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MLL encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis. De plus, nous expédions Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) Anticorps (61) et beaucoup plus de produits pour cette protéine.
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This study demonstrates a tractable approach for respecifying iPSC-derived blood cells into highly engraftable hematopoietic stem and progenitor cells (HSPCs) through transient expression of a single transcription factor, MLL-AF4
the influence of TGFbeta (Montrer TGFB1 Protéines)/SMADs on MLL- and MLL-AF4-mediated 5-LO (Montrer ALOX5 Protéines) promoter activation
FLT3 (Montrer FLT3 Protéines) cell-surface expression did not vary by FLT3 (Montrer FLT3 Protéines) mutational status, but high FLT3 (Montrer FLT3 Protéines) expression was strongly associated with KMT2A rearrangements. Our study found that there was no prognostic significance of FLT3 (Montrer FLT3 Protéines) cell surface expression in pediatric Acute Myeloid Leukemia (Montrer BCL11A Protéines)
results indicate that KMT2A promotes melanoma growth by activating the hTERT signaling, suggesting that the KMT2A/hTERT signaling pathway may be a potential therapeutic target for melanoma.
A novel regulatory pathway for MLL1, which may open a new therapeutic approach to MLL-rearrangement leukaemia.
data confirm MLL-PTD (Montrer BCS1L Protéines) and, to a lesser extent, FLT3 (Montrer FLT3 Protéines)-ITD as common events in +11 AML (Montrer RUNX1 Protéines).6, 7, 8 However, the high mutation frequencies of U2AF1 (Montrer U2AF1 Protéines) and genes involved in methylation (DNMT3A (Montrer DNMT3A Protéines), IDH2 (Montrer IDH2 Protéines)) have hitherto not been reported in +11 AML (Montrer RUNX1 Protéines)
It is, to our knowledge, the first case of B acute lymphoblastic leukemia with this fusion gene. At the molecular level, two rearrangements were detected using RNA sequencing juxtaposing exon 7 to exon 2 and exon 9 to intron 1-2 of the KMT2A and MAML2 genes respectively, and one rearrangement using Sanger sequencing juxtaposing exon 8 and exon 2.
IHC based post-Ki67 (Montrer MKI67 Protéines) levels may have distinct predictive power compared with the naive IHC Ki67 (Montrer MKI67 Protéines).
Data demonstrate an essential role for MLL1 and menin in mediating tumor maintenance and posterior HOXD gene activation in Ewing sarcoma.
The most common KMT2A breakpoint region was intron/exon 9 (3/8 patients), followed by intron/exon 11 and 10.
Kmt2a is also important in memory formation
Collectively, these data indicated that ATR or ATM (Montrer ATM Protéines) inhibition represent potential therapeutic strategies for the treatment of AML (Montrer RUNX1 Protéines), especially MLL-driven leukemias.
Epigenomic profiling indicates an abnormal H3K79me2 pattern on MLL-fusion targeted genes, but the molecular mechanism underlying this epigenetic dependency is not well understood.
NUP98 (Montrer NUP98 Protéines)-HOXA9 (Montrer HOXA9 Protéines) interacts with MLL via the NUP98 (Montrer NUP98 Protéines) second FG repeat domain. In the absence of MLL (in knockout mice), NUP98 (Montrer NUP98 Protéines)-HOXA9 (Montrer HOXA9 Protéines)-induced cell immortalization and leukemogenesis are severely inhibited. MLL is important for the recruitment of NUP98 (Montrer NUP98 Protéines)-HOXA9 (Montrer HOXA9 Protéines) to the HOXA locus and for NUP98 (Montrer NUP98 Protéines)-HOXA9 (Montrer HOXA9 Protéines)-induced HOXA gene expression. MLL is crucial for NUP98 (Montrer NUP98 Protéines)-HOXA9 (Montrer HOXA9 Protéines) leukemia initiation.
Atg5 (Montrer ATG5 Protéines)-dependent autophagy contributes to the development of acute myeloid leukemia (Montrer BCL11A Protéines) in an MLL-AF9 (Montrer MLLT3 Protéines)-driven mouse model.
These results reveal a cooperative transcriptional activation mechanism of AEP (Montrer LGMN Protéines) and DOT1L (Montrer DOT1L Protéines) and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L (Montrer DOT1L Protéines) for more effective treatment of MLL-rearranged leukemia.
This study demonstrated that Kmt2a regulates synaptic plasticity in striatal neurons and provides an epigenetic drug target for anxiety and dopamine-mediated behaviors.
Inactivation of Kmt2a in Men1-deficient mice accelerated pancreatic islet tumorigenesis and shortened the average life span. Increases in cell proliferation were observed in mouse pancreatic islet tumors upon inactivation of both Kmt2a and Men1.
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.
HoxBlinc RNA Recruits Set1/MLL Complexes to Activate Hox (Montrer MSH2 Protéines) Gene Expression Patterns and Mesoderm Lineage Development.
This gene encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis. The encoded protein contains multiple conserved functional domains. One of these domains, the SET domain, is responsible for its histone H3 lysine 4 (H3K4) methyltransferase activity which mediates chromatin modifications associated with epigenetic transcriptional activation. This protein is processed by the enzyme Taspase 1 into two fragments, MLL-C and MLL-N. These fragments reassociate and further assemble into different multiprotein complexes that regulate the transcription of specific target genes, including many of the HOX genes. Multiple chromosomal translocations involving this gene are the cause of certain acute lymphoid leukemias and acute myeloid leukemias. Alternate splicing results in multiple transcript variants.
CDK6/MLL fusion protein
, CXXC-type zinc finger protein 7
, MLL-AF4 der(11) fusion protein
, MLL/GAS7 fusion protein
, MLL/GMPS fusion protein
, histone-lysine N-methyltransferase 2A
, lysine N-methyltransferase 2A
, myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila)
, myeloid/lymphoid or mixed-lineage leukemia protein 1
, trithorax-like protein
, zinc finger protein HRX
, histone-lysine N-methyltransferase MLL
, myeloid/lymphoid or mixed-lineage leukemia 1
, trithorax Drosophila
, Mixed-lineage leukemia (also acute lymphocytic leukemia 1 or tritorax Drosophila gene)