AF9 (MLLT3) Antibody (Center V422) Blocking peptide
€293.00
In stock
SKU
AC-BP6190b
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.
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 AP6190b 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.
Type: Synthetic peptide
Primary Accession: P42568
Gene ID: 4300
Gene Name: MLLT3 {ECO:0000303|PubMed:16001262, ECO:0000312|HGNC:HGNC:7136}
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.
Bio 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).
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.
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 AP6190b 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.
Type: Synthetic peptide
Primary Accession: P42568
Gene ID: 4300
Gene Name: MLLT3 {ECO:0000303|PubMed:16001262, ECO:0000312|HGNC:HGNC:7136}
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.
Bio 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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