Parkin-mediated reduction of nuclear and soluble TDP-43 reverses behavioral decline in symptomatic mice

Tyrosine kinase inhibition increases functional parkin-Beclin-1 interaction and enhances amyloid clearance and cognitive performance

(2013) Irina Lonskaya et al.   EMBO Molecular Medicine

Nilotinib reverses loss of dopamine neurons and improves motor behavior via autophagic degradation of  -synuclein in Parkinson's disease models

(2013) M. L. Hebron et al.   HUMAN MOLECULAR GENETICS

Nilotinib-induced autophagic changes increase endogenous parkin level and ubiquitination, leading to amyloid clearance

(2013) Irina Lonskaya et al.   JOURNAL OF MOLECULAR MEDICINE-JMM

Parkin reverses TDP-43-induced cell death and failure of amino acid homeostasis

(2013) Michaeline Hebron et al.   JOURNAL OF NEUROCHEMISTRY

Ubiquitination Increases Parkin Activity to Promote Autophagic α-Synuclein Clearance

(2013) Irina Lonskaya et al.   PLoS One

Wild type TDP-43 induces neuro-inflammation and alters APP metabolism in lentiviral gene transfer models

(2012) Alexander M. Herman et al.   EXPERIMENTAL NEUROLOGY

parkin-induced defects in neurophysiology and locomotion are generated by metabolic dysfunction and not oxidative stress

(2012) A. Vincent et al.   HUMAN MOLECULAR GENETICS

Parkin Ubiquitinates Tar-DNA Binding Protein-43 (TDP-43) and Promotes Its Cytosolic Accumulation via Interaction with Histone Deacetylase 6 (HDAC6)

(2012) Michaeline L. Hebron et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Divergent roles of ALS-linked proteins FUS/TLS and TDP-43 intersect in processing long pre-mRNAs

(2012) Clotilde Lagier-Tourenne et al.   NATURE NEUROSCIENCE

Aggregation of the 35-kDa fragment of TDP-43 causes formation of cytoplasmic inclusions and alteration of RNA processing

(2011) Mei-Xia Che et al.   FASEB JOURNAL

Long pre-mRNA depletion and RNA missplicing contribute to neuronal vulnerability from loss of TDP-43

(2011) Magdalini Polymenidou et al.   NATURE NEUROSCIENCE

β-Amyloid1–42Gene Transfer Model Exhibits Intraneuronal Amyloid, Gliosis, Tau Phosphorylation, and Neuronal Loss

(2010) G. William Rebeck et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

TDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia

(2010) Ian RA Mackenzie et al.   LANCET NEUROLOGY

Phosphorylated and cleaved TDP-43 in ALS, FTLD and other neurodegenerative disorders and in cellular models of TDP-43 proteinopathy

(2010) Tetsuaki Arai et al.   NEUROPATHOLOGY

TDP-43 transgenic mice develop spastic paralysis and neuronal inclusions characteristic of ALS and frontotemporal lobar degeneration

(2010) Hans Wils et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration

(2009) I. Wegorzewska et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Mutations in FUS, an RNA Processing Protein, Cause Familial Amyotrophic Lateral Sclerosis Type 6

(2009) C. Vance et al.   SCIENCE

Mutations in the FUS/TLS Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis

(2009) T. J. Kwiatkowski et al.   SCIENCE

Disturbance of Nuclear and Cytoplasmic TAR DNA-binding Protein (TDP-43) Induces Disease-like Redistribution, Sequestration, and Aggregate Formation

(2008) Matthew J. Winton et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Imatinib for Newly Diagnosed Patients With Chronic Myeloid Leukemia: Incidence of Sustained Responses in an Intention-to-Treat Analysis

(2008) Hugues de Lavallade et al.   JOURNAL OF CLINICAL ONCOLOGY