Overview
Properties
Constituents: 0.1% Trifluoroacetic acid
Concentration information loading...Applications
Our Abpromise guarantee covers the use of ab73756 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Notes |
|---|---|
| SDS-PAGE | SDS-PAGE: Use at an assay dependent dilution. |
| Functional Studies | FuncS: Use at an assay dependent dilution. Biological Activity: The ED50 was determined by its ability to inhibit 5.0 ng/ml of BMP-4 induced alkaline phosphatase production by ATDC-5 chondrogenic cells. The expected ED50 for this effect is 0.05-0.08 µg/ml of Noggin. |
| WB | WB: Use at an assay dependent concentration. Ab73756 can be used as a WB positive control in conjunction with ab16054. |
Protein info
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Alternative names
- NOGNOGG_HUMANNoggin
- SYM 1SYM1Symphalangism 1 (proximal)Synostoses (multiple) syndrome 1SYNS 1SYNS1
see all
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.
Target information above from: UniProt accession
Q13253
The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010)
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Noggin protein (Active) images
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Anti-Noggin antibody (ab16054) at 1 µg/ml +
Noggin protein (Active) (ab73756) at 1 µg
Secondary
Goat polyclonal Secondary Antibody to Rabbit IgG - H&L (HRP), pre-adsorbed (ab97080) at 1/5000 dilution
developed using the ECL technique
Performed under reducing conditions.
Exposure time : 4 minutes
References for Noggin protein (Active) (ab73756)
ab73756 has not yet been referenced specifically in any publications.
