Nancy Y. Ip

TL;DR: It is shown that Cdk5-mediated phosphorylation of EndoB1 is essential for autophagy induction and neuronal loss in models of Parkinson’s disease.

TL;DR: In this paper, the authors summarize the latest advances in understanding of the role of autophagy deregulation in Parkinson's, Alzheimer's and Huntington's disease, and conclude that autophagous pathways, including macroautophagy and chaperone-mediated autophathy, are implicated in the turnover of proteins that are prone to aggregation in cellular or animal disease models.

TL;DR: Recent advances in the understanding of molecular and cellular events that mediate NMJ maturation and maintenance are reviewed and key molecular regulators at the presynaptic nerve terminal, synaptic cleft, and postsynaptic muscle membrane are discussed.

TL;DR: Recent research on the amyloid hypothesis and beta-amyloid-induced dysfunction of neuronal synapses through distinct cell surface receptors are reviewed and potential applications of disease-modifying strategies targeting synaptic failure for improved treatment of AD are proposed.

TL;DR: A physiological role of Cdk5 in regulating STAT3 phosphorylation and modulating its transcriptional activity is revealed and both the DNA-binding activity of STAT3 and the transcription of specific target genes, such as fibronectin, are reduced in Cdk 5-deficient muscle.