Reactive species
Human;Mouse;Rat;Dog
Antibody type
Polyclonal Antibody
Protein name
Runt-related transcription factor 2
Immunogen
The antiserum was produced against synthesized peptide derived from the Internal region of human RUNX2. AA range:201-250
Specificity
RUNX2 Polyclonal Antibody detects endogenous levels of RUNX2 protein.
Constitute
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Polyclonal, Rabbit,IgG
Dilution rate
IF: 1:50-200 Western Blot: 1/500 - 1/2000. ELISA: 1/20000. Not yet tested in other applications.
Purification process
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Other name
RUNX2; AML3; CBFA1; OSF2; PEBP2A; Runt-related transcription factor 2; Acute myeloid leukemia 3 protein; Core-binding factor subunit alpha-1; CBF-alpha-1; Oncogene AML-3Osteoblast-specific transcription factor 2; OSF-2; Polyomavirus enhancer-binding protein 2 alpha A subunit; PEA2-alpha A; PEBP2-alpha A; SL3-3 enhancer factor 1 alpha A subunit; SL3/AKV core-binding factor alpha A subunit
Background
This gene is a member of the RUNX family of transcription factors and encodes a nuclear protein with an Runt DNA-binding domain. This protein is essential for osteoblastic differentiation and skeletal morphogenesis and acts as a scaffold for nucleic acids and regulatory factors involved in skeletal gene expression. The protein can bind DNA both as a monomer or, with more affinity, as a subunit of a heterodimeric complex. Two regions of potential trinucleotide repeat expansions are present in the N-terminal region of the encoded protein, and these and other mutations in this gene have been associated with the bone development disorder cleidocranial dysplasia (CCD). Transcript variants that encode different protein isoforms result from the use of alternate promoters as well as alternate splicing. [provided by RefSeq, Jul 2016],
Function
disease:Defects in RUNX2 are the cause of cleidocranial dysplasia (CCD) [MIM:119600]. CCD 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.,domain:A proline/serine/threonine rich region at the C-terminus is necessary for transcriptional activation of target genes and contains the phosphorylation sites.,function:Transcription factor involved in osteoblastic differentiation and skeletal morphogenesis. Essential for the maturation of osteoblasts and both intramembranous a
