科研日报 2026-02-10
📅 Daily Report - 2026-02-10
今日筛选出 23 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: STAG2重构后在人类癌细胞中转录和基因组组织早期事件的RNA-Seq与Hi-C研究,揭示了基因组组织调控在癌症发生发展中的作用。
主要方向:
- 探索STAG2在癌细胞转录和基因组组织中的调控机制。
- 研究CFP1介导的H3K4me3宽域在早期B细胞谱系命运决定中的作用。
- 评估双靶向微球对肝细胞癌术后代谢-免疫微环境的重塑及疗效。
技术亮点:
- 空间转录组学技术应用于研究内脏利什曼病中巨噬细胞LPCAT2的表达。
- ATAC-seq和RNA-seq联合应用于TTNPB促进多能干细胞向神经干细胞转化的机制研究。
🧪 博客更新
今日焦点: 肠道细菌感知环境的新机制及其健康意义;芦荟化合物在阿尔茨海默病治疗中的潜力。
主要方向:
- 肠道微生物感知环境以维持生存和健康。
- 探索芦荟化合物(如β-谷甾醇)对抗阿尔茨海默病。
技术亮点:
- 揭示有益肠道微生物(特别是梭菌)感知环境的关键机制。
- 利用先进计算机模型发现芦荟化合物的治疗潜力。
📚 分类浏览
🧬 数据前沿 (21条)
详细内容(前10条)
1. ⭐ GSE318552 人类癌细胞中 STAG2 重组后转录和基因组组织的早期事件 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、RNA-seq、genome
- 📝 描述:Contributors : Tianyi Yang ; Jung-Sik Kim ; Clara Mellows ; Wanying Xu ; Alvin Ya ; Lisa Sadzewicz ; Luke Tallon ; Jann Sarkaria ; Fulai Jin ; Todd WaldmanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTruncating mutations of the tumor suppressor gene STAG2, encoding a component of the chromatin-bound cohesin complex, are present in many human cancer types. Here we report for the first time the early effects of reconstituting physiological levels of wild-type STAG2 in STAG2-mutant human cancer cells. Acute STAG2 reconstitution only modestly affected global gene expression - <1% of genes were altered by two-fold or greater. Only EFEMP1, encoding a secreted extracellular matrix glycoprotein, was induced by STAG2 in all experimental systems tested. There were similarly modest effects on chromatin loops - <1% of all chromatin loops were altered in intensity. and no loops were entirely STAG2-dependent. Loops strengthened by STAG2 reconstitution tended to be small, consistent with prior observations that STAG2-cohesin has less loop extrusion processivity than STAG1-cohesin. The STAG2-regulated “immediate early genes” were not accompanied by STAG2-regulated enhancer-promoter chromatin loops and no chromatin features were identified by integrative bioinformatics with newly generated ChIP-seq and ATAC-seq data that could explain their regulation by STAG2. Together these data indicate that the number of genes directly regulated by STAG2-cohesin is small, suggest that current models are likely insufficient to explain the mechanism of direct transcriptional regulation by STAG2-cohesin, and identify EFEMP1 as a potential effector of STAG2 tumor suppression.
- 🔗 查看原文
2. ⭐ GSE318550 人类癌细胞中 STAG2 重组后转录和基因组组织的早期事件 [Hi-C]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、Hi-C、genome
- 📝 描述:Contributors : Tianyi Yang ; Jung-Sik Kim ; Clara Mellows ; Wanying Xu ; Alvin Ya ; Lisa Sadzewicz ; Luke Tallon ; Jann Sarkaria ; Fulai Jin ; Todd WaldmanSeries Type : OtherOrganism : Homo sapiensTruncating mutations of the tumor suppressor gene STAG2, encoding a component of the chromatin-bound cohesin complex, are present in many human cancer types. Here we report for the first time the early effects of reconstituting physiological levels of wild-type STAG2 in STAG2-mutant human cancer cells. Acute STAG2 reconstitution only modestly affected global gene expression - <1% of genes were altered by two-fold or greater. Only EFEMP1, encoding a secreted extracellular matrix glycoprotein, was induced by STAG2 in all experimental systems tested. There were similarly modest effects on chromatin loops - <1% of all chromatin loops were altered in intensity. and no loops were entirely STAG2-dependent. Loops strengthened by STAG2 reconstitution tended to be small, consistent with prior observations that STAG2-cohesin has less loop extrusion processivity than STAG1-cohesin. The STAG2-regulated “immediate early genes” were not accompanied by STAG2-regulated enhancer-promoter chromatin loops and no chromatin features were identified by integrative bioinformatics with newly generated ChIP-seq and ATAC-seq data that could explain their regulation by STAG2. Together these data indicate that the number of genes directly regulated by STAG2-cohesin is small, suggest that current models are likely insufficient to explain the mechanism of direct transcriptional regulation by STAG2-cohesin, and identify EFEMP1 as a potential effector of STAG2 tumor suppression.
