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CBP-mediated acetylation of histone H3 lysine 27 antagonizes Drosophila Polycomb silencing
TLDR
It is proposed that TRX-dependent acetylation of H3K27 by CBP prevents H3k27me3 at Polycomb target genes and constitutes a key part of the molecular mechanism by which TRX antagonizes or prevents Polycomb silencing.
MLL repression domain interacts with histone deacetylases, the polycomb group proteins HPC2 and BMI-1, and the corepressor C-terminal-binding protein
TLDR
A model whereby recruitment of BMI-1 to the MLL protein may be able to modulate its function is suggested, whereby repression mediated by histone deacetylases and that mediated by polycomb group proteins may act either independently or together for MLL function in vivo.
Homozygous deletion of the alpha- and beta 1-interferon genes in human leukemia and derived cell lines.
TLDR
Evidence is presented of the homozygous deletion of the interferon genes in neoplastic hematopoietic cell lines and primary leukemia cells in the presence or absence of chromosomal deletions that are detectable at the level of the light microscope.
Rearrangements of the MLL gene in therapy-related acute myeloid leukemia in patients previously treated with agents targeting DNA- topoisomerase II
TLDR
The association of exposure to topo II- reactive chemotherapy with 11q23 rearrangements involving the MLL gene in t-AML suggests thatTopo II may play a role in the aberrant recombination events that occur in this region both in AML de novo and in t -AML.
Protein Interactions of the MLL PHD Fingers Modulate MLL Target Gene Regulation in Human Cells
TLDR
It is determined that the PHD fingers of the human MLL and Drosophila trx proteins mediate homodimerization and binding of MLL to Cyp33, a nuclear cyclophilin.
MLL2: A new mammalian member of the trx/MLL family of genes.
TLDR
A gene at chromosome band 19q13.1, MLL2, which is closely related to MLL is identified, which encodes a protein that exhibits a high level of similarity to M LL over several important protein domains.
Mapping chromosome band 11q23 in human acute leukemia with biotinylated probes: identification of 11q23 translocation breakpoints with a yeast artificial chromosome.
Translocations involving chromosome 11, band q23, are frequent recurring abnormalities in human acute lymphoblastic and acute myeloid leukemia. We used 19 biotin-labeled probes derived from genes and
Identification of a human gene (HCK) that encodes a protein-tyrosine kinase and is expressed in hemopoietic cells
TLDR
These findings add to the diversity of protein-tyrosine kinases that may serve specialized functions in hemopoietic cells, and they raise the possibility that damage to HCK may contribute to the pathogenesis of some human leukemias.
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