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AF9 (MLLT3) Antibody (Center H197) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | P42568 |
|---|---|
| Clone Names | 4091608 |
| Gene ID | 4300 |
|---|---|
| Other Names | Protein AF-9, ALL1-fused gene from chromosome 9 protein, Myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 3 protein, YEATS domain-containing protein 3, MLLT3, AF9, YEATS3 |
| Target/Specificity | The synthetic peptide sequence used to generate the antibody AP6190d was selected from the Center region of human MLLT3. 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 | MLLT3 {ECO:0000303|PubMed:16001262, ECO:0000312|HGNC:HGNC:7136} |
|---|---|
| Function | Chromatin reader component of the super elongation complex (SEC), a complex required to increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by the polymerase at multiple sites along the DNA (PubMed:20159561, PubMed:20471948, PubMed:25417107, PubMed:27105114, PubMed:27545619). Specifically recognizes and binds acylated histone H3, with a preference for histone H3 that is crotonylated (PubMed:25417107, PubMed:27105114, PubMed:27545619, PubMed:30374167, PubMed:30385749). Crotonylation marks active promoters and enhancers and confers resistance to transcriptional repressors (PubMed:25417107, PubMed:27105114, PubMed:27545619). Recognizes and binds histone H3 crotonylated at 'Lys-9' (H3K9cr), and with slightly lower affinity histone H3 crotonylated at 'Lys-18' (H3K18cr) (PubMed:27105114). Also recognizes and binds histone H3 acetylated and butyrylated at 'Lys-9' (H3K9ac and H3K9bu, respectively), but with lower affinity than crotonylated histone H3 (PubMed:25417107, PubMed:27105114, PubMed:30385749). In the SEC complex, MLLT3 is required to recruit the complex to crotonylated histones (PubMed:27105114, PubMed:27545619). Recruitment of the SEC complex to crotonylated histones promotes recruitment of DOT1L on active chromatin to deposit histone H3 'Lys-79' methylation (H3K79me) (PubMed:25417107). Plays a key role in hematopoietic stem cell (HSC) maintenance by preserving, rather than conferring, HSC stemness (PubMed:31776511). Acts by binding to the transcription start site of active genes in HSCs and sustaining level of H3K79me2, probably by recruiting DOT1L (PubMed:31776511). |
| Cellular Location | Nucleus {ECO:0000255|PROSITE-ProRule:PRU00376, ECO:0000269|PubMed:27105114}. Chromosome. Note=Colocalizes with acylated histone H3 (PubMed:25417107, PubMed:27105114). Colocalizes with histone H3 crotonylated at 'Lys-18' (H3K18cr) (PubMed:27105114) |
| Tissue Location | Enriched in undifferentiated hematopoietic stem cells in fetal liver, cord blood and bone marrow |
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Provided below are standard protocols that you may find useful for product applications.
Background
The human AF9 gene is one of the most common fusion partner genes with the ALL1 gene at 11q23 (also called MLL), resulting in the t(9;11)(p22;q23). The AF9 gene is more than 100 kb, and 2 patient breakpoint cluster regions (BCRs) have been identified; BCR1 is within intron 4, previously called site A, whereas BCR2 or site B spans introns 7 and 8. Several different structural elements have been identified in AF9, including a colocalizing in vivo DNA topo II cleavage site and an in vitro DNase I hypersensitive (DNase 1 HS) site in intron 7 in BCR2. Reversibility experiments demonstrated a religation of the topo II cleavage sites. In addition, 2 scaffold associated regions (SARs) are located centromeric to the topo II and DNase I HS cleavage sites and border breakpoint regions in 2 leukemic cells lines: SAR1 is located in intron 4, whereas SAR2 encompasses parts of exons 5-7. The patient breakpoint regions of AF9 share the same structural elements as the MLL BCR. A DNA breakage and repair model for nonhomologous recombination between MLL and its partner genes, particularly AF9, has been proposed.
References
Iida, S., et al., Oncogene 8(11):3085-3092 (1993).Nakamura, T., et al., Proc. Natl. Acad. Sci. U.S.A. 90(10):4631-4635 (1993).Strissel, P. L., et al., Hum. Molec. Genet. 9: 1671-1679 (2000).
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