- 🔗 查看原文
3. ⭐ GSE290324 实验性内脏利什曼病期间肉芽肿巨噬细胞中 LPCAT2 的个体发育非依赖性表达 [空间转录组学]
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Shoumit Dey ; Jian-Hua Cao ; Benjamin Balluff ; Gaia Mazza ; Helen Ashwin ; Lesley Gilbert ; Sally James ; Adam A Dowle ; Grant Calder ; Nidhi S Dey ; Peter O’Toole ; Ron Heeren ; Paul M KayeSeries Type : OtherOrganism : Mus musculusGranulomas are organized inflammatory lesions that form in response to persistent stimuli such as infections. Murine infection with Leishmania donovani results in the formation of granulomas around infected Kupffer cells in the liver and serves as a well-defined model of immune granuloma formation. The formation and resolution of granulomatous inflammation requires dynamic shifts in immune cell activation states, imposing significant metabolic demands. As mediators of energy homeostasis and cell signaling, lipids and lipid metabolism play a key role in regulating immune cell function during inflammation and the response to infection. However, the extent to which alterations in lipids are spatially linked to altered immune cell transcription has yet to be resolved. In this study, we performed a multimodal imaging analysis combining MALDI mass spectrometry, spatial and single cell transcriptomics, proteomics of flow-sorted macrophages and histopathology of L. donovani induced hepatic granulomas. Using this spatially-integrated approach, we identified LPCAT2-mediated membrane re-modelling of myeloid cells as a novel feature of these granulomas. Our study provides new insights into local immunometabolic changes associated with granuloma formation and macrophage activation.
- 🔗 查看原文
4. GSE289601 CFP1介导的H3K4me3广泛结构域控制早期B细胞谱系命运决定[RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:B cell、RNA-seq
- 📝 描述:Contributors : Wanyu Bai ; Yalin Yang ; Yanan Zhao ; Shuoxu Gong ; Yimiao Lu ; Zhonghui Xue ; Lie Wang ; Fei-Long Meng ; Chun Chen ; Junchao DongSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHistone H3K4me3 broad domain (BD) is a unique epigenetic feature to mark cell identity-associated genes, but its physiological role in lineage differentiation remains unclear. Here we show that CFP1, an integral component of the Setd1A/B methyltransferase complex, is critically required for functional H3K4me3-BD installation and B cell fate determination. Cfp1 deletion impairs H3K4me3-BDs on a subset of B-lineage genes and redistributes H3K4me3 from active genes to bivalent promoters. Transcription of subsets of H3K4me3-BD-bound gene is diminished in part due to reduced RNA Pol II at the promoter and gene body. Specifically, CFP1 ablation abolishes H3K4me3-BD at the recombination center and distal PAIR elements in the immunoglobulin heavy chain (IgH) gene, severely compromises its locus contraction for efficient V-to-DJ recombination and consequently arrests cells at the pro-B stage. Moreover, Cfp1-deficient pro-B cells upregulate a panel of progenitor and myeloid-specific genes with elevated H3K4me3 marks and can trans-differentiate into various myeloid cell types. Therefore, our study reveals pivotal roles for CFP1-mediated H3K4me3-BDs in the transcriptional regulation of cell lineage fate specification and commitment.
- 🔗 查看原文
5. GSE289599 CFP1介导的H3K4me3广泛结构域控制早期B细胞谱系命运决定[ChIP-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:B cell、ChIP-seq
- 📝 描述:Contributors : Wanyu Bai ; Yalin Yang ; Yanan Zhao ; Shuoxu Gong ; Yimiao Lu ; Zhonghui Xue ; Lie Wang ; Fei-Long Meng ; Chun Chen ; Junchao DongSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHistone H3K4me3 broad domain (BD) is a unique epigenetic feature to mark cell identity-associated genes, but its physiological role in lineage differentiation remains unclear. Here we show that CFP1, an integral component of the Setd1A/B methyltransferase complex, is critically required for functional H3K4me3-BD installation and B cell fate determination. Cfp1 deletion impairs H3K4me3-BDs on a subset of B-lineage genes and redistributes H3K4me3 from active genes to bivalent promoters. Transcription of subsets of H3K4me3-BD-bound gene is diminished in part due to reduced RNA Pol II at the promoter and gene body. Specifically, CFP1 ablation abolishes H3K4me3-BD at the recombination center and distal PAIR elements in the immunoglobulin heavy chain (IgH) gene, severely compromises its locus contraction for efficient V-to-DJ recombination and consequently arrests cells at the pro-B stage. Moreover, Cfp1-deficient pro-B cells upregulate a panel of progenitor and myeloid-specific genes with elevated H3K4me3 marks and can trans-differentiate into various myeloid cell types. Therefore, our study reveals pivotal roles for CFP1-mediated H3K4me3-BDs in the transcriptional regulation of cell lineage fate specification and commitment.
