What is he best known for?
The fields of study he is best known for:
His scientific interests lie mostly in Cell biology, DNA damage, Cell cycle, Cancer research and Molecular biology.
His research on Cell biology focuses in particular on Signal transduction.
Michael B. Kastan interconnects CHEK1, MDC1, DNA repair and Phosphorylation in the investigation of issues within DNA damage.
His work deals with themes such as Carcinogenesis and Mutation, which intersect with Cell cycle.
His studies deal with areas such as Ataxia-telangiectasia, c-Raf, Ataxia Telangiectasia Mutated Proteins, Cyclin-dependent kinase 4 and ASK1 as well as Cancer research.
His Molecular biology research includes elements of Translation, Messenger RNA, Untranslated region and Downregulation and upregulation.
His most cited work include:
- Participation of p53 Protein in the Cellular Response to DNA Damage (3461 citations)
- DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation (2832 citations)
- A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia (2773 citations)
What are the main themes of his work throughout his whole career to date?
Michael B. Kastan spends much of his time researching DNA damage, Cell biology, Cancer research, Molecular biology and Cell cycle.
His biological study spans a wide range of topics, including Gene, DNA repair, Kinase and Phosphorylation.
His Cell biology study which covers Autophagy that intersects with mTORC1.
His research in Cancer research intersects with topics in Cancer, Apoptosis, Ataxia-telangiectasia, Signal transduction and Tumor suppressor gene.
His Molecular biology research is multidisciplinary, incorporating perspectives in Cell culture, Progenitor cell, Translation, Messenger RNA and Oligonucleotide.
His Cell cycle research is multidisciplinary, relying on both Carcinogenesis, Mutation and DNA synthesis.
He most often published in these fields:
- DNA damage (39.91%)
- Cell biology (40.38%)
- Cancer research (31.92%)
What were the highlights of his more recent work (between 2012-2021)?
- Cell biology (40.38%)
- DNA damage (39.91%)
- Cancer research (31.92%)
In recent papers he was focusing on the following fields of study:
Michael B. Kastan focuses on Cell biology, DNA damage, Cancer research, DNA repair and DNA.
His Cell biology study incorporates themes from Peroxisome, Histone and Autophagy.
Michael B. Kastan has included themes like Gene and Alternative splicing in his DNA damage study.
His work carried out in the field of Cancer research brings together such families of science as Cancer, Immunology and Regulatory Pathway.
His research integrates issues of Molecular biology, Rad50, Homologous recombination and MDC1 in his study of DNA repair.
His DNA study combines topics from a wide range of disciplines, such as Cell, Gene mutation, Caspase, Kinase and Antitumor activity.
Between 2012 and 2021, his most popular works were:
- ATM functions at the peroxisome to induce pexophagy in response to ROS (219 citations)
- Strategies for optimizing the response of cancer and normal tissues to radiation. (214 citations)
- The DNA Damage Response: Implications for Tumor Responses to Radiation and Chemotherapy (197 citations)
In his most recent research, the most cited papers focused on:
His primary scientific interests are in Cell biology, Histone, Nucleotide excision repair, Replication protein A and Cancer research.
His Cell biology research incorporates themes from Peroxisome and Autophagy.
The study incorporates disciplines such as Homology directed repair, Double Strand Break Repair and DNA repair protein XRCC4 in addition to Histone.
His studies in Nucleotide excision repair integrate themes in fields like Eukaryotic DNA replication, Histone code, Chromatin, Chromatin remodeling and Molecular biology.
His Cancer research research integrates issues from MRE11 Homologue Protein, Synthetic lethality, Chemotherapy, DNA damage and Homologous recombination.
The concepts of his DNA damage study are interwoven with issues in MDC1, DNA repair, Ataxia Telangiectasia Mutated Proteins, Rad50 and MRN complex.
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