Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) (C-Term) antibody

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Antigen
  • fc39c11
  • wu:fc39c11
  • zgc:110210
  • AF9
  • YEATS3
  • 2210011H10Rik
  • 2610012I03Rik
  • 3830408D16Rik
  • Af9
  • D4Ertd321e
  • Af-9
  • myeloid/lymphoid or mixed lineage-leukemia translocation to 3 homolog (Drosophila)
  • myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 3
  • mllt3
  • MLLT3
  • Mllt3
Epitope
C-Term
31
14
10
8
6
5
4
4
4
4
3
2
2
1
1
1
1
1
Reactivity
Human
83
19
10
9
8
8
7
6
5
3
3
2
2
1
Host
Rabbit
80
3
Clonality
Polyclonal
Conjugate
Un-conjugated
3
3
3
2
2
2
1
1
1
1
1
1
1
1
1
1
1
Application
Enzyme Immunoassay (EIA), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Western Blotting (WB)
71
38
30
29
21
17
7
3
2
Options
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Immunogen This antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the C-terminal region of human MLLT3.
Isotype Ig
Specificity This antibody reacts to AF9 (MLLT3).
Cross-Reactivity (Details) Species reactivity (expected):Mouse.
Species reactivity (tested):Human.
Purification Protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS
Alternative Name MLLT3 / AF9 (MLLT3 Antibody Abstract)
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.Synonyms: ALL1 fused gene from chromosome 9 protein, Myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 3 protein, Protein AF-9, YEATS domain-containing protein 3, YEATS3
Molecular Weight 63351 Da
Gene ID 4300, 5874
UniProt P42568
Application Notes ELISA: 1/1,000. Immunohistochemistry: 1/50 - 1/100. Western Blot: 1/100 - 1/500.
Other applications not tested.
Optimal dilutions are dependent on conditions and should be determined by the user.
Restrictions For Research Use only
Format Liquid
Concentration 0.25 mg/mL
Buffer PBS, 0.09 % (W/V) Sodium Azide
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handling Advice Avoid repeated freezing and thawing.
Storage 4 °C/-20 °C
Storage Comment Store the antibody undiluted at 2-8 °C for one month or (in aliquots) at-20 °C for longer.
Supplier Images
 image for anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) (C-Term) antibody (ABIN358673) anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) (C-Term) antibody
 image for anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) (C-Term) antibody (ABIN358673) anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) (C-Term) antibody (Image 2)
Product cited in: Benedikt, Baltruschat, Scholz, Bursen, Arrey, Meyer, Varagnolo, Müller, Karas, Dingermann, Marschalek: "The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures." in: Leukemia, Vol. 25, Issue 1, pp. 135-44, 2011 (PubMed).

Background publications Bitoun, Oliver, Davies: "The mixed-lineage leukemia fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling." in: Human molecular genetics, Vol. 16, Issue 1, pp. 92-106, 2007 (PubMed).

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