Growth Factors & Cytokines Recombinant Proteins

Mouse Noggin Recombinant Protein (RPPB0805)

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RPPB0805

Description

system_update_altDatasheetsystem_update_altMSDS
Product Name:Mouse Noggin Recombinant Protein
Product Code:RPPB0805
Size:20µg
Species:Mouse
Target:Noggin
Synonyms:Noggin, SYM1, SYNS1, NOG.
Source:Escherichia Coli
Physical Appearance:Sterile Filtered White lyophilized (freeze-dried) powder.
Formulation:Lyophilized from a 0.2?m filtered solution in 30% acetonitrile, 0.1% TFA.
Solubility:It is recommended to be briefly centrifuged prior to opening to bring the contents to the bottom. Reconstitute in 10mM HAc to a concentration of 0.1-1.0 mg/ml. Further dilutions should be made in appropriate buffered solutions.
Stability:Lyophilized Mouse Noggin although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution Mouse Noggin should be stored at 4°C between 2-7 days and for future use below -18°C.For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA).Please prevent freeze-thaw cycles.
Purity:Greater than 95.0% as determined by SDS-PAGE.
Amino Acid Sequence:MQHYLHIRPAPSDNLPLVDLIEHPDPIFDPKEKDLNETLLRSLLGGHYDPGFMATSPPEDRPGGGGGPAGGAEDLAELDQLLRQRPSGAMPSEIKGLEFSEGLAQGKKQRLSKKLRRKLQMWLWSQTFCPVLYAWNDLGSRFWPRYVKVGSCFSKRSCSVPEGMVCKPSKSVHLTVLRWRCQRRGQRCGWIPIQYPIISECKCSC
Biological Activity:The ED50 as determined by inhibiting BMP-4-induced alkaline phosphatase production of murine ATDC5 cells is less than 2ng/ml, corresponding to a specific activity of > 5.0 � 105 IU/mg in the presence of 5ng/ml BMP-4.

The secreted polypeptide noggin, encoded by the NOG 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, noggin may have a principal role in creating morphogenic gradients. Noggin 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 noggin 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 NOG. All NOG mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of human noggin is highly homologous to that of Xenopus, rat and mouse.

Noggin Mouse Recombinant produced in E.Coli is a non-glycosylated, disulfide-linked protein consisting of two 206 amino acid polypeptide chains, having a total molecular mass of approximately 46.4 kDa (each chain 23.2 kDa).

UniProt Protein Function: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 peptideCellular Component: extracellular space; extracellular regionMolecular Function: protein homodimerization activity; cytokine binding; protein complex bindingBiological 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
UniProt Protein Details:
NCBI Summary:
UniProt Code:P97466
NCBI GenInfo Identifier:15214098
NCBI Gene ID:18121
NCBI Accession:P97466.1
UniProt Secondary Accession:P97466
UniProt Related Accession:P97466
Molecular Weight:25,770 Da
NCBI Full Name:Noggin
NCBI Synonym Full Names:noggin
NCBI Official Symbol:Nog��
NCBI Official Synonym Symbols:
NCBI Protein Information:noggin
UniProt Protein Name:Noggin
UniProt Synonym Protein Names:
Protein Family:Noggin
UniProt Gene Name:Nog��
UniProt Entry Name:NOGG_MOUSE
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Additional Information

Product Type:
Recombinant Protein
Species:
Mouse
Uniprot:
P97466
Research Area:
Growth Factors & Cytokines
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Growth Factors & Cytokines Recombinant Proteins

system_update_altDatasheetMouse Noggin/NOG Recombinant Protein Noggin is a secreted homodimeric glycoprotein that is an antagonist of bone morphogenetic proteins (BMPs). Mouse Noggin cDNA encodes