Harmonizome 3.0

noggin

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. [provided by RefSeq, Jul 2008]

From InterPro Predicted Protein Domain Annotations

proteins predicted to have the NOG, C-terminal protein domain from the InterPro Predicted Protein Domain Annotations dataset.

From CTD Gene-Disease Associations

genes/proteins associated with the disease NOG-Related-Symphalangism Spectrum Disorder from the curated CTD Gene-Disease Associations dataset.

From GeneRIF Biological Term Annotations

genes co-occuring with the biological term nog in literature-supported statements describing functions of genes from the GeneRIF Biological Term Annotations dataset.

From Pathway Commons Protein-Protein Interactions

interacting proteins for NOG from the Pathway Commons Protein-Protein Interactions dataset.

From CM4AI KOLF21J CRISPRi Gene Perturbation Atlas

genes differentially expressed following the NOG gene perturbation from the CM4AI KOLF21J CRISPRi Gene Perturbation Atlas.