科研日报 2026-08-26
📅 Daily Report - 2026-08-26
今日筛选出 62 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 多尺度空间转录组学技术(Visium HD, Visium, Xenium)首次解析了人杏仁核的细胞及分子精细结构;肿瘤细胞内源性应激状态驱动CAR-T疗法敏感性的机制被揭示。
主要方向:
- 解析人杏仁核的细胞及分子架构。
- 探究肿瘤细胞内源性应激状态对CAR-T疗法敏感性的影响。
- 研究 NSD2 蛋白在组蛋白修饰及重复序列表达中的空间调控作用。
- 揭示 SATB1 在 CD4+ T 细胞衰老过程中的 3D 染色质结构调控机制。
- 探索 KRAS 突变在结直肠癌中引起的差异性 mRNA 加工。
- 评估 BLVRB 靶向在单核细胞系急性髓系白血病免疫治疗中的潜力。
技术亮点:
- 整合多种空间转录组学技术(Visium HD, Visium, Xenium)实现多尺度解析。
- 结合 RNA-Seq, ChIP-Seq, Hi-C, ATAC-seq 等多组学技术进行综合研究。
🧪 博客更新
今日焦点: 肠道细菌能转化蔬菜中的硝酸盐和植物铁,生成有益心血管和代谢的保护性分子。某些常见药物可导致肠道菌群发生长期、持久的改变。
主要方向:
- 肠道菌群转化植物成分以促进心血管和代谢健康。
- 探索膳食氧化植物甾醇在诱导血管炎症中的作用机制。
- 研究常见药物对肠道微生物组的长期影响。
技术亮点:
- 利用单细胞RNA测序揭示7-酮基固醇诱导巨噬细胞极化和血管炎症的TLR4-IRF5信号通路。
- 通过RNA测序和Iso-Seq技术,提升马铃薯和番茄转录本注释的准确性,发现更多剪接异构体。
📚 分类浏览
🧬 数据前沿 (58条)
详细内容(前10条)
1. ⭐ GSE342738 多尺度空间转录组学解析人类杏仁核的细胞和分子结构 [Visium HD]
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、Visium、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Michael S Totty ; Svitlana V Bach ; Madeline R Valentine ; Madhavi Tippani ; Sarah E Maguire ; Ishbel Del Rosario Alvia ; Ryan A Miller ; Joel E Kleinman ; Kristen R Maynard ; Stephanie C Page ; Thomas M Hyde ; Stephanie C Hicks ; Keri MartinowichSeries Type : OtherOrganism : Homo sapiensThe amygdala is a central hub for emotional learning that is dysregulated across numerous psychiatric disorders, yet its molecular architecture in humans remains poorly defined. We here present a spatial transcriptomic atlas of the human amygdala from nine neurotypical donors. Integrating Visium, Xenium, and VisiumHD technologies, we profiled over 1.1 million cells across 13 spatial domains spanning the basolateral complex, central, medial, and cortical nuclei, as well as the intercalated islands, each defined by distinct marker genes and gene co-expression networks. By integrating snRNA-seq reference atlases, we found that each subdivision of the basolateral subnucleus contains distinct excitatory neuron classes. We additionally found three transcriptionally distinct populations of intercalated neuron types, two of which form spatially distinct islands neighboring the basolateral complex, and were able to refine cell type diversity across the central nucleus and related amygdalostriatal transition areas. Finally, we leveraged this atlas to spatially resolve the transcriptomic signatures of alcohol use disorder across cell types and subnuclei. Together, this atlas provides a foundational resource and framework for accelerating cross-species comparisons and human disease-focused investigations.
