When the single REP53 element was inserted into the pAZ1037 chloramphenicol acetyltransferase (CAT) expression vector immediately upstream of the chicken beta-actin promoter in either normal or inverted orientation and used to transfect K-562 erythroleukemia or HeLa cervical carcinoma cells, these modified vectors achieved 2 to 3-fold higher CAT activity than the parental pAZ1037 vector irrespective of orientation of the REP53.
When the single REP53 element was inserted into the pAZ1037 chloramphenicol acetyltransferase (CAT) expression vector immediately upstream of the chicken beta-actin promoter in either normal or inverted orientation and used to transfect K-562 erythroleukemia or HeLa cervical carcinoma cells, these modified vectors achieved 2 to 3-fold higher CAT activity than the parental pAZ1037 vector irrespective of orientation of the REP53.
When K562 human erythroleukemia cells were treated with the Oct-1 decoy oligonucleotide, significant increases in the level of the gamma-globin mRNA were observed.
When K562 human erythroleukemia cells were treated with the Oct-1 decoy oligonucleotide, significant increases in the level of the gamma-globin mRNA were observed.
When cultures were supplemented with TPA, CD30 transcript was downregulated in a dose- and time-dependent manner in the erythroleukemia cell line K562.
We then addressed the question of the protective role of peroxiredoxin-2 in erythropoiesis by exposing normal cells to oxidative stress and silencing peroxiredoxin-2 in human erythroleukemia K562 cells.
We studied RUNX1 binding to the <i>PCTP</i> promoter using DNA-protein binding studies and human erythroleukemia cells and promoter activity using luciferase reporter studies.
We show here that expression of the PML-RAR alpha protein in K562 erythroleukemia cells results in a reduced expression of erythroid differentiation markers and a reduced sensitivity to the erythroid differentiative action of heme.
We performed high-resolution mapping studies of the DNAse I-hypersensitive sites located just 5' to the human G gamma- and A gamma-globin genes of K562 erythroleukemia cells, in which these genes are constitutively expressed at low levels.
We now report the biochemical purification of SSP from K562 cell nuclear extract and demonstrate that the ubiquitously expressed transcription factor CP2 is pivotal to, but not sufficient for, SSP binding activity.
We investigated the activity of (E)-3(6-bromopyridin-2-yl)-2-cyano-N-(S0-1phenylethyl)acrylamide (WP1066), a novel analogue of the JAK2 inhibitor AG490, in JAK2V617F-positive erythroleukemia HEL cells and in blood cells from patients with polycythemia vera.
We hypothesized that Epo gene expression would be targeted to erythroid cells in these mice, resulting in autocrine stimulation of erythroid progenitor cell growth in culture, and that chronic autocrine Epo stimulation would result in erythroleukemia.
We have used DNase I footprinting with K562 erythroleukemia cell extracts to identify protein components of the minimal LCR element, hypersensitive site 2.
We have shown by immunoprecipitation analysis that the two complement receptors expressed by B lymphocytes, complement receptor 1 (CR1) and CR2, form a detergent-sensitive complex on the surface of tonsillar B lymphocytes and on K562 erythroleukemia cells that were co-transfected with cDNAs encoding CR1 and CR2.
We have reviewed the clinical, morphologic, immunophenotypic, and cytogenetic features of 52 patients with erythroleukemia (FAB Cooperative Group; AML-M6) studied by the Cancer and Leukemia Group B (CALGB).
We have isolated and sequenced cDNA clones from a human erythroleukemia cell line (K562) derived cDNA library, using different mouse bmi-1 cDNA fragments as a probe.
We have isolated and sequenced cDNA clones from a human erythroleukemia cell line (K562) derived cDNA library, using different mouse bmi-1 cDNA fragments as a probe.
We have analysed the expression of cloned human fetal gamma-globin genes introduced into murine erythroleukemia cells by a protoplast fusion procedure.
We further suggest that deregulated synthesis of Fli-1 may trigger a common mechanism contributing to erythroleukemia induced by either SFFV or F-MuLV.