[Google Scholar] Li T
Although astrocyte reactivity is likely in the first instance to be targeted at maintaining CNS homoeostasis and circuit functions, various mechanisms could alter astrocyte functions in potentially detrimental ways, including (i) persistent reactivity may contribute to chronic neurodegenerative disorders or chronic inflammation, (ii) ageing and cellular senescence which may alter and reduce astrocyte functional capacities, or (iii) genetic mutations in diseased astrocytes or polymorphisms may alter normal astrocyte functions or responses
The nonenzymatic functions of GSTs involve their interactions with cellular proteins, such as, Jun N-terminal kinase,(JNK), tumor necrosis factor receptor-associated factor-2 (TRAF2), apoptosis-signal-regulating kinase 1 (ASK), serine/threonine kinases (PKA, PKC), and tissue transglutaminase 2 (TGM2), during which, either the interacting protein partner undergoes functional alteration or the GST protein itself is post-translationally modified and/or functionally altered [53], [74]
Guo R, Luo J, Chang J, Rekhtman N, Arcila M, Drilon A
