MLLT6 Antibody (C-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | P55198 |
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Other Accession | NP_005928 |
Gene ID | 4302 |
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Other Names | Protein AF-17, ALL1-fused gene from chromosome 17 protein, MLLT6, AF17 |
Target/Specificity | The synthetic peptide sequence used to generate the antibody AP6192a was selected from the C-term region of human MLLT6 . 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 | MLLT6 |
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Synonyms | AF17 |
Cellular Location | Nucleus. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Band 11q23 chromosome locations are associated with approximately 10% of patients with acute lymphoblastic leukemia (ALL) and more than 5% of patients with acute myeloid leukemia (AML). 11q23 translocation associated leukemias typically jointly express lymphoid and myeloid markers and exhibit poor prognosis. The gene at 11q23 involved in the translocations is known by multiple names, including ALL1, HRX, MLL, and TRX1. One of the more infrequent translocations, t(11;17)(q23;q21), MLLT6, encodes a protein of 1,093 amino acids, containing a leucine-zipper dimerization motif 3-prime to the fusion point and a cysteine-rich domain at the end terminus that can be arranged in 3 zinc fingers. MMLT6 contains amino acid runs associated with domains involved in transcriptional repression or activation. It has been proposed that MLLT6 represses truncated ALL1 function or inhibits function of the normal protein in leukemic cells.
References
Prasad, R., et al., Proc. Natl. Acad. Sci. U.S.A. 91(17):8107-8111 (1994).
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