S100A6 participates in initiation of autoimmune encephalitis and is under epigenetic control DOI Creative Commons
Chih‐Hsiang Lin, Sung‐Chou Li, Ming‐Hong Lin

и другие.

Brain and Behavior, Год журнала: 2023, Номер 13(3)

Опубликована: Фев. 7, 2023

Abstract Introduction Autoimmune encephalitis (AE) is caused by autoantibodies attacking neuronal cell surface antigens and/or synaptic antigens. We previously demonstrated that S100A6 was hypomethylated in patients with AE and it promoted B lymphocyte infiltration through the simulated blood–brain barrier (BBB). In this study, we focused on epigenetic regulation of , process which affects infiltration, therapeutic potential antibodies. Methods enrolled collected serum from 10 healthy control (HC) subjects. Promoter methylation 5‐azacytidine treatment assays were conducted to observe . The effect lymphocytes analyzed using an adhesion assay leukocyte transendothelial migration (LTEM) assay. A LTEM also used compare effects HCs, patients, recombinant protein, antibodies lymphocytes. Result promoter confirmed regulated DNA methylation. study addition enhanced between a BBB endothelial line concentration‐dependent manner. showed as well S100A6, could be attenuated Conclusion clarified under helped adhere infiltrate layer, counteracted Therefore, profile marker activity AE, countering may target for AE.

Язык: Английский

Activation of Hypoxia Inducible Factor-1 Alpha-Mediated DNA Methylation Enzymes (DNMT3a and TET2) Under Hypoxic Conditions Regulates S100A6 Transcription to Promote Lung Cancer Cell Growth and Metastasis DOI
Tengfei Wang, Genbao Zhu, Bo Wang

и другие.

Antioxidants and Redox Signaling, Год журнала: 2024, Номер 41(1-3), С. 138 - 151

Опубликована: Фев. 1, 2024

This research was aimed at investigating the effects of hypoxia inducible factor-1 alpha (HIF-1α)-mediated DNA methylation enzymes (ten-eleven translocase-2 [TET2] and methyltransferase-3a [DNMT3a]) under hypoxic conditions on S100A6 transcription, thereby promoting growth metastasis lung cancer cells.

Язык: Английский

Процитировано

2
S100A6 participates in initiation of autoimmune encephalitis and is under epigenetic control DOI Creative Commons
Chih‐Hsiang Lin, Sung‐Chou Li, Ming‐Hong Lin

и другие.

Brain and Behavior, Год журнала: 2023, Номер 13(3)

Опубликована: Фев. 7, 2023

Abstract Introduction Autoimmune encephalitis (AE) is caused by autoantibodies attacking neuronal cell surface antigens and/or synaptic antigens. We previously demonstrated that S100A6 was hypomethylated in patients with AE and it promoted B lymphocyte infiltration through the simulated blood–brain barrier (BBB). In this study, we focused on epigenetic regulation of , process which affects infiltration, therapeutic potential antibodies. Methods enrolled collected serum from 10 healthy control (HC) subjects. Promoter methylation 5‐azacytidine treatment assays were conducted to observe . The effect lymphocytes analyzed using an adhesion assay leukocyte transendothelial migration (LTEM) assay. A LTEM also used compare effects HCs, patients, recombinant protein, antibodies lymphocytes. Result promoter confirmed regulated DNA methylation. study addition enhanced between a BBB endothelial line concentration‐dependent manner. showed as well S100A6, could be attenuated Conclusion clarified under helped adhere infiltrate layer, counteracted Therefore, profile marker activity AE, countering may target for AE.

Язык: Английский

Процитировано

2