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Noggin Protein, Antibody, ELISA Kit, cDNA Clone

Human Noggin Protein

Description: Active
Expression host: Human Cells
  • Slide 1
10267-H02H-50
10267-H02H-100
50 µg / $178
100 µg / $298
Add to Cart
Expression host: Human Cells
  • Slide 1
10267-H08H-100
10267-H08H-20
10267-H08H-500
10267-H08H-1
10267-H08H-5
100 µg / $548
20 µg / $138
500 µg / $1848
1 mg / $3098
5 µg / $38
Add to Cart

Mouse Noggin Protein

Expression host: Human Cells
  • Slide 1
  • Slide 1
50688-M02H-5
50688-M02H-100
50688-M02H-500
50688-M02H-1
50688-M02H-20
5 µg / $58
100 µg / $548
500 µg / $1848
1 mg / $3098
20 µg / $138
Add to Cart

Noggin Related Areas

Noggin Related Pathways

Noggin Related Product

Noggin Summary & Protein Information

Noggin Related Information

Noggin Background

Gene Summary: Noggin, the secreted polypeptide, encoded by this NOG gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, Noggin may have a principal role in creating morphogenic gradients. Noggin appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of the ortholog suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation. Recently, several dominant human NOG mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) were identified; both SYM1 and SYNS1 have multiple joint fusion as their principal feature, and map to the same region (17q22) as this gene. All of these mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of this human gene is highly homologous to that of Xenopus, rat and mouse.
General information above from NCBI
Subunit structure: Homodimer.
Subcellular location: Secreted.
Involvement in disease: Symphalangism proximal syndrome (SYM1) [MIM:185800]: 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. Note=The disease is caused by mutations affecting the gene represented in this entry.
Multiple synostoses syndrome 1 (SYNS1) [MIM:186500]: A bone disease characterized by multiple progressive joint fusions that commonly involve proximal interphalangeal, tarsal-carpal, humeroradial and cervical spine joints. Additional features can include progressive conductive deafness and facial dysmorphism. Note=The disease is caused by mutations affecting the gene represented in this entry.
Tarsal-carpal coalition syndrome (TCC) [MIM:186570]: 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. Note=The disease is caused by mutations affecting the gene represented in this entry.
Stapes ankylosis with broad thumb and toes (SABTS) [MIM:184460]: 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. Note=The disease is caused by mutations affecting the gene represented in this entry.
Brachydactyly B2 (BDB2) [MIM:611377]: A form of brachydactyly characterized by hypoplasia/aplasia of distal phalanges in combination with distal symphalangism, fusion of carpal/tarsal bones and partial cutaneous syndactyly. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Belongs to the noggin family.
General information above from UniProt

Noggin is a secreted protein involved at multiple stages of vertebrate embryonic development including neural induction and is known to exert its effects by inhibiting the bone morphogenetic protein (BMP)-signaling pathway. It binds several BMPs with very high (picomolar) affinities, with a marked preference for BMP2 and BMP4 over BMP7. By binding tightly to BMPs, Noggin prevents BMPs from binding their receptors. Noggin binds the bone morphogenetic proteins (BMP) such as BMP-4 and BMP-7, and inhibits BMP signaling by blocking the molecular interfaces of the binding epitopes for both type I and type II receptors. Interaction of BMP and its antagonist Noggin governs various developmental and cellular processes, including embryonic dorsal-ventral axis, induction of neural tissue, formation of joints in the skeletal system and neurogenesis in the adult brain. Noggin plays a key role in neural induction by inhibiting BMP4, along with other TGF-β signaling inhibitors such as chordin and follistatin. Mouse knockout experiments have demonstrated that noggin also plays a crucial role in bone development, joint formation, and neural tube fusion.

Noggin Alternative Name

Noggin Related Studies

  • Zimmerman LB, et al. (1996) The Spemann organizer signal noggin binds and inactivates bone morphogenetic protein 4. Cell. 86(4): 599-606.
  • Chandramore K, et al. (2010) Cloning of noggin gene from hydra and analysis of its functional conservation using Xenopus laevis embryos. Evol Dev. 12(3): 267-74.
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