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MLL encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis. Additionally we are shipping Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) Antibodies (53) and Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) Proteins (3) and many more products for this protein.
we report two boys with novel KMT2A mutations from Chinese origin for the first time. They do not show one of the characteristic WDSTS phenotype, cubiti hypertrichosis. Instead, both of them had absent palmar proximal transverse crease. The feature was not linked to WDSTS patients previously. Our findings extend the WDSTS phenotypic spectrum.
Whole exome sequencing allowed identifying a previously unreported de novo KMT2A missense mutation affecting the DNA binding domain of the methyltransferase. This finding expands the clinical phenotype associated with KMT2A mutations to include immunodeficiency and epilepsy as clinically relevant features for this disorder.
MLL rearrangement is associated with infant acute lymphoblastic leukemia.
These results reveal a cooperative transcriptional activation mechanism of AEP (show LGMN ELISA Kits) and DOT1L (show DOT1L ELISA Kits) and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L (show DOT1L ELISA Kits) for more effective treatment of MLL-rearranged leukemia.
this indicates that DOT1L (show DOT1L ELISA Kits) function, like MLL, does not completely rely on its methyltransferase activity. Nevertheless, the small molecule DOT1L (show DOT1L ELISA Kits) inhibition is sufficient to block the proliferation of MLL fusion-induced leukemia cells of murine and human origin
Studies demonstrate that histone methyl-transferase MLL1 coordinates with HIF1alpha (show HIF1A ELISA Kits) and histone acetyltransferase p300 (show EP300 ELISA Kits) and regulate hypoxia-induced HOTAIR expression. The hypoxia-induced upregulation of HOTAIR expression may contribute to its roles in tumorigenesis.
MLL1 and MLL2 (show MLL2 ELISA Kits) collaborate to regulate gene expression and leukemia maintenance not through redundancy, but through distinct pathways.
MLL1, deposits H3K4me2 at CpG-dense regions that could serve as polycomb (show CBX2 ELISA Kits) response elements.
A patient was diagnosed with Wiedemann-Steiner syndrome based on identification of a novel de novo pathogenic variant in the KMT2A gene.
MLL gene rearrangement is associated with acute lymphocytic leukemia.
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 (show NUP98 ELISA Kits)-HOXA9 (show HOXA9 ELISA Kits) interacts with MLL via the NUP98 (show NUP98 ELISA Kits) second FG repeat domain. In the absence of MLL (in knockout mice), NUP98 (show NUP98 ELISA Kits)-HOXA9 (show HOXA9 ELISA Kits)-induced cell immortalization and leukemogenesis are severely inhibited. MLL is important for the recruitment of NUP98 (show NUP98 ELISA Kits)-HOXA9 (show HOXA9 ELISA Kits) to the HOXA locus and for NUP98 (show NUP98 ELISA Kits)-HOXA9 (show HOXA9 ELISA Kits)-induced HOXA gene expression. MLL is crucial for NUP98 (show NUP98 ELISA Kits)-HOXA9 (show HOXA9 ELISA Kits) leukemia initiation.
Atg5 (show ATG5 ELISA Kits)-dependent autophagy contributes to the development of acute myeloid leukemia (show BCL11A ELISA Kits) in an MLL-AF9 (show MLLT3 ELISA Kits)-driven mouse model.
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 (show SETD1A ELISA Kits)/MLL Complexes to Activate Hox (show MSH2 ELISA Kits) Gene Expression Patterns and Mesoderm Lineage Development.
MLL1 and DOT1L (show DOT1L ELISA Kits) cooperate with meningioma-1 to induce acute myeloid leukemia (show BCL11A ELISA Kits).
Set1 role in cellular reprogramming and its interactions with Dpy30,Myc,Sox2 and Ash2l reprogramming factors
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)