Antibody-points Bulletin: Noggin
Jul-25-2017 0 comments Cube Biosystems
Antibody-points Bulletin: Noggin

Antibody-points Bulletin: Noggin

BOLO:

Name: Noggin

Noggin is suspected of inhibiting BMPs and being a cause of symphalangism.
Artist Rendering of Noggin (AA:28-232)
Source: Swiss-Model  
CC License

PID: Q13253

GID: 9241

Nicknames: Nog

AKA: SYM1, SYNS1, SYNS1A

Vitals:

   Origins: 17q22
   DNA: 1892 bp, NC_000017.11 (56593699..56595590)
   RNA: 1892 bp
   Exons: 0
   Protein: 282 aa, 25.8 kDa

Description:

Be on the lookout for NOG: The secreted polypeptide, encoded by this 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, this protein may have a principal role in creating morphogenic gradients. The protein 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.

Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite. Essential for cartilage morphogenesis and joint formation. Inhibits chondrocyte differentiation through its interaction with GDF5 and, probably, GDF6.

Mutations in Nog can cause symphalangism, a hereditary absence of the proximal interphalangeal joints. 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. Conductive hearing loss is seen and is due to fusion of the stapes to the petrous part of the temporal bone.

Protein of Interest in the Following Cases:

Noggin is suspected of inhibiting BMPs and being a cause of symphalangism.

Source: Open Targets Platform

Last Known Addresses:

  •  Secreted

Known Hangouts:

Noggin may most likely be found in normal adult endometrium, placent, skeletal muscle, lung, esophagus, and kidneys.

Source: Protein Atlas

Known Associates:

Noggin is suspected of inhibiting BMPs and being a cause of symphalangism.

Source: BioGrid

Gang Associations:

  •  BMP receptor signaling
  •  Cardiac Progenitor Differentiation
  •  Differentiation Pathway
  •  Endoderm Differentiation
  •  Mesodermal Commitment Pathway
  •  Signal Transduction
  •  TGF-beta Receptor Signaling

Known Weaknesses: Known

Reported Sightings:

Noggin is suspected of inhibiting BMPs and being a cause of symphalangism.

Source: Pubmed

Means of Capture:

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