Reactive gliosis surrounding amyloid beta (Abeta) plaques is an early feature of Alzheimer 's disease pathogenesis and has been postulated to represent activation of the innate immune system in an apparently ineffective attempt to clear or neutralize Abeta aggregates.
A balance in APP metabolism may influence the outcome between toxicity and protection to central nervous system (CNS) neurons in Alzheimer 's disease.
GeneChip analysis and in vitro kinase assays revealed potent APP-dependent repression of c-Jun , its target gene SPARC and reduced basal c-Jun N-terminal kinase (JNK) activity in PC12 cells overexpressing APP.
To study the role of c-Jun N-terminal kinase (JNK) and its relation to transcription factor AP-1 and Jun family proteins in hepatocellular carcinoma (HCC) with or without hepatitis B virus (HBV) infection.