The Experts below are selected from a list of 10119 Experts worldwide ranked by ideXlab platform
Hiroshi Sato - One of the best experts on this subject based on the ideXlab platform.
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Epstein‐barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2′-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
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Epstein-Barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line.
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2'-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
Tomokazu Yoshizaki - One of the best experts on this subject based on the ideXlab platform.
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Epstein‐barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2′-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
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Epstein-Barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line.
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2'-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
J. Leslie Redpath - One of the best experts on this subject based on the ideXlab platform.
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Loss of a Putative Tumor Suppressor Locus after Gamma-Ray-Induced Neoplastic Transformation of HeLa × Skin Fibroblast Human Cell Hybrids
Radiation research, 1995Co-Authors: Marc S. Mendonca, Clare L. Fasching, Eri S. Srivatsan, Eric J. Stanbridge, J. Leslie RedpathAbstract:The nontumorigenic HeLa × skin fibroblast Hybrid Cell Line, CGL1, can be induced to re-express HeLa tumor-associated Cell surface antigen, p75-IAP (intestinal alkaLine phosphatase), with resulting ...
Hazime Takeshita - One of the best experts on this subject based on the ideXlab platform.
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Epstein‐barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2′-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
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Epstein-Barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line.
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2'-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
Saichiro Tanaka - One of the best experts on this subject based on the ideXlab platform.
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Epstein‐barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2′-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
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Epstein-Barr virus lytic cycle spreads via Cell fusion in a nasopharyngeal carcinoma Hybrid Cell Line.
The Laryngoscope, 1994Co-Authors: Tomokazu Yoshizaki, Toru Takimoto, Hazime Takeshita, Saichiro Tanaka, Mitsuru Furukawa, Motoharu Seiki, Hiroshi SatoAbstract:NPC-KT cl.S61, a subclone derived from an epithelial-nasopharyngeal carcinoma Hybrid Cell Line NPC-KT, showed extensive Epstein-Barr virus (EBV) production and Cell fusion when the EBV replicative cycle was induced by 5-iodo-2'-deoxyuridine. On the contrary, parental NPC-KT Cells produced virus at a lower level and did not show Cell fusion. Cell fusion in cl.S61 Cells was blocked by 2-deoxyglucose and acyclovir, inhibitors of glycosylation and EBV DNA polymerase, respectively, with a concomitant decrease in the number of Cells expressing EBV growth-associated antigens. However, the frequency of virus antigen expression in parental NPC-KT Cells was not significantly affected by these drugs. This result suggests that efficient production of EBV from cl.S61 Cells is due to the spreading of viral replicative cycle via Cell fusion. It was also demonstrated by in situ autoradiography that cl.S61 Cells producing virus fused to not only EBV receptor/CR2 positive Raji and BJAB Cells, but also to receptor-negative Jurkat Cells. The possible mechanism of EBV entry into Cells devoid of virus receptor by Cell fusion is discussed.
