科研日报 2026-04-18
📅 Daily Report - 2026-04-18
今日筛选出 34 条内容,来自 3 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: DOT1L在肝细胞癌中双重抑制肿瘤免疫原性;新型Tn5技术实现大规模全基因组DNA甲基化测序。
主要方向:
- 肿瘤免疫微环境与治疗(肝癌、结直肠癌、淋巴水肿)
- 表观遗传学调控(DNA甲基化、组蛋白修饰、转录网络)
- 细胞代谢与信号通路(胱氨酸代谢、血管生成、粒细胞生成)
技术亮点:
- 基于Tn5转座酶的大规模全基因组DNA甲基化谱分析方法;
- 结合ChIP-seq、RNA-seq、ATAC-seq等多组学技术深入解析基因调控机制。
📊 学点生信
今日焦点: 首次利用R语言结合UniProt数据,实现跨蛋白质组的跨膜结构域(TMD)大规模扫描与计算。
主要方向:
- 蛋白质跨膜结构域(TMD)的全局鉴定与特性分析。
- 基于UniProt数据库的TMD信息自动化提取与计算。
技术亮点:
- 开发R语言脚本实现自动化TMD信息检索与分析。
- 整合UniProt数据库的丰富蛋白质信息,进行大规模TMD特征计算。
🧪 博客更新
今日焦点: 科学家成功增强免疫细胞杀伤癌细胞的效能与精准度;发现与细胞死亡相关的蛋白可作为延缓衰老新靶点。
主要方向:
- 肿瘤免疫疗法:通过优化免疫细胞信号通路,提升其抗肿瘤能力。
- 衰老机制研究:揭示特定蛋白对造血干细胞衰老的新型调控机制。
- 罕见病与癌症分子诊断:利用长读长RNA测序技术,精准识别致病性RNA剪接变异和基因融合。
技术亮点:
- 开发了通用且低成本的长读长RNA测序技术。
- 首次揭示“死亡”蛋白在延缓衰老中的潜在作用。
📚 分类浏览
🧬 数据前沿 (28条)
详细内容(前10条)
1. ⭐ GSE294356 DOT1L的双重功能抑制肝细胞癌的肿瘤内在免疫原性[ChIP-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、carcinoma、ChIP-seq
- 📝 描述:Contributors : Siyuan Xu ; Xianjiang LanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCheckpoint inhibitor therapy for Hepatocellular carcinoma (HCC) remains limited in patients’ overall response rate. Discovery and development of more effective combinatorial approaches in HCC checkpoint immunotherapy is urgent. Here, through CPlSPR/Cas9 genetic screens, we identify DOT1L as a versatile epigenetic factor that functions to suppress anti-tumor immunity through a dual mechanism. Depletion of DOT1L induces the expression of transposable elements and subsequent type-I interferon response, and meanwhile lowers ZEB1 levels to further unleash the expression of interferon simulated genes. In turn, we demonstrate that DOT1L loss or treatment with the selective DOT1L inhibitor EPZ-5676 sensitizes tumors to immune checkpoint blockade by increased immune infiltration in mouse. More importantly, EPZ-5676 treatment alone is sufficient to enhance antitumor immunity in humanized mouse model. These findings provide a rationale for targeting DOT1L to improve tumor immunogenicity and overcome immunotherapy resistance.
