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MLL encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis.
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Human Polyclonal MLL Primary Antibody for IHC - ABIN966301
Tkachuk, Kohler, Cleary: Involvement of a homolog of Drosophila trithorax by 11q23 chromosomal translocations in acute leukemias. in Cell 1992
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Human Polyclonal MLL Primary Antibody for ChIPSeq, ChIP - ABIN2668494
Ahmad, Katryniok, Scholz, Merkens, Löscher, Marschalek, Steinhilber: Inhibition of class I HDACs abrogates the dominant effect of MLL-AF4 by activation of wild-type MLL. in Oncogenesis 2014
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Human Polyclonal MLL Primary Antibody for - ABIN966302
Nilson, Löchner, Siegler, Greil, Beck, Fey, Marschalek: Exon/intron structure of the human ALL-1 (MLL) gene involved in translocations to chromosomal region 11q23 and acute leukaemias. in British journal of haematology 1996
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Human Monoclonal MLL Primary Antibody for IHC, ELISA - ABIN969286
Nigro, Sainati, Leszl, Mirabile, Spinelli, Consarino, Di Cataldo, Magro, Felix, Basso: Acute differentiated dendritic cell leukemia: a variant form of pediatric acute myeloid leukemia with MLL translocation. in Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 2007
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Human Monoclonal MLL Primary Antibody for ChIP, IP - ABIN2668648
Jin, Zhao, Yi, Nakata, Kalota, Gewirtz: c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis. in The Journal of clinical investigation 2010
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Human Monoclonal MLL Primary Antibody for ELISA, IHC - ABIN2869284
Partida-Pérez, Domínguez, Sánchez-Corona, Castañeda-Cisneros, García-González, López-Cardona, Rivera: Constitutional duplication 11q23 de novo involving the MLL gene. in Genetic counseling (Geneva, Switzerland) 2006
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FLT3 (show FLT3 Antibodies) cell-surface expression did not vary by FLT3 (show FLT3 Antibodies) mutational status, but high FLT3 (show FLT3 Antibodies) expression was strongly associated with KMT2A rearrangements. Our study found that there was no prognostic significance of FLT3 (show FLT3 Antibodies) cell surface expression in pediatric Acute Myeloid Leukemia (show BCL11A Antibodies)
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 (show BCS1L Antibodies) and, to a lesser extent, FLT3 (show FLT3 Antibodies)-ITD as common events in +11 AML (show RUNX1 Antibodies).6, 7, 8 However, the high mutation frequencies of U2AF1 (show U2AF1 Antibodies) and genes involved in methylation (DNMT3A (show DNMT3A Antibodies), IDH2 (show IDH2 Antibodies)) have hitherto not been reported in +11 AML (show RUNX1 Antibodies)
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 (show MAML2 Antibodies) genes respectively, and one rearrangement using Sanger sequencing juxtaposing exon 8 and exon 2.
IHC based post-Ki67 (show MKI67 Antibodies) levels may have distinct predictive power compared with the naive IHC Ki67 (show MKI67 Antibodies).
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.
study describes 2 patients with Wiedemann-Steiner syndrome who presented with variable severity; findings revealed a de novo nonsense mutation, p.Gln1978*, of KMT2A in the former, and a missense mutation, p.Gly1168Asp, in the latter
Comprehensive genetic analysis of donor cell derived leukemia with KMT2A rearrangement
Kmt2a is also important in memory formation
Collectively, these data indicated that ATR (show ATR Antibodies) or ATM (show ATM Antibodies) inhibition represent potential therapeutic strategies for the treatment of AML (show RUNX1 Antibodies), 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 (show NUP98 Antibodies)-HOXA9 (show HOXA9 Antibodies) interacts with MLL via the NUP98 (show NUP98 Antibodies) second FG repeat domain. In the absence of MLL (in knockout mice), NUP98 (show NUP98 Antibodies)-HOXA9 (show HOXA9 Antibodies)-induced cell immortalization and leukemogenesis are severely inhibited. MLL is important for the recruitment of NUP98 (show NUP98 Antibodies)-HOXA9 (show HOXA9 Antibodies) to the HOXA locus and for NUP98 (show NUP98 Antibodies)-HOXA9 (show HOXA9 Antibodies)-induced HOXA gene expression. MLL is crucial for NUP98 (show NUP98 Antibodies)-HOXA9 (show HOXA9 Antibodies) leukemia initiation.
Atg5 (show ATG5 Antibodies)-dependent autophagy contributes to the development of acute myeloid leukemia (show BCL11A Antibodies) in an MLL-AF9 (show MLLT3 Antibodies)-driven mouse model.
These results reveal a cooperative transcriptional activation mechanism of AEP (show LGMN Antibodies) and DOT1L (show DOT1L Antibodies) and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L (show DOT1L Antibodies) 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 (show SETD1A Antibodies)/MLL Complexes to Activate Hox (show MSH2 Antibodies) 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)