D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 53 Citations 11,772 99 World Ranking 11466 National Ranking 4929

Overview

What is she best known for?

The fields of study she is best known for:

  • Gene
  • DNA
  • Genetics

Her primary areas of study are C9orf72 Protein, C9orf72, Molecular biology, Amyotrophic lateral sclerosis and Trinucleotide repeat expansion. Her research in C9orf72 Protein focuses on subjects like Translation, which are connected to Plasma protein binding, Small molecule and Gene expression. Her C9orf72 research is multidisciplinary, relying on both RNA and DNA Repeat Expansion.

Her research integrates issues of Ran, Histone, Mitochondrion and Ectopic expression in her study of Molecular biology. Her Amyotrophic lateral sclerosis research focuses on Frontotemporal dementia and how it connects with Neurodegeneration and Astrogliosis. Her studies deal with areas such as Histone H3, Epigenetics, Histone methylation, DNA methylation and Chromatin immunoprecipitation as well as Trinucleotide repeat expansion.

Her most cited work include:

  • Unconventional Translation of C9ORF72 GGGGCC Expansion Generates Insoluble Polypeptides Specific to c9FTD/ALS (720 citations)
  • Aberrant Cleavage of TDP-43 Enhances Aggregation and Cellular Toxicity (422 citations)
  • Wild-Type Human TDP-43 Expression Causes TDP-43 Phosphorylation, Mitochondrial Aggregation, Motor Deficits, and Early Mortality in Transgenic Mice (364 citations)

What are the main themes of her work throughout her whole career to date?

C9orf72, Trinucleotide repeat expansion, Amyotrophic lateral sclerosis, Frontotemporal dementia and RNA are her primary areas of study. Her C9orf72 research is multidisciplinary, incorporating elements of C9orf72 Protein, Neurodegeneration and Cell biology. The Trinucleotide repeat expansion study combines topics in areas such as Molecular biology, Epigenetics, Computational biology and Bioinformatics.

Her study focuses on the intersection of Amyotrophic lateral sclerosis and fields such as C9orf72 Gene with connections in the field of Transcriptome. Tania F. Gendron has researched Frontotemporal dementia in several fields, including Phenotype and Genetic testing. Her RNA research includes themes of Gene knockdown, Small molecule and Pathogenesis.

She most often published in these fields:

  • C9orf72 (56.19%)
  • Trinucleotide repeat expansion (38.10%)
  • Amyotrophic lateral sclerosis (35.24%)

What were the highlights of her more recent work (between 2019-2021)?

  • Trinucleotide repeat expansion (38.10%)
  • C9orf72 (56.19%)
  • Amyotrophic lateral sclerosis (35.24%)

In recent papers she was focusing on the following fields of study:

Her main research concerns Trinucleotide repeat expansion, C9orf72, Amyotrophic lateral sclerosis, Neurodegeneration and RNA. Her Trinucleotide repeat expansion study necessitates a more in-depth grasp of Genetics. Her study on C9orf72 is mostly dedicated to connecting different topics, such as Cell biology.

Her Amyotrophic lateral sclerosis study contributes to a more complete understanding of Pathology. Her work carried out in the field of Neurodegeneration brings together such families of science as Ran, Spinocerebellar ataxia, Translation and Mutation. Her RNA study integrates concerns from other disciplines, such as Proteome and Frontotemporal dementia, TARDBP.

Between 2019 and 2021, her most popular works were:

  • Reduced C9ORF72 function exacerbates gain of toxicity from ALS/FTD-causing repeat expansion in C9orf72. (44 citations)
  • Nucleocytoplasmic Proteomic Analysis Uncovers eRF1 and Nonsense-Mediated Decay as Modifiers of ALS/FTD C9orf72 Toxicity. (25 citations)
  • C9orf72 poly(GR) aggregation induces TDP-43 proteinopathy (15 citations)

In her most recent research, the most cited papers focused on:

  • Gene
  • DNA
  • Gene expression

Tania F. Gendron spends much of her time researching C9orf72, Neurodegeneration, Cell biology, Amyotrophic lateral sclerosis and Trinucleotide repeat expansion. The study incorporates disciplines such as RNA and Nonsense-mediated decay in addition to C9orf72. Her study in Neurodegeneration is interdisciplinary in nature, drawing from both Translation, Spinocerebellar ataxia, Protein aggregation and Frontotemporal dementia.

Her work deals with themes such as Proteome, Endogeny, C9orf72 Protein, Genetically modified mouse and Neuroscience, which intersect with Cell biology. Her studies link Ran with Amyotrophic lateral sclerosis. Her Trinucleotide repeat expansion study combines topics in areas such as Double Strand Break Repair, DNA damage, DNA and Homologous recombination.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Unconventional Translation of C9ORF72 GGGGCC Expansion Generates Insoluble Polypeptides Specific to c9FTD/ALS

Peter E.A. Ash;Kevin F. Bieniek;Tania F. Gendron;Thomas Caulfield.
Neuron (2013)

1005 Citations

Aberrant Cleavage of TDP-43 Enhances Aggregation and Cellular Toxicity

Yong Jie Zhang;Ya Fei Xu;Casey Cook;Tania F. Gendron.
Proceedings of the National Academy of Sciences of the United States of America (2009)

602 Citations

Wild-Type Human TDP-43 Expression Causes TDP-43 Phosphorylation, Mitochondrial Aggregation, Motor Deficits, and Early Mortality in Transgenic Mice

Ya Fei Xu;Tania F. Gendron;Yong Jie Zhang;Wen Lang Lin.
The Journal of Neuroscience (2010)

525 Citations

Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS

Tania F Gendron;Kevin F. Bieniek;Yong-Jie Zhang;Karen Jansen-West.
Acta Neuropathologica (2013)

497 Citations

The role of tau in neurodegeneration

Tania F Gendron;Leonard Petrucelli.
Molecular Neurodegeneration (2009)

487 Citations

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

Jie Jiang;Jie Jiang;Qiang Zhu;Tania F. Gendron;Shahram Saberi.
Neuron (2016)

426 Citations

C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits

Jeannie Chew;Tania F. Gendron;Mercedes Prudencio;Hiroki Sasaguri.
Science (2015)

375 Citations

Modeling key pathological features of frontotemporal dementia with C9ORF72 repeat expansion in iPSC-derived human neurons

Sandra Almeida;Eduardo Gascon;Hélène Tran;Hsin Jung Chou.
Acta Neuropathologica (2013)

325 Citations

Discovery of a Biomarker and Lead Small Molecules to Target r(GGGGCC)-Associated Defects in c9FTD/ALS

Zhaoming Su;Yongjie Zhang;Tania F. Gendron;Peter O. Bauer.
Neuron (2014)

319 Citations

Distinct brain transcriptome profiles in C9orf72-associated and sporadic ALS

Mercedes Prudencio;Veronique V Belzil;Ranjan Batra;Christian A Ross.
Nature Neuroscience (2015)

306 Citations

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