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
Genetics and Molecular Biology D-index 68 Citations 12,973 119 World Ranking 1669 National Ranking 854

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Internal medicine

His scientific interests lie mostly in Mitochondrion, Cell biology, Molecular biology, Mitochondrial DNA and Amyotrophic lateral sclerosis. Giovanni Manfredi has researched Mitochondrion in several fields, including Oxidative phosphorylation, ATP synthase and SOD1. His research in SOD1 intersects with topics in Genetically modified mouse and Cytosol.

His work in Cell biology covers topics such as mitochondrial fusion which are related to areas like Human mitochondrial genetics, Inner mitochondrial membrane and Mitochondrial fission. His work in Mitochondrial DNA addresses issues such as Mutation, which are connected to fields such as Alpha-synuclein, Parkinson's disease, Proteasome and Kinase. The Amyotrophic lateral sclerosis study combines topics in areas such as Excitotoxicity, Motor neuron, Neuroscience and Mitochondrial transport.

His most cited work include:

  • Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice. (489 citations)
  • Cyclic AMP produced inside mitochondria regulates oxidative phosphorylation (350 citations)
  • Neuronal degeneration and mitochondrial dysfunction (299 citations)

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

The scientist’s investigation covers issues in Mitochondrion, Cell biology, Mitochondrial DNA, Biochemistry and Molecular biology. His Mitochondrion research is multidisciplinary, relying on both Oxidative phosphorylation, Amyotrophic lateral sclerosis, SOD1 and Neurodegeneration. His biological study spans a wide range of topics, including Autophagy, Downregulation and upregulation and Neuroprotection.

His Mitochondrial DNA study introduces a deeper knowledge of Genetics. His work on ATP synthase, Phosphorylation, Cytochrome c oxidase and Adenosine triphosphate as part of his general Biochemistry study is frequently connected to Soluble adenylyl cyclase, thereby bridging the divide between different branches of science. Giovanni Manfredi interconnects Mutation and Myopathy in the investigation of issues within Molecular biology.

He most often published in these fields:

  • Mitochondrion (43.11%)
  • Cell biology (29.78%)
  • Mitochondrial DNA (18.22%)

What were the highlights of his more recent work (between 2018-2021)?

  • Cell biology (29.78%)
  • SOD1 (12.44%)
  • Amyotrophic lateral sclerosis (12.44%)

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

His primary areas of study are Cell biology, SOD1, Amyotrophic lateral sclerosis, Internal medicine and Downregulation and upregulation. His Cell biology research integrates issues from Neurodegeneration and Programmed cell death. His work in SOD1 tackles topics such as Autophagy which are related to areas like Binding protein and TARDBP.

His Amyotrophic lateral sclerosis research includes elements of Degeneration, Neuroscience and Golgi apparatus. Giovanni Manfredi has included themes like Cancer research, Oxidative phosphorylation, Cysteine metabolism, Respiratory chain and Nitrosylation in his Downregulation and upregulation study. His research in the fields of Mitochondrial transport overlaps with other disciplines such as Mitochondrial intermembrane space.

Between 2018 and 2021, his most popular works were:

  • Lipid Deprivation Induces a Stable, Naive-to-Primed Intermediate State of Pluripotency in Human PSCs. (39 citations)
  • ALS/FTD mutant CHCHD10 mice reveal a tissue-specific toxic gain-of-function and mitochondrial stress response. (26 citations)
  • ALS-FTLD-linked mutations of SQSTM1/p62 disrupt selective autophagy and NFE2L2/NRF2 anti-oxidative stress pathway (21 citations)

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

  • Gene
  • Enzyme
  • Internal medicine

Giovanni Manfredi mainly investigates Cell biology, Reperfusion injury, Mitochondrial Complex I, Endocrinology and Internal medicine. His Cell biology study incorporates themes from Sequestosome 1, Growth factor and SOD1. His research investigates the link between SOD1 and topics such as Axoplasmic transport that cross with problems in Mitochondrion.

His Mitochondrion research includes themes of Mitophagy and Metabolism. In his research, Reactive oxygen species is intimately related to Neurological disability, which falls under the overarching field of Endocrinology. His work carried out in the field of Internal medicine brings together such families of science as Programmed cell death, Mitochondrial permeability transition pore and Intracellular.

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

Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice.

Marina Mattiazzi;Marilena D'Aurelio;Carl D. Gajewski;Katherine Martushova.
Journal of Biological Chemistry (2002)

643 Citations

Cyclic AMP produced inside mitochondria regulates oxidative phosphorylation

Rebeca Acin-Perez;Eric Salazar;Margarita Kamenetsky;Jochen Buck.
Cell Metabolism (2009)

450 Citations

Neuronal degeneration and mitochondrial dysfunction

Eric A. Schon;Giovanni Manfredi.
Journal of Clinical Investigation (2003)

430 Citations

Mitochondrial DNA and respiratory chain function in spinal cords of ALS patients

Falk R. Wiedemann;Giovanni Manfredi;Christian Mawrin;M. Flint Beal.
Journal of Neurochemistry (2002)

359 Citations

Positive Contribution of Pathogenic Mutations in the Mitochondrial Genome to the Promotion of Cancer by Prevention from Apoptosis

Yujiro Shidara;Kumi Yamagata;Takashi Kanamori;Kazutoshi Nakano.
Cancer Research (2005)

307 Citations

Proteolytic Cleavage of Opa1 Stimulates Mitochondrial Inner Membrane Fusion and Couples Fusion to Oxidative Phosphorylation

Prashant Mishra;Valerio Carelli;Giovanni Manfredi;David C. Chan.
Cell Metabolism (2014)

302 Citations

Rescue of a deficiency in ATP synthesis by transfer of MTATP6, a mitochondrial DNA-encoded gene, to the nucleus.

Giovanni Manfredi;Jin Fu;Jin Fu;Joseline Ojaimi;James E. Sadlock;James E. Sadlock.
Nature Genetics (2002)

295 Citations

Parkin overexpression selects against a deleterious mtDNA mutation in heteroplasmic cybrid cells

Der-Fen Suen;Derek P. Narendra;Atsushi Tanaka;Giovanni Manfredi.
Proceedings of the National Academy of Sciences of the United States of America (2010)

282 Citations

Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice.

Maria Damiano;Anatoly A. Starkov;Susanne Petri;Kathuna Kipiani.
Journal of Neurochemistry (2006)

275 Citations

Rescue of a mitochondrial deficiency causing Leber hereditary optic neuropathy

John Guy;Xiaoping Qi;Francesco Pallotti;Eric A. Schon.
Annals of Neurology (2002)

275 Citations

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