组蛋白甲基化：从染色质调控到靶向干预
组蛋白甲基化是调控染色质状态和基因表达的重要表观遗传机制。不同修饰位点及甲基化程度具有不同的转录效应，其异常与肿瘤发生、细胞分化障碍及基因组稳定性失衡密切相关。
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PRMT5
用于检测、定量和定位抗原与抗体的技术——ELISA、免疫印迹、免疫组化与流式细胞术。以下是我们知识库中标注该主题的实验方案、常见问题与技术文章。
8 项资源 · 实验方案、常见问题与文章
Histone Methylation: From Chromatin Regulation to Targeted Intervention
Histone methylation is an important epigenetic mechanism that regulates chromatin states and gene expression. Different modification sites and degrees of methylation produce distinct transcriptional effects, and their dysregulation is closely associated with tumorigenesis, impaired cell ...
How Does MTAP Loss Reshape PRMT5 Dependency?
MTAP loss disrupts the methionine salvage pathway, resulting in the accumulation of 5′-methylthioadenosine (MTA) and partial inhibition of PRMT5 activity. Cancer cells consequently enter a state with limited PRMT5 functional reserve and develop greater dependence on residual PRMT5 activity and ...
MTAP缺失如何重塑PRMT5依赖？
MTAP缺失可阻断甲硫氨酸补救代谢，使5′-甲硫腺苷（MTA）积累并部分抑制PRMT5活性。癌细胞由此进入PRMT5功能余量降低的状态，对剩余PRMT5活性及SAM供应形成更强依赖，使MTAP缺失成为可利用的肿瘤代谢脆弱性。
How Does MTAP Deletion Create a Therapeutic Window for PRMT5 Inhibition? — Mechanistic Basis from MTA Accumulation to MTA-Cooperative PRMT5 Inhibitors
In 2016, two independent studies published in Science found that cancer cells deficient in methylthioadenosine phosphorylase (MTAP) were more sensitive to partial depletion of protein arginine methyltransferase 5 (PRMT5).[1,2] This finding emerged from large-scale functional genomic screens and ...
MTAP缺失如何形成PRMT5抑制的治疗窗？——从MTA积累到MTA协同型PRMT5抑制剂的机制基础
2016 年，两项独立发表于 Science 的研究发现，甲硫腺苷磷酸化酶（methylthioadenosine phosphorylase，MTAP）缺失的癌细胞，对蛋白精氨酸甲基转移酶5（protein arginine methyltransferase 5，PRMT5）的部分降低表现出更高敏感性[1,2]。这一发现由大规模功能基因组筛选获得，并通过 MTAP ...
MAT-SAM轴在药物靶向与代谢干预中的研究潜力
MAT催化甲硫氨酸与 ATP 生成 S-腺苷甲硫氨酸（SAM），而 SAM 既是细胞内最核心的活性甲基供体之一，又处于一碳代谢、表观遗传调控和应激适应的交汇位置。随着 MAT1A/MAT2A 同工酶切换、MTAP 缺失相关 MAT2A 依赖以及 PRMT5 轴耦合机制逐步明确，MAT-SAM ...
The Research Potential of the MAT-SAM Axis in Drug Targeting and Metabolic Intervention
MAT catalyzes the conversion of methionine and ATP into S-adenosylmethionine (SAM). SAM is not only one of the most central active methyl donors in cells, but also lies at the intersection of one-carbon metabolism, epigenetic regulation, and stress adaptation. As mechanisms involving MAT1A/MAT2A ...
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