- 🔗 查看原文
2. ⭐ GSE342709 多尺度空间转录组学解析人类杏仁核的细胞和分子结构 [Visium]
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、Visium、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Michael S Totty ; Svitlana V Bach ; Ryan A Miller ; Madeline R Valentine ; Madhavi Tippani ; Sarah E Maguire ; Ishbel Del Rosario Alvia ; Joel E Kleinman ; Kristen R Maynard ; Stephanie C Page ; Thomas M Hyde ; Stephanie C Hicks ; Keri MartinowichSeries Type : OtherOrganism : Homo sapiensThe amygdala is a central hub for emotional learning that is dysregulated across numerous psychiatric disorders, yet its molecular architecture in humans remains poorly defined. We here present a spatial transcriptomic atlas of the human amygdala from nine neurotypical donors. Integrating Visium, Xenium, and VisiumHD technologies, we profiled over 1.1 million cells across 13 spatial domains spanning the basolateral complex, central, medial, and cortical nuclei, as well as the intercalated islands, each defined by distinct marker genes and gene co-expression networks. By integrating snRNA-seq reference atlases, we found that each subdivision of the basolateral subnucleus contains distinct excitatory neuron classes. We additionally found three transcriptionally distinct populations of intercalated neuron types, two of which form spatially distinct islands neighboring the basolateral complex, and were able to refine cell type diversity across the central nucleus and related amygdalostriatal transition areas. Finally, we leveraged this atlas to spatially resolve the transcriptomic signatures of alcohol use disorder across cell types and subnuclei. Together, this atlas provides a foundational resource and framework for accelerating cross-species comparisons and human disease-focused investigations.
- 🔗 查看原文
3. ⭐ GSE319162 肿瘤细胞内在应激状态驱动胰腺癌对 CAR T 细胞疗法的敏感性 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、cancer、T cell、RNA-seq
- 📝 描述:Contributors : Julia Fröse ; Evelyn Chen ; Charles Whittaker ; Paul Leclerc ; Sean Doherty ; Adam Langenbucher ; Jasmine Shao ; Riley Hellinger ; Daniel Goulet ; Tuomas Tammela ; Francisco Sánchez-Rivera ; Michael HemannSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic cancers, but has shown limited efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC). The cellular and molecular factors that influence CAR T cell therapy response remain largely unknown. By integrating modular in vivo CRISPR screens with single cell genomics and immunocompetent orthotopic models of PDAC, we uncover oxidative and proteotoxic stress pathways as previously unknown tumor-intrinsic modulators of CAR T cell therapy response. Disruption of stress-regulatory genes, particularly Keap1 and Slc33a1, sensitizes PDAC tumors to CAR T cell killing in vivo. Mechanistically, hyperactivation of the Nrf2 pathway by genetic ablation of the Keap1 tumor suppressor or endogenous engineering of a clinically observed Keap1 mutation enhances tumor susceptibility to CAR T cell therapy. Thus, tumor-intrinsic molecular stress phenotypes accompanying malignant tumor progression can induce unexpected cell state-specific vulnerabilities to cell-based immunotherapies. These findings provide a mechanistic molecular foundation to improve the efficacy of CAR T cell therapy in solid malignancies and to better stratify cancer patients by tumor genotype.
- 🔗 查看原文
4. ⭐ GSE304184 肿瘤细胞内在应激状态驱动胰腺癌对 CAR T 细胞疗法的敏感性 [scRNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、cancer、T cell、scRNA
- 📝 描述:Contributors : Julia Fröse ; Evelyn Chen ; Charles A Whittaker ; Paul Leclerc ; Sean Doherty ; Adam Langenbucher ; Jasmine Shao ; Riley D Hellinger ; Daniel Goulet ; Tuomas J Tammela ; Francisco J Sánchez-Rivera ; Michael T HemannSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChimeric antigen receptor (CAR) T cell therapy has transformed the treatment of hematologic cancers but has shown limited efficacy in solid tumors, including pancreatic ductal adenocarcinoma (PDAC). The cellular and molecular factors that influence CAR-T cell therapy response remain largely unknown. By integrating modular in vivo CRISPR screens with single cell genomics and immunocompetent models of PDAC, we uncover oxidative and proteotoxic stress pathways as previously unknown tumor-intrinsic modulators of CAR-T cell therapy response. Disruption of stress-regulatory genes, particularly Keap1 and Slc33a1, sensitizes PDAC tumors to CAR-T cell killing in vivo. Mechanistically, hyperactivation of the Nrf2 pathway by genetic ablation of the Keap1 tumor suppressor or endogenous engineering of a clinically observed Keap1 mutation enhances tumor susceptibility to CAR-T cell therapy. Thus, tumor-intrinsic molecular stress phenotypes accompanying malignant tumor progression can induce unexpected cell state-specific vulnerabilities to cell-based immunotherapies. These findings provide a mechanistic molecular foundation to improve the efficacy of CAR-T cell therapy in solid malignancies and better stratify cancer patients by tumor genotype.
