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MLL (HRX) Antibody (Center) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q03164 |
|---|---|
| Other Accession | NP_005924 |
| Clone Names | 2121603 |
| Gene ID | 4297 |
|---|---|
| Other Names | Histone-lysine N-methyltransferase 2A, Lysine N-methyltransferase 2A, ALL-1, CXXC-type zinc finger protein 7, Myeloid/lymphoid or mixed-lineage leukemia, Myeloid/lymphoid or mixed-lineage leukemia protein 1, Trithorax-like protein, Zinc finger protein HRX, MLL cleavage product N320, N-terminal cleavage product of 320 kDa, p320, MLL cleavage product C180, C-terminal cleavage product of 180 kDa, p180, KMT2A, ALL1, CXXC7, HRX, HTRX, MLL, MLL1, TRX1 |
| Target/Specificity | The synthetic peptide sequence used to generate the antibody AP1123c was selected from the Center region of human HRX . 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 | KMT2A |
|---|---|
| Synonyms | ALL1, CXXC7, HRX, HTRX, MLL, MLL1, TRX1 |
| Function | Histone methyltransferase that plays an essential role in early development and hematopoiesis (PubMed:15960975, PubMed:12453419, PubMed:15960975, PubMed:19556245, PubMed:19187761, PubMed:20677832, PubMed:21220120, PubMed:26886794). Catalytic subunit of the MLL1/MLL complex, a multiprotein complex that mediates both methylation of 'Lys- 4' of histone H3 (H3K4me) complex and acetylation of 'Lys-16' of histone H4 (H4K16ac) (PubMed:15960975, PubMed:12453419, PubMed:15960975, PubMed:19556245, PubMed:24235145, PubMed:19187761, PubMed:20677832, PubMed:21220120, PubMed:26886794). Catalyzes methyl group transfer from S-adenosyl-L-methionine to the epsilon-amino group of 'Lys-4' of histone H3 (H3K4) via a non-processive mechanism. Part of chromatin remodeling machinery predominantly forms H3K4me1 and H3K4me2 methylation marks at active chromatin sites where transcription and DNA repair take place (PubMed:25561738, PubMed:15960975, PubMed:12453419, PubMed:15960975, PubMed:19556245, PubMed:19187761, PubMed:20677832, PubMed:21220120, PubMed:26886794). Has weak methyltransferase activity by itself, and requires other component of the MLL1/MLL complex to obtain full methyltransferase activity (PubMed:19187761, PubMed:26886794). Has no activity toward histone H3 phosphorylated on 'Thr-3', less activity toward H3 dimethylated on 'Arg-8' or 'Lys-9', while it has higher activity toward H3 acetylated on 'Lys-9' (PubMed:19187761). Binds to unmethylated CpG elements in the promoter of target genes and helps maintain them in the nonmethylated state (PubMed:20010842). Required for transcriptional activation of HOXA9 (PubMed:12453419, PubMed:20677832, PubMed:20010842). Promotes PPP1R15A- induced apoptosis (PubMed:10490642). Plays a critical role in the control of circadian gene expression and is essential for the transcriptional activation mediated by the CLOCK-BMAL1 heterodimer (By similarity). Establishes a permissive chromatin state for circadian transcription by mediating a rhythmic methylation of 'Lys-4' of histone H3 (H3K4me) and this histone modification directs the circadian acetylation at H3K9 and H3K14 allowing the recruitment of CLOCK-BMAL1 to chromatin (By similarity). Also has auto-methylation activity on Cys-3882 in absence of histone H3 substrate (PubMed:24235145). |
| Cellular Location | Nucleus [MLL cleavage product C180]: Nucleus. Note=Localizes to a diffuse nuclear pattern when not associated with MLL cleavage product N320 |
| Tissue Location | Heart, lung, brain and T- and B-lymphocytes. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The gene variously symbolized ALL1, HRX, or MLL located on 11q23 has been demonstrated to be fused with a number of translocation partners in cases of leukemia. Tse et al. (1995) characterized 2 t(1;11)(q21;q23) translocations that fused the MLL gene to a gene on chromosomal band 1q21, AF1Q, in 2 infants with acute myelomonocytic leukemia. In one of these patients, the derivative chromosome 11 represented an in-frame fusion of the N-terminal portion of the MLL gene to the complete AF1Q open reading frame, whereas the derivative chromosome 1 did not give rise to an open reading frame. This observation suggested that the N-terminal portion of the MLL gene is critical for leukemogenesis in translocations involving band 11q23.
References
Megonigal, M.D., et al., Proc. Natl. Acad. Sci. U.S.A. 97(6):2814-2819 (2000).Pegram, L.D., et al., Blood 96(13):4360-4362 (2000).Sano, K., et al., Blood 95(3):1066-1068 (2000).Cui, X., et al., Nat. Genet. 18(4):331-337 (1998).Nilson, I., et al., Br. J. Haematol. 93(4):966-972 (1996).
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