- 🔗 查看原文
2. ⭐ GSE294355 DOT1L的双重功能抑制肝细胞癌的肿瘤内在免疫原性[RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、carcinoma、RNA-seq
- 📝 描述:Contributors : Siyuan Xu ; Xianjiang LanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusCheckpoint inhibitor therapy for Hepatocellular carcinoma (HCC) remains limited in patients’ overall response rate. Discovery and development of more effective combinatorial approaches in HCC checkpoint immunotherapy is urgent. Here, through CPlSPR/Cas9 genetic screens, we identify DOT1L as a versatile epigenetic factor that functions to suppress anti-tumor immunity through a dual mechanism. Depletion of DOT1L induces the expression of transposable elements and subsequent type-I interferon response, and meanwhile lowers ZEB1 levels to further unleash the expression of interferon simulated genes. In turn, we demonstrate that DOT1L loss or treatment with the selective DOT1L inhibitor EPZ-5676 sensitizes tumors to immune checkpoint blockade by increased immune infiltration in mouse. More importantly, EPZ-5676 treatment alone is sufficient to enhance antitumor immunity in humanized mouse model. These findings provide a rationale for targeting DOT1L to improve tumor immunogenicity and overcome immunotherapy resistance.
- 🔗 查看原文
3. ⭐ GSE294354 DOT1L 的双重功能抑制肝细胞癌的肿瘤内在免疫原性 [ATAC-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、carcinoma、ATAC-seq
- 📝 描述:Contributors : Siyuan Xu ; Xianjiang LanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCheckpoint inhibitor therapy for Hepatocellular carcinoma (HCC) remains limited in patients’ overall response rate. Discovery and development of more effective combinatorial approaches in HCC checkpoint immunotherapy is urgent. Here, through CPlSPR/Cas9 genetic screens, we identify DOT1L as a versatile epigenetic factor that functions to suppress anti-tumor immunity through a dual mechanism. Depletion of DOT1L induces the expression of transposable elements and subsequent type-I interferon response, and meanwhile lowers ZEB1 levels to further unleash the expression of interferon simulated genes. In turn, we demonstrate that DOT1L loss or treatment with the selective DOT1L inhibitor EPZ-5676 sensitizes tumors to immune checkpoint blockade by increased immune infiltration in mouse. More importantly, EPZ-5676 treatment alone is sufficient to enhance antitumor immunity in humanized mouse model. These findings provide a rationale for targeting DOT1L to improve tumor immunogenicity and overcome immunotherapy resistance.
- 🔗 查看原文
4. GSE320203 一种可扩展的基于Tn5的基因组DNA甲基化谱分析方法,用于发育和疾病研究
- ✍️ 作者:未知作者
- 🏷️ 关键词:genome、methylation
- 📝 描述:Contributors : Hanrong Hu ; Nahuel Simonet ; Ece Naz Bilgiç ; Heather Murray ; Fides Zenk ; Regina Reimann ; Markus RechsteinerSeries Type : OtherOrganism : Danio rerio ; Homo sapiensDNA methylation is a critical epigenetic modification involved in various diseases, including cancer, and serves as a biomarker for early disease detection. Traditional detection methods, such as bisulfite sequencing, offer base-pair resolution but are costly and require high sequencing depths. We developed CmeCUT&Tag, a novel approach using methylation-binding domain fusion proteins coupled to hyperactive Tn5 transposase that selectively targets methylated DNA regions in both chromatinized and isolated DNA. These fusion proteins insert sequencing adapters into methylated regions, allowing low-depth sequencing for quantitative methylation assessment or bisulfite treatment for base pair resolution. Our approach enables comprehensive genome-wide DNA methylation profiling with minimal sequencing coverage. We demonstrated its efficacy in detecting DNA methylation in human stem cells and organoid systems. The system exhibits a high correlation with traditional bisulfite sequencing. It efficiently identifies CpG islands and DNA methylation dynamics during brain organoid development, highlighting its potential for biomedical applications in disease monitoring and aging research.
