p(HGNC:MAPT, var("p.P301L"))

Entity

Name

MAPT

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Similarly, overexpressing the FTDP-17 mutant P301L tau in SH-SY5Y cells and then treating with lactacystin led to significantly increased tau levels (70). Lactacystin also caused accumulation of endogenous tau in the HT22 murine neuronal cell line (71). In immortalized mouse cortical neuronal cells inducibly expressing full-length wild-type tau, EPX slowed the degradation of full-length tau (72). PubMed:24027553

Stimulating autophagy either through serum withdrawal or rapamycin treatment in SH-SY5Y cells overexpressing P301L tau that had been induced to aggregate led to substantial reduction in aggregates that was prevented by 3-MA (70). PubMed:24027553

For example, it has been shown that the isomerase Pin1, which has been implicated in AD (30), had opposite effects on P301L and wild-type tau degradation (31). An alternative explanation for the effects of PSA may be that PSA is indirectly regulating tau degradation. PubMed:24027553

PSA was identified as a potential player in tau pathology through a microarray analysis of gene expression in disease-vulnerable vs. disease-resistant brain regions in JNPL3 mice that overexpress a mutant form of tau (P301L) found in the disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). These mice develop neurodegeneration in the cortex while the cerebellum is relatively spared [although in the original description of these animals pathology was found in the deep cerebellar nuclei (27)]. PubMed:24027553

PSA was identified as a potential player in tau pathology through a microarray analysis of gene expression in disease-vulnerable vs. disease-resistant brain regions in JNPL3 mice that overexpress a mutant form of tau (P301L) found in the disease frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). These mice develop neurodegeneration in the cortex while the cerebellum is relatively spared [although in the original description of these animals pathology was found in the deep cerebellar nuclei (27)]. PubMed:24027553