Ping-Ping Hui

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The expression of the human myeloid zinc finger gene (MZF-1) by human bone marrow cells is necessary for granulopoiesis. We have analyzed the structure and function of the MZF-1 gene by diagnostic polymerase chain reaction, genomic cloning, and promoter analysis. Comparison of human promyelocytic HL-60 cell cDNA with isolated MZF-1 genomic clones indicated(More)
Here we show that d,l-Threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), a glycosphingolipid biosynthesis inhibitor, increases the sensitivity of pancreatic cancer cells to the novel MEK-ERK inhibitor AZD-6244. AZD-6244 and PDMP co-administration induced massive pancreatic cancer cell death and apoptosis, more potently than either drug alone. We(More)
Lung cancer is a major cause of cancer-related mortality in the United States and around the world. Due to the pre-existing or acquired chemo-resistance, the current standard chemotherapy regimens only show moderate activity against lung cancer. In the current study, we explored the potential anti-lung cancer activity of cinobufotalin in vivo and in vitro,(More)
The inositol trisphosphate (InsP3) receptor is an essential regulator of intracellular calcium in many cells including chemoattractant- and cytokine-stimulated neutrophils and differentiated promyelocytic leukemic (HL-60) cells. We examined the expression and function of the InsP3 receptor and the transcriptional regulation of the InsP3 receptor gene in(More)
When treated with IL-3 plus GM-CSF, K562 myeloblast cells acquired the ability to mobilize nonmitochondrial stores of intracellular Ca2+ in response to added Ins (1, 4, 5) P3. Untreated K562 cells are capable of sequestering intracellular Ca2+ but released none of this Ca2+ in response to Ins (1, 4, 5) P3. Untreated K562 cells were shown to have no(More)
Human leukemic HL-60 cells were treated with 1,25-dihydroxyvitamin D3 (VitD3) to induce monocytic cell differentiation. Concomitant with differentiation there was increased inositol-1,4,5-trisphosphate (InsP3) receptor expression, as assessed by both [3H]InsP3 binding site density and maximal InsP3-mediated Ca2+ mobilization from intracellular stores.(More)
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