A5058025506- Alzheimer's disease research and treatments
- Computational Drug Discovery Methods
- Diabetes and associated disorders
- Pancreatic function and diabetes
- Biochemical Analysis and Sensing Techniques
- Diabetes Management and Research
- Supramolecular Self-Assembly in Materials
- Advanced biosensing and bioanalysis techniques
- Congenital heart defects research
- RNA modifications and cancer
- Cell death mechanisms and regulation
- Cholinesterase and Neurodegenerative Diseases
- Neurobiology and Insect Physiology Research
- Lipid Membrane Structure and Behavior
- Nuclear Receptors and Signaling
- Advanced Proteomics Techniques and Applications
- Olfactory and Sensory Function Studies
- Congenital Heart Disease Studies
- Immunotherapy and Immune Responses
- Monoclonal and Polyclonal Antibodies Research
- Neurological diseases and metabolism
Northwestern University
2011-2018
University of Chicago
2005-2007
May Institute
2006
Howard Hughes Medical Institute
2006
Conditional loss of BACE1 in adult mouse brain results abnormalities the hippocampal mossy fiber pathway, which is important for learning and memory.
Abstract Background The β-secretase, β-site amyloid precursor protein cleaving enzyme 1 (BACE1), is a prime therapeutic target for lowering cerebral β-amyloid (Aβ) levels in Alzheimer's disease (AD). Clinical development of BACE1 inhibitors being intensely pursued. However, little known about the physiological functions BACE1, and possibility exists that inhibition may cause mechanism-based side effects. Indeed, -/- mice exhibit complex neurological phenotype. Interestingly, co-localizes...
This paper describes a label-free assay for measuring endogenous caspase protease activities in cell lysates. The format, termed SAMDI-MS (self-assembled monolayers matrix assisted laser desorption ionization time-of-flight mass spectrometry), is based on the enzymatic modification of peptides immobilized to monolayer substrates, followed by direct detection products with spectrometry. Monolayers presenting peptide substrates either caspase-3 or -8 were treated lysates from Jurkat cells that...
Empirical evidence supporting a genetic basis for the etiology of congenital heart disease (CHD) is limited and few disease-causing mutations have been identified. To identify novel CHD genes, we performed forward screen to mutant mouse lines with heritable CHD. Lines recessive N-ethyl-N-nitrsourea-induced CHD-causing were identified using three-generation backcross. A hierarchical screening protocol was used test hypothesis that fetal-to-neonatal circulatory transition unmasks specific...