- 🔗 查看原文
6. GSE317124 双靶向微球重塑代谢免疫微环境并逆转肝细胞癌栓塞术后的多重困境_HCC VS TAE
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、metabolic
- 📝 描述:Contributor : Nan JiangSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusTransarterial embolization (TAE) efficacy in hepatocellular carcinoma (HCC) is limited by post-embolization hypoxia-driven angiogenesis and metabolic reprogramming. To address these challenges, pH-responsive gelatin microspheres encapsulating zinc sulfide (ZnS) nanoparticles (ZnS@GMs) were developed for the dual delivery of hydrogen sulfide (H2S) gas and Zn2+ ions.
- 🔗 查看原文
7. GSE317123 双靶向微球重塑代谢免疫微环境并逆转肝细胞癌栓塞术后的多重困境_GM VS GZM
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、metabolic
- 📝 描述:Contributor : Nan JiangSeries Type : Expression profiling by high throughput sequencingOrganism : Rattus norvegicusTransarterial embolization (TAE) efficacy in hepatocellular carcinoma (HCC) is limited by post-embolization hypoxia-driven angiogenesis and metabolic reprogramming. To address these challenges, pH-responsive gelatin microspheres encapsulating zinc sulfide (ZnS) nanoparticles (ZnS@GMs) were developed for the dual delivery of hydrogen sulfide (H2S) gas and Zn2+ ions.
- 🔗 查看原文
8. GSE301756 TTNPB 通过调节染色质可及性和胆碱代谢促进多能干细胞向神经干细胞的转变 [ATAC-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolism、ATAC-seq
- 📝 描述:Contributor : Yanglin ChenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensEfficient derivation of neural stem cells (NSCs) from human pluripotent stem cells (PSCs) is crucial for developmental biology and regenerative medicine. Here, we established a chemically defined system using CHIR99021 and TTNPB to generate advanced NSCs (ANSCs). Integrated chromatin accessibility, transcriptomic, and metabolomic analyses revealed molecular mechanisms underlying neural fate commitment. TTNPB synergistically enhanced CHIR99021-mediated neural induction by globally increasing chromatin accessibility and activating neural-specific transcription factors. Compared to NSCs and PSCs, ANSCs exhibited robust upregulation of neural markers and enhanced chromatin remodeling. Metabolomic profiling identified significant metabolic reprogramming during the PSC-to-ANSC transition, with specific enrichment of S-adenosylhomocysteine (SAH), ADP, and glutathione in ANSCs correlating with elevated neural gene expression. Functionally, choline supplementation—regulated via the PEMT pathway—enhanced NESTIN expression and promoted neuroectodermal fate commitment. Our findings establish CHIR99021/TTNPB as a potent synergistic pair for efficient NSC induction and identify choline metabolism as a critical axis governing neuroectodermal lineage specification.
- 🔗 查看原文
9. GSE301755 TTNPB 通过调节染色质可及性和胆碱代谢促进多能干细胞向神经干细胞的转变 [RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolism、RNA-seq
- 📝 描述:Contributor : Yanglin ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; RattusEfficient derivation of neural stem cells (NSCs) from human pluripotent stem cells (PSCs) is crucial for developmental biology and regenerative medicine. Here, we established a chemically defined system using CHIR99021 and TTNPB to generate advanced NSCs (ANSCs). Integrated chromatin accessibility, transcriptomic, and metabolomic analyses revealed molecular mechanisms underlying neural fate commitment. TTNPB synergistically enhanced CHIR99021-mediated neural induction by globally increasing chromatin accessibility and activating neural-specific transcription factors. Compared to NSCs and PSCs, ANSCs exhibited robust upregulation of neural markers and enhanced chromatin remodeling. Metabolomic profiling identified significant metabolic reprogramming during the PSC-to-ANSC transition, with specific enrichment of S-adenosylhomocysteine (SAH), ADP, and glutathione in ANSCs correlating with elevated neural gene expression. Functionally, choline supplementation—regulated via the PEMT pathway—enhanced NESTIN expression and promoted neuroectodermal fate commitment. Our findings establish CHIR99021/TTNPB as a potent synergistic pair for efficient NSC induction and identify choline metabolism as a critical axis governing neuroectodermal lineage specification.
