His primary scientific interests are in DNA damage, Genetics, DNA repair, Molecular biology and Cell cycle checkpoint. Anton Gartner has researched DNA damage in several fields, including Transcription factor and Gene. The Genetics study combines topics in areas such as NAD+ kinase and Sirtuin.
His DNA repair research includes elements of Phenotype, Model organism and Genome instability. The study incorporates disciplines such as Synapsis, Prophase and Synaptonemal complex in addition to Molecular biology. His Cell cycle checkpoint research incorporates themes from Origin of replication and Cell biology.
His scientific interests lie mostly in Cell biology, Genetics, DNA damage, Caenorhabditis elegans and DNA repair. His work deals with themes such as Chromatin and Apoptosis, Cell cycle, Cell cycle checkpoint, which intersect with Cell biology. His DNA damage research is multidisciplinary, relying on both G2-M DNA damage checkpoint, Transcription factor, Germline, Molecular biology and Germ cell.
His research in Molecular biology intersects with topics in Regulation of gene expression and DNA ligase. His Caenorhabditis elegans study combines topics in areas such as Oxidative stress, Dopaminergic, Proteomics and Programmed cell death. His DNA repair research is multidisciplinary, incorporating elements of Mutation, Mutagenesis and Homologous recombination.
His primary areas of investigation include Genetics, DNA repair, Cell biology, DNA and DNA damage. His DNA repair study frequently links to other fields, such as Homologous recombination. His biological study spans a wide range of topics, including Chromatin, Caenorhabditis elegans, Chromosome segregation and Enzyme.
His Caenorhabditis elegans study integrates concerns from other disciplines, such as Oxidative stress and Dopaminergic. His work focuses on many connections between DNA and other disciplines, such as Mutation rate, that overlap with his field of interest in Point mutation and Whole genome sequencing. In his work, Hsp70 and Carcinogenesis is strongly intertwined with APAF1, which is a subfield of DNA damage.
His main research concerns Mutation, Cell biology, DNA repair, DNA damage and Genetics. His research integrates issues of Genome and Methylation in his study of Mutation. His Cell biology research integrates issues from Ubiquitin, Homologous recombination, Chromosome segregation, Chromatin and APAF1.
His DNA repair research incorporates elements of Whole genome sequencing, Mutation rate and Point mutation. His DNA damage study incorporates themes from Apoptosis, NEDD8, Chaperone, Enzyme and Hsp70. His DNA sequencing, Gene knockout and DNA mismatch repair study in the realm of Genetics interacts with subjects such as CpG site and Somatic hypermutation.
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A conserved checkpoint pathway mediates DNA damage--induced apoptosis and cell cycle arrest in C. elegans.
Anton Gartner;Stuart Milstein;Stuart Milstein;Shawn Ahmed;Jonathan Hodgkin.
Molecular Cell (2000)
FAR1 links the signal transduction pathway to the cell cycle machinery in yeast
Matthias Peter;Anton Gartner;Joe Horecka;Gustav Ammerer.
Excess Mcm2–7 license dormant origins of replication that can be used under conditions of replicative stress
Anna M. Woodward;Thomas Göhler;M. Gloria Luciani;Maren Oehlmann.
Journal of Cell Biology (2006)
The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis
Björn Schumacher;Kay Hofmann;Simon Boulton;Anton Gartner.
Current Biology (2001)
Signal transduction in Saccharomyces cerevisiae requires tyrosine and threonine phosphorylation of FUS3 and KSS1.
Anton Gartner;Kim Nasmyth;Gustav Ammerer.
Genes & Development (1992)
Identification of KIAA1018/FAN1, a DNA Repair Nuclease Recruited to DNA Damage by Monoubiquitinated FANCD2
Craig MacKay;Anne-Cécile Déclais;Cecilia Lundin;Ana Agostinho.
Combined Functional Genomic Maps of the C. elegans DNA Damage Response
Simon J. Boulton;Anton Gartner;Jérôme Reboul;Philippe Vaglio.
MSG5, a novel protein phosphatase promotes adaptation to pheromone response in S. cerevisiae.
Kentaro Doi;Anton Gartner;Gustav Ammerer;Beverly Errede.
The EMBO Journal (1994)
Combined hereditary and somatic mutations of replication error repair genes result in rapid onset of ultra-hypermutated cancers.
Adam Shlien;Brittany B Campbell;Richard de Borja;Ludmil B Alexandrov.
Nature Genetics (2015)
Caenorhabditis elegans HUS-1 is a DNA damage checkpoint protein required for genome stability and EGL-1-mediated apoptosis
E. R. Hofmann;E. R. Hofmann;S. Milstein;S. Milstein;S. Milstein;S. J. Boulton;M. J. Ye.
Current Biology (2002)
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