Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles.

By Jonathan C. Cruz, H. Tseng, J. A. Goldman, H. Shih, Li-Huei Tsai. Neuron, 2003

614 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/36e3d9ad4484f66ac58be1fd82d38e6692a3d131

How researchers see this paper

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

In Genetics

1. Aviv Regev
2. Martin Hemberg
3. R. Ransohoff

In Molecular Biology

1. Fei Liu
2. C. Gong
3. K. Iqbal
4. I. Grundke‐Iqbal
5. Aviv Regev
6. Li-Huei Tsai
7. Martin Hemberg
8. F. LaFerla

In Oncology

1. Li-Huei Tsai
2. R. Ransohoff

Citations in the corpus

• Age-Dependent Neurofibrillary Tangle Formation, Neuron Loss, and Memory Impairment in a Mouse Model of Human Tauopathy (P301L) (2005, background): “F, 40 ; G, H, 100 . neg, Negative; pos, positive. been shown to be central to the process of neurodegeneration following in a recent study that showed neuronal loss in the brains of inducible transgenic mice overexpressing the Cdk5 regulator p25 (Cruz et al., 2003).”
• Temporal Tracking of Microglia Activation in Neurodegeneration at Single-Cell Resolution (2017, background): “Additional AD-like phenotypes found in 6-week induced CK-p25 mice include forebrain atrophy, astrogliosis, aberrant APP processing, and hyperphosphorylation of tau (Cruz et al., 2003, 2006).”
• Post-translational modifications of tau protein: implications for Alzheimer's disease. (2011, neutral): “A role of CDK5 in tau phosphorylation and NFT formation has been clearly established in transgenic mice (Cruz et al., 2003; Noble et al., 2003).”
• Lipopolysaccharide-Induced Inflammation Exacerbates Tau Pathology by a Cyclin-Dependent Kinase 5-Mediated Pathway in a Transgenic Model of Alzheimer's Disease (2005, methodology): “Immunoprecipitation and kinase assays were performed as described previously with a slight modification (Cruz et al., 2003; Noble et al., 2003).”
• DNA damage and its links to neurodegeneration (2014, neutral): “…express p25 in a forebrain-specific manner and systematically recapitulate various AD-like pathologies including the accumulation of amyloid-β peptides, neurofibrillary tau tangles, astrogliosis, reduced synaptic density and neuronal loss in the forebrain (Cruz et al., 2006; Cruz et al., 2003).”
• Mechanisms of tau-induced neurodegeneration (2009, neutral): “Overexpression of p25 in transgenic mice, which results in an increase in the activity of cdk5, also produces hyperphosphorylation of tau [32, 136].”
• Tau pathology in Alzheimer disease and other tauopathies. (2005, background): “Overexpression of p25 in transgenic mice, which results in an increase in the activity of this enzyme, also produces hyperphosphorylation of tau [51,52].”