James G. Burchfield

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Since generation of reliable ground truth annotation of fluo-rescence microscopy sequences is usually a laborious and expensive task, many proposed detection and tracking methods have been evaluated using synthetic data with known ground truth. However, differences between real and synthetic images may lead to inaccurate judgment about the performance of an(More)
Total Internal Reflection Fluorescence Microscopy (TIRFM) is imposing itself as the tool of choice for studying biological activity in close proximity to the plasma membrane. For example, the exquisite selectivity of TIRFM allows monitoring the diffusion of GFP-phogrin vesicles and their recruitment to the plasma membrane in pancreatic β-cells. We present a(More)
  • James Cantley, James G. Burchfield, Gemma L. Pearson, Carsten Schmitz-Peiffer, Michael Leitges, Trevor J. Biden
  • 2009
OBJECTIVE—Insufficient insulin secretion is a hallmark of type 2 diabetes, and exposure of ␤-cells to elevated lipid levels (lipotoxicity) contributes to secretory dysfunction. Functional ablation of protein kinase C ε (PKCε) has been shown to improve glucose homeostasis in models of type 2 diabetes and, in particular, to enhance glucose-stimulated insulin(More)
MOTIVATION With the advancement of high-throughput techniques, large-scale profiling of biological systems with multiple experimental perturbations is becoming more prevalent. Pathway analysis incorporates prior biological knowledge to analyze genes/proteins in groups in a biological context. However, the hypotheses under investigation are often confined to(More)
The Niemann-Pick disease, type C1 (NPC1) gene encodes a transmembrane protein involved in cholesterol efflux from the lysosome. SNPs within NPC1 have been associated with obesity and type 2 diabetes, and mice heterozygous or null for NPC1 are insulin resistant. However, the molecular mechanism underpinning this association is currently undefined. This study(More)
Transglutaminase type 2 (TG2) has been reported to be a candidate gene for maturity onset diabetes of the young (MODY) because three different mutations that impair TG2 transamidase activity have been found in 3 families with MODY. TG2 null (TG2(-/-)) mice have been reported to be glucose intolerant and have impaired glucose-stimulated insulin secretion(More)
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