What is she best known for?
The fields of study she is best known for:
Laura J. Niedernhofer spends much of her time researching DNA repair, Nucleotide excision repair, DNA damage, Cancer research and Progeria.
Her DNA repair study frequently draws connections between adjacent fields such as Cell aging.
Her study in Nucleotide excision repair is interdisciplinary in nature, drawing from both Molecular biology, Genome instability and Homologous recombination.
Her research integrates issues of Cell biology and Longevity in her study of DNA damage.
Her Cancer research research incorporates themes from Apoptosis and Senolytic.
Her Progeria study combines topics in areas such as Endocrinology, Senescence, Internal medicine, Ageing and Progeroid syndromes.
Her most cited work include:
- The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs (759 citations)
- A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis (538 citations)
- Senolytics improve physical function and increase lifespan in old age (517 citations)
What are the main themes of her work throughout her whole career to date?
The scientist’s investigation covers issues in DNA repair, DNA damage, Cell biology, Senescence and Nucleotide excision repair.
Her DNA repair research is multidisciplinary, relying on both Molecular biology, Cancer research, Progeria and Genome instability.
Her research in DNA damage intersects with topics in Oxidative stress, Internal medicine and NF-κB.
In her study, Pathology, Tobacco smoke, Matrix metalloproteinase and Homeostasis is strongly linked to Intervertebral disc, which falls under the umbrella field of Cell biology.
Her work in Senescence addresses subjects such as Senolytic, which are connected to disciplines such as Apoptosis.
Her work deals with themes such as Xeroderma pigmentosum, Homologous recombination and Bioinformatics, which intersect with Nucleotide excision repair.
She most often published in these fields:
- DNA repair (38.97%)
- DNA damage (38.97%)
- Cell biology (37.95%)
What were the highlights of her more recent work (between 2018-2021)?
- Senescence (35.90%)
- Cell biology (37.95%)
- DNA damage (38.97%)
In recent papers she was focusing on the following fields of study:
Laura J. Niedernhofer mostly deals with Senescence, Cell biology, DNA damage, Progeria and Phenotype.
Her Senescence study incorporates themes from Cell, Senolytic, Stem cell and Bioinformatics.
Her Cell biology research is multidisciplinary, incorporating perspectives in Oxidative stress, Adult stem cell, Transcription factor, Programmed cell death and In vivo.
Her DNA damage study combines topics from a wide range of disciplines, such as NF-κB, Signal transduction, Endogeny, DNA repair and Kinase.
Laura J. Niedernhofer is interested in Genotoxic Stress, which is a field of DNA repair.
Her Progeria research includes elements of Lamin, Cell growth, Progenitor cell, Progerin and Nuclear lamina.
Between 2018 and 2021, her most popular works were:
- Cellular Senescence: Defining a Path Forward (329 citations)
- Systemic clearance of p16INK4a -positive senescent cells mitigates age-associated intervertebral disc degeneration (43 citations)
- Tissue specificity of senescent cell accumulation during physiologic and accelerated aging of mice. (33 citations)
In her most recent research, the most cited papers focused on:
Senescence, Cell biology, DNA damage, Health span and Phenotype are her primary areas of study.
Her biological study spans a wide range of topics, including Senolytic, Model organism, mTORC1, Tissue homeostasis and Signal transduction.
Her Senolytic research is multidisciplinary, incorporating elements of Cell, Clinical trial, Bioinformatics, Senescent cell and Disease.
Her studies deal with areas such as Oxidative stress, Progeria, Apoptosis and Adult stem cell as well as Cell biology.
The concepts of her Progeria study are interwoven with issues in Lamin, Cell growth, DNA repair, Genotoxic Stress and Messenger RNA.
Laura J. Niedernhofer has researched DNA damage in several fields, including Transcription factor, NF-κB, Stem cell, Mediator and Kinase.
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