详细内容（前10条）

1. ⭐ GSE326241 多模态单细胞转录组和染色质可及性分析揭示缺血性中风后单核细胞衍生巨噬细胞的动态变化 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、monocyte、single-cell、scRNA
• 📝 描述：Contributors : Milton Hamblin ; Jean-Pyo LeeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIschemic stroke promotes monocyte recruitment to the injured brain and their differentiation into monocyte-derived macrophages (MDMs). These cells contribute to debris clearance but may also exacerbate neuroinflammation. However, the heterogeneity of macrophage subsets and the phenotypic transitions that shape MDM functional states during the subacute phase of stroke remain incompletely characterized. To address this, we first performed single-cell RNA sequencing (scRNA-seq) to define the transcriptional landscape of the mouse brain 48 hours after transient middle cerebral artery occlusion/reperfusion compared with sham controls. Reclustering of macrophage-lineage cells identified multiple monocyte-derived subsets, including a distinct Cd68hi/Ctsdhi MDM subset enriched for lysosomal and lipid-processing gene expression programs. Cell trajectory inference supported a transition from inflammatory infiltrates toward the Cd68hi/Ctsdhi state, accompanied by induction of transcriptomic networks that drive macrophage function to favor a clearance-competent phenotype in response to ischemic stroke. Complementary single-cell ATAC sequencing (scATAC-seq) demonstrated cell type-specific chromatin remodeling after stroke and revealed MDM subclusters with accessibility at key loci regulating lysosomal function and lipid metabolism. Together, our findings define a cellular and regulatory framework of the subacute post-stroke brain and identify a lysosome-enriched Cd68hi/Ctsdhi MDM trajectory, highlighting endolysosomal and lipid-processing programs during early stroke recovery.
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2. ⭐ GSE326118 多模态单细胞转录组和染色质可及性分析揭示缺血性卒中后单核细胞衍生巨噬细胞的动态变化 [scATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、monocyte、single-cell、scATAC
• 📝 描述：Contributors : Milton Hamblin ; Jean-Pyo LeeSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusIschemic stroke promotes monocyte recruitment to the injured brain and their differentiation into monocyte-derived macrophages (MDMs). These cells contribute to debris clearance but may also exacerbate neuroinflammation. However, the heterogeneity of macrophage subsets and the phenotypic transitions that shape MDM functional states during the subacute phase of stroke remain incompletely characterized. To address this, we first performed single-cell RNA sequencing (scRNA-seq) to define the transcriptional landscape of the mouse brain 48 hours after transient middle cerebral artery occlusion/reperfusion compared with sham controls. Reclustering of macrophage-lineage cells identified multiple monocyte-derived subsets, including a distinct Cd68hi/Ctsdhi MDM subset enriched for lysosomal and lipid-processing gene expression programs. Cell trajectory inference supported a transition from inflammatory infiltrates toward the Cd68hi/Ctsdhi state, accompanied by induction of transcriptomic networks that drive macrophage function to favor a clearance-competent phenotype in response to ischemic stroke. Complementary single-cell ATAC sequencing (scATAC-seq) demonstrated cell type-specific chromatin remodeling after stroke and revealed MDM subclusters with accessibility at key loci regulating lysosomal function and lipid metabolism. Together, our findings define a cellular and regulatory framework of the subacute post-stroke brain and identify a lysosome-enriched Cd68hi/Ctsdhi MDM trajectory, highlighting endolysosomal and lipid-processing programs during early stroke recovery.
