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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) Proteins (3) and many more products for this protein.
Showing 10 out of 54 products:
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
Show all 7 Pubmed References
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
Show all 5 Pubmed References
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
Show all 4 Pubmed References
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
Show all 4 Pubmed References
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
Data show that expression of myeloid-lymphoid leukemia protein (MLL) fusion protein does neither influence DNA signaling nor DNA double strand breaks (DNA-DSBs) repair.
In this case study, we diagnosed t-MN with KMT2A rearrangement in a patient with history of B-ALL with 9p deletion and gain of X chromosome. Unusual features associated with this case are discussed
Identification of novel biomarkers for MLL-translocated acute myeloid leukemia (show BCL11A Antibodies).
Collectively, these data indicated that ATR (show ANTXR1 Antibodies) or ATM (show ATM Antibodies) inhibition represent potential therapeutic strategies for the treatment of AML (show RUNX1 Antibodies), especially MLL-driven leukemias.
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.
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.
MLL1 and DOT1L (show DOT1L Antibodies) cooperate with meningioma-1 to induce acute myeloid leukemia (show BCL11A Antibodies).
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)