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mouse homolog regulates pattern formation during embryogenesis [RGD, Feb 2006].. 再加上，我们可以发Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 抗体 (84)和数多这个蛋白质的别的产品。
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MLL (显示 MLL 蛋白)-AF9 fusion is associated with acute myeloid leukemia (显示 BCL11A 蛋白).
Structural insights into H3 histone (显示 HIST1H3B 蛋白) 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 (显示 MLL 蛋白)-AF9 expression in mouse long-term hematopoietic stem cells causes invasive, chemoresistant acute myeloid leukemia (显示 BCL11A 蛋白) that expresses genes related to epithelial-mesenchymal transition.
Results show that MLL (显示 MLL 蛋白)-AF9 reduces Id2 and increases E2-2 (显示 TCF4 蛋白) expression to drive and sustain leukemia stem cell potential in MLL (显示 MLL 蛋白)-rearranged acute myeloid leukemia (显示 BCL11A 蛋白) (AML (显示 RUNX1 蛋白)). Low expression of Id2 or of an Id2 gene signature is associated with poor prognosis in not only MLL (显示 MLL 蛋白)-rearranged but also t(8;21) AML (显示 RUNX1 蛋白) 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 (显示 DOT1L 蛋白)-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 (显示 KAT6B 蛋白) cells harbouring the MLL (显示 MLL 蛋白)-AF9 oncogene (显示 RAB1A 蛋白).
Atg5 (显示 ATG5 蛋白)-dependent autophagy contributes to the development of acute myeloid leukemia (显示 BCL11A 蛋白) in an MLL (显示 MLL 蛋白)-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 (显示 PDPK1 蛋白) conditional deletion MLL (显示 MLL 蛋白)-AF9 murine AML (显示 RUNX1 蛋白) model, we revealed that the deletion of PDK1 (显示 PDPK1 蛋白) prolonged the survival of AML (显示 RUNX1 蛋白) mice by inducing LSC (显示 ARHGEF1 蛋白) apoptosis
define a specific pairing of two amino acids that creates a salt bridge between MLLT1 (显示 MLLT1 蛋白)/3 and AFF proteins that is critically important for MLL (显示 MLL 蛋白)-mediated transformation of HPCs
Af9 mediates site-selective physical and functional recruitment of Rnf2 (显示 RNF2 蛋白) to the alpha-ENaC (显示 SCNN1A 蛋白) promoter to constrain basal alpha-ENaC (显示 SCNN1A 蛋白) transcription in collecting duct cells.
Impaired alphaENaC (显示 SCNN1A 蛋白) 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 (显示 MLL 蛋白)-AF9 requires RUVBL2 (RuvB-like 2 (显示 RUVBL2 蛋白)), an AAA (显示 AAAS 蛋白)+ 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 (显示 EDN1 蛋白) 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 (显示 SCNN1A 蛋白)-subunit (显示 POLG 蛋白) represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit (显示 POLG 蛋白) 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