Recombinant Human RUNX1 / AML1 protein is a Human Full Length protein, in the 2 to 250 aa range, expressed in Escherichia coli, with >90% purity and suitable for SDS-PAGE, FuncS.
2 9 a a _ T a g _ R I P V D A S T S R R F T P P S T A L S P G K M S E A L P L G A P D A G A A L A G K L R S G D R S M V E V L A D H P G E L V R T D S P N F L C S V L P T H W R C N K T L P I A F K V V A L G D V P D G T L V T V M A G N D E N Y S A E L R N A T A A M K N Q V A R F N D L R F V G R S G R G K S F T L T I T V F T N P P Q V A T Y H R A I K I T V D G P R E P R R H R Q K L D D Q T K P G S L S F S E R L S E L E Q L R R T A M R V S P H H P A P T P N P R A S L N H S T A F N P Q P Q S Q M Q E E D T A P W R C L E E S G G G G S P G R R R R R R R R R R R
| Application | Reactivity | Dilution info | Notes |
|---|---|---|---|
Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application FuncS | Reactivity Reacts | Dilution info 2.00000-8.00000 µg/mL | Notes For studying Human hematopoietic cell differentiation in vitro. |
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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). Isoform AML-1G shows higher binding activities for target genes and binds TCR-beta-E2 and RAG-1 target site with threefold higher affinity than other isoforms. It is less effective in the context of neutrophil terminal differentiation. Isoform AML-1L interferes with the transactivation activity of RUNX1.
AML1, CBFA2, RUNX1, Runt-related transcription factor 1, Acute myeloid leukemia 1 protein, Core-binding factor subunit alpha-2, Oncogene AML-1, Polyomavirus enhancer-binding protein 2 alpha B subunit, SL3-3 enhancer factor 1 alpha B subunit, SL3/AKV core-binding factor alpha B subunit, CBF-alpha-2, PEA2-alpha B, PEBP2-alpha B
Recombinant Human RUNX1 / AML1 protein is a Human Full Length protein, in the 2 to 250 aa range, expressed in Escherichia coli, with >90% purity and suitable for SDS-PAGE, FuncS.
pH: 8
Constituents: 0.32% Tris HCl
ab134873 was expressed in E. coli as inclusion bodies, refolded using unique temperature shift inclusion body refolding technology, chromatographically purified and sterile-filtered.
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).
Phosphorylated in its C-terminus upon IL-6 treatment. Phosphorylation enhances interaction with KAT6A.
RUNX1 also known as AML1 is a transcription factor with a molecular weight of approximately 48 kDa. It belongs to the Runt-related transcription factor family and plays a critical role in hematopoiesis. RUNX1 is expressed in hematopoietic stem cells and various other tissues where it regulates the expression of genes involved in the differentiation and proliferation of blood cells. It exerts its function by binding to specific DNA sequences thereby controlling the transcriptional activity necessary for normal hematopoietic development.
RUNX1 is essential in the formation of blood cells and is part of the core-binding factor (CBF) complex. This complex is a heterodimer comprising RUNX1 and the CBFβ subunit. The interaction between RUNX1 and CBFβ stabilizes the DNA binding capability of RUNX1 facilitating the activation of target gene transcription. The proper functioning of RUNX1 is necessary for the maintenance of normal lineage specification of hematopoietic progenitors affecting both myeloid and lymphoid cell lineages.
RUNX1 plays a significant role in the Wnt signaling pathway and the TGF-beta signaling pathway. RUNX1 interacts with several proteins in these pathways including SMAD proteins and β-catenin which are important for transmitting extracellular signals that regulate cell growth and differentiation. RUNX1’s role in these pathways highlights its importance not only in hematopoiesis but also in preventing abnormal cell proliferation.
RUNX1 mutations are strongly associated with acute myeloid leukemia (AML) and familial platelet disorder. In AML RUNX1 mutations disrupt normal hematopoiesis leading to the uncontrolled proliferation of immature blood cells. RUNX1-related proteins such as the GM-CSF receptor can contribute to disease progression by altering cytokine signaling. RUNX1's involvement in familial platelet disorder reflects its importance in maintaining normal blood cell counts and function as loss of RUNX1 function leads to predisposition to leukemia.
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