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Phospho-RUNX1(S276) Antibody Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q01196 |
|---|---|
| Other Accession | NP_001745 |
| Clone Names | 80118190 |
| Gene ID | 861 |
|---|---|
| Other Names | Runt-related transcription factor 1, Acute myeloid leukemia 1 protein, Core-binding factor subunit alpha-2, CBF-alpha-2, Oncogene AML-1, Polyomavirus enhancer-binding protein 2 alpha B subunit, PEA2-alpha B, PEBP2-alpha B, SL3-3 enhancer factor 1 alpha B subunit, SL3/AKV core-binding factor alpha B subunit, RUNX1, AML1, CBFA2 |
| Target/Specificity | The synthetic peptide sequence used to generate the antibody AP3672a was selected from the region of human Phospho-RUNX1-S276. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | RUNX1 |
|---|---|
| Synonyms | AML1, CBFA2 |
| Function | Forms the heterodimeric complex core-binding factor (CBF) with CBFB. 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 (Probable). Essential for the development of normal hematopoiesis (PubMed:17431401). Acts synergistically with ELF4 to transactivate the IL-3 promoter and with ELF2 to transactivate the BLK promoter (PubMed:10207087, PubMed:14970218). Inhibits KAT6B-dependent transcriptional activation (By similarity). Involved in lineage commitment of immature T cell precursors. 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. CBF complexes binding to the transcriptional silencer is essential for recruitment of nuclear protein complexes that catalyze epigenetic modifications to establish epigenetic ZBTB7B silencing (By similarity). Controls the anergy and suppressive function of regulatory T-cells (Treg) by associating with FOXP3. Activates the expression of IL2 and IFNG and down-regulates the expression of TNFRSF18, IL2RA and CTLA4, in conventional T-cells (PubMed:17377532). Positively regulates the expression of RORC in T-helper 17 cells (By similarity). |
| Cellular Location | Nucleus. |
| Tissue Location | Expressed in all tissues examined except brain and heart. Highest levels in thymus, bone marrow and peripheral blood |
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Provided below are standard protocols that you may find useful for product applications.
Background
AML1/Runx1 binds DNA as a monomer and through the Runt domain. DNA binding is increased by heterodimerization with CBFB. Isoform AML1L can neither bind DNA nor heterodimerize and interferes with the transactivation activity of AML1/Runx1. 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, LCK, IL3 and GMCSF promoters. The alpha subunit binds DNA and appears to have a role in the development of normal hematopoiesis. AML1/Runx1 is expressed in a wide variety of tissues and is expressed at the highest levels in thymus, bone marrow and peripheral blood. Defects in AML1/Runx1 are the cause of familial platelet disorder with associated myeloid malignancy, an autosomal dominant disease characterized by qualitative and quantitative platelet defects, and propensity to develop acute myelogenous leukemia.
References
Roberts,K.E., et.al., Gastroenterology (2010) In pressKonn,Z.J., et.al., Genes Chromosomes Cancer 49 (3), 253-259 (2010)
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