The Experts below are selected from a list of 222 Experts worldwide ranked by ideXlab platform
Dora B Krimer - One of the best experts on this subject based on the ideXlab platform.
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Differential gene expression analysis by RNA-seq reveals the importance of actin cytoskeletal proteins in Erythroleukemia Cells
PeerJ Inc., 2017Co-Authors: Vanessa Fernández-calleja, Pablo HernÁndez, Jorge B. Schvartzman, Mario García De Lacoba, Dora B KrimerAbstract:Development of drug resistance limits the effectiveness of anticancer treatments. Understanding the molecular mechanisms triggering this event in tumor Cells may lead to improved therapeutic strategies. Here we used RNA-seq to compare the transcriptomes of a murine Erythroleukemia Cell line (MEL) and a derived Cell line with induced resistance to differentiation (MEL-R). RNA-seq analysis identified a total of 596 genes (Benjamini–Hochberg adjusted p-value
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Protein kinase clk/STY is differentially regulated during Erythroleukemia Cell differentiation: a bias toward the skipped splice variant characterizes postcommitment stages
Cell Research, 2005Co-Authors: Ana GarcÍa-sacristÁn, María J FernÁndez-nestosa, Pablo HernÁndez, Jorge B Schvartzman, Dora B KrimerAbstract:Clk/STY is a LAMMER protein kinase capable to phosphorylate serine/arginine-rich (SR) proteins that modulate prem-RNA splicing. Clk/STY alternative splicing generates transcripts encoding a full-length kinase and a truncated catalytically inactive protein. Here we showed that clk/STY, as well as other members of the family (e.g. clk2, clk3 and clk4), are up-regulated during HMBA-induced Erythroleukemia Cell differentiation. mRNAs coding for the full-length and the truncated forms were responsible for the overall increased expression. In clk/STY, however, a switch was observed for the ratio of the two alternative spliced products. In undifferentiated Cells the full-length transcript was more abundant whereas the transcript encoding for the truncated form predominated at latter stages of differentiation. Surprisingly, overexpression of clk/STY did not alter the splicing switch upon differentiation in MEL Cells. These results suggest that clk/STY might contribute to control erythroid differentiation by a mechanism that implicates a balance between these two isoforms.
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protein kinase clk sty is differentially regulated during Erythroleukemia Cell differentiation a bias toward the skipped splice variant characterizes postcommitment stages
Cell Research, 2005Co-Authors: Ana Garciasacristan, Jorge B Schvartzman, Maria Jose Fernandeznestosa, Pablo E Hernandez, Dora B KrimerAbstract:Clk/STY is a LAMMER protein kinase capable to phosphorylate serine/arginine-rich (SR) proteins that modulate pre-mRNA splicing. Clk/STY alternative splicing generates transcripts encoding a full-length kinase and a truncated catalytically inactive protein. Here we showed that clk/STY, as well as other members of the family (e.g. clk2, clk3 and clk4), are up-regulated during HMBA-induced Erythroleukemia Cell differentiation. mRNAs coding for the full-length and the truncated forms were responsible for the overall increased expression. In clk/STY, however, a switch was observed for the ratio of the two alternative spliced products. In undifferentiated Cells the full-length transcript was more abundant whereas the transcript encoding for the truncated form predominated at latter stages of differentiation. Surprisingly, overexpression of clk/STY did not alter the splicing switch upon differentiation in MEL Cells. These results suggest that clk/STY might contribute to control erythroid differentiation by a mechanism that implicates a balance between these two isoforms.
Masabumi Shibuya - One of the best experts on this subject based on the ideXlab platform.
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amplification and rearrangement of melf mouse cd43 leukosialin gene encoding a highly glycosylated membrane protein gp120 in friend Erythroleukemia Cells
Oncogene, 1992Co-Authors: Y Misawa, Masabumi ShibuyaAbstract:Using a differential hybridization method, we isolated a cDNA (melF) overexpressed in a murine Friend Erythroleukemia Cell line, F5-5. Southern blotting and sequence analysis revealed that the melF cDNA encodes a membrane protein of 395 amino acids that is the couterpart to human CD43 (leukosialin) surface antigen of lymphocytes in mice. The melF/mouse CD43 (mCD43) gene was found to be amplified eight- to 10-fold not only in F5-5 Cells, but also in their sib Cell lines, including the earliest clone established. This indicates that the amplification of melF/mCD43 gene occurred at an early stage of malignant transformation of the F5-5 family. Furthermore, the same gene was rearranged in another Friend Erythroleukemia Cell line TSA8. In both Cell lines, F5-5 and TSA8, the levels of melF/mCD43 mRNA were 30- to 50-fold higher than that in uninfected spleen Cells. Among normal tissues examined, the expression of melF/mCD43 gene was restricted to hematopoietic tissues. These results suggest that melF/mCD43 gene has an important role in progression of leukemic Cells in the erythroid lineage and also has a physiological function in normal hematopoiesis.
