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One or more keywords matched the following properties of Bosco, Daryl


Daryl Bosco received her Ph.D. (bio-organic chemistry) in 2003 from Brandeis University, where she used NMR spectroscopy to study enzyme dynamics. From 2003-2005, Dr. Bosco was a post-doctoral fellow in the lab of Jeffery W. Kelly at the Scripps Research Institute, where she studied the effect of oxidative cholesterol metabolites on the mis-folding of alpha-synuclein, a Parkinson's disease-associated protein. Prior to joining the faculty at UMMS in 2008, Dr. Bosco was an Instructor of Neurology at Harvard Medical School and worked on various aspects of ALS in the Cecile B. Day lab directed by Dr. Robert H. Brown, Jr. at the Massachusetts General Hospital.


Our lab is investigating the pathogenic mechanisms of ALS-associated proteins SOD1, FUS/TLS, profilin-1 and TDP-43.  ALS (amyotrophic lateral sclerosis), also known as Lou Gehrig’s disease, is a fatal neurodegenerative disorder that targets motor neurons.  Motor neuron death culminates in paralysis and eventual death, usually 2-3 years after symptom onset.  To date, there is no cure or effective therapy for ALS.  Our ultimate goal is to translate our basic-research findings into therapies for this devastating disease.   We use a multidisciplinary approach involving biochemistry, cell biology (including iPS cell technology), biophysics and in vivo model systems for our investigations. See our lab webpage for more information on Research Projects: https://www.umassmed.edu/boscolab

One or more keywords matched the following items that are connected to Bosco, Daryl
Item TypeName
Academic Article Paraoxonase gene mutations in amyotrophic lateral sclerosis.
Academic Article Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS.
Academic Article A yeast model of FUS/TLS-dependent cytotoxicity.
Academic Article Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis.
Academic Article Mutant FUS proteins that cause amyotrophic lateral sclerosis incorporate into stress granules.
Academic Article Genetic determinants of amyotrophic lateral sclerosis as therapeutic targets.
Academic Article Mutational analysis reveals the FUS homolog TAF15 as a candidate gene for familial amyotrophic lateral sclerosis.
Academic Article Anti-superoxide dismutase antibodies are associated with survival in patients with sporadic amyotrophic lateral sclerosis.
Academic Article Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis.
Academic Article Inhibition of fast axonal transport by pathogenic SOD1 involves activation of p38 MAP kinase.
Concept Amyotrophic Lateral Sclerosis
Academic Article Amyotrophic lateral sclerosis-linked FUS/TLS alters stress granule assembly and dynamics.
Academic Article Identification of a misfolded region in superoxide dismutase 1 that is exposed in amyotrophic lateral sclerosis.
Academic Article Functions of FUS/TLS from DNA repair to stress response: implications for ALS.
Academic Article Autophagy meets fused in sarcoma-positive stress granules.
Academic Article Structural basis for mutation-induced destabilization of profilin 1 in ALS.
Academic Article Human C9ORF72 Hexanucleotide Expansion Reproduces RNA Foci and Dipeptide Repeat Proteins but Not Neurodegeneration in BAC Transgenic Mice.
Academic Article ALS-linked FUS exerts a gain of toxic function involving aberrant p38 MAPK activation.
Academic Article Endoplasmic reticulum stress leads to accumulation of wild-type SOD1 aggregates associated with sporadic amyotrophic lateral sclerosis.
Academic Article Translation dysregulation in neurodegenerative disorders.
Academic Article Quantitative proteomics identifies proteins that resist translational repression and become dysregulated in ALS-FUS.
Academic Article The RNA-binding protein FUS/TLS undergoes calcium-mediated nuclear egress during excitotoxic stress and is required for GRIA2 mRNA processing.
Academic Article Phenotypic Suppression of ALS/FTD-Associated Neurodegeneration Highlights Mechanisms of Dysfunction.
Academic Article ALS-linked PFN1 variants exhibit loss and gain of functions in the context of formin-induced actin polymerization.
Academic Article Interactions between ALS-linked FUS and nucleoporins are associated with defects in the nucleocytoplasmic transport pathway.
Academic Article Excessive release of inorganic polyphosphate by ALS/FTD astrocytes causes non-cell-autonomous toxicity to motoneurons.
Academic Article Anti-SOD1 Nanobodies That Stabilize Misfolded SOD1 Proteins Also Promote Neurite Outgrowth in Mutant SOD1 Human Neurons.
Academic Article Interactions between FUS and the C-terminal Domain of Nup62 are Sufficient for their Co-phase Separation into Amorphous Assemblies.
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  • Motor Neuron Disease