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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Myeloid/lymphoid or mixed-lineage leukemia

MLL, ALL-1, HRX
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.[provided by RefSeq, Oct 2010] (from NCBI)
Top mentioned proteins: Histone, CAN, HAD, AML1, Fel
Papers using MLL antibodies
Genome regulation by polycomb and trithorax proteins.
Supplier
Tarnopolsky Mark A., In PLoS ONE, 2006
... Louis, MO), anti-MLL-5 antibody from Orbigen (San Diego, CA), antibodies ...
Papers on MLL
Systematic Classification of Mixed-Lineage Leukemia Fusion Partners Predicts Additional Cancer Pathways.
Review
New
Marschalek, Frankfurt am Main, Germany. In Ann Lab Med, Mar 2016
Chromosomal translocations of the human mixed-lineage leukemia (MLL) gene have been analyzed for more than 20 yr at the molecular level.
Mutations in epigenetic modifiers in acute myeloid leukemia and their clinical utility.
New
Tien et al., Taipei, Taiwan. In Expert Rev Hematol, Feb 2016
Somatic mutations in epigenetic modifiers, including IDH1, IDH2, TET2, DNAMT3A, ASXL1, MLL and EZH2 are enriched in patients with acute myeloid leukemia (AML), especially those with intermediate-risk cytogenetics.
H3K4 Methyltransferase Set1a Is A Key Oct4 Coactivactor Essential for Generation of Oct4 Positive Inner Cell Mass.
New
Wong et al., Shanghai, China. In Stem Cells, Feb 2016
We found that among the SET1/MLL family H3K4 methyltransferases, Set1a specifically interacts with Oct4 and this interaction is independent of Wdr5.
PBX3 and MEIS1 cooperate in hematopoietic cells to drive acute myeloid leukemias characterized by a core transcriptome of the MLL-rearranged disease.
New
Chen et al., Chapel Hill, United States. In Cancer Res, Feb 2016
UNASSIGNED: Overexpression of HOXA/MEIS1/PBX3 homeobox genes is the hallmark of mixed lineage leukemia (MLL)-rearranged acute myeloid leukemia (AML).
Property focused structure-based optimization of small molecule inhibitors of the protein-protein interaction between menin and Mixed Lineage Leukemia (MLL).
New
Grembecka et al., In J Med Chem, Feb 2016
Here, we report synthesis and structure-based optimization of new thienopyrimidine class of compounds, which block the protein-protein interaction between menin and MLL fusion proteins that plays an important role in acute leukemias with MLL translocations.
Revisiting the biology of infant t(4;11)/MLL-AF4+ B-cell acute lymphoblastic leukemia.
Review
New
Menéndez et al., Barcelona, Spain. In Blood, Jan 2016
The genetic hallmark of most infant B-ALL is chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene.
Synthetic lethal targeting of oncogenic transcription factors in acute leukemia by PARP inhibitors.
New
Impact
So et al., Hong Kong, Hong Kong. In Nat Med, Dec 2015
In contrast, leukemia driven by mixed-lineage leukemia (MLL, encoded by KMT2A) fusions with dominant transactivation ability is proficient in DDR and insensitive to PARP inhibition.
The leukemogenic fusion gene MLL-AF9 alters microRNA expression pattern and inhibits monoblastic differentiation via miR-511 repression.
New
Schmid et al., München, Germany. In J Exp Clin Cancer Res, Dec 2015
BACKGROUND: In this study we explored the role of microRNAs (miRNAs) as mediators of leukemogenic effects of the fusion gene MLL-AF9, which results from a frequent chromosomal translocation in infant and monoblastic acute myeloid leukemia (AML).
Hematopoietic Differentiation Is Required for Initiation of Acute Myeloid Leukemia.
New
Impact
Tenen et al., Boston, United States. In Cell Stem Cell, Dec 2015
Using murine MLL-AF9 and MOZ-TIF2 AML models, we show that myeloid differentiation to granulocyte macrophage progenitors (GMPs) is critical for LSC generation.
AMPK Protects Leukemia-Initiating Cells in Myeloid Leukemias from Metabolic Stress in the Bone Marrow.
