ADORA2B介导的抗炎细胞因子产生
中文名称
通路描述
腺苷受体A2B（ADORA2B）的天然配体是胞外腺苷（Ad-Rib），由ENTDP酶将ATP还原形成。ATP在寄生虫感染、组织损伤、凋亡等应激因素下进入细胞外空间，具有趋化性和兴奋性作用（Cekic et al. 2016）。ATP还原为Ad-Rib被认为是诱导抗炎细胞因子合成的调节机制，同时关闭了杀伤机制（Figueiredo et al. 2016）。因此，单核细胞中ADORA2B的表达增加与莱什曼原虫L. donovani载量增加及IL-10产生增加相关（Vijayamahantesh et al. 2016）。L. amazonensis感染小鼠病变的加重也与高浓度的Ad-Rib相关（Figueiredo et al. 2016）。
英文描述
Regulation of TP53 Activity through Methylation TP53 (p53) undergoes methylation on several lysine and arginine residues, which modulates its transcriptional activity.PRMT5, recruited to TP53 as part of the ATM-activated complex that includes TTC5, JMY and EP300 (p300), methylates TP53 arginine residues R333, R335 and R337. PRMT5-mediated methylation promotes TP53-stimulated expression of cell cycle arrest genes (Shikama et al. 1999, Demonacos et al. 2001, Demonacos et al. 2004, Adams et al. 2008, Adams et al. 2012). SETD9 (SET9) methylates TP53 at lysine residue K372, resulting in increased stability and activity of TP53 (Chuikov et al. 2004, Couture et al. 2006, Bai et al. 2011).TP53 transcriptional activity is repressed by SMYD2-mediated methylation of TP53 at lysine residue K370 (Huang et al. 2006). Dimethylation of TP53 at lysine residue K373 by the complex of methyltransferases EHMT1 and EHMT2 also represses TP53-mediated transcription (Huang et al. 2010). The chromatin compaction factor L3MBTL1 binds TP53 monomethylated at lysine K382 by SETD8 (SET8) and, probably through changing local chromatin architecture, represses transcription of TP53 targets (West et al. 2010). The histone lysine-specific demethylase LSD1 interacts with TP53 and represses p53-mediated transcriptional activation (Huang et al. 2007). PRMT1 and CARM1 can also modulate p53 functions in a cooperative manner (An et al. 2004).
所含基因
19 个基因