John M. Sedivy spends much of his time researching Cell biology, Senescence, Signal transduction, Molecular biology and Cell cycle. His Cell biology study combines topics from a wide range of disciplines, such as Cyclin-dependent kinase and Downregulation and upregulation. His Senescence research is multidisciplinary, incorporating perspectives in Cell cycle checkpoint, DNA damage, Somatic cell, Chromatin and Telomere.
His DNA damage research includes themes of CHEK1 and Oxidative stress. His Signal transduction research incorporates themes from Cancer research, Prostate, Kinase and Small interfering RNA. His Cell cycle research focuses on Cell culture and how it connects with Gene, Gene targeting and Cell growth.
John M. Sedivy focuses on Cell biology, Molecular biology, Senescence, Genetics and Gene. His biological study spans a wide range of topics, including Cell cycle and DNA damage. His research in Cell cycle intersects with topics in Cell culture and Cell growth.
His research integrates issues of Transfection and Ectopic expression in his study of Molecular biology. John M. Sedivy interconnects Cell cycle checkpoint, Somatic cell, Chromatin, Telomere and Epigenetics in the investigation of issues within Senescence. In Signal transduction, John M. Sedivy works on issues like Cancer research, which are connected to Gene knockdown, Immunology and Apoptosis.
Cell biology, Senescence, DNA damage, Cell aging and Epigenetics are his primary areas of study. He combines Cell biology and Glutamine in his research. His Senescence research is multidisciplinary, incorporating elements of Molecular biology, Cell cycle, Gene and Infarcted heart.
His DNA damage study results in a more complete grasp of DNA. His research investigates the connection with Cell aging and areas like Telomere which intersect with concerns in Rotenone, In vitro, Gene expression profiling and Phenotype. His Epigenetics study incorporates themes from Cancer research, DNA methylation, Epigenome, Chromatin and Histone.
His primary scientific interests are in Cell biology, Senescence, Chromatin, Cancer research and Retrotransposon. The study incorporates disciplines such as Inflammation, Interferon, Transcription factor and DNA damage in addition to Cell biology. His Senescence study combines topics in areas such as Cell cycle checkpoint, Developmental biology, Senolytic and Mitochondrion.
His Chromatin research incorporates elements of Cell, Cell aging, Computational biology, Regulation of gene expression and Epigenetics. John M. Sedivy combines subjects such as Protein kinase B, Epigenomics, DNA methylation, Transcriptome and Molecular biology with his study of Cancer research. His studies examine the connections between Retrotransposon and genetics, as well as such issues in Human genome, with regards to Repeated sequence, Genome evolution and Genome instability.
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Requirement for p53 and p21 to Sustain G2 Arrest After DNA Damage
Fred Bunz;A. Dutriaux;C. Lengauer;T. Waldman.
Mitochondrial DNA Mutations, Oxidative Stress, and Apoptosis in Mammalian Aging
G. C. Kujoth;A. Hiona;T. D. Pugh;S. Someya.
Telomere Shortening Triggers Senescence of Human Cells through a Pathway Involving ATM, p53, and p21CIP1, but Not p16INK4a
Utz Herbig;Wendy A Jobling;Benjamin P.C Chen;David J Chen.
Molecular Cell (2004)
Cellular senescence in aging primates.
Utz Herbig;Mark Ferreira;Laura Condel;Dee Carey.
Bypass of Senescence After Disruption of p21CIP1/WAF1 Gene in Normal Diploid Human Fibroblasts
Jeremy P. Brown;Wenyi Wei;John M. Sedivy.
Suppression of Raf-1 kinase activity and MAP kinase signalling by RKIP
Kam Yeung;Thomas Seitz;Shengfeng Li;Petra Janosch.
Dissociation among in vitro telomerase activity, telomere maintenance, and cellular immortalization
Christopher M. Counter;William C. Hahn;Wenyi Wei;Stephanie Dickinson Caddle.
Proceedings of the National Academy of Sciences of the United States of America (1998)
Accumulation of senescent cells in mitotic tissue of aging primates.
Jessie C. Jeyapalan;Mark Ferreira;John M. Sedivy;Utz Herbig.
Mechanisms of Ageing and Development (2007)
Stat3-mediated Myc expression is required for Src transformation and PDGF-induced mitogenesis
Tammy Bowman;Martin A. Broome;Dominic Sinibaldi;Walker Wharton.
Proceedings of the National Academy of Sciences of the United States of America (2001)
Phenotypes of c-Myc-deficient rat fibroblasts isolated by targeted homologous recombination
Maria K. Mateyak;Alvaro J. Obaya;Susumu Adachi;John M. Sedivy.
Cell Growth & Differentiation (1997)
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