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3. ⭐ GSE295950 单细胞 RNA 测序揭示代谢功能障碍相关脂肪肝疾病肝脏中单核细胞来源巨噬细胞的异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：monocyte、metabolic、sequencing、single-cell
• 📝 描述：Contributors : Haozhe Xu ; Lu Yang ; Guangyong SunSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMonocyte-derived macrophages (MoMFs) orchestrate inflammation and fibrogenesis in metabolic dysfunction-associated steatotic liver disease (MASLD). However, current therapeutic strategies targeting macrophage-mediated inflammation have shown limited clinical efficacy in MASLD. Using single-cell RNA sequencing (scRNA-seq) analysis of liver-infiltrating MoMFs from MASLD mouse models, we identified seven distinct clusters (c0-c6) with unique molecular signatures. Among these, the predominant CD14+CCR2+ (c0) showed multifaceted functions in fibrosis, lipid phagocytosis, and antigen presentation beyond inflammation. We identified two distinct clusters, CCR3+ (c3) and CCR7+ (c4) MoMFs, which exhibited enhanced pro-inflammatory/oxidative stress activity and specialized antigen-presenting capacity, respectively. Pseudotime analysis revealed that the resident basal cluster (c1) could give rise to both CD14+CCR2+ (c0) and CCR7+ (c4) MoMFs during disease progression, challenging the traditional view that CCR2+ MoMFs exclusively originate from bone marrow. Notably, these MoMFs subsets and their dynamic changes during disease progression were conserved between mouse models and human MASLD samples. These findings expand our understanding of MoMFs heterogeneity and suggest new therapeutic strategies for MASLD.
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4. ⭐ GSE301840 挽救生命的左心室辅助装置促进有利于心脏脂肪酸代谢、修复和抗炎的转录组特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、metabolism、cardiac
• 📝 描述：Contributors : Pauline Mury ; Olina Dagher ; Pierre-Emmanuel Noly ; Anique Ducharme ; Shreya Gramolini ; Filio Billia ; Eric ThorinSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensIn this study, we performed single-nuclei RNA sequencing on heart samples from 6 end-stage heart failure patients (3 ischemic cardiomyopathy and 3 non-ischemic cardiomyopathy). Each of these patients was treated with a left ventricular assist device (LVAD). Analysis of the longitudinal effect of LVAD at the transcriptomic level revealed a common signature profile related to the glucocorticoid receptor, independent of etiologies. Specifically, four genes promoting cardiac fatty acid metabolism, repair, and anti-inflammatory action were highlighted: FKBP5, ZBTB16, FOXO3, and PDK4.
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5. ⭐ GSE267599 AP-1 介导致癌转录并预测肺鳞状细胞癌患者的死亡率 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、regex:onco(logy|logist|gene|genic)、RNA-seq
• 📝 描述：Contributor : Xianglong TanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDespite the growing volume of genomic data, there remains a gap in our understanding of the mechanisms driving oncogenic transcription during non-small cell lung cancer (NSCLC) progression. In this study, we employed a model cell line-guided, multi-omic approach including promoter-capture Hi-C, ATAC-Seq, transcriptomics, and epigenomics, to uncover the epigenomic and three-dimensional (3D) genomic alterations on oncogenes in NSCLC patients from the Cancer Genome Atlas (TCGA). Our model cell lines recapitulate key aspects of the transcriptomic and chromatin-accessibility changes observed in NSCLC patients. ChIP-Seq analysis in model cell lines, revealed increased activity at promoters and enhancers, but decreased activity at insulators in NSCLC patients. We identified several increased promoter-enhancer interaction events in upregulated oncogenes. These aberrant enhancer-promoter looping events were mediated by the transcription factor AP-1. Survival analysis revealed a significant correlation between AP-1 expression levels and mortality in lung squamous carcinoma patients, but not in lung adenocarcinoma patients. Inhibition of AP-1, using AP-1 or JNK inhibitors, suggests that the abnormal activity of AP-1 is modulated by JNK kinases within the MAPK pathway, which promotes oncogenic transcription in NSCLC. These findings highlight the role of AP-1 in promoting lung squamous cell carcinoma progression and suggest that AP-1 and JNK inhibitors could be useful in treating high AP-1 lung squamous cell cancers.