- 🔗 查看原文
5. ⭐ GSE342289 多尺度空间转录组学解析人类杏仁核的细胞和分子结构 [Xenium]
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Michael S Totty ; Svitlana V Bach ; Madeline R Valentine ; Madhavi Tippani ; Sarah E Maguire ; Ishbel Del Rosario Alvia ; Ryan A Miller ; Joel E Kleinman ; Kristen R Maynard ; Stephanie C Page ; Thomas M Hyde ; Stephanie C Hicks ; Keri MartinowichSeries Type : OtherOrganism : Homo sapiensThe amygdala is a central hub for emotional learning that is dysregulated across numerous psychiatric disorders, yet its molecular architecture in humans remains poorly defined. We here present a spatial transcriptomic atlas of the human amygdala from nine neurotypical donors. Integrating Visium, Xenium, and VisiumHD technologies, we profiled over 1.1 million cells across 13 spatial domains spanning the basolateral complex, central, medial, and cortical nuclei, as well as the intercalated islands, each defined by distinct marker genes and gene co-expression networks. By integrating snRNA-seq reference atlases, we found that each subdivision of the basolateral subnucleus contains distinct excitatory neuron classes. We additionally found three transcriptionally distinct populations of intercalated neuron types, two of which form spatially distinct islands neighboring the basolateral complex, and were able to refine cell type diversity across the central nucleus and related amygdalostriatal transition areas. Finally, we leveraged this atlas to spatially resolve the transcriptomic signatures of alcohol use disorder across cell types and subnuclei. Together, this atlas provides a foundational resource and framework for accelerating cross-species comparisons and human disease-focused investigations.
- 🔗 查看原文
6. ⭐ GSE303602 NSD2 的空间分区沉积 H3K36me2 作为活性组蛋白标记促进重复序列表达 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:RNA-seq、spatial、histone
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHistone H3 lysine 36 dimethylation (H3K36me2) plays a key role in transcriptional elongation and chromatin organization, yet how its deposition is spatially controlled across the genome remains unclear. Here, we identify TOP1 as a critical recruiter of the H3K36me2 methyltransferase NSD2 to gene bodies. Disruption of the TOP1–NSD2 interaction reduces H3K36me2 at gene bodies, impairs RNA Polymerase II release, and represses transcription. Remarkably, loss of this recruitment increases H3K36me2 at repetitive sequences, licensing their aberrant transcriptional activation. Subsequently, we identify MTA1 as a principal recruiter of NSD2 at these repetitive sequences through the recognition of consensus sequence GATC. Together, we demonstrate that TOP1 and MTA1 orchestrate NSD2 binding to direct its genomic distribution. Our study elucidates a complex recruitment mechanism that spatially partitions NSD2, thereby establishing the bifunctional role of H3K36me2 in regulating canonical gene expression and serving as an active mark for the transcriptional activation of repetitive sequences.
- 🔗 查看原文
7. ⭐ GSE303598 NSD2 沉积 H3K36me2 作为活性组蛋白标记促进重复序列表达的空间分区 [ChIP-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:ChIP-seq、spatial、histone
- 📝 描述:Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHistone H3 lysine 36 dimethylation (H3K36me2) plays a key role in transcriptional elongation and chromatin organization, yet how its deposition is spatially controlled across the genome remains unclear. Here, we identify TOP1 as a critical recruiter of the H3K36me2 methyltransferase NSD2 to gene bodies. Disruption of the TOP1–NSD2 interaction reduces H3K36me2 at gene bodies, impairs RNA Polymerase II release, and represses transcription. Remarkably, loss of this recruitment increases H3K36me2 at repetitive sequences, licensing their aberrant transcriptional activation. Subsequently, we identify MTA1 as a principal recruiter of NSD2 at these repetitive sequences through the recognition of consensus sequence GATC. Together, we demonstrate that TOP1 and MTA1 orchestrate NSD2 binding to direct its genomic distribution. Our study elucidates a complex recruitment mechanism that spatially partitions NSD2, thereby establishing the bifunctional role of H3K36me2 in regulating canonical gene expression and serving as an active mark for the transcriptional activation of repetitive sequences.
