Dr. Jean Charron is an investigator at the Research Centre of the CHU of Québec-Université Laval in the Oncology axis. He is also Professor at the Department of molecular biology, medical biochemistry and pathology in the Faculty of medicine at Université Laval. His research activities focus on the functional characterization of the decision-making mechanisms of the ERK/MAPK signaling pathway in cells when exposed to developmental or environmental cues. These mechanisms are essential for embryonic development and homeostasis of every living throughout life. Any failure of interpretation of cell signalling leads to malformations or pathologies.
Role of the ERK/MAPK pathway in lung development
The development of the respiratory tract is complex and requires several steps of morphogenesis, differentiation and maturation to form the definitive lung. The integration of signals induces by the interaction of secreted factors with their receptors or by cell-cell interactions is essential for lung formation. Dr. Charron’s laboratory examines the role of the ERK/MAPK pathway in lung development using the mouse as a model. His team has already highlighted the role of the ERK/MAPK pathway in lung morphogenesis during bronchial branching and the formation of tracheal cartilage. These defects faithfully recapitulate the phenotypes of significant and costly human diseases, including lung hypoplasia, lung agenesis and tracheomalacia, each representing a major public health concern. These studies will play an increasingly important role in providing insights into the molecular mechanisms underlying fetal and neonatal diseases and in allowing development of novel targeted therapies.
Role of the ERK/MAPK path in the development of autoimmune diseases
The work of the team of Dr. Charron has also shown that decreased ERK/MAPK signaling in hematopoietic cells causes the abnormal production of autoantibodies directed against nuclear proteins and DNA double strand in mice. Over time, these mice develop a glomerulonephritis leading to kidney failure and severe anemia. These symptoms are similar to those of systemic lupus erythematosus (SLE), a severe auto-immune disease more frequent in women than in men. In the murine model generated in the laboratory of Dr. Charron, the females are also 5 times more likely to develop the disease than males. Work is in progress in Dr. Charron’s laboratory to identify which immune cell types are involved in the onset of the auto-immune disease and which molecular mechanisms are involved. This study will provide understanding of the molecular processes leading to the development of autoimmune diseases, and will eventually lead to new therapeutic approaches adapted to sex.
9, rue McMahon
Canada G1R 2J6
Identification of N-myc regulatory regions involved in embryonic expressionJournal Article
Pediatr Res, 51 (1), 2002.
Phosphorylation is involved in the activation of metal-regulatory transcription factor 1 in response to metal ionsJournal Article
J Biol Chem, 276 (45), 2001.
N-Myc shares cellular functions wiht c-MycJournal Article
DNA Cell Biol, 19 (6), 2000.
Le rôle essentiel de MEK1 lors de l’angiogénèse placentaireJournal Article
Med Sci (Paris), 15 , 1999.
Embryonic death of Mek1-deficient mice reveals a role for this kinase in angiogenesis in the labyrinthine region of the placentaJournal Article
Curr Biol, 9 (7), 1999.
Defective development of the embryonic liver in N-myc-deficient miceJournal Article
Dev Biol, 195 (1), 1998.
Generation of normal lymphocytes derived from N-myc-deficient embryonic stem cellsJournal Article
Int Immunol, 7 (10), 1995.
Specification of axial identity in the mouse: role of the Hoxa-5 (Hox1.3) geneJournal Article
Genes Dev, 7 (11), 1993.
Embryonic lethality in mice homozygous for a targeted disruption of the N-myc geneJournal Article
Genes Dev, 6 (12A), 1992.
RAG-2-deficient mice lack mature lymphocytes owing to inability to initiate V(D)J rearrangementJournal Article
Cell, 68 (5), 1992.
Recently finished projects
- Role of the ERK/MAPK pathway in intestine development and homeostasis., from 2016-04-01 to 2022-03-31