详细内容（前10条）

1. ⭐ GSE327611 KAT7 对小胶质细胞线粒体免疫的表观遗传控制驱动阿尔茨海默病的发病机制 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、Alzheimer、scRNA、epigenetic
• 📝 描述：Contributor : Yongqing LiuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer’s disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of Cmpk2, a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 expression, impairs mtDNA replication and release, and consequently suppresses cGAS-STING and NLRP3 signaling. Importantly, both microglia-specific deletion and pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced neuroinflammation, decrease amyloid-β burden, restore synaptic plasticity, and improve cognitive function in 5×FAD mice. Together, these findings uncover an epigenetic-mitochondrial axis sustaining microglial pathogenicity and establish KAT7 as a promising therapeutic target for AD.
• 🔗 查看原文

2. ⭐ GSE327604 KAT7 对小胶质细胞线粒体免疫的表观遗传控制驱动阿尔茨海默病的发病机制 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、Alzheimer、RNA-seq、epigenetic
• 📝 描述：Contributor : Yongqing LiuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer’s disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of Cmpk2, a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 expression, impairs mtDNA replication and release, and consequently suppresses cGAS-STING and NLRP3 signaling. Importantly, both microglia-specific deletion and pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced neuroinflammation, decrease amyloid-β burden, restore synaptic plasticity, and improve cognitive function in 5×FAD mice. Together, these findings uncover an epigenetic-mitochondrial axis sustaining microglial pathogenicity and establish KAT7 as a promising therapeutic target for AD.
• 🔗 查看原文

3. ⭐ GSE327681 JMJD1C介导的表观遗传控制自身免疫和HIT抗体产生[RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：antibody、RNA-seq、epigenetic
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHeparin-induced thrombocytopenia (HIT) is a common drug-induced immune disorder occurring in a subset of heparin-treated patients. Immune complexes comprising heparin, platelet factor 4 (PF4), and PF4/heparin-reactive antibodies are central to its pathogenesis. However, the role of epigenetic modification in HIT remains unexplored. Our study identified JMJD1C, a member of the lysine-specific histone demethylase 3 subfamily, as an essential regulator of PF4/heparin-specific antibody production. While JMJD1C was expressed throughout B-cell development and was dispensable for normal B-cell development, its deficiency disrupted immune tolerance and promoted production of self-reactive antibodies in systemic autoimmune diseases, including PF4/heparin-specific platelet-activating antibodies, a hallmark of pathogenic HIT antibodies. JMJD1C-deficient B cells were hyperresponsive, characterized by enhanced B-cell receptor (BCR)-induced proliferation. Transcriptomic analysis (RNA-Seq) revealed upregulation of pathways associated with BCR signaling, NF-kB activation, the cell cycle, and systemic lupus erythematosus (SLE). CUT&Tag profiling demonstrated that JMJD1C deficiency increased H3K36me1 modification at gene start sites in these pathways, indicating that epigenetic dysregulation drives B-cell hyperactivation. Importantly, transcriptional profiling and regulon analysis of B cells from HIT patients showed enrichment of BCR signaling, cell-cycle, NF-κB, and SLE-associated pathways, closely mirroring those in JMJD1C-deficient B cells. Epigenetic analyses further revealed enhanced promoter chromatin accessibility and elevated H3K36me1 deposition at promoter-TSS regions in HIT B cells. Together, these findings establish a strong molecular overlap between JMJD1C deficiency and human HIT B cells and reveal a previously unrecognized epigenetic mechanism underlying HIT pathogenesis. Our study provides the first evidence linking epigenetic regulation to HIT, offering new insights into its pathophysiology.
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4. ⭐ GSE328012 从单细胞测序推断涌现的时空过程揭示了从头 DNA 甲基化和染色质凝聚体之间的反馈 [亚硫酸氢盐测序 2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、methylation
• 📝 描述：Contributors : Fabrizio Olmeda ; Tim Lohoff ; Ioannis Kafetzopoulos ; Stephen J Clark ; Laura Benson ; Fatima Santos ; Felix Krueger ; Simon Walker ; Wolf Reik ; Steffen RulandsSeries Type : Methylation profiling by high throughput sequencingOrganism : Mus musculusRecent breakthroughs in single-cell genomics allow probing molecular states of cells with unprecedented detail along the sequence of the DNA. Biological function relies, however, on emergent processes in the three-dimensional space of the nucleus, such as droplet formation through phase separation. Here, we use single-cell multi-omics sequencing to develop a theoretical framework to rigorously map epigenome profiling along the DNA sequence onto a description of the emergent spatial dynamics in the nucleus. Drawing on scNMT-seq multi-omics sequencing in vitro and in vivo we exemplify our approach in the context of exit from pluripotency and global de novo methylation of the genome. We show how DNA methylation patterns of the embryonic genome are established through the interplay between spatially correlated DNA methylation and topological changes to the DNA. This feedback leads to the predicted formation of 30-40nm sized condensates of methylated DNA and determines genome-scale DNA methylation rates. We verify these findings with orthogonal single cell multi-omics data that combine the methylome with HiC measurements. Notably, this scale of chromatin organization has recently been described by super-resolution microscopy. Using this framework, we identify local methylation correlations in gene bodies that precede transcriptional changes at the exit from pluripotency. Our work provides a general framework of how mechanistic insights into emergent processes underlying cell fate decisions can be gained by the combination of single-cell multi-omics and methods from theoretical physics that have not been applied in the context of genomics before.
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5. ⭐ GSE304750 Arid3b 通过 Runx3 抑制微卫星稳定型结直肠癌中 CD8+ T 细胞的浸润和功能 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、RNA-seq
• 📝 描述：Contributors : Shuo Wang ; Sen Hou ; Ce Luo ; Yingjiang Ye ; Zexian Zeng ; Zhidong GaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMicrosatellite stable/proficient mismatch repair (MSS/pMMR) colorectal cancer (CRC) is characterized by a cold tumor microenvironment, marked by sparse CD8⁺ T cell infiltration and resistance to immune checkpoint inhibitors (ICIs). To uncover regulators that limit CD8⁺ T cell infiltration in MSS CRC, we conducted an in vivo CRISPR/Cas9 screen targeting genes in CD8⁺ T cells using a CMT93 cell-derived tumor model. This screen identified Arid3b as a key negative regulator of CD8⁺ T cell tumor infiltration and antitumor activity. Genetic ablation of Arid3b in CD8⁺ T cells significantly enhanced their intratumoral accumulation and mediated robust tumor control. Mechanistically, Arid3b deficiency upregulated Runx3, promoting a tissue-resident memory phenotype and effector function. Notably, the benefits conferred by Arid3b knockout were abrogated by Runx3 deletion, indicating a Runx3-dependent mechanism. In summary, targeting ARID3B could offer a promising strategy to reshape the tumor microenvironment and sensitize MSS CRC to immunotherapy.
• 🔗 查看原文

