Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136021 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the mechanism of telomerase regulation in BCR-ABL positive cells due to its clinical value, we studied the catalytic component of telomerase, TERT. Our results suggest that BCR-ABL plays an important role in regulating hTERT in K562 (BCR-ABL positive human leukemia) cells. When Gleevec inhibited the tyrosine kinase activity of BCR-ABL, phosphorylation of hTERT was downregulated, therefore suggesting a positive correlation between BCR-ABL and hTERT. Gleevec treatment inhibited hTERT at the mRNA level and significantly reduced telomerase activity (TA) in K562 cells, but not in HL60 or Jurkat cells. TRAP assay also revealed that Gleevec treatment significantly reduced TA specifically in K562 cells. Furthermore, translocation of hTERT from nucleoli to nucleoplasm was observed in K562 cells induced by Gleevec. Although Gleevec down-regulated hTERT mRNA level, the protein level of hTERT remained unchanged. Therefore, Gleevec-induced-TA decrease is not due to the alteration in telomerase subunits expression. It could be presumably due to posttranslational modification of hTERT, possibly through multiple signaling pathways. We have found that Gleevec reduced the tyrosine phosphorylation of hTERT by BCR-ABL, which is associated with the nucleoplasm localization of hTERT from nucleoli sequesters. These findings reveal unknown functions and regulations of telomerase by BCR-ABL. Using cRNA microarray, gene expression of Gleevec-treated and non-treated K562 (BCR-ABL positive) cells were compared against Gleevec-treated and non-treated HL60 (BCR-ABL deficient) cells.
2011-12-15 | E-GEOD-26821 | biostudies-arrayexpress
Project description:To investigate the mechanism of telomerase regulation in BCR-ABL positive cells due to its clinical value, we studied the catalytic component of telomerase, TERT. Our results suggest that BCR-ABL plays an important role in regulating hTERT in K562 (BCR-ABL positive human leukemia) cells. When Gleevec inhibited the tyrosine kinase activity of BCR-ABL, phosphorylation of hTERT was downregulated, therefore suggesting a positive correlation between BCR-ABL and hTERT. Gleevec treatment inhibited hTERT at the mRNA level and significantly reduced telomerase activity (TA) in K562 cells, but not in HL60 or Jurkat cells. TRAP assay also revealed that Gleevec treatment significantly reduced TA specifically in K562 cells. Furthermore, translocation of hTERT from nucleoli to nucleoplasm was observed in K562 cells induced by Gleevec. Although Gleevec down-regulated hTERT mRNA level, the protein level of hTERT remained unchanged. Therefore, Gleevec-induced-TA decrease is not due to the alteration in telomerase subunits expression. It could be presumably due to posttranslational modification of hTERT, possibly through multiple signaling pathways. We have found that Gleevec reduced the tyrosine phosphorylation of hTERT by BCR-ABL, which is associated with the nucleoplasm localization of hTERT from nucleoli sequesters. These findings reveal unknown functions and regulations of telomerase by BCR-ABL.
2011-12-15 | GSE26821 | GEO
Project description:Comparative analysis of BCR-ABL tyrosine kinase inhibitors in BCR-ABL positive K562 cells
| PRJNA92407 | ENA
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
2011-08-25 | GSE23936 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs. One-condition experment, gene expression of 3A6
2010-09-25 | E-GEOD-24338 | biostudies-arrayexpress
Project description:K562 cells were treated with the BCR-ABL kinase inhibitor dasatinib over an extended period of time to determine how BCR-ABL inhibition affects BCR-ABL-dependent negative feedback and erythropoietin receptor (EPO-R) signaling. Specifically, what types of changes (upregulation versus downregulation) occur in both the negative and positive regulators of growth-factor receptor signaling. Total RNA was extracted from K562 cells treated with 0.2% DMSO for 24hrs or 100nM dasatinib for 4hrs, 8hrs, and 24hrs.
2013-09-24 | E-GEOD-51083 | biostudies-arrayexpress
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs. Two-condition experiment, KP MSCs vs. 3A6 MSCs.
2011-08-24 | E-GEOD-23936 | biostudies-arrayexpress
Project description:K562 cells were treated with the BCR-ABL kinase inhibitor dasatinib over an extended period of time to determine how BCR-ABL inhibition affects BCR-ABL-dependent negative feedback and erythropoietin receptor (EPO-R) signaling. Specifically, what types of changes (upregulation versus downregulation) occur in both the negative and positive regulators of growth-factor receptor signaling.
2013-09-24 | GSE51083 | GEO
Project description:LncRNA-IIRX plays critical role in Bcr-Abl-induced tumorigenesis. To discover its mechanisms underlying cellular transformation by Bcr-Abl oncogene, genome-wide mRNA expression was measured by RNA-seq in K562 cells expressing shRNA targeting lncRNA-IIRX and control cells. We identified many genes with differential expression in K562 cells after knocking down lncRNA-IIRX.
2019-04-17 | GSE120337 | GEO