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MLL encodes a transcriptional coactivator that plays an essential role in regulating gene expression during early development and hematopoiesis. 再加上，我们可以发Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila) 蛋白 (3)和数多这个蛋白质的别的产品。
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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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Identification of novel biomarkers for MLL-translocated acute myeloid leukemia (显示 BCL11A 抗体).
Collectively, these data indicated that ATR (显示 ANTXR1 抗体) or ATM (显示 ATM 抗体) inhibition represent potential therapeutic strategies for the treatment of AML (显示 RUNX1 抗体), 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.
These results reveal a cooperative transcriptional activation mechanism of AEP (显示 LGMN 抗体) and DOT1L (显示 DOT1L 抗体) and suggest a molecular rationale for the simultaneous inhibition of the MLL fusion-AF4 complex and DOT1L (显示 DOT1L 抗体) for more effective treatment of MLL-rearranged leukemia.
this indicates that DOT1L (显示 DOT1L 抗体) function, like MLL, does not completely rely on its methyltransferase activity. Nevertheless, the small molecule DOT1L (显示 DOT1L 抗体) 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 (显示 HIF1A 抗体) and histone acetyltransferase p300 (显示 EP300 抗体) and regulate hypoxia-induced HOTAIR expression. The hypoxia-induced upregulation of HOTAIR expression may contribute to its roles in tumorigenesis.
MLL1 and MLL2 (显示 MLL2 抗体) 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 (显示 CBX2 抗体) response elements.
Collectively, these data indicated that ATR (显示 ATR 抗体) or ATM (显示 ATM 抗体) inhibition represent potential therapeutic strategies for the treatment of AML (显示 RUNX1 抗体), 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 (显示 NUP98 抗体)-HOXA9 (显示 HOXA9 抗体) interacts with MLL via the NUP98 (显示 NUP98 抗体) second FG repeat domain. In the absence of MLL (in knockout mice), NUP98 (显示 NUP98 抗体)-HOXA9 (显示 HOXA9 抗体)-induced cell immortalization and leukemogenesis are severely inhibited. MLL is important for the recruitment of NUP98 (显示 NUP98 抗体)-HOXA9 (显示 HOXA9 抗体) to the HOXA locus and for NUP98 (显示 NUP98 抗体)-HOXA9 (显示 HOXA9 抗体)-induced HOXA gene expression. MLL is crucial for NUP98 (显示 NUP98 抗体)-HOXA9 (显示 HOXA9 抗体) leukemia initiation.
Atg5 (显示 ATG5 抗体)-dependent autophagy contributes to the development of acute myeloid leukemia (显示 BCL11A 抗体) in an MLL-AF9 (显示 MLLT3 抗体)-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 (显示 SETD1A 抗体)/MLL Complexes to Activate Hox (显示 MSH2 抗体) Gene Expression Patterns and Mesoderm Lineage Development.
MLL1 and DOT1L (显示 DOT1L 抗体) cooperate with meningioma-1 to induce acute myeloid leukemia (显示 BCL11A 抗体).
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)