Cell Death Differ: The function of RPS23RG1 in neurodegenerative diseases.

Tau protein lesions (tauopathy) are a group of neurodegenerative diseases characterized by excessive phosphatation of the micro-tube binding protein tau, which is usually characterized by axon damage and synapse dysfunction.
cdk5 (cell cycle protein-dependent kinase 5) is an important tau kinase whose activity needs to be regulated by p35 or p25.
P35 is able to rapidly degrade proteases in the form of membrane binding and is cut into stable p25s by calcipase (calpain) under pressure, resulting in abnormal activation of Cdk5 and excessive phosphateization of tau.
RPS23RG1 is an IB-type trans-membrane protein that is expressed highly in the central nervous system, including neuronal cells, astoninal glial cells, and small glial cells.
previous studies have found a decrease in expression levels of RPS23RG1 in Alzheimer's disease (AD) brain tissue.
the function of RPS23RG1 in AD and Tau protein lesions-related diseases has yet to be further studied.
study found that the axon growth of the Rps23rg1 gene knockout (KO) mice was blocked, protein expression levels increased at p35 and p25, and phosphate levels at the main CDk5 phosphateation point of the tau protein.
the expression of p35 and the use of cdk5 inhibitor roscovitine can reduce the phosphorylation level of tau protein in Rps23rg1 KO mouse neurons and relieve the growth of axon obstruction.
interesting is that the interaction between the end of the RPS23RG1 carboxyl and the end of the p35 amino promotes the degradation of the upper membrane and protease of proteases.
addition, the P301L tau genetically modified (Tg) mouse model shows that tau's high phosphate levels increase, RPS? The expression level of 23RG1 is reduced and impaired with axon growth.
expression RPS23RG1 can significantly reduce tau's excessive phosphorication and axon growth in P301L tau Tg neurons.
, the results show that RPS23RG1 has a crucial role in Tau protein lesions-related diseases, which can inhibit excessive phosphorylation of tau protein by mediating p35 degradation and inhibiting Cdk5 activation.
lowering the level of RPS23RG1 triggers abnormal activation of Cdk5-p35, accompanied by tau's excessive phosphatization and blocked axon growth, suggesting that RPS23RG1 may be a potential therapeutic target for tauopathy disease.
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