Nicotinamide Mononucleotide Adenylyl Transferase-Mediated Axonal Protection Requires Enzymatic Activity But Not Increased Levels of Neuronal Nicotinamide Adenine DinucleotideYo Sasaki, Jeffrey Milbrandt, Bhupinder P. S. Vohra et al.|Journal of Neuroscience|2009Cited by 259
Transgenic Mice Expressing the Nmnat1 Protein Manifest Robust Delay in Axonal Degeneration<i>In Vivo</i>Yo Sasaki, Jeffrey Milbrandt, Bhupinder P. S. Vohra et al.|Journal of Neuroscience|2009Cited by 154
Amyloid Precursor Protein Cleavage-Dependent and -Independent Axonal Degeneration Programs Share a Common Nicotinamide Mononucleotide Adenylyltransferase 1-Sensitive PathwayBhupinder P. S. Vohra, Jeffrey Milbrandt, Yo Sasaki et al.|Journal of Neuroscience|2010Cited by 103
Image-based Screening Identifies Novel Roles for IκB Kinase and Glycogen Synthase Kinase 3 in Axonal DegenerationJosiah Gerdts, Jeffrey Milbrandt, Yo Sasaki et al.|Journal of Biological Chemistry|2011Cited by 69
Protein Kinase Cζ and Glycogen Synthase Kinase-3β Control Neuronal Polarity in Developing Rodent Enteric Neurons, whereas SMAD Specific E3 Ubiquitin Protein Ligase 1 Promotes Neurite Growth But Does Not Influence PolarityBhupinder P. S. Vohra, Robert O. Heuckeroth|Journal of Neuroscience|2007Cited by 38