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NOGGIN, Human
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Species | Human |
|---|---|
| Sequence | MQHYLHIRPA PSDNLPLVDL IEHPDPIFDP KEKDLNETLL RSLLGGHYDP GFMATSPPED RPGGGGGAAG GAEDLAELDQ LLRQRPSGAM PSEIKGLEFS EGLAQGKKQR LSKKLRRKLQ MWLWSQTFCP VLYAWNDLGS RFWPRYVKVG SCFSKRSCSV PEGMVCKPSK SVHLTVLRWR CQRRGGQRCG WIPIQYPIIS ECKCSC |
| Purity | > 95 % by SDS-PAGE and HPLC analyses. |
| Endotoxin Level | Less than 1 EU/ µg of rHuNoggin as determined by LAL method. |
| Formulation | Lyophilized from a 0.2 µm filtered concentrated solution in 30 % acetonitrile, 0.1 % TFA. |
| Reconstitution | We recommend that this vial 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. Stock solutions should be apportioned into working aliquots and stored at ≤ -20 °C. Further dilutions should be made in appropriate buffered solutions. |
| Target Background | Noggin belongs to a group of diffusible proteins which bind to ligands of the TGF-ß family and regulate their activity by inhibiting their access to signaling receptors. 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. |
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Research Areas
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Cat# PVGS1066
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