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Amplification and rearrangement of melF/mouse CD43 (leukosialin) gene encoding a highly glycosylated membrane protein gp120 in Friend Erythroleukemia Cells.
Oncogene, 1992Co-Authors: Y Misawa, Masabumi ShibuyaAbstract:Using a differential hybridization method, we isolated a cDNA (melF) overexpressed in a murine Friend Erythroleukemia Cell line, F5-5. Southern blotting and sequence analysis revealed that the melF cDNA encodes a membrane protein of 395 amino acids that is the couterpart to human CD43 (leukosialin) surface antigen of lymphocytes in mice. The melF/mouse CD43 (mCD43) gene was found to be amplified eight- to 10-fold not only in F5-5 Cells, but also in their sib Cell lines, including the earliest clone established. This indicates that the amplification of melF/mCD43 gene occurred at an early stage of malignant transformation of the F5-5 family. Furthermore, the same gene was rearranged in another Friend Erythroleukemia Cell line TSA8. In both Cell lines, F5-5 and TSA8, the levels of melF/mCD43 mRNA were 30- to 50-fold higher than that in uninfected spleen Cells. Among normal tissues examined, the expression of melF/mCD43 gene was restricted to hematopoietic tissues. These results suggest that melF/mCD43 gene has an important role in progression of leukemic Cells in the erythroid lineage and also has a physiological function in normal hematopoiesis.
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Unregulated expression of the erythropoietin receptor gene caused by insertion of spleen focus-forming virus long terminal repeat in a murine Erythroleukemia Cell line.
Molecular and Cellular Biology, 1991Co-Authors: Masayuki Hino, Arinobu Tojo, Y Misawa, H Morii, Fumimaro Takaku, Masabumi ShibuyaAbstract:A murine Erythroleukemia (MEL) Cell line, F5-5, expressed 10,000 binding sites for erythropoietin (EPO) per Cell, 10-fold more than was expressed by other murine Erythroleukemia Cell lines and normal erythroid progenitors. Northern (RNA) and Southern blot analyses revealed overexpression of mRNA for the EPO receptor (EPOR) and rearrangement of one of the EPOR gene alleles in F5-5 Cells, respectively. Molecular cloning of F5-5-derived cDNA encoding EPOR revealed that the 5' noncoding region of the EPOR cDNA corresponds to the 3' long terminal repeat sequence of the polycythemic strain of Friend spleen focus-forming virus (F-SFFVP). The aberrant EPOR transcripts containing the 3' long terminal repeat sequence were mainly expressed in F5-5 Cells. The same integration upstream of the EPOR gene was also observed in other subclones and the parent Cell line. It is possible that overexpression of EPOR by viral promoter insertion will confer growth advantage to an F-SFFVP-infected erythroid progenitor Cell, leading to positive clonal selection through further leukemogenic steps.
Jeanpierre Cartron - One of the best experts on this subject based on the ideXlab platform.
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Putative Oncogenic Role of the Erythropoietin Receptor in Murine and Human Erythroleukemia Cells
Blood, 1994Co-Authors: S Chretien, Sylvie Gisselbrecht, P Mayeux, Jeanpierre Cartron, Françoise Moreau-gachelin, F Apiou, Geneviève Courtois, B Dutrillaux, Claire LacombeAbstract:To determine whether the erythropoietin receptor (Epo-R) plays a role in the course of malignant erythropoietic disorders, this gene was studied in murine and human Erythroleukemia Cells. An altered Epo-R gene was found in a murine Friend Erythroleukemia Cell line, FCL1, due to a spleen focus-forming virus (SFFV) long terminal repeat insertion within the noncoding region of the first exon, leading to Epo-R mRNA overexpression. A similar mechanism of Epo-R activation has previously been described in the T3CL-2 Friend Erythroleukemia Cell line. An elevated number of Epo-binding sites has been observed in two human Erythroleukemia Cell lines, TF-1 and UT7. In UT7 Cells, homogeneously staining region of the short arm of chromosome 19 [hsr (19)] was evidenced, which contained an amplification of the Epo-R gene. This Epo- R gene amplification was confirmed by the quantification of Southern blots in which the intensity of the Epo-R signal was compared in UT7 DNA and in DNA from normal Cells. The Epo-R gene was present in UT7 at a mean number of seven to eight copies per Cell. Interestingly, the Epo- R gene was rearranged; the breakpoint region was located near the 3′ end of the gene, 3 kb downstream from the end of the last exon. Taken together, these results suggest that, in both murine and human systems, genetic alterations of the Epo-R gene are not rare events and could be involved in the occurrence of the erythroleukemic process.