New
Impact
Nakada et al., Houston, United States. In Cell Stem Cell, Dec 2015
Upon dietary restriction, MLL-AF9-induced murine acute myeloid leukemia (AML) activated AMPK and maintained leukemogenic potential.
CD93 Marks a Non-Quiescent Human Leukemia Stem Cell Population and Is Required for Development of MLL-Rearranged Acute Myeloid Leukemia.
New
Impact
Cleary et al., Stanford, United States. In Cell Stem Cell, Nov 2015
Here, we show that acute myeloid leukemias (AMLs) with genomic rearrangements of the MLL gene contain a non-quiescent LSC population.
Recent progress in the treatment of infant acute lymphoblastic leukemia.
Review
New
Tomizawa, Tokyo, Japan. In Pediatr Int, Oct 2015
Treatment of infants with acute lymphoblastic leukemia (ALL), especially those with mixed lineage leukemia (MLL) rearrangement (MLL-r), which account for approximately 80% of cases, is still a major challenge for pediatric hematologists and oncologists worldwide.
Transcriptional plasticity promotes primary and acquired resistance to BET inhibition.
New
Impact
Zuber et al., Vienna, Austria. In Nature, Oct 2015
To identify factors involved in primary and acquired BET resistance in leukaemia, here we perform a chromatin-focused RNAi screen in a sensitive MLL-AF9;Nras(G12D)-driven AML mouse model, and investigate dynamic transcriptional profiles in sensitive and resistant mouse and human leukaemias.
Childhood Acute Lymphoblastic Leukemia: Progress Through Collaboration.
Review
New
Impact
Mullighan et al., Memphis, United States. In J Clin Oncol, Oct 2015
As a result, treatment strategies have been improved for several subtypes of ALL, such as infant, MLL-rearranged, Philadelphia chromosome-positive, and Philadelphia chromosome-like ALL.
Leukemogenic rearrangements at the mixed lineage leukemia gene (MLL)-multiple rather than a single mechanism.
Review
Wiesmüller et al., Ulm, Germany. In Front Cell Dev Biol, 2014
Rearrangements involving a short telomeric <1 kb region of the mixed lineage leukemia (MLL) gene are the most frequently observed molecular changes in secondary as well as infant acute leukemia.
The super elongation complex (SEC) family in transcriptional control.
Review
Impact
GeneRIF
Shilatifard et al., Kansas City, United States. In Nat Rev Mol Cell Biol, 2012
Studies indicate that the super elongation complex (SEC) consisting of ELL, P-TEFb (CDK9) and MLL required for rapid transcriptional induction in the presence or absence of paused RNA polymerase II (Pol II).
De novo mutations in MLL cause Wiedemann-Steiner syndrome.
GeneRIF
Simpson et al., London, United Kingdom. In Am J Hum Genet, 2012
De novo mutations in MLL cause Wiedemann-Steiner syndrome.
Mll partial tandem duplication and Flt3 internal tandem duplication in a double knock-in mouse recapitulates features of counterpart human acute myeloid leukemias.
GeneRIF
Caligiuri et al., Columbus, United States. In Blood, 2012
Here we demonstrate, for the first time, that Mll partial tandem duplication contributes to leukemogenesis as a gain-of-function mutation and describe a novel murine model closely recapitulating human acute myeloid leukemia.
Stress hematopoiesis reveals abnormal control of self-renewal, lineage bias, and myeloid differentiation in Mll partial tandem duplication (Mll-PTD) hematopoietic stem/progenitor cells.
GeneRIF
Huang et al., Cincinnati, United States. In Blood, 2012
The underlying pathogenic role of MLL partial tandem duplication in the clonal evolution of human leukemia.
Rearrangement of the myeloid/lymphoid leukemia gene in therapy-related myelodysplastic syndrome in patients previously treated with agents targeting DNA topoisomerase II.
GeneRIF
Zaky et al., Asyūţ, Egypt. In Oncology, 2011
the MLL gene is etiopathogenetically relevant for hematological neoplasias transformation and survival
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