstitution with further dilution in a buffer containing a carrier protein (example 0.1% BSA). Store working aliquots at -20°C to -80°C. Avoid repeated freeze-thaw cycles. The product can then be stored for 3 months.
General Info
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Alternative names
- Nog
- NOGG_HUMAN
- Noggin
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
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
References (0)
ab134390 has not yet been referenced specifically in any publications.