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Showing 141-160 of 160 results
  1. Histone methylase MLL1 has critical roles in tumor growth and angiogenesis and its knockdown suppresses tumor growth in vivo

    Mixed lineage leukemias (MLLs) are human histone H3 lysine-4-specific methyl transferases that have critical roles in gene expression, epigenetics...

    K I Ansari, S Kasiri, S S Mandal in Oncogene
    Article 27 August 2012
  2. Abstracts

    Article 21 October 2012
  3. Deregulated transcription factors in leukemia

    Specific chromosomal translocations and other mutations associated with acute myeloblastic leukemia (AML) often involve transcription factors and...

    Yutaka Shima, Issay Kitabayashi in International Journal of Hematology
    Article 09 August 2011
  4. The heterogeneity of pediatric MLL-rearranged acute myeloid leukemia

    Translocations involving the mixed-lineage leukemia ( MLL ) gene, localized at 11q23, comprise 15 to 20% of all pediatric acute myeloid leukemia (AML)...

    B V Balgobind, C M Zwaan, ... M M Van den Heuvel-Eibrink in Leukemia
    Article 13 May 2011
  5. Mutation spectrum of MLL2 in a cohort of kabuki syndrome patients

    Background

    Kabuki syndrome (Niikawa-Kuroki syndrome) is a rare, multiple congenital anomalies/mental retardation syndrome characterized by a peculiar...

    Lucia Micale, Bartolomeo Augello, ... Giuseppe Merla in Orphanet Journal of Rare Diseases
    Article Open access 09 June 2011
  6. Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

    MOZ and MLL , encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal...

    J Paggetti, A Largeot, ... L Delva in Oncogene
    Article 28 June 2010
  7. The heterodimerization domains of MLL—FYRN and FYRC—are potential target structures in t(4;11) leukemia

    The chromosomal translocation t(4;11)(q21;q23) is a frequent genetic aberration of the mixed lineage leukemia ( MLL) gene, predominantly associated...

    B Pless, C Oehm, ... R Marschalek in Leukemia
    Article 14 January 2011
  8. Abstracts

    Article 29 May 2014
  9. The leukemogenic AF4–MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures

    Expression of the AF4–MLL fusion protein in murine hematopoietic progenitor/stem cells results in the development of proB acute lymphoblastic...

    A Benedikt, S Baltruschat, ... R Marschalek in Leukemia
    Article 29 October 2010
  10. Camptothecin-induced downregulation of MLL5 contributes to the activation of tumor suppressor p53

    Mixed lineage leukemia 5 (MLL5) has been implicated in multiple aspects of cell physiology, such as hematopoiesis, cell cycle control and chromatin...

    F Cheng, J Liu, ... L-W Deng in Oncogene
    Article 21 March 2011
  11. Genetic analysis of vertebral trabecular bone density and cross-sectional area in older men

    Summary

    We investigated 383 bone candidate genes for associations between single nucleotide polymorphisms and vertebral trabecular volumetric bone...

    J. M. Zmuda, L. M. Yerges-Armstrong, ... E. S. Orwoll in Osteoporosis International
    Article 09 December 2010
  12. Abstracts

    Article 02 May 2013
  13. Impaired recruitment of the histone methyltransferase DOT1L contributes to the incomplete reactivation of tumor suppressor genes upon DNA demethylation

    Understanding the mechanisms that link changes in DNA methylation with histone modifications is particularly relevant in the case of tumor suppressor...

    F V Jacinto, E Ballestar, M Esteller in Oncogene
    Article 07 September 2009
  14. Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-κB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes

    Constitutive nuclear factor (NF)-κB activation in haematological malignancies is caused in several cases by loss of function mutations within the...

    I Robert, M Aussems, ... A Chariot in Oncogene
    Article 16 February 2009
  15. Alterations of the CxxC domain preclude oncogenic activation of mixed-lineage leukemia 2

    The mixed-lineage leukemia (MLL) family of histone methyltransferases has become notorious for the participation of the founding member, MLL, in...

    C Bach, D Mueller, ... R K Slany in Oncogene
    Article 08 December 2008
  16. Young carers in Germany: to live on as normal as possible – a grounded theory study

    Background

    In contrast to a growing body of research on the situation of adult family care givers, in Germany hardly anything is known about the...

    Sabine Metzing-Blau, Wilfried Schnepp in BMC Nursing
    Article Open access 24 December 2008
  17. Genome-wide identification of aberrantly methylated promoter associated CpG islands in acute lymphocytic leukemia

    We performed a genome-wide analysis of promoter associated CpG island methylation using methylated CpG island amplification (MCA) coupled to...

    S-Q Kuang, W-G Tong, ... G Garcia-Manero in Leukemia
    Article 05 June 2008
  18. Males absent on the first (MOF): from flies to humans

    Histone modifications such as acetylation, methylation and phosphorylation have been implicated in fundamental cellular processes such as epigenetic...

    S Rea, G Xouri, A Akhtar in Oncogene
    Article 13 August 2007
  19. Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia

    Fusion of the mixed lineage leukemia protein (MLL) to one of over 50 different translocation partners converts it into a potent leukemogenic...

    Yali Dou, Jay L. Hess in International Journal of Hematology
    Article 04 December 2007
  20. Mechanisms of Disease: multiple endocrine neoplasia type 1—relation to chromatin modifications and transcription regulation

    Multiple endocrine neoplasia type 1 (MEN1) is a hereditary tumor syndrome characterized by tumors of the parathyroid glands, the pancreatic islets,...

    Koen MA Dreijerink, Jo WM Höppener, ... Cornelis JM Lips in Nature Clinical Practice Endocrinology & Metabolism
    Article 01 October 2006
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