What is he best known for?
The fields of study he is best known for:
His primary scientific interests are in DNA repair, Molecular biology, Genetics, Nucleotide excision repair and Xeroderma pigmentosum.
He interconnects Complementation and Ubiquitin in the investigation of issues within DNA repair.
The concepts of his Molecular biology study are interwoven with issues in Homologous recombination, Carcinogenesis, Biochemistry, Chromosome and Gene product.
His work on Gene, Genetic linkage, Phenotype and Chromosomal translocation as part of general Genetics study is frequently linked to Transcription, therefore connecting diverse disciplines of science.
His Nucleotide excision repair research is multidisciplinary, relying on both Pyrimidine dimer, RNA polymerase II and Helicase.
Xeroderma pigmentosum is the subject of his research, which falls under DNA damage.
His most cited work include:
- A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia (1169 citations)
- Mammalian Cry1 and Cry2 are essential for maintenance of circadian rhythms. (1093 citations)
- Xeroderma Pigmentosum Group C Protein Complex Is the Initiator of Global Genome Nucleotide Excision Repair (759 citations)
What are the main themes of his work throughout his whole career to date?
His primary areas of investigation include Molecular biology, Genetics, DNA repair, Xeroderma pigmentosum and Gene.
Dirk Bootsma has included themes like DNA, Chinese hamster, Nucleotide excision repair and Chromosome, Chromosome 22 in his Molecular biology study.
His research in Chromosome tackles topics such as Chromosomal translocation which are related to areas like Chromosome 9.
As part of his studies on Genetics, Dirk Bootsma often connects relevant areas like Cancer research.
His DNA repair research incorporates themes from Mutation and DNA synthesis.
His biological study spans a wide range of topics, including Complementation and Complementation group.
He most often published in these fields:
- Molecular biology (49.21%)
- Genetics (45.03%)
- DNA repair (33.51%)
What were the highlights of his more recent work (between 1996-2009)?
- Nucleotide excision repair (28.80%)
- DNA repair (33.51%)
- Genetics (45.03%)
In recent papers he was focusing on the following fields of study:
Dirk Bootsma focuses on Nucleotide excision repair, DNA repair, Genetics, Molecular biology and Xeroderma pigmentosum.
His Nucleotide excision repair study integrates concerns from other disciplines, such as Carcinogenesis, Cell biology and Pyrimidine dimer.
His DNA repair course of study focuses on RNA polymerase II and Transcription factor.
His research links Enzyme with Genetics.
His studies in Molecular biology integrate themes in fields like Homologous recombination, General transcription factor and DNA replication.
His Xeroderma pigmentosum research includes elements of Chiasma and DNA repair synthesis.
Between 1996 and 2009, his most popular works were:
- Mammalian Cry1 and Cry2 are essential for maintenance of circadian rhythms. (1093 citations)
- Xeroderma Pigmentosum Group C Protein Complex Is the Initiator of Global Genome Nucleotide Excision Repair (759 citations)
- Disruption of Mouse RAD54 Reduces Ionizing Radiation Resistance and Homologous Recombination (403 citations)
In his most recent research, the most cited papers focused on:
Dirk Bootsma mainly focuses on Molecular biology, Nucleotide excision repair, DNA damage, Genetics and Homologous recombination.
In his work, Transcription factor II H, ERCC6 and Cockayne syndrome is strongly intertwined with Carcinogenesis, which is a subfield of Molecular biology.
His Nucleotide excision repair study is concerned with the field of DNA repair as a whole.
His DNA repair research is multidisciplinary, incorporating elements of RNA polymerase II and General transcription factor.
His DNA damage research includes themes of Gene targeting and Saccharomyces cerevisiae.
His study in the field of Photolyase also crosses realms of ARNTL Transcription Factors, Oscillating gene, Translation and Cryptochrome-1.
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