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mouse homolog regulates pattern formation during embryogenesis [RGD, Feb 2006].. Zusätzlich bieten wir Ihnen und viele weitere Produktgruppen zu diesem Protein an.
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miR (zeige MLXIP Proteine)-564 inhibited metastasis and proliferation of prostate cancer by targeting MLLT3
MLL (zeige MLL Proteine)-AF9 fusion is associated with acute myeloid leukemia (zeige BCL11A Proteine).
Structural insights into H3 histone (zeige HIST1H3B Proteine) 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 (zeige MLL Proteine)-AF9 expression in mouse long-term hematopoietic stem cells causes invasive, chemoresistant acute myeloid leukemia (zeige BCL11A Proteine) that expresses genes related to epithelial-mesenchymal transition.
Results show that MLL (zeige MLL Proteine)-AF9 reduces Id2 and increases E2-2 (zeige TCF4 Proteine) expression to drive and sustain leukemia stem cell potential in MLL (zeige MLL Proteine)-rearranged acute myeloid leukemia (zeige BCL11A Proteine) (AML (zeige RUNX1 Proteine)). Low expression of Id2 or of an Id2 gene signature is associated with poor prognosis in not only MLL (zeige MLL Proteine)-rearranged but also t(8;21) AML (zeige RUNX1 Proteine) 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 (zeige DOT1L Proteine)-mediated H3K79 methylation in transcription control.
AF9 and its homolog ENL directly interact with AF4.
Atg5 (zeige ATG5 Proteine)-dependent autophagy contributes to the development of acute myeloid leukemia (zeige BCL11A Proteine) in an MLL (zeige MLL Proteine)-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 (zeige PDPK1 Proteine) conditional deletion MLL (zeige MLL Proteine)-AF9 murine AML (zeige RUNX1 Proteine) model, we revealed that the deletion of PDK1 (zeige PDPK1 Proteine) prolonged the survival of AML (zeige RUNX1 Proteine) mice by inducing LSC (zeige ARHGEF1 Proteine) apoptosis
define a specific pairing of two amino acids that creates a salt bridge between MLLT1 (zeige MLLT1 Proteine)/3 and AFF proteins that is critically important for MLL (zeige MLL Proteine)-mediated transformation of HPCs
Af9 mediates site-selective physical and functional recruitment of Rnf2 (zeige RNF2 Proteine) to the alpha-ENaC (zeige SCNN1A Proteine) promoter to constrain basal alpha-ENaC (zeige SCNN1A Proteine) transcription in collecting duct cells.
Impaired alphaENaC (zeige SCNN1A Proteine) 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 (zeige MLL Proteine)-AF9 requires RUVBL2 (RuvB-like 2 (zeige RUVBL2 Proteine)), an AAA (zeige AAAS Proteine)+ 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 (zeige EDN1 Proteine) 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 (zeige SCNN1A Proteine)-subunit (zeige POLG Proteine) represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit (zeige POLG Proteine) 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