- 🔗 查看原文
10. GSE318493 唾液酸化的 CD43 形成糖免疫屏障,抑制抗白血病免疫
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、immunity
- 📝 描述:Contributors : Jooho Chung ; Mounica Vallurupalli ; Ashwin V Kammula ; Todd R Golub ; Robert T MangusoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMacrophages exert anti-tumorigenic activity through phagocytosis, but phagocytosis-enhancing therapeutics have not improved acute myeloid leukemia (AML) outcomes. To identify phagocytosis regulators, we performed CRISPR knockout screens in human AML cells co-cultured with human macrophages. We found that the “don’t eat me” signal CD47 inhibited mouse but not human macrophage phagocytosis. However, O-linked glycosylation and sialylation were strong negative regulators of phagocytosis. In AML, the cell surface mucin-like glycoprotein CD43 was the major effector of these pathways. Inhibition of phagocytosis by CD43 was dependent on the length of its ectodomain and independent of the macrophage sialic acid receptors SIGLEC-1, SIGLEC-7, and SIGLEC-9. The inhibitory effects of CD43 extended beyond human macrophages to natural killer and T cells. Thus, CD43 forms a glyco-immune barrier that restrains both innate and adaptive anti-leukemic immunity.
- 🔗 查看原文
💡 该来源还有 11 条内容,详见 文末
🧪 博客更新 (2条)
详细内容(全部2条)
1. ⭐ 肠道细菌能够感知周围环境,这对你的健康至关重要。
- ✍️ 作者:未知作者
- 🏷️ 关键词:bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
- 📝 描述:Your gut is home to trillions of bacteria that constantly “sense” their surroundings to survive and thrive. New research shows that beneficial gut microbes, especially common Clostridia bacteria, can detect a surprisingly wide range of chemical signals produced during digestion, including byproducts of fats, proteins, sugars, and even DNA. These microbes use specialized sensors to move toward valuable nutrients, with lactate and formate standing out as especially important fuel sources.
- 🔗 查看原文
2. 芦荟中一种隐藏的化合物有望对抗阿尔茨海默病
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer
- 📝 描述:Scientists have uncovered promising clues that compounds found in Aloe vera could play a role in fighting Alzheimer’s disease. Using advanced computer modeling, researchers discovered that beta-sitosterol—a natural plant compound—strongly interacts with two key enzymes involved in memory loss and cognitive decline. The compound showed stability, strong binding, and favorable safety indicators, making it a standout candidate for future drug development.
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| B cell | 6 |
| RNA-seq | 4 |
| immune | 3 |
| ChIP-seq | 2 |
| metabolic | 2 |
| metabolism | 2 |
| cancer | 2 |
| genome | 2 |
| scRNA | 2 |
| Alzheimer | 1 |
| ATAC-seq | 1 |
| bacteria | 1 |
| regex:bacter(ia | ial |
| gut | 1 |
| regex:gut(-?microbiome)? | 1 |
| Hi-C | 1 |
| immunity | 1 |
| carcinoma | 1 |
| sequencing | 1 |
| transcriptome | 1 |
📎 更多内容
🧬 数据前沿 其他内容 (11条)
- GSE318418 在索拉非尼和纳武利尤单抗联合治疗的 II 期试验中,肝功能障碍的肝细胞癌患者体内免疫抑制性单核细胞富集 [scRNA-Seq]
- GSE309480 WT iPSCs 和 R693Q iPSCs 的转录组测序研究
- GSE289627 CFP1介导的H3K4me3广域调控早期B细胞谱系命运决定
- GSE289602 CFP1介导的H3K4me3广泛结构域控制早期B细胞谱系命运决定[VDJ-Seq]
- GSE289600 CFP1介导的H3K4me3广泛结构域控制早期B细胞谱系命运决定[Cut&Tag]
- GSE289597 CFP1介导的H3K4me3广泛结构域控制早期B细胞谱系命运决定[4C-Seq]
- GSE315663 ACSS2 介导的赖氨酸巴豆酰化可减轻衰老并增强脂肪来源干细胞在炎症性肠病中的治疗效果 [RNA-Seq]
- GSE315662 ACSS2 介导的赖氨酸巴豆酰化可减轻衰老并增强脂肪来源干细胞在炎症性肠病中的治疗效果 [ChIP-Seq]
- GSE302482 9p缺失通过伴随Pax5和Cd72的丢失驱动B细胞白血病
- GSE290325 实验性内脏利什曼病期间肉芽肿巨噬细胞中 LPCAT2 的个体发育非依赖性表达 [scRNA-seq]
- GSE246657 神经元 TDP-43 通过神经连接蛋白 1 mRNA 稳定作用调节髓鞘形成
📅 报告生成时间:2026-02-09 22:00
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