Francesca Bianchi
Milan, 20132, Italy
Last Updated: 09/26/2026
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Found 10 publications
Activation of XBP1s attenuates disease severity in models of proteotoxic Charcot-Marie-Tooth type 1B.
Journal: bioRxiv : the preprint server for biology
Published: February 14, 2024
Activation of XBP1s attenuates disease severity in models of proteotoxic Charcot-Marie-Tooth type 1B.
Journal: Brain : a journal of neurology
Published: February 02, 2024
Structured wound angiogenesis instructs mesenchymal barrier compartments in the regenerating nerve.
Journal: Neuron
Published: April 26, 2023
A novel mouse model of CMT1B identifies hyperglycosylation as a new pathogenetic mechanism.
Journal: Human molecular genetics
Published: March 22, 2022
Treatment with IFB-088 Improves Neuropathy in CMT1A and CMT1B Mice.
Journal: Molecular neurobiology
Published: December 23, 2021
Dysregulation of myelin synthesis and actomyosin function underlies aberrant myelin in CMT4B1 neuropathy.
Journal: Proceedings of the National Academy of Sciences of the United States of America
Published: March 03, 2021
Phosphorylation of eIF2α Promotes Schwann Cell Differentiation and Myelination in CMT1B Mice with Activated UPR.
Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience
Published: April 23, 2020
Schwann cells ER-associated degradation contributes to myelin maintenance in adult nerves and limits demyelination in CMT1B mice.
Journal: PLoS genetics
Published: September 24, 2018
Enhanced axonal neuregulin-1 type-III signaling ameliorates neurophysiology and hypomyelination in a Charcot-Marie-Tooth type 1B mouse model.
Journal: Human molecular genetics
Published: August 29, 2018
Loss of Fig4 in both Schwann cells and motor neurons contributes to CMT4J neuropathy.
Journal: Human molecular genetics
Published: September 05, 2014
Showing 1-10 of 10
Last Updated: 09/26/2026