- 🔗 查看原文
5. GSE327961 淋巴水肿中由抗原呈递样脂肪基质细胞定义的免疫偏倚基质-免疫轴
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、antigen
- 📝 描述:Contributors : Nam Hyunsung ; Choi Una ; Ha Eun Hee ; Lee Brian Hyohyong ; Ko Jaecheon ; Kim Hyun Je ; Hong Ki YongSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground Lymphedema, a chronic and progressive disease, is characterized by lymphatic dysfunction, persistent inflammation, fibrosis, and pathological adipose tissue remodeling. Although adipose-derived stromal cells (ASCs) are implicated in disease progression, the stromal cell states and stromal–immune interactions that sustain chronic fibro-inflammatory remodeling remain poorly defined. Methods Single-cell RNA sequencing was performed of the stromal vascular fraction isolated from anatomically matched human subcutaneous adipose tissues. These tissues were obtained from patients with advanced-stage lymphedema and healthy individuals to delineate disease-associated stromal heterogeneity at single-cell resolution. Results A disease-expanded ASC progenitor population (ASC_c2) that exhibits pronounced transcriptional reprogramming in lymphedema was identified. The ASC_c2 population segregated into two mutually exclusive pathological subsets: a VCAM1⁺ vascular-interacting stromal population (V-ASCs) associated with ECM remodeling and CD74⁺HLA class II–expressing subset (I-ASCs) with antigen-presentation-like features. I-ASCs displayed a robust interferon-responsive transcriptional program consistent with immune priming and preferentially expressed the CXCL14 chemokine. Ligand–receptor interaction analysis revealed biased stromal–immune interactions between I-ASCs and CD8⁺ T cells, suggesting a skewed immune microenvironment in lymphedematous adipose tissue. Conclusions Our findings suggest an immune-skewed stromal–immune axis in lymphedema, driven by immune-primed, antigen-presentation-like ASCs. The study findings suggest a cellular framework linking stromal reprogramming to chronic immune dysregulation and fibrosis in human lymphedema, offering insights into potential therapeutic targets for interrupting pathological stromal–immune crosstalk.
- 🔗 查看原文
6. GSE318632 小鼠口咽癌单细胞RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:carcinoma、scRNA
- 📝 描述:Contributors : Carlos Silvestre-Roig ; Jadwiga Jablonska ; Raphael Chevre ; Alexander BenderSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusWe performed scRNA-seq analysis using the 10X genomics platform of mice following injection of mouse oropharyngeal carcinoma cell line MOPC in the flank of C57BL6/J to generate a model of murine oropharyngeal carcinoma. Here, we isolated bone marrow, spleen, blood and tumor from Gr1+and cKit+-enriched cells to investigate the dynamics of production across both sites of origin.
- 🔗 查看原文
7. GSE316605 高胆固醇血症小鼠免疫细胞和结构细胞的单细胞RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、scRNA
- 📝 描述:Contributors : Alexander Bender ; Celia Borja Almarcha ; Raphael Chevre ; Carlos Silvestre-Roig ; Oliver SoehnleinSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusWe performed scRNA-seq analysis using the 10X genomics platform of ApoE-/- mice fed for 16 weeks with high-fat diet (HFD). In these mice, we isolated brachiocephalic artery (BCA, digested), blood, bone marrow, spleen as well as perfusates of lung and liver at two times of the day (ZT1 and ZT13). For BCA cells, not-enriched cells and enriched cells (neutrophils, B- and T-cells, F4/80+ macrophages, CD31+ endothelial cells and CD31- stromal cells) were isolated and loaded for processing. For blood, bone marrow, spleen and the lung and liver perfusates, Lineage- Gr1+ were sorted together with enriched cKit+ cells.
- 🔗 查看原文
8. GSE295105 对 pfap2-g 报告基因系的分析揭示了疟原虫恶性疟原虫性决定的表观遗传机制 [RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:RNA-seq、epigenetic
- 📝 描述:Contributors : Elvira Carrió ; Martijn van den Broek ; Beatriz Graça ; Jonas Gockel ; Sylwia D boltryk ; Richárd Bártfai ; Till VossSeries Type : Expression profiling by high throughput sequencingOrganism : Plasmodium falciparumThis study aimed to investigate the changes occuring in parasites that are commited to express the sexual commitment transcription factor: ap2g.
