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mouse homolog regulates pattern formation during embryogenesis. Additionally we are shipping Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 Proteins (4) and many more products for this protein.
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Human Polyclonal MLLT3 Primary Antibody for IHC (p), WB - ABIN390128
Iida, Seto, Yamamoto, Komatsu, Tojo, Asano, Kamada, Ariyoshi, Takahashi, Ueda: MLLT3 gene on 9p22 involved in t(9;11) leukemia encodes a serine/proline rich protein homologous to MLLT1 on 19p13. in Oncogene 1993
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Human Polyclonal MLLT3 Primary Antibody for EIA, WB - ABIN358674
Nakamura, Alder, Gu, Prasad, Canaani, Kamada, Gale, Lange, Crist, Nowell: Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs. in Proceedings of the National Academy of Sciences of the United States of America 1993
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Human Polyclonal MLLT3 Primary Antibody for ICC, IF - ABIN151110
Lin, Hemenway: Hsp90 directly modulates the spatial distribution of AF9/MLLT3 and affects target gene expression. in The Journal of biological chemistry 2010
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Human Polyclonal MLLT3 Primary Antibody for EIA, WB - ABIN358675
Strissel, Strick, Tomek, Roe, Rowley, Zeleznik-Le: DNA structural properties of AF9 are similar to MLL and could act as recombination hot spots resulting in MLL/AF9 translocations and leukemogenesis. in Human molecular genetics 2000
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Human Polyclonal MLLT3 Primary Antibody for EIA, IHC (p) - ABIN358673
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 2007
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Cow (Bovine) Polyclonal MLLT3 Primary Antibody for WB - ABIN2780604
Wei, Wunderlich, Fox, Alvarez, Cigudosa, Wilhelm, Zheng, Cancelas, Gu, Jansen, Dimartino, Mulloy: Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia. in Cancer cell 2008
MLL (show MLL Antibodies)-AF9 fusion is associated with acute myeloid leukemia (show BCL11A Antibodies).
Structural insights into H3 histone (show HIST1H3B Antibodies) crotonyl-lysine recognition by the AF9 YEATS domain have been presented.
A luciferase reporter gene assay revealed that hsp70 promoter activation is enhanced by the transcriptional co-activator AF9 and splicing mediator SNRPE, but suppressed by the coiled-coil domain-containing protein CCDC127.
YEATS domain of AF9 directly links histone crotonylation to active transcription.
Results show that human MLL (show MLL Antibodies)-AF9 expression in mouse long-term hematopoietic stem cells causes invasive, chemoresistant acute myeloid leukemia (show BCL11A Antibodies) that expresses genes related to epithelial-mesenchymal transition.
Results show that MLL (show MLL Antibodies)-AF9 reduces Id2 and increases E2-2 (show TCF4 Antibodies) expression to drive and sustain leukemia stem cell potential in MLL (show MLL Antibodies)-rearranged acute myeloid leukemia (show BCL11A Antibodies) (AML (show RUNX1 Antibodies)). Low expression of Id2 or of an Id2 gene signature is associated with poor prognosis in not only MLL (show MLL Antibodies)-rearranged but also t(8;21) AML (show RUNX1 Antibodies) patients.
Exploring the mechanism how AF9 recognizes and binds H3K9ac by molecular dynamics simulations and free energy calculations.
Studies identified the evolutionarily conserved Af9 YEATS domain as a novel acetyllysine-binding module and established a direct link between histone acetylation and DOT1L (show DOT1L Antibodies)-mediated H3K79 methylation in transcription control.
AF9 and its homolog ENL directly interact with AF4.
Abrogation of Rac1 signaling causes DNA double-strand breaks in acute monocytic leukemia (show KAT6B Antibodies) cells harbouring the MLL (show MLL Antibodies)-AF9 oncogene (show RAB1A Antibodies).
Data suggest that RAS-homolog enriched in brain protein (Rheb1) promotes MLL-AF9 fusion protein initiated acute myeloid leukemia (AML) progression through target of rapamycin complex 1 (mTORC1) signaling pathway.
Using a PDK1 (show PDPK1 Antibodies) conditional deletion MLL (show MLL Antibodies)-AF9 murine AML (show RUNX1 Antibodies) model, we revealed that the deletion of PDK1 (show PDPK1 Antibodies) prolonged the survival of AML (show RUNX1 Antibodies) mice by inducing LSC (show ARHGEF1 Antibodies) apoptosis
define a specific pairing of two amino acids that creates a salt bridge between MLLT1 (show MLLT1 Antibodies)/3 and AFF proteins that is critically important for MLL (show MLL Antibodies)-mediated transformation of HPCs
Af9 mediates site-selective physical and functional recruitment of Rnf2 (show RNF2 Antibodies) to the alpha-ENaC (show SCNN1A Antibodies) promoter to constrain basal alpha-ENaC (show SCNN1A Antibodies) transcription in collecting duct cells.
Impaired alphaENaC (show SCNN1A Antibodies) expression due to failure to inhibit Dot1a-Af9 may play an important role in the early stages of pseudohypoaldosteronism type 1 in MR(-/-) mice.
We demonstrate that leukemogenic activity of MLL (show MLL Antibodies)-AF9 requires RUVBL2 (RuvB-like 2 (show RUVBL2 Antibodies)), an AAA (show AAAS Antibodies)+ ATPase (show DNAH8 Antibodies) family member that functions in a wide range of cellular processes, including chromatin remodeling and transcriptional regulation.
Therefore, Dot1a and Af9 as aldosterone-downregulated targets are negative regulators of endothelin-1 (show EDN1 Antibodies) transcription in vitro and in vivo, and may be considered as new potential therapeutic targets of kidney injury in diabetes.
It was concluded that +78/+92 of the epithelial Na+ channel alpha (show SCNN1A Antibodies)-subunit (show POLG Antibodies) represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit (show POLG Antibodies) transcription.
PRC2 supports aberrant self-renewal in a mouse model of MLL (show MLL Antibodies)-AF9;Nras (show NRAS Antibodies)(G12D) acute myeloid leukemia (show BCL11A Antibodies).
mouse homolog regulates pattern formation during embryogenesis
, ALL1-fused gene from chromosome 9 protein
, YEATS domain-containing protein 3
, myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog); translocated to, 3
, myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 3 protein
, myeloid/lymphoid or mixed lineage-leukemia translocation to 3 homolog
, myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 3 protein homolog
, myeloid/lymphoid or mixed-lineage leukemia, translocated to, 3
, myeloid/lymphoid or mixed-lineage leukemia,translocated to, 3 (trithorax homolog, Drosophila)
, translocated to, 3