6. ⭐ GSE327640 靶向 UBE2F 诱导增强 CD8 T 细胞免疫的韧性程序 [批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、T cell、RNA-seq
• 📝 描述：Contributor : Xiaonan MaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCD8 memory T cells (TMEM) and exhausted T cells (TEX) are essential for host defense against infection and cancer, yet their therapeutic potential is often limited by insufficient persistence and sustained functional capacity. Strategies to enhance the longevity of both populations remain scarce. Here, we demonstrate that ablation of UBE2F, a neddylation E2 enzyme, induces a resilience program in CD8 T cells that operates across both TMEM and TEX compartments, resulting in improved viral and tumor control. This resilience state is characterized by enhanced self-renewal and survival without perturbing the conventional CD8 T cell differentiation trajectories. Mechanistically, UBE2F deficiency inhibited neddylation of CUL5, leading to accumulation of JUNB and upregulation of IL-2Rβ. The increased IL-2Rβ expression hypersensitizes CD8 T cells to physiological IL-15, thereby conferring the resilience features. Together, these findings identify the UBE2F-CUL5-JUNB-IL-2Rβ axis as a conserved post-translational mechanism regulating CD8 T cell longevity across memory and exhausted states, providing a novel strategy for enhancing antiviral and antitumor immunity.
• 🔗 查看原文

7. ⭐ GSE327608 KAT7 对小胶质细胞线粒体免疫的表观遗传调控驱动阿尔茨海默病的发病机制 [Cut & Tag]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、Alzheimer、epigenetic
• 📝 描述：Contributor : Yongqing LiuSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusMitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer’s disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of Cmpk2, a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 expression, impairs mtDNA replication and release, and consequently suppresses cGAS-STING and NLRP3 signaling. Importantly, both microglia-specific deletion and pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced neuroinflammation, decrease amyloid-β burden, restore synaptic plasticity, and improve cognitive function in 5×FAD mice. Together, these findings uncover an epigenetic-mitochondrial axis sustaining microglial pathogenicity and establish KAT7 as a promising therapeutic target for AD.
• 🔗 查看原文

