|Calculated MW||21508 Da|
|Positive Control||ELISA: Peptides, ChIP: SKNO-1 cells.|
|Application & Usage||ChIP: 4 µl/ChIP, ELISA: 1:500.|
|Other Names||PEBP2B, CBF-beta, PEA2-beta, PEB2-beta|
|Formulation||In PBS with 0.05% (W/V) sodium azide.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||CBFb polyclonal antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Forms the heterodimeric complex core-binding factor (CBF) with RUNX family proteins (RUNX1, RUNX2, and RUNX3). RUNX members modulate the transcription of their target genes through recognizing the core consensus binding sequence 5'-TGTGGT-3', or very rarely, 5'-TGCGGT-3', within their regulatory regions via their runt domain, while CBFB is a non-DNA-binding regulatory subunit that allosterically enhances the sequence-specific DNA- binding capacity of RUNX. The heterodimers bind to the core site of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, LCK, IL3 and GM-CSF promoters. CBF complexes repress ZBTB7B transcription factor during cytotoxic (CD8+) T cell development. They bind to RUNX-binding sequence within the ZBTB7B locus acting as transcriptional silencer and allowing for cytotoxic T cell differentiation.|
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Provided below are standard protocols that you may find useful for product applications.
CBFb represents the beta subunit of a heterodimeric core-binding transcription factor belonging to the PEBP2/CBF transcription factor family. These transcription factors regulate a host of genes specific to hematopoiesis (e.g. RUNX1) and osteogenesis (e.g. RUNX2). The beta subunit is the regulatory subunit which allosterically enhances the activity of the DNA binding alpha subunit as the complex binds to the core site of various enhancers and promoters. CBFb can be involved in a chromosomal rearrangement of chromosome 16 (inv(16)(p13q22)) which produces a fusion protein consisting of the N terminus of CBFb and the C-terminal portion of MYH11. This chromosomal rearrangement is associated with acute myeloid leukemia of the M4Eo subtype.
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