NP_032737.1
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Related Accession #
Molecular Weight
25,770 Da
NCBI Official Full Name
noggin
NCBI Official Synonym Full Names
noggin
NCBI Protein Information
noggin
UniProt Protein Name
Noggin
UniProt Entry Name
NOGG_MOUSE
UniProt Comments for NOG
NOG: Essential for cartilage morphogenesis and joint formation. Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite. Defects in NOG are a cause of symphalangism proximal syndrome (SYM1). SYM1 is 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. Defects in NOG are the cause of multiple synostoses syndrome type 1 (SYNS1); 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). 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); 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). 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. Belongs to the noggin family.
Protein type: Secreted, signal peptide; Secreted
Cellular Component: extracellular space; extracellular region
Molecular Function: protein homodimerization activity; cytokine binding; protein complex binding
Biological Process: neural tube development; limb development; axon guidance; central nervous system development; wound healing; somatic stem cell maintenance; regulation of neuron differentiation; embryonic skeletal development; multicellular organismal development; regulation of BMP signaling pathway; motor axon guidance; middle ear morphogenesis; negative regulation of transcription from RNA polymerase II promoter; negative regulation of BMP signaling pathway; BMP signaling pathway; notochord morphogenesis; cell differentiation in hindbrain; ureteric bud development; negative regulation of cardiac muscle cell proliferation; axial mesoderm development; anatomical structure formation; negative regulation of osteoblast differentiation; cell differentiation; negative regulation of cell migration; skeletal development; neural plate morphogenesis; in utero embryonic development; pattern specification process; osteoblast differentiation; negative regulation of cell differentiation; mesenchymal cell differentiation; mesoderm formation; dorsal/ventral pattern formation; endoderm formation; spinal cord development; pituitary gland development; cartilage development; negative regulation of astrocyte differentiation; neural tube closure; epithelial to mesenchymal transition; positive regulation of transcription from RNA polymerase II promoter; brain development; embryonic digit morphogenesis; urogenital system development; positive regulation of epithelial cell proliferation
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Pathways associated with NOG elisa kit
Diseases associated with NOG elisa kit
Organs/Tissues associated with NOG elisa kit
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