What is she best known for?
The fields of study she is best known for:
Karlene A. Cimprich focuses on DNA repair, DNA damage, DNA replication, Genetics and Ataxia telangiectasia and Rad3 related.
Her DNA repair research incorporates themes from G2-M DNA damage checkpoint, Replication protein A, Genome instability and Molecular biology.
Her DNA damage research includes themes of Histone, Genome, Genomics and Computational biology.
Her work carried out in the field of DNA replication brings together such families of science as CHEK1 and Cell biology.
In the subject of general Genetics, her work in Pre-replication complex, Replication fork protection and DNA re-replication is often linked to Context and Somatic hypermutation, thereby combining diverse domains of study.
Her work deals with themes such as Regulator, Ataxia Telangiectasia Mutated Proteins and DNA replication checkpoint, which intersect with Ataxia telangiectasia and Rad3 related.
Her most cited work include:
- Activation of the ATM Kinase by Ionizing Radiation and Phosphorylation of p53 (1780 citations)
- ATR: an essential regulator of genome integrity (1327 citations)
- Causes and consequences of replication stress. (959 citations)
What are the main themes of her work throughout her whole career to date?
Her scientific interests lie mostly in Cell biology, DNA damage, DNA replication, DNA repair and Genetics.
Her studies in Cell biology integrate themes in fields like Cell cycle checkpoint, Cell cycle, Eukaryotic DNA replication, Xenopus and Biochemistry.
Her study in DNA damage is interdisciplinary in nature, drawing from both G2-M DNA damage checkpoint and CHEK1.
Her DNA replication study combines topics from a wide range of disciplines, such as Cilium, Cyclin-dependent kinase and DNA synthesis.
Her DNA repair research is multidisciplinary, relying on both Rad50 and Ataxia telangiectasia and Rad3 related.
Her studies deal with areas such as Ataxia Telangiectasia Mutated Proteins and DNA replication checkpoint as well as Ataxia telangiectasia and Rad3 related.
She most often published in these fields:
- Cell biology (57.75%)
- DNA damage (52.11%)
- DNA replication (40.85%)
What were the highlights of her more recent work (between 2017-2021)?
- Cell biology (57.75%)
- DNA damage (52.11%)
- DNA replication (40.85%)
In recent papers she was focusing on the following fields of study:
The scientist’s investigation covers issues in Cell biology, DNA damage, DNA replication, Transcription and Genome instability.
Much of her study explores Cell biology relationship to Cell cycle.
Particularly relevant to Replication fork reversal is her body of work in DNA replication.
Her Transcription study deals with Computational biology intersecting with Nucleic acid and DNA.
Her Genome instability study combines topics in areas such as Carcinogenesis, REV1 and DNA repair.
The various areas that she examines in her DNA repair study include Base pair, Peroxisome proliferator-activated receptor, Regulation of gene expression and Homeostasis.
Between 2017 and 2021, her most popular works were:
- R-Loops as Cellular Regulators and Genomic Threats. (160 citations)
- An intrinsic S/G2 checkpoint enforced by ATR (106 citations)
- HLTF Promotes Fork Reversal, Limiting Replication Stress Resistance and Preventing Multiple Mechanisms of Unrestrained DNA Synthesis. (22 citations)
In her most recent research, the most cited papers focused on:
Her primary scientific interests are in DNA damage, Cell biology, DNA replication, Genome instability and R-loop.
Her study in Cell cycle extends to DNA damage with its themes.
Karlene A. Cimprich combines subjects such as Metaphase, Mitosis and Chromosome segregation with her study of Cell cycle.
Her R-loop study integrates concerns from other disciplines, such as Computational biology, Base pair, DNA repair, Regulation of gene expression and Transcription.
Many of her studies involve connections with topics such as DNA and Computational biology.
Her research in Replication fork reversal intersects with topics in Carcinogenesis, REV1 and DNA synthesis.
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