Histone H3 (Acetyl Lys27) 兔多克隆抗體
引言
組蛋白修飾是表觀遺傳調(diào)控的核心機制，其中 H3K27ac（組蛋白H3第27位賴氨酸乙?；?/strong> 作為活性增強子的標志物，在基因轉(zhuǎn)錄激活、細胞分化及發(fā)育中起關(guān)鍵作用[1]。該修飾通過破壞染色質(zhì)壓縮結(jié)構(gòu)，促進轉(zhuǎn)錄因子與DNA結(jié)合，從而調(diào)控基因表達[2]。H3K27ac特異性抗體（如兔多克隆抗體）已成為表觀遺傳研究的重要工具，廣泛應(yīng)用于染色質(zhì)免疫沉淀（ChIP）、免疫細胞化學(xué)（ICC）等實驗[3][4]。
一、抗體基礎(chǔ)特性
1. 分子識別特異性
- 靶向H3K27ac位點，對非乙?；?、單/雙甲基化H3K27無交叉反應(yīng)[5]。
- 可區(qū)分活性增強子（H3K27ac?）與靜息/預(yù)備增強子（僅含H3K4me1）[1]。
2. 實驗適用性
- ChIP-seq：用于繪制全基因組增強子圖譜（如胚胎干細胞分化研究）[1][6]。
- 免疫熒光/組化：檢測組織切片（如睪丸、腦腫瘤）中H3K27ac的空間分布[3][7]。
- 稀釋比例：典型工作濃度為1:50–1:500（依實驗優(yōu)化）[3][4]。
二、作用機制
1. 表觀遺傳調(diào)控
- H3K27ac與H3K27me3（三甲基化）拮抗：乙酰化中和賴氨酸正電荷，開放染色質(zhì)；甲基化介導(dǎo)基因沉默[2][8]。
- 協(xié)同轉(zhuǎn)錄因子（如p300）維持增強子活性，驅(qū)動發(fā)育相關(guān)基因表達[1][9]。
2. 生物學(xué)功能
- 干細胞多能性：維持胚胎干細胞活性增強子網(wǎng)絡(luò)，重置核重編程過程[1]。
- 性別染色體逃逸基因：與RNF8/SCML2協(xié)同調(diào)控減數(shù)分裂中X/Y染色體基因激活[3]。
三、臨床應(yīng)用
1. 疾病診斷標志物
- 膠質(zhì)瘤分型：H3K27ac與H3K27M突變、H3K27me3聯(lián)合檢測，輔助鑒別兒童彌漫性中線膠質(zhì)瘤[7]。
- 心肌衰老：端粒縮短導(dǎo)致H3K27ac減少，驅(qū)動FOXC1依賴性心肌細胞衰老[4]。
2. 治療靶點探索
- 動脈粥樣硬化：視黃酸信號通過調(diào)節(jié)H3K27ac重塑平滑肌細胞表型[10]。
- 前列腺癌：JAK-STAT通路異常激活致H3K27ac重分布，促進干細胞樣態(tài)及耐藥性[5]。
四、未來展望
1. 技術(shù)創(chuàng)新
- 單細胞表觀組學(xué)：結(jié)合scChIP-seq/scCUT&Tag提升細胞異質(zhì)性解析[4]。
- 多維組學(xué)整合：聯(lián)合ATAC-seq、RNA-seq揭示H3K27ac動態(tài)調(diào)控網(wǎng)絡(luò)[11]。
2. 疾病治療
- 靶向表觀編輯器：開發(fā)CRISPR/dCas9-p300乙酰轉(zhuǎn)移酶復(fù)合物，精準修復(fù)H3K27ac異常[9][10]。
- 天然代謝物調(diào)控：利用卟啉代謝物靶向G4結(jié)構(gòu)，間接調(diào)控H3K27ac修飾[12]。
結(jié)語
H3K27ac兔多克隆抗體是表觀遺傳研究的關(guān)鍵試劑，其應(yīng)用深化了對基因調(diào)控、疾病機制的理解。隨著表觀編輯技術(shù)與多組學(xué)整合分析的發(fā)展，該抗體將繼續(xù)推動精準醫(yī)療與靶向治療創(chuàng)新。
參考文獻
1. Histone H3K27ac separates active from poised enhancers and predicts developmental state. Creyghton MP, et al. PNAS. 2010 Nov 24; 107(50):21931–21936. [PMID: 211067?59]
2. Characterization of an antagonistic switch between histone H3 lysine 27 methylation and acetylation in the transcriptional regulation of Polycomb group target genes. Pasini D, et al. Nucleic Acids Research. 2010 Apr 12; 38(15):4958–4962. [PMID: 20385?581]
3. RNF8 and SCML2 cooperate to regulate ubiquitination and H3K27 acetylation for escape gene activation on the sex chromosomes. Adams SR, et al. Genes & Development. 2018 Feb 01; 32(3-4):255–267. [PMID: 294?83155]
4. Proximal telomeric decompaction due to telomere shortening drives FOXC1-dependent myocardial senescence. Li B, et al. Circulation Research. 2024 Apr 18; 134(8):e1–e17. [PMID: 38629?201]
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6. GmMDE genes bridge the maturity gene E1 and florigens in photoperiodic regulation of flowering in soybean. Zhai H, et al. Plant Physiol. 2022 Jun 1;189(2):1021-1036. [PMID: 35234946]
7. Proteolipid Protein 2 Overexpression Indicates Aggressive Tumor Behavior and Adverse Prognosis in Human Gliomas. Chen YH, et al. Journal of Neuropathology & Experimental Neurology. 2018 Oct 26; 77(11):1045–1058. [PMID: 30203?052]
8. The histone H3K27 methylation mark regulates intestinal epithelial cell density-dependent proliferation and the inflammatory response. Turgeon N, et al. J Cell Biochem. 2013 May;114(5):1203-15. [PMID: 23192652]
9. PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression. Mittal P, et al. Nat Commun. 2024 Aug 24;15(1):7303. [PMID: 39181868]
10. Retinoic acid signaling modulates smooth muscle cell phenotypic switching in atherosclerosis through epigenetic regulation of gene expression. Pan H, et al. Nature Cardiovascular Research. 2022 Nov 10; 1(11):1030–1043. [PMID: 36?632201]
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