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spleen focus forming virus long terminal repeat insertional activation of the murine erythropoietin receptor gene in the t3cl 2 friend leukemia Cell line
Journal of Biological Chemistry, 1991Co-Authors: Catherine Lacombe, Sylvie Gisselbrecht, S Chretien, V Lemarchandel, P Mayeux, Paulhenri Romeo, Jeanpierre CartronAbstract:Abstract We have characterized the structure of the erythropoietin receptor gene promoter in normal murine erythroid tissues and in Friend-induced tumor Cells. Using primer extension analysis, we identified two distinct transcriptional start sites, which were located 2 base pairs apart in anemic spleens, fetal liver, Friend-induced tumoral spleens, and mouse erythro-leukemia Cells. In contrast, transcription was initiated 37 base pairs upstream of the normal cap sites in T3Cl-2, a Friend virus-induced murine Erythroleukemia Cell line. Also, the erythropoietin receptor mRNA in T3Cl-2 was overexpressed when compared with other Erythroleukemia Cell lines. We found that abnormal transcription occurring in T3Cl-2 Cells resulted from an erythropoietin receptor gene alteration. Indeed, one erythropoietin receptor allele was rearranged by insertion of a spleen focus-forming virus long terminal repeat within the noncoding region of the first exon, 45 bases upstream of the ATG initiation codon and in the same 5'----3' orientation. The transcription of the rearranged allele was shown to be directed from the long terminal repeat promoter, leading to a long terminal repeat-erythropoietin receptor fusion transcript, whereas the normal erythropoietin receptor allele was weakly transcribed. Such altered receptor gene activation may provide a positive pressure in the development of tumorigenic Erythroleukemia.
Jorge B Schvartzman - One of the best experts on this subject based on the ideXlab platform.
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Protein kinase clk/STY is differentially regulated during Erythroleukemia Cell differentiation: a bias toward the skipped splice variant characterizes postcommitment stages
Cell Research, 2005Co-Authors: Ana GarcÍa-sacristÁn, María J FernÁndez-nestosa, Pablo HernÁndez, Jorge B Schvartzman, Dora B KrimerAbstract:Clk/STY is a LAMMER protein kinase capable to phosphorylate serine/arginine-rich (SR) proteins that modulate prem-RNA splicing. Clk/STY alternative splicing generates transcripts encoding a full-length kinase and a truncated catalytically inactive protein. Here we showed that clk/STY, as well as other members of the family (e.g. clk2, clk3 and clk4), are up-regulated during HMBA-induced Erythroleukemia Cell differentiation. mRNAs coding for the full-length and the truncated forms were responsible for the overall increased expression. In clk/STY, however, a switch was observed for the ratio of the two alternative spliced products. In undifferentiated Cells the full-length transcript was more abundant whereas the transcript encoding for the truncated form predominated at latter stages of differentiation. Surprisingly, overexpression of clk/STY did not alter the splicing switch upon differentiation in MEL Cells. These results suggest that clk/STY might contribute to control erythroid differentiation by a mechanism that implicates a balance between these two isoforms.
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protein kinase clk sty is differentially regulated during Erythroleukemia Cell differentiation a bias toward the skipped splice variant characterizes postcommitment stages
Cell Research, 2005Co-Authors: Ana Garciasacristan, Jorge B Schvartzman, Maria Jose Fernandeznestosa, Pablo E Hernandez, Dora B KrimerAbstract:Clk/STY is a LAMMER protein kinase capable to phosphorylate serine/arginine-rich (SR) proteins that modulate pre-mRNA splicing. Clk/STY alternative splicing generates transcripts encoding a full-length kinase and a truncated catalytically inactive protein. Here we showed that clk/STY, as well as other members of the family (e.g. clk2, clk3 and clk4), are up-regulated during HMBA-induced Erythroleukemia Cell differentiation. mRNAs coding for the full-length and the truncated forms were responsible for the overall increased expression. In clk/STY, however, a switch was observed for the ratio of the two alternative spliced products. In undifferentiated Cells the full-length transcript was more abundant whereas the transcript encoding for the truncated form predominated at latter stages of differentiation. Surprisingly, overexpression of clk/STY did not alter the splicing switch upon differentiation in MEL Cells. These results suggest that clk/STY might contribute to control erythroid differentiation by a mechanism that implicates a balance between these two isoforms.
