Difference between revisions of "Pu-erh tea"
From MyWiki
(Created page with "Information on nutritional supplements people with ALS have been taking [https://en.wikipedia.org/wiki/Pu-erh_tea Wikipedia page] == Effects on ALS == Pu-erh tea may h...") |
m (Reverted edits by 45.146.26.46 (talk) to last revision by Leevi) |
||
| (6 intermediate revisions by 3 users not shown) | |||
| Line 1: | Line 1: | ||
[[Information on nutritional supplements people with ALS have been taking]] | [[Information on nutritional supplements people with ALS have been taking]] | ||
| − | [https://en.wikipedia.org/wiki/Pu-erh_tea Wikipedia page] | + | * [https://en.wikipedia.org/wiki/Pu-erh_tea Wikipedia page] |
| − | |||
== Effects on ALS == | == Effects on ALS == | ||
| Line 8: | Line 7: | ||
Pu-erh tea may have beneficial health effects, including preventing the onset of FET family protein-associated neurodegenerative diseases and delaying the progression of ALS by inhibiting the cytoplasmic aggregation of FET family proteins. | Pu-erh tea may have beneficial health effects, including preventing the onset of FET family protein-associated neurodegenerative diseases and delaying the progression of ALS by inhibiting the cytoplasmic aggregation of FET family proteins. | ||
| − | FET family proteins consist of fused in sarcoma/translocated in liposarcoma (FUS/TLS), Ewing's sarcoma (EWS), and TATA-binding protein-associated factor 15 (TAF15). Mutations in the copper/zinc superoxide dismutase (SOD1), TAR DNA-binding protein 43 (TDP-43), and FET family proteins are associated with the development of ALS. | + | FET family proteins consist of fused in sarcoma/translocated in liposarcoma (FUS/TLS), Ewing's sarcoma (EWS), and TATA-binding protein-associated factor 15 (TAF15). Mutations in the copper/zinc superoxide dismutase (SOD1), TAR DNA-binding protein 43 (TDP-43), and FET family proteins are associated with the development of ALS.{{#pmid: 24804206|Yu2014}} |
== Discussion threads on the ALSTDI forum == | == Discussion threads on the ALSTDI forum == | ||
== Regulated pathways == | == Regulated pathways == | ||
| − | |||
== References == | == References == | ||
| − | [ | + | [[Category:Supplement data pages]] |
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
Latest revision as of 17:58, 17 July 2022
Information on nutritional supplements people with ALS have been taking
Contents
Effects on ALS[edit]
Pu-erh tea may have beneficial health effects, including preventing the onset of FET family protein-associated neurodegenerative diseases and delaying the progression of ALS by inhibiting the cytoplasmic aggregation of FET family proteins.
FET family proteins consist of fused in sarcoma/translocated in liposarcoma (FUS/TLS), Ewing's sarcoma (EWS), and TATA-binding protein-associated factor 15 (TAF15). Mutations in the copper/zinc superoxide dismutase (SOD1), TAR DNA-binding protein 43 (TDP-43), and FET family proteins are associated with the development of ALS.[1]
Discussion threads on the ALSTDI forum[edit]
Regulated pathways[edit]
References[edit]
- ↑ Yu et al.: Pu-erh tea extract induces the degradation of FET family proteins involved in the pathogenesis of amyotrophic lateral sclerosis. Biomed Res Int 2014;2014:254680. PMID: 24804206. DOI. FET family proteins consist of fused in sarcoma/translocated in liposarcoma (FUS/TLS), Ewing's sarcoma (EWS), and TATA-binding protein-associated factor 15 (TAF15). Mutations in the copper/zinc superoxide dismutase (SOD1), TAR DNA-binding protein 43 (TDP-43), and FET family proteins are associated with the development of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease. There is currently no cure for this disease and few effective treatments are available. Epidemiological studies indicate that the consumption of tea is associated with a reduced risk of developing neurodegenerative diseases. The results of this study revealed that components of a pu-erh tea extract (PTE) interacted with FET family proteins but not with TDP-43 or SOD1. PTE induced the degradation of FET family proteins but had no effects on TDP-43 or SOD1. The most frequently occurring ALS-linked FUS/TLS mutant protein, R521C FUS/TLS, was also degraded in the presence of PTE. Furthermore, ammonium chloride, a lysosome inhibitor, but not lactacystin, a proteasome inhibitor, reduced the degradation of FUS/TLS protein by PTE. PTE significantly reduced the incorporation of R521C FUS/TLS into stress granules under stress conditions. These findings suggest that PTE may have beneficial health effects, including preventing the onset of FET family protein-associated neurodegenerative diseases and delaying the progression of ALS by inhibiting the cytoplasmic aggregation of FET family proteins.
