Recombinant Murine NOGGIN

For Research Use Only. Not for use in diagnostic procedures.

E Coli

Above 95% as determined by SDS-PAGE Analysis.

At -20 degree C

Small volumes of NOGGIN recombinant protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Noggin belongs to a group of diffusible proteins which bind to ligands of the TGF-beta family and regulate their activity by inhibiting their access to signaling receptors. The interplay between TGF-beta ligands and their natural antagonists has major biological significance during development processes, in which cellular response can vary considerably depending upon the local concentration of the signaling molecule. Noggin was originally identified as a BMP-4 antagonist whose action is critical for proper formation of the head and other dorsal structures. Consequently, Noggin has been shown to modulate the activities of other BMPs including BMP-2, -7, -13, and -14. Targeted deletion of Noggin in mice results in prenatal death and recessive phenotype displaying a severely malformed skeletal system. Conversely, transgenic mice over-expressing Noggin in mature osteoblasts display impaired osteoblastic differentiation, reduced bone formation, and severe osteoporosis. Recombinant murine Noggin is a 46.4 kDa disulfide-linked homodimer consisting of two 206 amino acid polypeptide chains.

Stem Cell Research; Bone Biology

25,770 Da

noggin

noggin

Noggin

NOGG_MOUSE

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; Secreted, signal peptide

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; multicellular organismal development; embryonic skeletal 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; negative regulation of cardiac muscle cell proliferation; ureteric bud development; axial mesoderm development; anatomical structure formation; negative regulation of osteoblast differentiation; cell differentiation; skeletal development; negative regulation of cell migration; in utero embryonic development; neural plate morphogenesis; pattern specification process; osteoblast differentiation; negative regulation of cell differentiation; mesenchymal cell differentiation; dorsal/ventral pattern formation; mesoderm formation; pituitary gland development; endoderm formation; spinal cord development; cartilage development; neural tube closure; negative regulation of astrocyte differentiation; 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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