8. GSE326619 JMJD1C介导的表观遗传调控自身免疫和HIT抗体产生

• ✍️ 作者：未知作者
• 🏷️ 关键词：antibody、epigenetic
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHeparin-induced thrombocytopenia (HIT) is a common drug-induced immune disorder occurring in a subset of heparin-treated patients. Immune complexes comprising heparin, platelet factor 4 (PF4), and PF4/heparin-reactive antibodies are central to its pathogenesis. However, the role of epigenetic modification in HIT remains unexplored. Our study identified JMJD1C, a member of the lysine-specific histone demethylase 3 subfamily, as an essential regulator of PF4/heparin-specific antibody production. While JMJD1C was expressed throughout B-cell development and was dispensable for normal B-cell development, its deficiency disrupted immune tolerance and promoted production of self-reactive antibodies in systemic autoimmune diseases, including PF4/heparin-specific platelet-activating antibodies, a hallmark of pathogenic HIT antibodies. JMJD1C-deficient B cells were hyperresponsive, characterized by enhanced B-cell receptor (BCR)-induced proliferation. Transcriptomic analysis (RNA-Seq) revealed upregulation of pathways associated with BCR signaling, NF-kB activation, the cell cycle, and systemic lupus erythematosus (SLE). CUT&Tag profiling demonstrated that JMJD1C deficiency increased H3K36me1 modification at gene start sites in these pathways, indicating that epigenetic dysregulation drives B-cell hyperactivation. Importantly, transcriptional profiling and regulon analysis of B cells from HIT patients showed enrichment of BCR signaling, cell-cycle, NF-κB, and SLE-associated pathways, closely mirroring those in JMJD1C-deficient B cells. Epigenetic analyses further revealed enhanced promoter chromatin accessibility and elevated H3K36me1 deposition at promoter-TSS regions in HIT B cells. Together, these findings establish a strong molecular overlap between JMJD1C deficiency and human HIT B cells and reveal a previously unrecognized epigenetic mechanism underlying HIT pathogenesis. Our study provides the first evidence linking epigenetic regulation to HIT, offering new insights into its pathophysiology.
• 🔗 查看原文

9. GSE304035 Arid3b 通过 Runx3 抑制微卫星稳定型结直肠癌中 CD8+ T 细胞的浸润和功能

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell
• 📝 描述：Contributors : Shuo Wang ; Sen Hou ; Ce Luo ; Yiteng Jin ; Yingjiang Ye ; Zexian Zeng ; Zhidong GaoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusMicrosatellite stable/proficient mismatch repair (MSS/pMMR) colorectal cancer (CRC) is characterized by a cold tumor microenvironment, marked by sparse CD8⁺ T cell infiltration and resistance to immune checkpoint inhibitors (ICIs). To uncover regulators that limit CD8⁺ T cell infiltration in MSS CRC, we conducted an in vivo CRISPR/Cas9 screen targeting genes in CD8⁺ T cells using a CMT93 cell-derived tumor model. This screen identified Arid3b as a key negative regulator of CD8⁺ T cell tumor infiltration and antitumor activity. Genetic ablation of Arid3b in CD8⁺ T cells significantly enhanced their intratumoral accumulation and mediated robust tumor control. Mechanistically, Arid3b deficiency upregulated Runx3, promoting a tissue-resident memory phenotype and effector function. Notably, the benefits conferred by Arid3b knockout were abrogated by Runx3 deletion, indicating a Runx3-dependent mechanism. In summary, targeting ARID3B could offer a promising strategy to reshape the tumor microenvironment and sensitize MSS CRC to immunotherapy.
• 🔗 查看原文

10. GSE303137 HNRNPH 在转录组范围内协同控制可变剪接 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、transcriptome
• 📝 描述：Contributors : Kerstin Tretow ; Mario Keller ; Mirko Brüggemann ; Simon Braun ; Anke Busch ; Kathi Zarnack ; Julian KönigSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo investigate alternative splicing regulation mediated by HNRNPH, we gradually decreased and increased HNRNPH protein concentration in MCF7 cells. Then, we performed splicing analysis using the data from the RNA-Seq.
• 🔗 查看原文

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1. ⭐ 和你同住的人可能会改变你的肠道菌群。

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
• 📝 描述：Spending time with close companions might do more than strengthen bonds—it could also reshape your gut bacteria. In a study of island birds, those with stronger social ties shared more gut microbes, especially types that require direct contact to spread. This suggests that social interaction itself—not just shared space—drives microbial exchange. The same process may be happening in human households through everyday closeness.
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2. ⭐ 桑格研究所空间转录组学发展史

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：At the Wellcome Sanger Institute, advances in spatial transcriptomics and RNA sequencing enable detailed mapping of gene expression and cellular interactions within complex tissues…
• 🔗 查看原文

3. 阻断单一蛋白质即可显著增强免疫系统对抗癌症的能力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Scientists have discovered a way to supercharge the immune system’s T cells by blocking a protein called Ant2, forcing the cells to rewire how they generate energy. This shift makes them more powerful, resilient, and effective at finding and destroying cancer cells.
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4. PhytoCell——一种用于识别植物单细胞RNA测序数据中细胞状态的集成学习框架

