The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Additional notesBest use within three months from the date of receipt of this protein.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
pH: 8.00 Constituents: 0.31% Glutathione, 0.79% Tris HCl
Acute myeloid leukemia 3 protein
Alpha subunit 1
CBF alpha 1
Cleidocranial dysplasia 1
Core binding factor
Core binding factor runt domain alpha subunit 1
Core binding factor subunit alpha 1
Core-binding factor subunit alpha-1
Oncogene AML 3
Osteoblast specific transcription factor 2
Osteoblast-specific transcription factor 2
PEA2 alpha A
PEBP2 alpha A
Polyomavirus enhancer binding protein 2 alpha A subunit
Polyomavirus enhancer-binding protein 2 alpha A subunit
Runt related transcription factor 2
Runt-related transcription factor 2
SL3 3 enhancer factor 1 alpha A subunit
SL3-3 enhancer factor 1 alpha A subunit
SL3/AKV core binding factor alpha A subunit
SL3/AKV core-binding factor alpha A subunit
FunctionTranscription factor involved in osteoblastic differentiation and skeletal morphogenesis. Essential for the maturation of osteoblasts and both intramembranous and endochondral ossification. CBF binds to the core site, 5'-PYGPYGGT-3', of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, osteocalcin, osteopontin, bone sialoprotein, alpha 1(I) collagen, LCK, IL-3 and GM-CSF promoters (By similarity). Inhibits MYST4-dependent transcriptional activation.
Tissue specificitySpecifically expressed in osteoblasts.
Involvement in diseaseDefects in RUNX2 are the cause of cleidocranial dysplasia (CLCD) [MIM:119600]; also known as cleidocranial dysostosis (CCD). CLCD is an autosomal dominant skeletal disorder with high penetrance and variable expressivity. It is due to defective endochondral and intramembranous bone formation. Typical features include hypoplasia/aplasia of clavicles, patent fontanelles, wormian bones (additional cranial plates caused by abnormal ossification of the calvaria), supernumerary teeth, short stature, and other skeletal changes. In some cases defects in RUNX2 are exclusively associated with dental anomalies.
Sequence similaritiesContains 1 Runt domain.
DomainA proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes and contains the phosphorylation sites.
Post-translational modificationsPhosphorylated; probably by MAP kinases (MAPK) (By similarity). Isoform 3 is phosphorylated on Ser-340.