Caroline Reisacher
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Caroline Reisacher has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Iñigo Casafont
Cell and Tissue Biology Group, Anatomy and Cell Biology Department, University of Cantabria-IDIVAL, 39011 Santander, Spain
1 shared publication - Jorge Mata-Garrido
Cell and Tissue Biology Group, Anatomy and Cell Biology Department, University of Cantabria-IDIVAL, 39011 Santander, Spain
1 shared publication - Laura Frizzi
Université Paris Cité, INSERM, CNRS, Institut Necker Enfants Malades, 75015 Paris, France
1 shared publication - Laurence Arbibe
Université Paris Cité, INSERM, CNRS, Institut Necker Enfants Malades
1 shared publication - Thien Nguyen
Université Paris Cité, INSERM, CNRS, Institut Necker Enfants Malades, 75015 Paris, France
1 shared publication - Xiangyan He
Université Paris Cité, INSERM, CNRS, Institut Necker Enfants Malades, 75015 Paris, France
1 shared publication
Latest Publications
- Open Access
- 16 April 2023
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 24 (8) , 7347
HP1γ Prevents Activation of the cGAS/STING Pathway by Preserving Nuclear Envelope and Genomic Integrity in Colon Adenocarcinoma Cells
Chronic inflammatory processes in the intestine result in serious conditions such as inflammatory bowel disease (IBD) and cancer. An increased detection of cytoplasmic DNA sensors has been reported in the IBD colon mucosa, suggesting their contribution in mucosal inflammation. Yet, the mechanisms altering DNA homeostasis and triggering the activation of DNA sensors remain poorly understood. In this study, we show that the epigenetic regulator HP1γ plays a role in preserving nuclear envelope and genomic integrity in enterocytic cells, thereby protecting against the presence of cytoplasmic DNA. Accordingly, HP1 loss of function led to the increased detection of cGAS/STING, a cytoplasmic DNA sensor that triggers inflammation. Thus, in addition to its role as a transcriptional silencer, HP1γ may also exert anti-inflammatory properties by preventing the activation of the endogenous cytoplasmic DNA response in the gut epithelium.
- 16 April 2023
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 24 (8) , 7347
Open AccessHP1γ Prevents Activation of the cGAS/STING Pathway by Preserving Nuclear Envelope and Genomic Integrity in Colon Adenocarcinoma Cells
Chronic inflammatory processes in the intestine result in serious conditions such as inflammatory bowel disease (IBD) and cancer. An increased detection of cytoplasmic DNA sensors has been reported in the IBD colon mucosa, suggesting their contribution in mucosal inflammation. Yet, the mechanisms altering DNA homeostasis and triggering the activation of DNA sensors remain poorly understood. In this study, we show that the epigenetic regulator HP1γ plays a role in preserving nuclear envelope and genomic integrity in enterocytic cells, thereby protecting against the presence of cytoplasmic DNA. Accordingly, HP1 loss of function led to the increased detection of cGAS/STING, a cytoplasmic DNA sensor that triggers inflammation. Thus, in addition to its role as a transcriptional silencer, HP1γ may also exert anti-inflammatory properties by preventing the activation of the endogenous cytoplasmic DNA response in the gut epithelium.