Proteasome expression

Kwak MK, Wakabayashi N, Greenlaw JL, Yamamoto M, Kensler TW. 2003. Antioxidants enhance mammalian proteasome expression through the Keapl-Nrf2 signaling pathway. Mol Cell Biol 23 8786-8794. 

Kumamoto, T., Fujimoto, S., Ito, T., Horinouchi, H., Ueyama, H., and Tsuda, T., 2000, Proteasome expression in the skeletal muscles of patients with muscular dystrophy, Acta Neuropathol (Berl), 100, pp 595-602. 

Proteasomal pathways degrade the oxidized and misfolded proteins. The partial loss of proteasomal expression and function has been described in the retinae of elderly rats (Louie et al., 2002). Oxidative and metabolic stress can have a cumulative effect. Accumulation of oxidatively damaged molecules can lead to the dysfunction of various metabolic and signaling pathways. 

Keller JN, Huang FF, Markesbery WR. Decreased levels of proteasome activity and proteasome expression in aging spinal cord. Neuroscience 2000 98(1) 149-156. 

Oxidative damage to cells is a common phenomenon, and quality control of modified proteins is important to maintain normal cellular functions. In the cytoplasm, nucleus, and endoplasmic reticulum, the proteasome is involved in the removal of various types of proteins such as ubiquinated, misfolded, or unfolded proteins, and oxidized proteins. Abnormal inhibition of proteasome may contribute to neuro-degenerative diseases such as Alzheimer disease, Parkinson disease, Lewy body dementia, and Huntington disease [31-40]. Neuromuscular diseases, such as sporadic inclusion-body myositis (s-IBM) share several phenotypes described in the brain tissues of Alzheimer and Parkinson disease patients [41]. One such similarity to Alzheimer disease is the accumulation of amyloid-P (AP), phosphory-lated tau (p-tau), and ubiquitin, which are often found within these aggregates [42, 43]. In s-IBM patients, significant proteasome abnormalities were identified including, increased 26 S proteasome expression and abnormal accumulation of 26S proteasome, but reduced proteasome activities [44]. The inverse relationship between increased expression... 

Ferrer I, MartinB, Castano JG et al. (2004) Proteasomal expression, induction of immunoproteasome suhunits, and local MHC class I presentation in myofibrillar myopathy and inclusion body myositis. J Neuropathol Exp Neurol 63, 484-498. 

F-adjacent Transcript-10 (FAT 10) is composed of two ubiquitin-like domains and capable to mark conjugated proteins for proteasomal degradation independent of ubiquitin. FAT10 is inducible by IFN-y and TNF and induces apoptosis when over expressed. 

Robust decreases in the expression of the various proteasome subunits and ubiquitin-conjugating enzymes have been described in prefrontal cortex in schizophrenia. Neuronal ubiquitin and proteasomes play an important role in the assembly, function and plasticity of the synapse. Structural proteins including tubulin and a-spectrin also show decreased expression in prefrontal cortex. 

Meinees, S. et al. Inhibition of proteasome activity induces concerted expression of proteasome genes and de novo formation of Mammalian proteasomes. J Biol Chem 2003, 278, 21517-25. 

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