The Experts below are selected from a list of 90 Experts worldwide ranked by ideXlab platform
John M. Lehman - One of the best experts on this subject based on the ideXlab platform.
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Induction of tetraploid DNA content by simian virus 40 is dependent on T-Antigen Function in the G2 phase of the cell cycle
Journal of virology, 1994Co-Authors: Thomas D. Friedrich, Judith Laffin, John M. LehmanAbstract:Previous experiments with the simian virus 40 mutant tsA357R-K (tsA30) demonstrated a T-Antigen Function that is required for production of cells with a greater-than-G2-phase DNA content. In this study, temperature shift experiments indicated that the temperature-sensitive Function of tsA357R-K, which is necessary for entry into the greater-than-G2 phase, is not required in G1 or S but must be supplied in the G2 phase.
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Simian virus 40 large T-Antigen Function is required for induction of tetraploid DNA content during lytic infection.
Journal of virology, 1992Co-Authors: Thomas D. Friedrich, Judith Laffin, John M. LehmanAbstract:Infection of quiescent CV-1 cells with simian virus 40 mutant tsA30 at 37 degrees C resulted in the induction of two rounds of cellular DNA synthesis in T-Antigen-positive cells, as previously described for wild-type simian virus 40. Following infection with tsA30 at 40.5 degrees C, T-Antigen-positive cells were induced into S phase and reached a diploid G2 DNA content; however, a second S phase was not initiated. The failure of tsA30-infected CV-1 cells to enter tetraploid S phase at 40.5 degrees C identifies a T-Antigen Function, distinct from T-Antigen Functions responsible for stimulation of cell DNA synthesis, which is required for initiation of a second round of DNA synthesis without mitosis.
Rati Fotedar - One of the best experts on this subject based on the ideXlab platform.
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Growth inhibition by CDK-cyclin and PCNA binding domains of p21 occurs by distinct mechanisms and is regulated by ubiquitin-proteasome pathway
Oncogene, 1999Co-Authors: Denis Rousseau, Dominique Cannella, Jerome Boulaire, Patrick Fitzgerald, Arun Fotedar, Rati FotedarAbstract:The CDK inhibitor, p21^WAF1/Cip1 blocks cell cycle progression. In vitro , the N-terminus of p21 binds and inhibits CDK-cyclin kinase activity, whereas the C-terminus binds and inhibits PCNA (proliferating cell nuclear Antigen) Function. PCNA is essential for processivity of both DNA polymerase δ and ε. We have performed a detailed analysis of growth inhibition by the N- and C-terminal regions of p21, and determined whether the N- and C-terminal regions mediate this effect by different mechanisms. Expression of either the N- or the C-terminal region of p21 inhibits DNA synthesis and cell growth, but not as efficiently as full length p21. The effectiveness of the two p21 domains is dependent on their stability which is determined by the ubiquitin-proteasome pathway. The stabilization of the N- and C-terminal region of p21 increases their effectiveness as inhibitors of DNA synthesis to levels comparable to full length p21. Inhibition of DNA synthesis by the N-terminal region of p21 involves suppression of E2F activity. In contrast, inhibition by the C-terminal region of p21 is not accompanied by suppression of E2F activity, but is mediated via PCNA binding. The C-terminal region of p21 therefore inhibits cell growth by a mechanism distinct from that of the N-terminal region containing the CDK-cyclin inhibitory domain.
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Growth inhibition by CDK-cyclin and PCNA binding domains of p21 occurs by distinct mechanisms and is regulated by ubiquitin-proteasome pathway.
Oncogene, 1999Co-Authors: Denis Rousseau, Dominique Cannella, Jerome Boulaire, Patrick Fitzgerald, Arun Fotedar, Rati FotedarAbstract:The CDK inhibitor, p21(WAF1/Cip1) blocks cell cycle progression. In vitro, the N-terminus of p21 binds and inhibits CDK-cyclin kinase activity, whereas the C-terminus binds and inhibits PCNA (proliferating cell nuclear Antigen) Function. PCNA is essential for processivity of both DNA polymerase delta and epsilon. We have performed a detailed analysis of growth inhibition by the N- and C-terminal regions of p21, and determined whether the N- and C-terminal regions mediate this effect by different mechanisms. Expression of either the N- or the C-terminal region of p21 inhibits DNA synthesis and cell growth, but not as efficiently as full length p21. The effectiveness of the two p21 domains is dependent on their stability which is determined by the ubiquitin-proteasome pathway. The stabilization of the N- and C-terminal region of p21 increases their effectiveness as inhibitors of DNA synthesis to levels comparable to full length p21. Inhibition of DNA synthesis by the N-terminal region of p21 involves suppression of E2F activity. In contrast, inhibition by the C-terminal region of p21 is not accompanied by suppression of E2F activity, but is mediated via PCNA binding. The C-terminal region of p21 therefore inhibits cell growth by a mechanism distinct from that of the N-terminal region containing the CDK-cyclin inhibitory domain.
Thomas D. Friedrich - One of the best experts on this subject based on the ideXlab platform.
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Induction of tetraploid DNA content by simian virus 40 is dependent on T-Antigen Function in the G2 phase of the cell cycle
Journal of virology, 1994Co-Authors: Thomas D. Friedrich, Judith Laffin, John M. LehmanAbstract:Previous experiments with the simian virus 40 mutant tsA357R-K (tsA30) demonstrated a T-Antigen Function that is required for production of cells with a greater-than-G2-phase DNA content. In this study, temperature shift experiments indicated that the temperature-sensitive Function of tsA357R-K, which is necessary for entry into the greater-than-G2 phase, is not required in G1 or S but must be supplied in the G2 phase.
