|Other Names||Afadin, ALL1-fused gene from chromosome 6 protein, Protein AF-6, MLLT4, AF6|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP6191b was selected from the N-term region of human MLLT4. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|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.|
|Function||Belongs to an adhesion system, probably together with the E-cadherin-catenin system, which plays a role in the organization of homotypic, interneuronal and heterotypic cell-cell adherens junctions (AJs). Nectin- and actin-filament-binding protein that connects nectin to the actin cytoskeleton.|
|Cellular Location||Cell junction, adherens junction. Note=Not found at cell-matrix AJs|
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Most acute leukemias in infancy and at least 5% of acute lymphoblastic leukemias and acute myeloid leukemias of older children and adults show abnormalities of chromosome band 11q23. In these cases, translocation results in fusion of a gene at 11q23, variously called ALL1, MLL, and the human homolog of Drosophila trithorax, with part of a gene on chromosome 4, chromosome 9, or chromosome 19. The cloning and characterization of the partner gene involved in a fourth common translocation involving 11q23, t(6;11)(q27;q23) has been described. The gene, designated MLLT4 or alternatively AF6, expressed in a variety of cell types and encoded a protein of 1,612 amino acids. The protein contains short stretches rich in proline, charged amino acids, serines, or glutamines. In addition, the AF6 protein contains the GLGF motif shared with several proteins of vertebrates and invertebrates thought to be involved in signal transduction at special cell-cell junctions. Using rapid amplification of cDNA ends (RACE) by PCR, the breakpoint in AF6 was confirmed and a cDNA clone that was used as a probe to screen a chromosome 6 cosmid library was identified. By fluorescence in situ hybridization, the single clone that was isolated was found to map distal to the critically deleted region associated with ovarian malignancies. AF6 is therefore distinct from and lies telomeric to that region.
Beausoleil, S.A., et al., Proc. Natl. Acad. Sci. U.S.A. 101(33):12130-12135 (2004).Mungall, A.J., et al., Nature 425(6960):805-811 (2003).Saito, S., et al., DNA Res. 5(2):115-120 (1998).Prasad, R., et al., Cancer Res. 53(23):5624-5628 (1993).Takai, Y., et al., J. Cell. Sci. 116 (PT 1), 17-27 (2003).
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