We are analyzing https://link.springer.com/article/10.1007/s12185-015-1774-4.

Title:
Molecular mechanisms of MLL-associated leukemia | International Journal of Hematology
Description:
Gene rearrangements of the mixed lineage leukemia (MLL) gene cause aggressive leukemia. The fusion of MLL and its partner genes generates various MLL fusion genes, and their gene products trigger aberrant self-renewal of hematopoietic progenitors leading to leukemia. Since the identification of the MLL gene two decades ago, a substantial amount of information has been obtained regarding the mechanisms by which MLL mutations cause leukemia. Wild-type MLL maintains the expression of Homeobox (HOX) genes during development. MLL activates the expression of posterior HOX-A genes in the hematopoietic lineage to stimulate the expansion of immature progenitors. MLL fusion proteins constitutively activate the HOX genes, causing aberrant self-renewal. The modes of transcriptional activation vary depending on the fusion partners and can be categorized into at least four groups. Here I review the recent progress in research related to the molecular mechanisms of MLL fusion-dependent leukemogenesis.
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Keywords {🔍}

mll, pubmed, article, google, scholar, cas, fusion, proteins, central, domain, cell, leukemia, genes, complex, family, gene, expression, mllaf, hematopoietic, transformation, progenitors, target, histone, dotl, fig, activity, cells, protein, mol, transcriptional, myeloid, hoxa, methyltransferase, transcription, hox, activation, cleary, mechanisms, mllassociated, acute, biol, binding, pwwp, cancer, leukemogenesis, model, required, menin, hkme, development,

Topics {✒️}

pdz psd-95/dlg/zo-1 domain 11q23 chromosomal translocations corepressor c-terminal-binding protein mll-af4 b-cell tumourigenesis ell/p-tefb elongation complex nonmethyl-cpg-binding cxxc domain high-affinity menin-binding motif previously-active gene promoters activate mll-target genes p-tefb facilitates oncogenic mll-af6-transformed cells resulted c-terminal homology domain leukaemia mouse embryonic fibroblasts weak tri-methyltransferase activity mll-af1p fusion proteins wild-type mll maintains wild-type mll regulate mll-af9-induced leukemogenesis mll-cbp family proteins mll-af10 family proteins ibd integrase-binding domain menin-deficient mouse lines ash2l/rbbp5 heterodimer stimulates mll-af9 gene fusion mll-deficient embryos produce intra-molecular interaction stabilizes wild-type mll allele physiologic mll-dependent transcription human mll-af4 leukemias article yokoyama menin-dependent pathway appears leukemia proto-oncoprotein mll typical mll-null phenotype mll-aep fusion proteins mll-af6 complex formed set domain-truncated form chromosome 11q23 translocations mll fusion/menin complex position-specific expression patterns mll-af6 fusion protein gene knockout-rescue experiment retrovirally transduced hrx-enl hsc program genes mll fusion-dependent leukemogenesis structure/function analysis revealed mll-af9-mediated leukemogenesis calm-af10-mediated transformation proto-oncoprotein mll binds mll-af5q31 activates hoxa9

Schema {🗺️}

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         headline:Molecular mechanisms of MLL-associated leukemia
         description:Gene rearrangements of the mixed lineage leukemia (MLL) gene cause aggressive leukemia. The fusion of MLL and its partner genes generates various MLL fusion genes, and their gene products trigger aberrant self-renewal of hematopoietic progenitors leading to leukemia. Since the identification of the MLL gene two decades ago, a substantial amount of information has been obtained regarding the mechanisms by which MLL mutations cause leukemia. Wild-type MLL maintains the expression of Homeobox (HOX) genes during development. MLL activates the expression of posterior HOX-A genes in the hematopoietic lineage to stimulate the expansion of immature progenitors. MLL fusion proteins constitutively activate the HOX genes, causing aberrant self-renewal. The modes of transcriptional activation vary depending on the fusion partners and can be categorized into at least four groups. Here I review the recent progress in research related to the molecular mechanisms of MLL fusion-dependent leukemogenesis.
         datePublished:2015-03-17T00:00:00Z
         dateModified:2015-03-17T00:00:00Z
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            Leukemia
            Cellular memory
            Transcription
            Epigenetics
            Hematology
            Oncology
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      headline:Molecular mechanisms of MLL-associated leukemia
      description:Gene rearrangements of the mixed lineage leukemia (MLL) gene cause aggressive leukemia. The fusion of MLL and its partner genes generates various MLL fusion genes, and their gene products trigger aberrant self-renewal of hematopoietic progenitors leading to leukemia. Since the identification of the MLL gene two decades ago, a substantial amount of information has been obtained regarding the mechanisms by which MLL mutations cause leukemia. Wild-type MLL maintains the expression of Homeobox (HOX) genes during development. MLL activates the expression of posterior HOX-A genes in the hematopoietic lineage to stimulate the expansion of immature progenitors. MLL fusion proteins constitutively activate the HOX genes, causing aberrant self-renewal. The modes of transcriptional activation vary depending on the fusion partners and can be categorized into at least four groups. Here I review the recent progress in research related to the molecular mechanisms of MLL fusion-dependent leukemogenesis.
      datePublished:2015-03-17T00:00:00Z
      dateModified:2015-03-17T00:00:00Z
      pageStart:352
      pageEnd:361
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      keywords:
         MLL
         Leukemia
         Cellular memory
         Transcription
         Epigenetics
         Hematology
         Oncology
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         name:Springer Japan
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            name:Akihiko Yokoyama
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                     type:PostalAddress
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      email:[email protected]
PostalAddress:
      name:Laboratory for Malignancy Control Research, Kyoto University Graduate School of Medicine, Kyoto, Japan

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