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Simian virus 40 large T-Antigen Function is required for induction of tetraploid DNA content during lytic infection.
Journal of virology, 1992Co-Authors: Thomas D. Friedrich, Judith Laffin, John M. LehmanAbstract:Infection of quiescent CV-1 cells with simian virus 40 mutant tsA30 at 37 degrees C resulted in the induction of two rounds of cellular DNA synthesis in T-Antigen-positive cells, as previously described for wild-type simian virus 40. Following infection with tsA30 at 40.5 degrees C, T-Antigen-positive cells were induced into S phase and reached a diploid G2 DNA content; however, a second S phase was not initiated. The failure of tsA30-infected CV-1 cells to enter tetraploid S phase at 40.5 degrees C identifies a T-Antigen Function, distinct from T-Antigen Functions responsible for stimulation of cell DNA synthesis, which is required for initiation of a second round of DNA synthesis without mitosis.
Denis Rousseau - One of the best experts on this subject based on the ideXlab platform.
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Growth inhibition by CDK-cyclin and PCNA binding domains of p21 occurs by distinct mechanisms and is regulated by ubiquitin-proteasome pathway
Oncogene, 1999Co-Authors: Denis Rousseau, Dominique Cannella, Jerome Boulaire, Patrick Fitzgerald, Arun Fotedar, Rati FotedarAbstract:The CDK inhibitor, p21^WAF1/Cip1 blocks cell cycle progression. In vitro , the N-terminus of p21 binds and inhibits CDK-cyclin kinase activity, whereas the C-terminus binds and inhibits PCNA (proliferating cell nuclear Antigen) Function. PCNA is essential for processivity of both DNA polymerase δ and ε. We have performed a detailed analysis of growth inhibition by the N- and C-terminal regions of p21, and determined whether the N- and C-terminal regions mediate this effect by different mechanisms. Expression of either the N- or the C-terminal region of p21 inhibits DNA synthesis and cell growth, but not as efficiently as full length p21. The effectiveness of the two p21 domains is dependent on their stability which is determined by the ubiquitin-proteasome pathway. The stabilization of the N- and C-terminal region of p21 increases their effectiveness as inhibitors of DNA synthesis to levels comparable to full length p21. Inhibition of DNA synthesis by the N-terminal region of p21 involves suppression of E2F activity. In contrast, inhibition by the C-terminal region of p21 is not accompanied by suppression of E2F activity, but is mediated via PCNA binding. The C-terminal region of p21 therefore inhibits cell growth by a mechanism distinct from that of the N-terminal region containing the CDK-cyclin inhibitory domain.
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Growth inhibition by CDK-cyclin and PCNA binding domains of p21 occurs by distinct mechanisms and is regulated by ubiquitin-proteasome pathway.
Oncogene, 1999Co-Authors: Denis Rousseau, Dominique Cannella, Jerome Boulaire, Patrick Fitzgerald, Arun Fotedar, Rati FotedarAbstract:The CDK inhibitor, p21(WAF1/Cip1) blocks cell cycle progression. In vitro, the N-terminus of p21 binds and inhibits CDK-cyclin kinase activity, whereas the C-terminus binds and inhibits PCNA (proliferating cell nuclear Antigen) Function. PCNA is essential for processivity of both DNA polymerase delta and epsilon. We have performed a detailed analysis of growth inhibition by the N- and C-terminal regions of p21, and determined whether the N- and C-terminal regions mediate this effect by different mechanisms. Expression of either the N- or the C-terminal region of p21 inhibits DNA synthesis and cell growth, but not as efficiently as full length p21. The effectiveness of the two p21 domains is dependent on their stability which is determined by the ubiquitin-proteasome pathway. The stabilization of the N- and C-terminal region of p21 increases their effectiveness as inhibitors of DNA synthesis to levels comparable to full length p21. Inhibition of DNA synthesis by the N-terminal region of p21 involves suppression of E2F activity. In contrast, inhibition by the C-terminal region of p21 is not accompanied by suppression of E2F activity, but is mediated via PCNA binding. The C-terminal region of p21 therefore inhibits cell growth by a mechanism distinct from that of the N-terminal region containing the CDK-cyclin inhibitory domain.
Judith Laffin - One of the best experts on this subject based on the ideXlab platform.
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Induction of tetraploid DNA content by simian virus 40 is dependent on T-Antigen Function in the G2 phase of the cell cycle
Journal of virology, 1994Co-Authors: Thomas D. Friedrich, Judith Laffin, John M. LehmanAbstract:Previous experiments with the simian virus 40 mutant tsA357R-K (tsA30) demonstrated a T-Antigen Function that is required for production of cells with a greater-than-G2-phase DNA content. In this study, temperature shift experiments indicated that the temperature-sensitive Function of tsA357R-K, which is necessary for entry into the greater-than-G2 phase, is not required in G1 or S but must be supplied in the G2 phase.
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Simian virus 40 large T-Antigen Function is required for induction of tetraploid DNA content during lytic infection.
Journal of virology, 1992Co-Authors: Thomas D. Friedrich, Judith Laffin, John M. LehmanAbstract:Infection of quiescent CV-1 cells with simian virus 40 mutant tsA30 at 37 degrees C resulted in the induction of two rounds of cellular DNA synthesis in T-Antigen-positive cells, as previously described for wild-type simian virus 40. Following infection with tsA30 at 40.5 degrees C, T-Antigen-positive cells were induced into S phase and reached a diploid G2 DNA content; however, a second S phase was not initiated. The failure of tsA30-infected CV-1 cells to enter tetraploid S phase at 40.5 degrees C identifies a T-Antigen Function, distinct from T-Antigen Functions responsible for stimulation of cell DNA synthesis, which is required for initiation of a second round of DNA synthesis without mitosis.