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. [provided by RefSeq, Jul 2008]

Noggin

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 (PubMed:21976273, PubMed:26643732).

Atrial cardiac muscle tissue morphogenesisISS:BHF-UCL
Axial mesoderm developmentIEA:Ensembl
BMP signaling pathway involved in heart developmentISS:BHF-UCL
Cartilage developmentIEA:UniProtKB-KW
Cell differentiation in hindbrainManual Assertion Based On ExperimentIMP:BHF-UCL
Cell population proliferationIEA:Ensembl
Cranial skeletal system developmentIEA:Ensembl
Dorsal/ventral pattern formationManual Assertion Based On ExperimentIDA:BHF-UCL
Embryonic digit morphogenesisManual Assertion Based On ExperimentIMP:BHF-UCL
Embryonic skeletal joint morphogenesisManual Assertion Based On ExperimentIMP:BHF-UCL
Embryonic skeletal system developmentManual Assertion Based On ExperimentIMP:BHF-UCL
Endocardial cushion morphogenesisISS:BHF-UCL
Endoderm formationIEA:Ensembl
Epithelial to mesenchymal transitionISS:UniProtKB
Exploration behaviorIEA:Ensembl
Face morphogenesisIEA:Ensembl
Fibroblast growth factor receptor signaling pathway involved in neural plate anterior/posterior pattern formationManual Assertion Based On ExperimentIMP:BHF-UCL
Heart trabecula morphogenesisISS:BHF-UCL
In utero embryonic developmentIEA:Ensembl
Limb developmentManual Assertion Based On ExperimentIMP:BHF-UCL
Long-term synaptic potentiationIEA:Ensembl
Lung morphogenesisIEA:Ensembl
Membranous septum morphogenesisISS:BHF-UCL
Mesoderm formationIEA:Ensembl
Middle ear morphogenesisManual Assertion Based On ExperimentIMP:BHF-UCL
Motor neuron axon guidanceIEA:Ensembl
Negative regulation of apoptotic signaling pathwayIEA:Ensembl
Negative regulation of astrocyte differentiationISS:UniProtKB
Negative regulation of BMP signaling pathwayManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of canonical Wnt signaling pathwayManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of cardiac muscle cell proliferationISS:UniProtKB
Negative regulation of cartilage developmentIEA:Ensembl
Negative regulation of cell migrationManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of cytokine activityManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of epithelial to mesenchymal transition involved in endocardial cushion formationISS:BHF-UCL
Negative regulation of gene expressionIEA:Ensembl
Negative regulation of osteoblast differentiationManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of pathway-restricted SMAD protein phosphorylationManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of transcription by RNA polymerase IIISS:BHF-UCL
Nervous system developmentManual Assertion Based On ExperimentTAS:ProtInc
Neural plate morphogenesisIEA:Ensembl
Neural tube closureIEA:Ensembl
Notochord morphogenesisIEA:Ensembl
Osteoblast differentiationISS:UniProtKB
Outflow tract morphogenesisISS:BHF-UCL
Pharyngeal arch artery morphogenesisISS:BHF-UCL
Pituitary gland developmentIEA:Ensembl
Positive regulation of branching involved in ureteric bud morphogenesisISS:UniProtKB
Positive regulation of epithelial cell proliferationIEA:Ensembl
Positive regulation of gene expressionISS:BHF-UCL
Positive regulation of glomerulus developmentISS:UniProtKB
Positive regulation of transcription by RNA polymerase IIIEA:Ensembl
Presynaptic modulation of chemical synaptic transmissionIEA:Ensembl
Prostatic bud formationIEA:Ensembl
Regulation of fibroblast growth factor receptor signaling pathway involved in neural plate anterior/posterior pattern formationManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of neuronal synaptic plasticityIEA:Ensembl
Short-term synaptic potentiationIEA:Ensembl
Skeletal system developmentManual Assertion Based On ExperimentTAS:ProtInc
Smoothened signaling pathwayIEA:Ensembl
Somatic stem cell population maintenanceManual Assertion Based On ExperimentIMP:BHF-UCL
Somite developmentIEA:Ensembl
Spinal cord developmentIEA:Ensembl
Ureteric bud formationIEA:Ensembl
Ventricular compact myocardium morphogenesisISS:BHF-UCL
Ventricular septum morphogenesisISS:BHF-UCL
Visual learningIEA:Ensembl
Wound healingISS:UniProtKB

Secreted

Symphalangism, proximal 1A (SYM1A):
A disease characterized by the 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.
Multiple synostoses syndrome 1 (SYNS1):
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.
Tarsal-carpal coalition syndrome (TCC):
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.
Stapes ankylosis with broad thumb and toes (SABTS):
An autosomal dominant disorder characterized by hyperopia, a hemicylindrical nose, broad thumbs, great toes, and other minor skeletal anomalies but lacked carpal and tarsal fusion and symphalangism.
Brachydactyly B2 (BDB2):
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.