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mouse homolog regulates pattern formation during embryogenesis. De plus, nous expédions Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 Protéines (4) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal MLLT3 Primary Antibody pour ICC, IF - ABIN151110
Lin, Hemenway: Hsp90 directly modulates the spatial distribution of AF9/MLLT3 and affects target gene expression. dans The Journal of biological chemistry 2010
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Human Polyclonal MLLT3 Primary Antibody pour 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. dans Oncogene 1993
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Human Polyclonal MLLT3 Primary Antibody pour 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. dans Human molecular genetics 2007
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MLL (Montrer MLL Anticorps)-AF9 fusion is associated with acute myeloid leukemia (Montrer BCL11A Anticorps).
Structural insights into H3 histone (Montrer HIST1H3B Anticorps) 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 (Montrer MLL Anticorps)-AF9 expression in mouse long-term hematopoietic stem cells causes invasive, chemoresistant acute myeloid leukemia (Montrer BCL11A Anticorps) that expresses genes related to epithelial-mesenchymal transition.
Results show that MLL (Montrer MLL Anticorps)-AF9 reduces Id2 and increases E2-2 (Montrer TCF4 Anticorps) expression to drive and sustain leukemia stem cell potential in MLL (Montrer MLL Anticorps)-rearranged acute myeloid leukemia (Montrer BCL11A Anticorps) (AML (Montrer RUNX1 Anticorps)). Low expression of Id2 or of an Id2 gene signature is associated with poor prognosis in not only MLL (Montrer MLL Anticorps)-rearranged but also t(8;21) AML (Montrer RUNX1 Anticorps) 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 (Montrer DOT1L Anticorps)-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 (Montrer KAT6B Anticorps) cells harbouring the MLL (Montrer MLL Anticorps)-AF9 oncogene (Montrer RAB1A Anticorps).
Atg5 (Montrer ATG5 Anticorps)-dependent autophagy contributes to the development of acute myeloid leukemia (Montrer BCL11A Anticorps) in an MLL (Montrer MLL Anticorps)-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 (Montrer PDPK1 Anticorps) conditional deletion MLL (Montrer MLL Anticorps)-AF9 murine AML (Montrer RUNX1 Anticorps) model, we revealed that the deletion of PDK1 (Montrer PDPK1 Anticorps) prolonged the survival of AML (Montrer RUNX1 Anticorps) mice by inducing LSC (Montrer ARHGEF1 Anticorps) apoptosis
define a specific pairing of two amino acids that creates a salt bridge between MLLT1 (Montrer MLLT1 Anticorps)/3 and AFF proteins that is critically important for MLL (Montrer MLL Anticorps)-mediated transformation of HPCs
Af9 mediates site-selective physical and functional recruitment of Rnf2 (Montrer RNF2 Anticorps) to the alpha-ENaC (Montrer SCNN1A Anticorps) promoter to constrain basal alpha-ENaC (Montrer SCNN1A Anticorps) transcription in collecting duct cells.
Impaired alphaENaC (Montrer SCNN1A Anticorps) 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 (Montrer MLL Anticorps)-AF9 requires RUVBL2 (RuvB-like 2 (Montrer RUVBL2 Anticorps)), an AAA (Montrer AAAS Anticorps)+ ATPase (Montrer DNAH8 Anticorps) 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 (Montrer EDN1 Anticorps) 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 (Montrer SCNN1A Anticorps)-subunit (Montrer POLG Anticorps) represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit (Montrer POLG Anticorps) 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