D. A. Bosco

Robert H. Brown, B. Hyman, D. A. Bosco, 2011, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS

Jeffery N Agar, Robert H. Brown, D. A. Bosco, 2010, Nature Neuroscience.

Identification of Human Monoclonal Antibodies Specific for Human SOD1 Recognizing Distinct Epitopes and Forms of SOD1

D. A. Bosco, C. Matthews, Can Kayatekin, 2013, PloS one.

Structural basis for mutation-induced destabilization of profilin 1 in ALS

D. A. Bosco, C. Schiffer, J. Landers, 2015, Proceedings of the National Academy of Sciences.

ALS-linked PFN1 variants exhibit loss and gain of functions in the context of formin-induced actin polymerization

D. A. Bosco, O. Bilsel, F. Massi, 2021, Proceedings of the National Academy of Sciences.

Differential association of baseline body weight and body-weight loss with neurological deficits, histology, and death after repetitive closed head traumatic brain injury

D. A. Bosco, N. Henninger, J. Bouley, 2021, Neuroscience Letters.

A reference human induced pluripotent stem cell line for large-scale collaborative studies.

Sonja W. Scholz, M. Nalls, D. Vitale, 2022, Cell stem cell.

Elevated levels of oxidized cholesterol metabolites in Lewy body disease brains accelerate α-synuclein fibrilization

R. Lerner, D. A. Bosco, J. Nieva, 2006, Nature chemical biology.

Localized Thermodynamic Coupling between Hydrogen Bonding and Microenvironment Polarity Substantially Stabilizes Proteins

Jianmin Gao, D. A. Bosco, J. Kelly, 2009, Nature Structural &Molecular Biology.

Catalysis and binding of cyclophilin A with different HIV-1 capsid constructs.

D. A. Bosco, D. Kern, 2004, Biochemistry.

Dissecting the microscopic steps of the cyclophilin A enzymatic cycle on the biological HIV-1 capsid substrate by NMR.

D. A. Bosco, E. Eisenmesser, D. Kern, 2010, Journal of molecular biology.

Interactions between ALS-linked FUS and nucleoporins are associated with defects in the nucleocytoplasmic transport pathway

Eric N. Anderson, Nicolas L. Fawzi, D. A. Bosco, 2021, Nature Neuroscience.

Excessive release of inorganic polyphosphate by ALS/FTD astrocytes causes non-cell-autonomous toxicity to motoneurons

Robert H. Brown, D. A. Bosco, F. González-Nilo, 2022, Neuron.

Paraoxonase gene mutations in amyotrophic lateral sclerosis

Robert H. Brown, D. A. Bosco, J. Glass, 2010, Annals of neurology.

Phenotypic Suppression of ALS/FTD-Associated Neurodegeneration Highlights Mechanisms of Dysfunction

D. A. Bosco, Nicole F. Liachko, C. Lagier-Tourenne, 2019, The Journal of Neuroscience.

The RNA-binding protein FUS/TLS undergoes calcium-mediated nuclear egress during excitotoxic stress and is required for GRIA2 mRNA processing

D. A. Bosco, J. Landers, C. Fallini, 2019, The Journal of Biological Chemistry.

Quantitative proteomics identifies proteins that resist translational repression and become dysregulated in ALS-FUS.

D. A. Bosco, J. Landers, R. Parker, 2019, Human molecular genetics.

FUS/TLS undergoes calcium-mediated nuclear egress during excitotoxic stress and is required for Gria2 mRNA processing

D. A. Bosco, J. Landers, C. Fallini, 2018, bioRxiv.

ALS-linked FUS exerts a gain of toxic function involving aberrant p38 MAPK activation

D. A. Bosco, J. Landers, C. Fallini, 2017, Scientific Reports.

A loss of FUS/TLS function leads to impaired cellular proliferation

D. A. Bosco, J. Landers, S. Shaffer, 2014, Cell Death and Disease.

Functions of FUS/TLS From DNA Repair to Stress Response: Implications for ALS

D. A. Bosco, C. Ward, R. R. K. Sama, 2014, ASN neuro.

Amyotrophic lateral sclerosis-linked FUS/TLS alters stress granule assembly and dynamics

D. A. Bosco, A. Quaresma, J. Nickerson, 2013, Molecular Neurodegeneration.

Mutations in the Profilin 1 Gene Cause Familial Amyotrophic Lateral Sclerosis

S. C. Chafe, D. Goldstein, Robert H. Brown, 2012, Nature.

Proteostasis and movement disorders: Parkinson's disease and amyotrophic lateral sclerosis.

G. Petsko, D. Ringe, D. A. Bosco, 2011, Cold Spring Harbor perspectives in biology.

Mutational analysis reveals the FUS homolog TAF15 as a candidate gene for familial amyotrophic lateral sclerosis

Robert H. Brown, D. A. Bosco, C. Shaw, 2011, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

A Yeast Model of FUS/TLS-Dependent Cytotoxicity

Daniel F Tardiff, G. Petsko, Robert H. Brown, 2011, PLoS biology.

Mutant FUS proteins that cause amyotrophic lateral sclerosis incorporate into stress granules.

Robert H. Brown, D. A. Bosco, L. Hayward, 2010, Human molecular genetics.

Human C9ORF72 Hexanucleotide Expansion Reproduces RNA Foci and Dipeptide Repeat Proteins but Not Neurodegeneration in BAC Transgenic Mice

H. Horvitz, Robert H. Brown, L. Petrucelli, 2015, Neuron.

Anti-SOD1 Nanobodies That Stabilize Misfolded SOD1 Proteins Also Promote Neurite Outgrowth in Mutant SOD1 Human Neurons

D. A. Bosco, D. Golebiowski, M. Sena-Esteves, 2022, International journal of molecular sciences.

Small molecule oxidation products trigger disease-associated protein misfolding.

R. Lerner, D. A. Bosco, J. Kelly, 2006, Accounts of chemical research.

Inhibition of Fast Axonal Transport by Pathogenic SOD1 Involves Activation of p38 MAP Kinase

Robert H. Brown, D. A. Bosco, A. Tiwari, 2013, PloS one.