Y Misawa - One of the best experts on this subject based on the ideXlab platform.
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amplification and rearrangement of melf mouse cd43 leukosialin gene encoding a highly glycosylated membrane protein gp120 in friend Erythroleukemia Cells
Oncogene, 1992Co-Authors: Y Misawa, Masabumi ShibuyaAbstract:Using a differential hybridization method, we isolated a cDNA (melF) overexpressed in a murine Friend Erythroleukemia Cell line, F5-5. Southern blotting and sequence analysis revealed that the melF cDNA encodes a membrane protein of 395 amino acids that is the couterpart to human CD43 (leukosialin) surface antigen of lymphocytes in mice. The melF/mouse CD43 (mCD43) gene was found to be amplified eight- to 10-fold not only in F5-5 Cells, but also in their sib Cell lines, including the earliest clone established. This indicates that the amplification of melF/mCD43 gene occurred at an early stage of malignant transformation of the F5-5 family. Furthermore, the same gene was rearranged in another Friend Erythroleukemia Cell line TSA8. In both Cell lines, F5-5 and TSA8, the levels of melF/mCD43 mRNA were 30- to 50-fold higher than that in uninfected spleen Cells. Among normal tissues examined, the expression of melF/mCD43 gene was restricted to hematopoietic tissues. These results suggest that melF/mCD43 gene has an important role in progression of leukemic Cells in the erythroid lineage and also has a physiological function in normal hematopoiesis.
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Amplification and rearrangement of melF/mouse CD43 (leukosialin) gene encoding a highly glycosylated membrane protein gp120 in Friend Erythroleukemia Cells.
Oncogene, 1992Co-Authors: Y Misawa, Masabumi ShibuyaAbstract:Using a differential hybridization method, we isolated a cDNA (melF) overexpressed in a murine Friend Erythroleukemia Cell line, F5-5. Southern blotting and sequence analysis revealed that the melF cDNA encodes a membrane protein of 395 amino acids that is the couterpart to human CD43 (leukosialin) surface antigen of lymphocytes in mice. The melF/mouse CD43 (mCD43) gene was found to be amplified eight- to 10-fold not only in F5-5 Cells, but also in their sib Cell lines, including the earliest clone established. This indicates that the amplification of melF/mCD43 gene occurred at an early stage of malignant transformation of the F5-5 family. Furthermore, the same gene was rearranged in another Friend Erythroleukemia Cell line TSA8. In both Cell lines, F5-5 and TSA8, the levels of melF/mCD43 mRNA were 30- to 50-fold higher than that in uninfected spleen Cells. Among normal tissues examined, the expression of melF/mCD43 gene was restricted to hematopoietic tissues. These results suggest that melF/mCD43 gene has an important role in progression of leukemic Cells in the erythroid lineage and also has a physiological function in normal hematopoiesis.
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Unregulated expression of the erythropoietin receptor gene caused by insertion of spleen focus-forming virus long terminal repeat in a murine Erythroleukemia Cell line.
Molecular and Cellular Biology, 1991Co-Authors: Masayuki Hino, Arinobu Tojo, Y Misawa, H Morii, Fumimaro Takaku, Masabumi ShibuyaAbstract:A murine Erythroleukemia (MEL) Cell line, F5-5, expressed 10,000 binding sites for erythropoietin (EPO) per Cell, 10-fold more than was expressed by other murine Erythroleukemia Cell lines and normal erythroid progenitors. Northern (RNA) and Southern blot analyses revealed overexpression of mRNA for the EPO receptor (EPOR) and rearrangement of one of the EPOR gene alleles in F5-5 Cells, respectively. Molecular cloning of F5-5-derived cDNA encoding EPOR revealed that the 5' noncoding region of the EPOR cDNA corresponds to the 3' long terminal repeat sequence of the polycythemic strain of Friend spleen focus-forming virus (F-SFFVP). The aberrant EPOR transcripts containing the 3' long terminal repeat sequence were mainly expressed in F5-5 Cells. The same integration upstream of the EPOR gene was also observed in other subclones and the parent Cell line. It is possible that overexpression of EPOR by viral promoter insertion will confer growth advantage to an F-SFFVP-infected erythroid progenitor Cell, leading to positive clonal selection through further leukemogenic steps.