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6. ⭐ GSE267597 AP-1 介导致癌转录并预测肺鳞状细胞癌患者的死亡率 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、regex:onco(logy|logist|gene|genic)、ChIP-seq
• 📝 描述：Contributor : Xianglong TanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensDespite the growing volume of genomic data, there remains a gap in our understanding of the mechanisms driving oncogenic transcription during non-small cell lung cancer (NSCLC) progression. In this study, we employed a model cell line-guided, multi-omic approach including promoter-capture Hi-C, ATAC-Seq, transcriptomics, and epigenomics, to uncover the epigenomic and three-dimensional (3D) genomic alterations on oncogenes in NSCLC patients from the Cancer Genome Atlas (TCGA). Our model cell lines recapitulate key aspects of the transcriptomic and chromatin-accessibility changes observed in NSCLC patients. ChIP-Seq analysis in model cell lines, revealed increased activity at promoters and enhancers, but decreased activity at insulators in NSCLC patients. We identified several increased promoter-enhancer interaction events in upregulated oncogenes. These aberrant enhancer-promoter looping events were mediated by the transcription factor AP-1. Survival analysis revealed a significant correlation between AP-1 expression levels and mortality in lung squamous carcinoma patients, but not in lung adenocarcinoma patients. Inhibition of AP-1, using AP-1 or JNK inhibitors, suggests that the abnormal activity of AP-1 is modulated by JNK kinases within the MAPK pathway, which promotes oncogenic transcription in NSCLC. These findings highlight the role of AP-1 in promoting lung squamous cell carcinoma progression and suggest that AP-1 and JNK inhibitors could be useful in treating high AP-1 lung squamous cell cancers.
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7. ⭐ GSE267596 AP-1 介导致癌转录并预测肺鳞状细胞癌患者的死亡率 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、regex:onco(logy|logist|gene|genic)、ATAC-seq
• 📝 描述：Contributor : Xianglong TanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensDespite the growing volume of genomic data, there remains a gap in our understanding of the mechanisms driving oncogenic transcription during non-small cell lung cancer (NSCLC) progression. In this study, we employed a model cell line-guided, multi-omic approach including promoter-capture Hi-C, ATAC-Seq, transcriptomics, and epigenomics, to uncover the epigenomic and three-dimensional (3D) genomic alterations on oncogenes in NSCLC patients from the Cancer Genome Atlas (TCGA). Our model cell lines recapitulate key aspects of the transcriptomic and chromatin-accessibility changes observed in NSCLC patients. ChIP-Seq analysis in model cell lines, revealed increased activity at promoters and enhancers, but decreased activity at insulators in NSCLC patients. We identified several increased promoter-enhancer interaction events in upregulated oncogenes. These aberrant enhancer-promoter looping events were mediated by the transcription factor AP-1. Survival analysis revealed a significant correlation between AP-1 expression levels and mortality in lung squamous carcinoma patients, but not in lung adenocarcinoma patients. Inhibition of AP-1, using AP-1 or JNK inhibitors, suggests that the abnormal activity of AP-1 is modulated by JNK kinases within the MAPK pathway, which promotes oncogenic transcription in NSCLC. These findings highlight the role of AP-1 in promoting lung squamous cell carcinoma progression and suggest that AP-1 and JNK inhibitors could be useful in treating high AP-1 lung squamous cell cancers.
• 🔗 查看原文

8. ⭐ GSE294606 通过转录组测序分析鉴定与主动脉夹层中程序性细胞死亡相关的生物标志物 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、RNA-seq、transcriptome
• 📝 描述：Contributors : Yukui Du ; Dongqing Chang ; Bofeng Yu ; Li Zhang ; Liang He ; Fengxia Wang ; Shaoyan ChangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Aortic dissection (AD) seriously threatens human health. Programmed cell death (PCD) plays a crucial role in AD development. This study aimed to identify biomarkers associated with PCD-related genes (PCD-RGs) in AD, providing new targets and strategies for therapeutic intervention. Methods: Transcriptome sequencing data from 5 control samples and 8 AD samples were analyzed. Candidate genes were identified by intersecting PCD-RGs with differentially expressed genes (DEGs). Biomarkers were found through PPI analysis and gene expression analysis. Functional enrichment, immune infiltration, regulatory network, and drug prediction analyses further elucidated AD mechanisms. Results: IL6, IL10, and TLR4 were identified as biomarkers for AD. IL6/IL10 had high expression in AD samples, while TLR4 had lower expression. Notably, these biomarkers are enriched in the “MYC Targets V1” pathway. Additionally, 5 immune cells with significant different were identified between AD and control samples. Correlation analysis indicated that IL10 had the strongest positive correlation with memory B cells and the strongest negative correlation with endothelial cells. Furthermore, 30 TFs targeting IL6, 23 targeting IL10, and 5 targeting TLR4 were identified. 6 key miRNAs targeting biomarkers and 5 key lncRNAs targeting the key miRNAs were also identified. This information was employed to construct regulatory networks, elucidating the mechanisms underlying these biomarkers. Finally, a total of 48, 20, and 23 drugs targeting IL6, IL10, and TLR4 were identified, which provided potential therapeutic targets for AD. Conclusion: IL6, IL10, and TLR4 were identified as biomarkers for AD, providing a promising foundation for targeted treatments.
