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Gisèle Bonne

Gisèle Bonne

D-Index & Metrics

Molecular Biology

D-Index
73
Citations
20015
World Ranking
1273
National Ranking
40

Overview

Gisèle Bonne is affiliated with Sorbonne University in France and conducts research primarily in the field of Biochemistry, Genetics and Molecular Biology, with a focus on various subfields such as Molecular Biology, Genetics, Cell Biology, Cardiology and Cardiovascular Medicine, and Cellular and Molecular Neuroscience.

The main research topics covered in their publications include:

  • Nuclear Structure and Function
  • RNA Research and Splicing
  • Muscle Physiology and Disorders
  • Genomics and Rare Diseases
  • Cardiomyopathy and Myosin Studies
  • Mitochondrial Function and Pathology
  • Genetic Neurodegenerative Diseases

Significant recent papers authored or co-authored by Gisèle Bonne include:

  • "Solve-RD: systematic pan-European data sharing and collaborative analysis to solve rare diseases" (2021), published in European Journal of Human Genetics
  • "Solving patients with rare diseases through programmatic reanalysis of genome-phenome data" (2021), published in European Journal of Human Genetics
  • "The 2021 version of the gene table of neuromuscular disorders (nuclear genome)" (2020), published in Neuromuscular Disorders
  • "The 2022 version of the gene table of neuromuscular disorders (nuclear genome)" (2021), published in Neuromuscular Disorders
  • "Targeting the histone demethylase LSD1 prevents cardiomyopathy in a mouse model of laminopathy" (2021), published in Journal of Clinical Investigation

Frequent collaborators include:

  • Rabah Ben Yaou
  • Isabelle Nelson
  • Louise Benarroch
  • Tanya Stojkovic
  • Mridul Johari

The scientist often publishes in the following venues:

  • Neuromuscular Disorders
  • bioRxiv (Cold Spring Harbor Laboratory)
  • European Journal of Human Genetics
  • médecine/sciences
  • Cells

Best Publications

  • Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy

    Gisèle Bonne;M R Di Barletta;S Varnous;H M Bécane

  • "Laminopathies": a wide spectrum of human diseases.

    Howard J. Worman;Gisèle Bonne;Gisèle Bonne

  • Mandibuloacral Dysplasia Is Caused by a Mutation in LMNA-Encoding Lamin A/C

    Giuseppe Novelli;Antoine Muchir;Federica Sangiuolo;Anne Helbling-Leclerc

  • Cardiac myosin binding protein-C gene splice acceptor site mutation is associated with familial hypertrophic cardiomyopathy.

    Bonne G;Bercovici J;Cruaud C

  • Clinical and molecular genetic spectrum of autosomal dominant Emery‐Dreifuss muscular dystrophy due to mutations of the lamin A/C gene

    Bonne G;Mercuri E;Muchir A;Urtizberea A

  • Different Mutations in the LMNA Gene Cause Autosomal Dominant and Autosomal Recessive Emery-Dreifuss Muscular Dystrophy

    Marina Raffaele di Barletta;Enzo Ricci;Giuliana Galluzzi;Pietro Tonali

  • Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies

    Takuro Arimura;Anne Helbling-Leclerc;Catherine Massart;Shaida Varnous

  • Organization and Sequence of Human Cardiac Myosin Binding Protein C Gene (MYBPC3) and Identification of Mutations Predicted to Produce Truncated Proteins in Familial Hypertrophic Cardiomyopathy

    G Bonne;E Bährend;B Yu

  • The Ig-like Structure of the C-Terminal Domain of Lamin A/C, Mutated in Muscular Dystrophies, Cardiomyopathy, and Partial Lipodystrophy

    Isabelle Krimm;Cecilia Östlund;Bernard Gilquin;Joël Couprie

  • Activation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy

    Antoine Muchir;Paul Pavlidis;Valérie Decostre;Alan J. Herron

  • De Novo LMNA Mutations Cause a New Form of Congenital Muscular Dystrophy

    Susana Quijano-Roy;Blaise Mbieleu;Carsten G. Bönnemann;Pierre Yves Jeannet

  • Properties of lamin A mutants found in Emery-Dreifuss muscular dystrophy, cardiomyopathy and Dunnigan-type partial lipodystrophy

    Cecilia Östlund;Gisèle Bonne;Ketty Schwartz;Howard J. Worman

  • Mutations of the FHL1 Gene Cause Emery-Dreifuss Muscular Dystrophy

    Lucie Gueneau;Lucie Gueneau;Anne T. Bertrand;Anne T. Bertrand;Jean-Philippe Jais;Mustafa A. Salih

  • Autophagic degradation of nuclear components in mammalian cells.

    Young-Eun Park;Yukiko K Hayashi;Gisèle Bonne;Takuro Arimura

  • Zidovudine myopathy: a distinctive disorder associated with mitochondrial dysfunction.

    C. Mhiri;M. Baudrimont;G. Bonne;C. Geny

  • Nuclear envelope alterations in fibroblasts from LGMD1B patients carrying nonsense Y259X heterozygous or homozygous mutation in lamin A/C gene.

    Antoine Muchir;Baziel G van Engelen;Martin Lammens;John M Mislow

  • Mitogen-Activated Protein Kinase Inhibitors Improve Heart Function and Prevent Fibrosis in Cardiomyopathy Caused by Mutation in Lamin A/C Gene

    Wei Wu;Antoine Muchir;Jian Shan;Gisèle Bonne

  • Inhibition of extracellular signal-regulated kinase signaling to prevent cardiomyopathy caused by mutation in the gene encoding A-type lamins

    Antoine Muchir;Jian Shan;Gisèle Bonne;Gisèle Bonne;Stephan E. Lehnart

  • Identification of two novel mutations in the ventricular regulatory myosin light chain gene (MYL2) associated with familial and classical forms of hypertrophic cardiomyopathy.

    Jeanne Flavigny;Pascale Richard;Richard Isnard;Lucie Carrier

  • LMNA mutations in atypical Werner's syndrome [5] (multiple letters)

    C. Vigouroux;F. Caux;J. Capeau;S. Christin-Maitre

Frequent Co-Authors

Ketty Schwartz
Ketty Schwartz Grenoble Alpes University
Bruno Eymard
Bruno Eymard Université Paris Cité
Francesco Muntoni
Francesco Muntoni University College London
Luciano Merlini
Luciano Merlini University of Bologna
Thomas Voit
Thomas Voit University College London
Pascale Guicheney
Pascale Guicheney Sorbonne University
Caroline Sewry
Caroline Sewry Great Ormond Street Hospital
Howard J. Worman
Howard J. Worman Columbia University
Ichizo Nishino
Ichizo Nishino Tokyo Medical University
Daniela Toniolo
Daniela Toniolo Vita-Salute San Raffaele University

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