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16 results on '"Dalfo, Esther"'

3. The Small GTPase RAC1/CED-10 Is Essential in Maintaining Dopaminergic Neuron Function and Survival Against α-Synuclein-Induced Toxicity

Author

Kim, Hanna, Calatayud, Carles, Guha, Sanjib, Fernández-Carasa, Irene, Berkowitz, Laura, Carballo-Carbajal, Iria, Ezquerra, Mario, Fernández-Santiago, Rubén, Kapahi, Pankaj, Raya, Ángel, Miranda-Vizuete, Antonio, Lizcano, Jose Miguel, Vila, Miquel, Caldwell, Kim A., Caldwell, Guy A., Consiglio, Antonella, and Dalfo, Esther

Published
2018
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4. Correction to: The Small GTPase RAC1/CED-10 Is Essential in Maintaining Dopaminergic Neuron Function and Survival Against α-Synuclein-Induced Toxicity

Author

Kim, Hanna, Calatayud, Carles, Guha, Sanjib, Fernández-Carasa, Irene, Berkowitz, Laura, Carballo-Carbajal, Iria, Ezquerra, Mario, Fernández-Santiago, Rubén, Kapahi, Pankaj, Raya, Ángel, Miranda-Vizuete, Antonio, Lizcano, Jose Miguel, Vila, Miquel, Caldwell, Kim A., Caldwell, Guy A., Consiglio, Antonella, and Dalfo, Esther

Published
2018
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5. Anti-oxidant MitoQ rescue of AWB chemosensory neuron impairment in a C. elegans model of X-linked Adrenoleukodystrophy

Author

Guha, Sanjib, Pujol, Aurora, and Dalfo, Esther

Subjects
New Finding, Models of Human Disease, Phenotype Data
Abstract

X-linked Adrenoleukodystrophy (X-ALD) is a neurometabolic disorder caused by a defective peroxisomal ABCD1 transporter of very long-chain fatty acids (VLCFAs). We have characterized a nematode model of X-ALD with loss of the pmp-4 gene, the worm orthologue of ABCD1. These mutants recapitulated the key hallmarks of X-ALD and importantly mitochondria targeted antioxidant MitoQ prevented axonal degeneration and locomotor disability. In this study, we further demonstrated that the AWB chemosensory neuron of the pmp-4 mutant worm is defective, both in morphology and function. Interestingly, MitoQ could rescue both the phenotypes. Collectively, our results suggest that C. elegans' chemosensation might provide a novel setting for exploring peroxisomal disease related disorders.​

Published
2021

8. Transgenic mice overexpressing the full-length neurotrophin receptor TrkC exhibit increased catecholaminergic neuron density in specific brain areas and increased anxiety-like behavior and panic reaction

Author

Dierssen, Mara, Gratacòs, Mònica, Sahún, Ignasi, Martín, Miguel, Gallego, Xavier, Amador-Arjona, Alejandro, Martínez de Lagrán, María, Murtra, Patricia, Martí, Eulalia, Pujana, Miguel A., Ferrer, Isidre, Dalfó, Esther, Martínez-Cué, Carmen, Flórez, Jesús, Torres-Peraza, Jesús F., Alberch, Jordi, Maldonado, Rafael, Fillat, Cristina, and Estivill, Xavier

Published
2006
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10. ZPD-2, a Small Compound That Inhibits α-Synuclein Amyloid Aggregation and Its Seeded Polymerization

Author

Peña-Díaz, Samuel, primary, Pujols, Jordi, additional, Conde-Giménez, María, additional, Čarija, Anita, additional, Dalfo, Esther, additional, García, Jesús, additional, Navarro, Susanna, additional, Pinheiro, Francisca, additional, Santos, Jaime, additional, Salvatella, Xavier, additional, Sancho, Javier, additional, and Ventura, Salvador, additional

Published
2019
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14. PDR-1/hParkin negatively regulates the phagocyosis of apoptotic cell corpses in Caenorhabditis elegans

Author

Cabello, J., Sämann, J., Gómez-Orte, E., Erazo, Tatiana, Coppa, A., Pujol, Aurora, Büssing, I, Schulze, B., Lizcano de Vega, José Miguel, Ferrer, I, Baumeister, R., Dalfo, Esther, and Universitat de Barcelona

Subjects
0301 basic medicine, rac1 GTP-Binding Protein, Cancer Research, proteasomal degradation, Engulfment, Cell, Homeòstasi, Apoptosis, Proteasomal degradation, Cell Movement, Homeostasis, Small GTPase, Cytoskeleton, Tissue homeostasis, Caenorhabditis elegans, Cell biology, rac GTP-Binding Proteins, medicine.anatomical_structure, Mort cel·lular, C. elegans, Original Article, Proteasome Inhibitors, Rac1, Signal Transduction, Cell death, Programmed cell death, Proteasome Endopeptidase Complex, Ubiquitin-Protein Ligases, Immunology, RAC1, Biology, Transfection, 03 medical and health sciences, Cellular and Molecular Neuroscience, Phagocytosis, medicine, Animals, Humans, Caenorhabditis elegans Proteins, Parkin, Cell growth, Ubiquitination, Cell Biology, biology.organism_classification, 030104 developmental biology, HEK293 Cells, engulfment, Mutation, Proteolysis
Abstract

Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. In Caenorhabditis elegans, two parallel and partly redundant conserved pathways act in cell corpse engulfment. The pathway for cytoskeletal rearrangement requires the small GTPase CED-10 Rac1 acting for an efficient surround of the dead cell. The CED-10 Rac pathway is also required for the proper migration of the distal tip cells (DTCs) during the development of the C. elegans gonad. Parkin, the mammalian homolog of the C. elegans PDR-1, interacts with Rac1 in aged human brain and it is also implicated with actin dynamics and cytoskeletal rearrangements in Parkinsons's disease, suggesting that it might act on engulfment. Our genetic and biochemical studies indicate that PDR-1 inhibits apoptotic cell engulfment and DTC migration by ubiquitylating CED-10 for degradation.

Published
2014

16. Anti-oxidant MitoQ rescue of AWB chemosensory neuron impairment in a C. elegans model of X-linked Adrenoleukodystrophy.

Author

Guha S, Pujol A, and Dalfo E

Abstract

X-linked Adrenoleukodystrophy (X-ALD) is a neurometabolic disorder caused by a defective peroxisomal ABCD1 transporter of very long-chain fatty acids (VLCFAs). We have characterized a nematode model of X-ALD with loss of the pmp-4 gene, the worm orthologue of ABCD1 . These mutants recapitulated the key hallmarks of X-ALD and importantly mitochondria targeted antioxidant MitoQ prevented axonal degeneration and locomotor disability. In this study, we further demonstrated that the AWB chemosensory neuron of the pmp-4 mutant worm is defective, both in morphology and function. Interestingly, MitoQ could rescue both the phenotypes. Collectively, our results suggest that C. elegans' chemosensation might provide a novel setting for exploring peroxisomal disease related disorders.​., (Copyright: © 2021 by the authors.)

Published
2021
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