• ✍️ 作者：未知作者
• 🏷️ 关键词：scRNA
• 📝 描述：PhytoCell uses machine learning with RNA sequencing to identify marker genes and classify plant cell subpopulations, improving accuracy in complex single-cell datasets…
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5. 终生坚持这样做，或许能降低患阿尔茨海默病的风险38%。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：A lifetime of mental stimulation—like reading, writing, and learning new skills—may help protect the brain as we age. People with the highest levels of cognitive enrichment had a much lower risk of Alzheimer’s and experienced symptoms years later than those with the lowest levels.
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• GSE328023 利用 IgD 和 IgM 抗体衍生标签对人骨髓 B 细胞进行单细胞 CITE-seq 分析
• GSE327341 Surfaceome CRISPR激活筛选揭示了调控肿瘤对NK细胞杀伤敏感性的配体
• GSE326887 同源异构体水平的单细胞映射解析了同基因和半同种异体妊娠期间母胎界面处的细胞因子网络
• GSE320270 TFR 细胞通过 IL-10 调节肠道中抗共生菌 IgA 的特异性并抑制全身 IgA 反应
• GSE310745 CCM3 敲除内皮细胞的肿瘤样增殖：来自塞马西尼治疗和共培养转录组分析的启示
• GSE294111 慢性抗原驱动的人类T细胞功能障碍的翻译后调控图谱
• GSE293948 空间组织数百万愈伤组织细胞，识别核心网络，使番茄芽再生[空间]
• GSE293947 空间组织数百万愈伤组织细胞，识别出能够促进番茄芽再生的核心网络 [RNA-Seq 2]
• GSE293946 空间组织数百万愈伤组织细胞，识别出能够促进番茄芽再生的核心网络 [scRNA-Seq]
• GSE291545 体外研究从U87MG细胞系分选的CD133+VE细胞的化疗耐药性和干性相关的表观遗传调控因子
• GSE271813 位置至关重要：肌成纤维细胞的空间依赖性效应决定乳腺癌患者的生存率
• GSE327717 血清尿酸与心血管危险因素的关联以及痛风患者循环tsRNA生物标志物的鉴定
• GSE316230 Gene expression profile on a single-cell level of monocytes isolated from dura mater of mice infected with group B streptococci
• GSE309834 Massively multiplex multi-modal chemical screens at single-cell resolution with DOGMA-plex
• GSE300551 Massively multiplex multi-modal chemical screens at single-cell resolution with icCITE-plex
• GSE328010 对幼稚、活化和 HIV-1 感染的 CD4+ T 细胞进行 RNA 测序
• GSE313714 牙根表面无细胞牙骨质形成成牙骨质细胞的 Wnt 依赖性个体发育 [scRNA-seq]
• GSE304967 HNRNPH 在转录组范围内协同控制可变剪接 [RTstop 分析]
• GSE304723 HNRNPH 在转录组范围内协同控制可变剪接 [体外 iCLIP]
• GSE303138 HNRNPH 在转录组范围内协同控制可变剪接
• GSE303135 HNRNPH 在转录组范围内协同控制可变剪接 [iCLIP]
• GSE300647 Ryder：表观基因组标准化和可变特征识别
• GSE296450 小鼠持续低剂量电离辐射引起的免疫紊乱有限
• GSE286266 年龄影响 CMV 特异性 NK 和 CD8 T 细胞记忆命运（NK 细胞）
• GSE286265 年龄影响 CMV 特异性 NK 和 CD8 T 细胞记忆命运（OT-Is）
• GSE163010 内聚素环挤出在分化早期增强子激活基因表达中发挥作用（ATAC-seq）
• GSE163008 内聚素环挤出在分化早期增强子激活基因表达中发挥作用（ChIP-seq）
• GSE327705 肥大细胞选择性地将细胞外囊泡包裹的mRNA递送至结直肠癌细胞
• GSE327600 氯法齐明治疗对肝细胞癌细胞功能基因转录的影响评价
• GSE327595 内质网应激和自噬的稳态调控肝细胞癌细胞中的功能基因转录
• GSE326939：体外对甲硝唑表现出低、中、高耐药性的阴道毛滴虫分离株的转录组特征
• GSE319562 外周血转录组特征在慢性过敏性肺炎中的预后准确性
• GSE315295 通过亚群特异性转录组适应揭示伤害感受器在炎症和瘙痒中的不同作用
• GSE293577 拟南芥突变体 nac42-L1 和 nac42-L2 在温带和地中海驯化后接种核盘菌的全局转录组
• GSE230419 IBD 患者肠道活检固有层单核细胞的单细胞水平基因表达谱。