AF4 (MLLT2) Antibody (C-term)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| IHC-P, E |
---|---|
Primary Accession | P51825 |
Other Accession | NP_005926 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 131422 Da |
Antigen Region | 1181-1210 aa |
Gene ID | 4299 |
---|---|
Other Names | AF4/FMR2 family member 1, ALL1-fused gene from chromosome 4 protein, Protein AF-4, Protein FEL, Proto-oncogene AF4, AFF1, AF4, FEL, MLLT2, PBM1 |
Target/Specificity | This AF4 (MLLT2) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1181~1210 amino acids from the C-terminal region of human MLLT2. |
Dilution | IHC-P~~1:50~100 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | AF4 (MLLT2) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | AFF1 |
---|---|
Synonyms | AF4, FEL, MLLT2, PBM1 |
Cellular Location | Nucleus. |
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Provided below are standard protocols that you may find useful for product applications.
Background
MLLT2 is involved in acute leukemias through a chromosomal translocation t(4;11)(q21;q23) that involves mllt2 and mll/hrx. AF-4 (MLLT2), AF-9, and ENL proteins contain nuclear targeting sequences as well as serine-rich and proline-rich regions. Stretches abundant in basic amino acids are also present in the three proteins. These results suggest that the different proteins fused to ALL-1 polypeptide(s) provide similar functional domains. AF4 is a serine- and proline-rich putative transcription factor with a glutamine-rich carboxyl terminus. The composition of the complete MLL-AF4 fusion product argues that it may act through either a gain-of-function or a dominant negative mechanism in leukemogenesis.
References
Domer, P.H., et al., Proc. Natl. Acad. Sci. U.S.A. 90(16):7884-7888 (1993).
Nakamura, T., et al., Proc. Natl. Acad. Sci. U.S.A. 90(10):4631-4635 (1993).
Morrissey, J., et al., Blood 81(5):1124-1131 (1993).
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