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mouse homolog regulates pattern formation during embryogenesis [RGD, Feb 2006].. Additionally we are shipping Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 Antibodies (84) and many more products for this protein.
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MLL (show MLL Proteins)-AF9 fusion is associated with acute myeloid leukemia (show BCL11A Proteins).
Structural insights into H3 histone (show HIST1H3B Proteins) 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 Proteins)-AF9 expression in mouse long-term hematopoietic stem cells causes invasive, chemoresistant acute myeloid leukemia (show BCL11A Proteins) that expresses genes related to epithelial-mesenchymal transition.
Results show that MLL (show MLL Proteins)-AF9 reduces Id2 and increases E2-2 (show TCF4 Proteins) expression to drive and sustain leukemia stem cell potential in MLL (show MLL Proteins)-rearranged acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)). Low expression of Id2 or of an Id2 gene signature is associated with poor prognosis in not only MLL (show MLL Proteins)-rearranged but also t(8;21) AML (show RUNX1 Proteins) 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 Proteins)-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 Proteins) cells harbouring the MLL (show MLL Proteins)-AF9 oncogene (show RAB1A Proteins).
Atg5 (show ATG5 Proteins)-dependent autophagy contributes to the development of acute myeloid leukemia (show BCL11A Proteins) in an MLL (show MLL Proteins)-AF9-driven mouse model.
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 Proteins) conditional deletion MLL (show MLL Proteins)-AF9 murine AML (show RUNX1 Proteins) model, we revealed that the deletion of PDK1 (show PDPK1 Proteins) prolonged the survival of AML (show RUNX1 Proteins) mice by inducing LSC (show ARHGEF1 Proteins) apoptosis
define a specific pairing of two amino acids that creates a salt bridge between MLLT1 (show MLLT1 Proteins)/3 and AFF proteins that is critically important for MLL (show MLL Proteins)-mediated transformation of HPCs
Af9 mediates site-selective physical and functional recruitment of Rnf2 (show RNF2 Proteins) to the alpha-ENaC (show SCNN1A Proteins) promoter to constrain basal alpha-ENaC (show SCNN1A Proteins) transcription in collecting duct cells.
Impaired alphaENaC (show SCNN1A Proteins) 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 Proteins)-AF9 requires RUVBL2 (RuvB-like 2 (show RUVBL2 Proteins)), an AAA (show AAAS Proteins)+ ATPase 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 Proteins) 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 Proteins)-subunit (show POLG Proteins) represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit (show POLG Proteins) transcription.
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