- 🔗 查看原文
8. ⭐ GSE300662 幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变 3D 染色质结构并促进 T 细胞衰老 [Hi-C]
- ✍️ 作者:未知作者
- 🏷️ 关键词:aging、T cell、Hi-C
- 📝 描述:Contributors : Bao Wang ; Qian BianSeries Type : OtherOrganism : Mus musculusT cell aging significantly increases the incidence of infections, tumors, and autoimmune diseases in elderly individuals. However, the regulatory factors and molecular mechanisms that influence T cell aging remain unclear. We have previously discovered that the nuclear matrix-binding protein SATB1, a regulatory protein essential for the three-dimensional (3D) genome organization of T cells, plays a pivotal role in T cell activation and the expression of inflammatory genes. Our preliminary results further indicate that during T cell aging, SATB1 expression markedly decreases, resulting in alterations in the 3D genome organization through modulation of CTCF-mediated chromatin interactions. These structural changes subsequently affect the gene expression profile of T cells, thereby promoting the progression of T cell aging. This study aims to further elucidate the molecular mechanisms by which the downregulation of SATB1 remodels the 3D genome organization of T cells, and investigate the protective effects of restoring SATB1 expression on T cell aging. These findings will provide new insights into the mechanisms of T cell aging and may unveil potential therapeutic target for the clinical management of age-related immune decline.
- 🔗 查看原文
9. ⭐ GSE298137 幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变 3D 染色质结构并促进 T 细胞衰老 [ATAC-seq 2]
- ✍️ 作者:未知作者
- 🏷️ 关键词:aging、T cell、ATAC-seq
- 📝 描述:Contributors : Bao Wang ; Qian BianSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusT cell aging significantly increases the incidence of infections, tumors, and autoimmune diseases in elderly individuals. However, the regulatory factors and molecular mechanisms that influence T cell aging remain unclear. We have previously discovered that the nuclear matrix-binding protein SATB1, a regulatory protein essential for the three-dimensional (3D) genome organization of T cells, plays a pivotal role in T cell activation and the expression of inflammatory genes. Our preliminary results further indicate that during T cell aging, SATB1 expression markedly decreases, resulting in alterations in the 3D genome organization through modulation of CTCF-mediated chromatin interactions. These structural changes subsequently affect the gene expression profile of T cells, thereby promoting the progression of T cell aging. This study aims to further elucidate the molecular mechanisms by which the downregulation of SATB1 remodels the 3D genome organization of T cells, and investigate the protective effects of restoring SATB1 expression on T cell aging. These findings will provide new insights into the mechanisms of T cell aging and may unveil potential therapeutic target for the clinical management of age-related immune decline.
- 🔗 查看原文
10. ⭐ GSE297890 幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变 3D 染色质结构并促进 T 细胞衰老 [ATAC-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:aging、T cell、ATAC-seq
- 📝 描述:Contributors : Bao Wang ; Qian BianSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusT cell aging significantly increases the incidence of infections, tumors, and autoimmune diseases in elderly individuals. However, the regulatory factors and molecular mechanisms that influence T cell aging remain unclear. We have previously discovered that the nuclear matrix-binding protein SATB1, a regulatory protein essential for the three-dimensional (3D) genome organization of T cells, plays a pivotal role in T cell activation and the expression of inflammatory genes. Our preliminary results further indicate that during T cell aging, SATB1 expression markedly decreases, resulting in alterations in the 3D genome organization through modulation of CTCF-mediated chromatin interactions. These structural changes subsequently affect the gene expression profile of T cells, thereby promoting the progression of T cell aging. This study aims to further elucidate the molecular mechanisms by which the downregulation of SATB1 remodels the 3D genome organization of T cells, and investigate the protective effects of restoring SATB1 expression on T cell aging. These findings will provide new insights into the mechanisms of T cell aging and may unveil potential therapeutic target for the clinical management of age-related immune decline.
- 🔗 查看原文
💡 该来源还有 48 条内容,详见 文末
🧪 博客更新 (4条)
详细内容(全部4条)
1. ⭐ 肠道细菌或许能揭示蔬菜的隐藏益处
- ✍️ 作者:未知作者
- 🏷️ 关键词:bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
- 📝 描述:Gut bacteria can transform nitrate and plant-based iron from vegetables and other foods into protective molecules that may benefit the heart and metabolism. In experimental models, higher levels of these compounds were linked to lower blood pressure, better blood sugar control, healthier blood vessels, and less liver fat.
