Valentina Romano
Trieste, 34149, Italy
Last Updated: 09/26/2026
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Found 8 publications
Thioridazine reverts the phenotype in cellular and Drosophila models of amyotrophic lateral sclerosis by enhancing TDP-43 aggregate clearance.
Journal: Neurobiology of disease
Published: December 17, 2020
Point mutations in the N-terminal domain of transactive response DNA-binding protein 43 kDa (TDP-43) compromise its stability, dimerization, and functions.
Journal: The Journal of biological chemistry
Published: January 09, 2017
A novel Drosophila model of TDP-43 proteinopathies: N-terminal sequences combined with the Q/N domain induce protein functional loss and locomotion defects.
Journal: Disease models & mechanisms
Published: September 24, 2015
The TDP-43 N-terminal domain structure at high resolution.
Journal: The FEBS journal
Published: August 13, 2015
The structural integrity of TDP-43 N-terminus is required for efficient aggregate entrapment and consequent loss of protein function.
Journal: Prion
Published: January 31, 2015
TDP-43 loss of cellular function through aggregation requires additional structural determinants beyond its C-terminal Q/N prion-like domain.
Journal: Human molecular genetics
Published: August 15, 2014
Cellular model of TAR DNA-binding protein 43 (TDP-43) aggregation based on its C-terminal Gln/Asn-rich region.
Journal: The Journal of biological chemistry
Published: January 12, 2012
Showing 1-8 of 8
Last Updated: 09/26/2026