Neurotoxicity induces cleavage of p35 to p25 by calpain

By M. Lee, Y. T. Kwon, Mingwei Li, Junmin Peng, R. Friedlander, Li-Huei Tsai. Nature, 2000

1,125 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience

View Paper: https://www.semanticscholar.org/paper/da58726a2b4eaf30642485be1efc049832ec6c19

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. Li-Huei Tsai
2. Junying Yuan
3. Philip C. Wong
4. R. Dhavan
5. R. Kaufman

In Cellular and Molecular Neuroscience

1. D. Sinclair
2. E. Masliah
3. Shu Zhang
4. Li-Huei Tsai
5. Y. Wang
6. T. Lai
7. R. Dhavan

Citations in the corpus

• Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Phosphorylation of tau is regulated by several kinases, including GSK3β and cdk5, both of which are activated by extracellular Aβ (Hernandez & Avila 2008, Lee et al. 2000).”
• SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis (2007, methodology): “These specific stresses have previously been shown to trigger the deterioration of neuronal morphology and the formation of p25 in cultured neurons (Kusakawa et al, 2000; Lee et al, 2000; Nath et al, 2000).”
• The calpain system. (2003, background): “Tau is a substrate of CDK5, and p25 accumulates in brains of Alzheimer’s patients (237), suggesting that calpain-cleaved p25 is responsible for the hyperphos-”
• Molecular mechanisms of neurodegeneration in Alzheimer's disease. (2010, background): “Abnormal activation of signaling pathways might lead to synaptic failure and altered neurogenesis by promoting abnormal Tau phosphorylation and aggregation (126–128), cytoskeletal abnormalities (129), activating caspase pro-apototic pathways (130–132) and activating calcium and calpain dependent pro”
• Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles. (2003, background): “…that in pri-Boston, Massachusetts 02115 mary neurons, p25 is produced by calpain cleavage of p35 between residues 98 and 99 upon neurotoxic insults, including oxidative stress, excitoxicity, and -amyloid (A )Summary peptide treatment (Kusakawa et al., 2000; Lee et al., 2000; Nath et al., 2000).”
• A decade of CDK5 (2001, background): “p25 is produced by neurotoxic insults, and is generated by H 2 O 2 , glutamate, maitotoxin and ionomycin treatments of cultured primary neuron”
• Excitotoxicity and stroke: identifying novel targets for neuroprotection. (2014, positive): “dependent calpain-mediated proteolytic cleavage of p35 into a smaller 25-kDa form (p25) (Lee et al., 2000; O’Hare et al., 2005), which induces neuronal death, in part by aberrant activation and target-redirection of cdk5 (Patrick et al.”
• Lipopolysaccharide-Induced Inflammation Exacerbates Tau Pathology by a Cyclin-Dependent Kinase 5-Mediated Pathway in a Transgenic Model of Alzheimer's Disease (2005, background): “First, the steady-state levels of p25 were markedly higher in the LPS-treated mice, which is significant because elevated levels of p25 cause a prolonged activation of cdk5 (Tsai et al., 1994; Alvarez et al., 1999; Ahlijanian et al., 2000; Lee et al., 2000).”
• Cross-Talk between Two Cysteine Protease Families (2000, background): “Recently, calpain has been shown to cleave p35 to generate a toxic p25 fragment under neurotoxic conditions including ischemia and amyloidb treatment (Patrick et al., 1999; Lee et al., 2000).”