RGD Reference Report - Activation and redistribution of c-jun N-terminal kinase/stress activated protein kinase in degenerating neurons in Alzheimer's disease. - Rat Genome Database

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Activation and redistribution of c-jun N-terminal kinase/stress activated protein kinase in degenerating neurons in Alzheimer's disease.

Authors: Zhu, X  Raina, AK  Rottkamp, CA  Aliev, G  Perry, G  Boux, H  Smith, MA 
Citation: Zhu X, etal., J Neurochem. 2001 Jan;76(2):435-41.
RGD ID: 10412676
Pubmed: PMID:11208906   (View Abstract at PubMed)

Cellular responses to increased oxidative stress appear to be a mechanism that contributes to the varied cytopathology of Alzheimer's disease (AD). In this regard, we suspect that c-Jun N-terminal kinase/Stress activated protein kinase (JNK/SAPK), a major cellular stress response protein induced by oxidative stress, plays an important role in Alzheimer disease in susceptible neurons facing the dilemma of proliferation or death. We found that JNK2/SAPK-alpha and JNK3/SAPK-beta were related to neurofibrillary pathology and JNK1/SAP-Kgamma related to Hirano bodies in cases of AD but were only weakly diffuse in the cytoplasm in all neurons in control cases and in non-involved neurons in diseased brain. In this regard, in hippocampal and cortical regions of individuals with severe AD, the activated phospho-JNK/SAPK was localized exclusively in association with neurofibrillar alterations including neurofibrillary tangles, senile plaque neurites, neuropil threads and granulovacuolar degeneration structures (GVD), completely overlapping with tau-positive neurofibrillary pathology, but was virtually absent in these brain regions in younger and age-matched controls without pathology. However, in control patients with some pathology, as well as in mild AD cases, there was nuclear phospho-JNK/SAPK and translocation of phospho-JNK/SAPK from nuclei to cytoplasm, respectively, indicating that the activation and re-distribution of JNK/SAPK correlates with the progress of the disease. By immunoblot analysis, phospho-JNK/SAPK is significantly increased in AD over control cases. Together, these findings suggest that JNK/SAPK dysregulation, probably resulting from oxidative stress, plays an important role in the increased phosphorylation of cytoskeletal proteins found in AD.



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Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
MAPK10HumanAlzheimer's disease  IEP protein:increased expression:CA1 field of hippocampus:RGD 
MAPK8HumanAlzheimer's disease disease_progressionIEP protein:increased expression:brain and CA1 field of hippocampus:RGD 
MAPK9HumanAlzheimer's disease  IEP protein:increased expression:brain and CA1 field of hippocampus:RGD 
Mapk10RatAlzheimer's disease  ISOMAPK10 (Homo sapiens)protein:increased expression:CA1 field of hippocampus:RGD 
Mapk10MouseAlzheimer's disease  ISOMAPK10 (Homo sapiens)protein:increased expression:CA1 field of hippocampus:RGD 
Mapk8RatAlzheimer's disease disease_progressionISOMAPK8 (Homo sapiens)protein:increased expression:brain and CA1 field of hippocampus:RGD 
Mapk8MouseAlzheimer's disease disease_progressionISOMAPK8 (Homo sapiens)protein:increased expression:brain and CA1 field of hippocampus:RGD 
Mapk9RatAlzheimer's disease  ISOMAPK9 (Homo sapiens)protein:increased expression:brain and CA1 field of hippocampus:RGD 
Mapk9MouseAlzheimer's disease  ISOMAPK9 (Homo sapiens)protein:increased expression:brain and CA1 field of hippocampus:RGD 
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Genes (Rattus norvegicus)
Mapk10  (mitogen activated protein kinase 10) Mapk8  (mitogen-activated protein kinase 8) Mapk9  (mitogen-activated protein kinase 9)

Genes (Mus musculus)
Mapk10  (mitogen-activated protein kinase 10) Mapk8  (mitogen-activated protein kinase 8) Mapk9  (mitogen-activated protein kinase 9)

Genes (Homo sapiens)
MAPK10  (mitogen-activated protein kinase 10) MAPK8  (mitogen-activated protein kinase 8) MAPK9  (mitogen-activated protein kinase 9)