The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Information available upon request.
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
Transcription 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.
Specifically expressed in osteoblasts.
Involvement in disease
Defects 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.
Contains 1 Runt domain.
A proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes and contains the phosphorylation sites.
Phosphorylated; probably by MAP kinases (MAPK) (By similarity). Isoform 3 is phosphorylated on Ser-340.
David V et al. Mechanical loading down-regulates peroxisome proliferator-activated receptor gamma in bone marrow stromal cells and favors osteoblastogenesis at the expense of adipogenesis. Endocrinology148:2553-62 (2007).
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