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Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression
TLDR
It is suggested that C CDC26 controls growth of myeloid leukemia cells through regulation of KIT expression, and a KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered. Expand
Genes encoded within 8q24 on the amplicon of a large extrachromosomal element are selectively repressed during the terminal differentiation of HL-60 cells.
TLDR
The results suggest that the Myc, NSMCE2, CCDC26 and LOC389637 and TRIB1 genes were selected during the development of amplicons and might be amplified and, sometimes, truncated to contribute to the maintenance of HL-60 cells in an undifferentiated state. Expand
Loss of amplified c-myc genes in the spontaneously differentiated HL-60 cells.
TLDR
It is shown that the spontaneous differentiation could be a result of extensive losses of amplified c-myc genes by the findings: the spontaneously differentiated HL-60 cells express Mac-1 (CR3, CD11b/CD18) antigen, irreversibly stop the uptake of [3H]thymidine, and die by apoptosis. Expand
Expression profile of active genes in granulocytes.
TLDR
An expression profile of 748 different species of active genes in human peripheral granulocytes obtained by analyzing a 3'-directed cDNA library that faithfully represents the mRNA population in the source cells showed similarities and dissimilarities of gene expressions. Expand
Granulocytic differentiation of HL-60 cells, both spontaneous and drug-induced, might require loss of extrachromosomal DNA encoding a gene(s) not c-MYC.
TLDR
It is shown that a gene(s) in other extrachromosomal, acentromeric DNA can be assumed to be necessary and sufficient for the expression of the above phenotypes by resolving the paradox of loss of c-MYC copies in double minutes via micronuclei. Expand
Survival by Mac-1-mediated Adherence and Anoikis in Phorbol Ester-treated HL-60 Cells*
TLDR
It is shown that the adherent cells rapidly died by apoptosis after forced detachment, indicating that phorbol diester induced apoptosis by default, and suggests that the commitment signal of apoptosisBy default is lost faster than the survival signal by adherence. Expand
Involvement of Mac-1-mediated adherence and sphingosine 1-phosphate in survival of phorbol ester-treated U937 cells.
TLDR
The plastic adherence of phorbol ester-treated U937 cells is mediated by expression of integrin Mac-1 (CD11b/CD18) on the cell surface and these adherent cells exhibit anoikis (apoptosis when adherent cells are detached or adherence is inhibited). Expand
Evolution of large extrachromosomal elements in HL-60 cells during culture and the associated phenotype alterations.
In the HL-60 sublines that were isolated after a long-term continuous culture, abnormally stained or abnormally banded regions on chromosomes replaced extrachromosomal double minutes. The c-MYC geneExpand
Co-localization of mitochondrial and double minute DNA in the nuclei of HL-60 cells but not normal cells.
TLDR
It is shown that amplified mtDNA sequences were localized in nuclei and micronuclei of HL-60 and COLO 320DM cells, but not in nucleo of WI-38 normal human fibroblasts or peripheral blood T-cells, and the mechanisms of nuclear retention of mtDNA and Dmin DNA and the resulting influence on tumorigenesis are discussed. Expand
An Active C-Terminally Truncated Form of Ca2+/Calmodulin-Dependent Protein Kinase Phosphatase-N (CaMKP-N/PPM1E)
TLDR
The truncated CaMKP-N showed Mn2+ or Mg2+-dependent phosphatase activity with a strong preference for phospho-Thr residues and was severely inhibited by NaF, but not by okadaic acid, calyculin A, or 1-amino-8-naphthol-2,4-disulfonic acid, a specific inhibitor of CaMKp. Expand
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