- 🔗 查看原文
9. GSE295104 对 pfap2-g 报告基因系的分析揭示了疟原虫恶性疟原虫性决定的表观遗传机制 [ChIP-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:ChIP-seq、epigenetic
- 📝 描述:Contributors : Elvira Carrió ; Martijn van den Broek ; Beatriz Graça ; Jonas Gockel ; Sylwia D boltryk ; Richárd Bártfai ; Till VossSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Plasmodium falciparumThis study aimed to investigate the changes occuring in parasites that are commited to express the sexual commitment transcription factor: ap2g.
- 🔗 查看原文
10. GSE305827 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,确保血管生长和修复 [HUVEC_Ribo_ext553]
- ✍️ 作者:未知作者
- 🏷️ 关键词:histone
- 📝 描述:Contributor : Sofia-Iris BibliSeries Type : OtherOrganism : Homo sapiensEndothelial metabolic reprogramming is essential for vascular growth and critical for organ (re)generation, health and life span. Here, we identify a nuclear oxidative catabolic pathway that links cystine metabolism to endothelial gene regulation and angiogenesis. Endothelial cells preparing to proliferate, increase the translation of the transporter (SLC)7A11 to import cystine, which is further oxidatively catabolized by cystathionine gamma lyase (CSE) within the nuclear compartment. This process, preserved in young but not aged tissues, generates acetyl moieties in a pyruvate dehydrogenase dependent manner and initiates specific histone H3 lysine acetylation, leading to chromatin reorganization. Such changes solidify endothelial cell transcriptional programmes and maintain cell proliferation. Combined deletion of the SLC7A11 and CSE causes embryonic lethality and abrogates vascular growth. While SLC7A11 deficiency triggers compensatory de novo cysteine synthesis from methionine, partially preserving angiogenesis; CSE deletion disrupts nuclear cystine oxidative catabolism, endothelial transcription, and vessel formation. Therapeutically, oral cystine supplementation in models of retinopathy of prematurity, acute myocardial infraction and vascular injury in aging promotes vascular growth and repair. Together, our study highlights the role of cyst(e)ine nuclear oxidative catabolism in robust control of endothelial gene transcription, vessel growth and repair.
- 🔗 查看原文
💡 该来源还有 18 条内容,详见 文末
📊 学点生信 (1条)
详细内容(全部1条)
1. 我的研究领域:跨膜结构域的蛋白质组范围扫描
- ✍️ 作者:未知作者
- 🏷️ 关键词:proteome
- 📝 描述:I wanted to know: After a little bit of searching, I couldn’t find any answers. So I decided to use R to retrieve the necessary info from Uniprot and calculate it myself. I thought I’d post it here in case it’s useful for others. Human We’ll … Continue reading: My Domain: proteome-wide scanning of TMDs
- 🔗 查看原文
🧪 博客更新 (5条)
详细内容(全部5条)
1. 科学家们增强免疫细胞功能,使其能更有效地摧毁癌细胞。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、immune
- 📝 描述:Researchers have found a way to make cancer-killing immune cells more powerful and precise. By adding specific signaling components, they boosted the cells’ readiness to attack tumors. Surprisingly, briefly suppressing the cells with a drug before use made them even more effective later. The approach could help create safer, stronger next-gen cancer treatments.
- 🔗 查看原文
2. 费城儿童医院 (CHOP) 的研究人员开发出用途广泛且成本低廉的靶向长读长 RNA 测序技术
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing
- 📝 描述:Long-read RNA sequencing improves rare disease diagnosis by resolving transcript isoforms and variant effects, enabling more accurate interpretation of pathogenic splicing…
- 🔗 查看原文
3. IMA组织学检查结果应提示对非小细胞肺癌患者进行RNA测序——原因如下
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing
- 📝 描述:RNA sequencing enables detection of NRG1 fusions in invasive mucinous adenocarcinoma, ensuring accurate molecular profiling and identification of actionable targets often missed by DNA-based testing…
- 🔗 查看原文
4. 一种“死亡”蛋白或许是延缓衰老根源的关键。
- ✍️ 作者:未知作者
- 🏷️ 关键词:aging
- 📝 描述:Scientists have discovered that a protein linked to cell death is secretly driving the aging of blood stem cells in a completely different way. Instead of killing the cells, it damages their mitochondria, sapping their energy and weakening the immune system over time. When this protein was turned off, stem cells remained stronger and more balanced, even under stress. The findings point to a new strategy for slowing aging at its source.