- 🔗 查看原文
2. 膳食中氧化的植物甾醇会改变巨噬细胞状态,从而促进主动脉炎症。
- ✍️ 作者:未知作者
- 🏷️ 关键词:macrophage、inflammation
- 📝 描述:Single-cell RNA sequencing reveals how dietary 7-ketositosterol promotes inflammatory macrophage polarization and vascular inflammation through the TLR4-IRF5 signaling pathway…
- 🔗 查看原文
3. 常用药物可能会在数年内改变你的肠道菌群。
- ✍️ 作者:未知作者
- 🏷️ 关键词:gut、regex:gut(-?microbiome)?
- 📝 描述:Common medications may reshape the gut microbiome long after the last dose is taken. In a study of more than 2,500 people, researchers found lasting microbial changes linked not only to antibiotics, but also to antidepressants, beta-blockers, acid-reducing drugs, and benzodiazepines. Some effects were still detectable years later, suggesting past medication use may strongly influence the gut bacteria people carry today.
- 🔗 查看原文
4. PotatoRTD 和 TomatoRTD:用于精确转录组分析和异构体发现的综合参考转录组数据集
- ✍️ 作者:未知作者
- 🏷️ 关键词:transcriptome
- 📝 描述:RNA sequencing and Iso-Seq improve potato and tomato transcript annotations, revealing additional isoforms and enabling more accurate analysis of gene expression and alternative splicing…
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| RNA-seq | 10 |
| T cell | 9 |
| aging | 8 |
| spatial | 7 |
| regex:immuno(logy | therapy |
| leukemia | 7 |
| immune | 6 |
| cancer | 6 |
| transcriptome | 5 |
| single-cell | 5 |
| transcriptomics | 4 |
| histone | 4 |
| sequencing | 4 |
| regex:intestin(e | al) |
| spatial transcriptomics | 3 |
| ChIP-seq | 3 |
| gut | 3 |
| regex:gut(-?microbiome)? | 3 |
| ATAC-seq | 3 |
| macrophage | 2 |
📎 更多内容
🧬 数据前沿 其他内容 (48条)
- GSE297889 幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变 3D 染色质结构并促进 T 细胞衰老 [RNA-seq]
- GSE107605 致癌KRAS差异性mRNA加工在结肠癌中的作用
- GSE344640 未经治疗的人类高级别浆液性卵巢癌的单细胞RNA测序
- GSE344578 EBV 再激活启动多发性硬化症复发中的外周免疫系统 [CD19+ B 细胞批量 RNA 测序]
- GSE344484 人类胎儿和新生儿初始CD4+ T细胞倾向于肠道迁移,并表现出易于被肠道激活的特征
- GSE344417 CD163/pAPN 双敲除猪背最长肌全转录组测序数据集 [RNA-seq]
- GSE307025 对经 PBS 或 OM-85 处理的 KrasG12D Tgfbr2-/- 肺腺癌小鼠模型中的免疫细胞进行单细胞 RNA 测序分析
- GSE344787 解码生物材料介导的骨再生中免疫细胞亚群的相互作用:中性粒细胞-巨噬细胞的顺序两阶段回路
- GSE344299 利用单细胞分辨率对秀丽隐杆线虫胚胎肠道进行高通量转录组分析
- GSE328697 通过阻断盘状结构域受体 2 改善卵巢癌免疫疗法
- GSE315606 靶向 BLVRB 可克服免疫抑制并增强单核细胞急性髓系白血病的免疫治疗效果
- GSE310226 靶向 BLVRB 可克服免疫抑制并增强单核细胞急性髓系白血病的免疫疗法 [bulk_atac_THP1]
