What is he best known for?
The fields of study he is best known for:
His main research concerns Tumor necrosis factor alpha, Cell biology, Receptor, Signal transduction and Apoptosis.
His Tumor necrosis factor alpha research incorporates elements of Cytokine, Cell culture, Immune system and Programmed cell death.
His study looks at the relationship between Programmed cell death and fields such as NFKB1, as well as how they intersect with chemical problems.
His work on NF-κB is typically connected to Context as part of general Cell biology study, connecting several disciplines of science.
The study incorporates disciplines such as Molecular biology, Stimulation and Antigen in addition to Receptor.
He studied Signal transduction and Cancer research that intersect with Caspase 8.
His most cited work include:
- Tumor necrosis factor signaling. (1836 citations)
- THE TRANSMEMBRANE FORM OF TUMOR NECROSIS FACTOR IS THE PRIME ACTIVATING LIGAND OF THE 80 KDA TUMOR NECROSIS FACTOR RECEPTOR (1112 citations)
- NF-kappaB inducers upregulate cFLIP, a cycloheximide-sensitive inhibitor of death receptor signaling (547 citations)
What are the main themes of his work throughout his whole career to date?
Peter Scheurich mainly investigates Tumor necrosis factor alpha, Cell biology, Receptor, Apoptosis and Signal transduction.
The concepts of his Tumor necrosis factor alpha study are interwoven with issues in Molecular biology, Cancer research, Antibody and Cytokine.
He combines subjects such as Cell, Fas ligand, Fas receptor, FADD and Death domain with his study of Cell biology.
His Endocrinology research extends to Receptor, which is thematically connected.
His work carried out in the field of Apoptosis brings together such families of science as Crosstalk and Signalling.
His Signal transduction research is multidisciplinary, incorporating perspectives in Kinase, Protein kinase A, Downregulation and upregulation, Transcription factor and Tumor Necrosis Factor Receptor-Associated Factors.
He most often published in these fields:
- Tumor necrosis factor alpha (46.05%)
- Cell biology (41.45%)
- Receptor (36.18%)
What were the highlights of his more recent work (between 2006-2021)?
- Cell biology (41.45%)
- Tumor necrosis factor alpha (46.05%)
- Apoptosis (26.32%)
In recent papers he was focusing on the following fields of study:
Peter Scheurich mostly deals with Cell biology, Tumor necrosis factor alpha, Apoptosis, Signal transduction and Receptor.
His Cell biology study combines topics from a wide range of disciplines, such as Fas ligand, Programmed cell death, Death domain and Immune system.
His Tumor necrosis factor alpha study improves the overall literature in Immunology.
His Apoptosis study incorporates themes from Cell, Downregulation and upregulation and Crosstalk.
His Signal transduction research includes elements of Transcription factor, Neurodegeneration, Molecular biology, FADD and Internalization.
His Receptor research entails a greater understanding of Biochemistry.
Between 2006 and 2021, his most popular works were:
- TNFR1‐induced activation of the classical NF‐κB pathway (172 citations)
- ON/OFF and Beyond - A Boolean Model of Apoptosis (147 citations)
- Single-Chain TNF, a TNF Derivative with Enhanced Stability and Antitumoral Activity (82 citations)
In his most recent research, the most cited papers focused on:
His primary areas of investigation include Tumor necrosis factor alpha, Cell biology, Signal transduction, Immunology and Receptor.
His Tumor necrosis factor alpha research is multidisciplinary, incorporating elements of Humanized antibody, Tissue homeostasis, Cytokine and Fragment crystallizable region.
His studies in Cell biology integrate themes in fields like Inhibitor of apoptosis, Apoptosis, Programmed cell death and TRADD.
He has researched Apoptosis in several fields, including Transcription factor and Neuroscience.
His Signal transduction study is concerned with Biochemistry in general.
The various areas that Peter Scheurich examines in his Receptor study include Extracellular, Cell membrane and Binding site.
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