- 🔗 查看原文
5. 气泡水能促进新陈代谢并帮助减肥吗?
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolism
- 📝 描述:Sparkling water is often seen as a simple, healthy drink—but could it also help with weight loss? New research suggests it may slightly boost how the body processes blood sugar and energy. However, the effect is very small, meaning it’s no substitute for diet and exercise.
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| histone | 7 |
| carcinoma | 4 |
| RNA-seq | 4 |
| tumor | 3 |
| ChIP-seq | 3 |
| immune | 3 |
| cancer | 3 |
| scRNA | 3 |
| sequencing | 2 |
| genome | 2 |
| ATAC-seq | 2 |
| epigenetic | 2 |
| regex:intestin(e | al) |
| proteome | 1 |
| methylation | 1 |
| antigen | 1 |
| monocyte | 1 |
| resistance | 1 |
| aging | 1 |
| metabolism | 1 |
📎 更多内容
🧬 数据前沿 其他内容 (18条)
- GSE305826 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,并确保血管生长和修复 [MLEC_WT_ACT]
- GSE305824 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,并确保血管生长和修复 [MLEC_WT_CSE-KO_ACT]
- GSE305823 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,并确保血管生长和修复 [Human_young_old_ATAC_ext353]
- GSE305822 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,并确保血管生长和修复 [MLEC_WT_CSE-KO_ATAC_ext251]
- GSE305820 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,并确保血管生长和修复 [MLEC_WT_CSE-KO_H3K9ac_CnR_ext577]
- GSE305819 胱氨酸输入和氧化分解代谢促进营养反应性组蛋白乙酰化,从而解锁内皮细胞位点的染色质,并确保血管生长和修复 [MLEC_WT_CSE-KO_RNA_ext248]
- GSE327886 脑-脾轴紊乱会损害单核细胞-小胶质细胞通讯并加速淀粉样变性小鼠模型的疾病进展
- GSE327697 肥大细胞与结直肠癌细胞直接相互作用,促进上皮间质转化
- GSE327665 研究发现,溃疡性结肠炎患者对乌司奴单抗的耐药性与促炎性黏膜调节性T细胞亚群的改变有关。
- GSE327273 逐步DNA解旋调控TnpB基因组编辑活性
- GSE318435 ATAC-seq of the granulopoiesis lineage from different organs
- GSE317310 scRNA-seq of bone marrow and splenic emergency granulopoiesis
- GSE294920 可扩展的微阵列类器官平台用于精确模拟肠上皮损伤和恢复
- GSE286910 人类排卵卵泡中孕酮受体 (PGR) 介导的转录网络:鉴定 SOX9 为一种新的 PGR 下游介质 [ChIP-seq]
- GSE286909 人类排卵卵泡中孕酮受体 (PGR) 介导的转录网络:鉴定 SOX9 为一种新的 PGR 下游介质 [RNA-seq]
- GSE328248 基于基因表达的胃癌患者个体化致癌过程
- GSE322512 Engrailed-1 增强线粒体移植在脊髓缺血再灌注损伤中的神经保护作用 [RNA-Seq]
- GSE288972 罗伊氏乳杆菌来源的胞外多糖促进化疗药物暴露造成的肠道上皮屏障损伤的修复
📅 报告生成时间:2026-04-17 22:04
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