- GSE300571 靶向 BLVRB 可克服免疫抑制并增强单核细胞急性髓系白血病的免疫疗法 [bulk_rna_patient]
- GSE300570 靶向 BLVRB 可克服免疫抑制并增强单核细胞急性髓系白血病的免疫疗法 [bulk_rna_CART]
- GSE300569 靶向 BLVRB 可克服免疫抑制并增强单核细胞急性髓系白血病的免疫疗法 [bulk_rna_THP1]
- GSE300568 靶向 BLVRB 可克服免疫抑制并增强单核细胞急性髓系白血病的免疫疗法 [CITE-seq]
- GSE320191 高剂量维生素 D3 补充剂与多发性硬化症中的先天免疫染色质重塑和背景依赖性转录组反应相关 [ATAC-seq]
- GSE320190 高剂量维生素 D3 补充剂与多发性硬化症中的先天免疫染色质重塑和背景依赖性转录组反应相关 [RNA-seq]
- GSE303600 NSD2 沉积 H3K36me2 作为活性组蛋白标记促进重复序列表达的空间分区 [CUT&Tag]
- GSE303597 NSD2 的空间分区沉积 H3K36me2 作为活性组蛋白标记促进重复序列表达 [TT-Seq]
- GSE300830 研究发现,幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变其三维染色质结构并促进 T 细胞衰老。
- GSE298143 幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变 3D 染色质结构并促进 T 细胞衰老 [CUT&Tag 2]
- GSE297892 幼稚 CD4+ T 细胞中 SATB1 的缺乏会改变 3D 染色质结构并促进 T 细胞衰老 [CUT&Tag]
- GSE262411 单细胞转录组学揭示高脂饮食对下丘脑(ARC)和后脑(DVC)葡萄糖感知的影响
- GSE344611 Id2 调控致病性 Th2 细胞中 IL-33 驱动的代谢重编程 (ChIP-seq)
- GSE344508 RNA-seq 分析了用 17-羟基jolkinolide B 处理的人类胶质瘤 LN229 细胞。
- GSE344418 CD163/pAPN 双敲除猪背最长肌全转录组测序数据集 [miRNA-seq]
- GSE343535 对稳定感染牛白血病病毒 (BLV) 的三种人类细胞系进行全转录组分析,揭示了新的凋亡相关因子
- GSE338895 表观遗传重编程改变袋状炎中人类肠道干细胞的命运
- GSE344333 ATRX 缺陷通过 cGAS 依赖性转录失调驱动 I 型干扰素信号异常 [RNA-seq]
- GSE330583 转录因子 Helios 对器官特异性自身免疫中的 T 调节细胞效应分化至关重要 [ChIP-seq]
- GSE313945 重组鞭毛蛋白FLAMOD对原代人呼吸道细胞的局部耐受性和高效先天免疫激活
- GSE212922 突变型和野生型 ATRX 细胞在神经元发育不同阶段的差异基因表达分析
- GSE343621:母体暴露于 HIV 和未暴露于 HIV 的儿童的 NK 细胞和经典单核细胞的 DNA 甲基化谱分析
- GSE343384 HIV暴露儿童和未暴露儿童NK细胞和经典单核细胞的转录组分析
- GSE272761 ATR-tBid复合物在细胞线粒体中的积累是细胞衰老和老化的标志,与通过逃避细胞凋亡而发生的年龄相关自发性肿瘤发生有关。
- GSE344539 NCOR1 通过 ERRα-RASSF1-Hippo/YAP 通路在体内外缓解骨关节炎软骨退化
- GSE344441 Eurotium cristatum 通过微生物组衍生的代谢组重编程改善高尿酸血症引起的肾脏焦亡。
- GSE344082 皱褶欧氏菌通过微生物组衍生的代谢组重编程改善高尿酸血症诱导的肾细胞焦亡
- GSE336129 11-羟基茉莉酸途径扩展了拟南芥中茉莉酸分解代谢的途径,从而减弱了应激特异性激素的表达
- GSE327308 丁酸盐通过促进 PLEKHG3-肌动蛋白结合来对抗母体肥胖引起的心脏缺陷
- GSE308826 EZH2-TTP-mTORC1轴驱动致命性前列腺癌的表型可塑性和治疗脆弱性
- GSE305941 miR-29c-3p上调对胃癌细胞增殖和转移过程中基因表达的影响
- GSE305782 泛素化凝聚体通过非酶促染色质机制塑造基因组结构
- GSE297820:不同分化和成熟方案下iPSC衍生树突状细胞的单细胞RNA测序
- GSE342086 HP1 二聚化驱动 H3K9me 标记染色质的凝聚和分离 [RNA-seq]
- GSE336656 RNA-seq 分析人类滋养层干细胞和绒毛外滋养层细胞中 EP300 和 CREBBP 敲低
- GSE328924 酮体介导的肾脏 mTORC1 信号通路调控在近端肾小管特异性 Tsc1 敲除小鼠中的单细胞转录组图谱
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