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9. ⭐ GSE214527 组蛋白伴侣 ASF1B 在胎儿和成人红细胞生成过程中招募不同的表观遗传因子来调控组蛋白变体 H3.3 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、epigenetic、histone
• 📝 描述：Contributor : Xiang GuoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTo identify the role of ASF1B in regulation of histone modification during murine erythropoiesis, H3K27ac and H3.3 ChIP-seq was performed in the WT and ASF1B KO E14.5 fetal liver and bone marrow cells. ASF1B was found bind to the promoter and potential enhancer region. Loss of ASF1B impaired H3.3 and H3K27ac enrichments during development.
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10. ⭐ GSE214526 组蛋白伴侣 ASF1B 在胎儿和成人红细胞生成过程中招募不同的表观遗传因子来调控组蛋白变体 H3.3 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq、epigenetic、histone
• 📝 描述：Contributor : Xiang GuoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTo determine ASF1B function in chromatin accessbility, ATAC Seq was performed in both WT and ASF1B KO mouse liver. Loss of ASF1B caused generally decresed of chrmoatin accessbility on the promoters.
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1. 使用 R 包 crossvalidation 进行概率时间序列交叉验证

• ✍️ 作者：未知作者
• 🏷️ 关键词：R package
• 📝 描述：Examples of use of R package crossvalidation for Probabilistic Time Series Cross-Validation (measuring coverage and Winkler score) Continue reading: Probabilistic Time Series Cross-Validation with R package crossvalidation
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1. RNA的微小变化，对先天免疫力产生巨大影响

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity
• 📝 描述：RNA sequencing and protein interaction analyses reveal how a single nucleotide at the start of RNA can alter antiviral immune signaling and influence therapeutic RNA design…
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2. 科学家发现维生素B2可能有助于癌细胞存活

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have uncovered a surprising dark side to vitamin B2: it may help cancer cells stay alive. The vitamin supports a cellular shield that protects tumors from ferroptosis, a form of programmed cell death linked to cancer suppression. In lab tests, researchers used a vitamin B2-like compound called roseoflavin to break down that protection and trigger cancer cell death.
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• GSE330648 四价体内 CAR-巨噬细胞通过抗原扩散抑制实体瘤并克服肿瘤异质性
• GSE330471 单细胞转录组分析揭示 KLF2 限制肝细胞癌中肿瘤细胞的可塑性
• GSE331048 可配体结合的 PNT 结构域证实 ERG 是前列腺癌中可直接靶向的致癌驱动因子
• GSE304049 H3K27me3介导的FgHMG1表观遗传沉默使真菌能够逃避宿主免疫攻击
• GSE301437 USP7增强WTAP稳定性，通过激活AKT信号通路促进前列腺癌对恩扎卢胺的耐药性
• GSE299684 复发性小细胞肺癌患者标本的单细胞RNA测序分析
• GSE293015 创伤诱导急性肾损伤大鼠模型中空间分辨的肾脏转录组特征
• GSE292717 超级增强子驱动的 SOX4/SMAD3 通过膜磷脂重塑增强 AXL 信号传导，加速白血病进展 [RNA-Seq]
• GSE292716 超级增强子驱动的 SOX4/SMAD3 通过膜磷脂重塑增强 AXL 信号传导，加速白血病进展 [ChIP-seq]
• GSE288291 单细胞 RNA 测序 - 幼鼠和老鼠肠道
• GSE267598 AP-1 介导致癌转录并预测肺鳞状细胞癌患者的死亡率 [pcHi-C]
• GSE256530 代谢检查点控制造血干细胞复制寿命（scRNA-Seq）
• GSE256529 代谢检查点控制造血干细胞复制寿命（批量RNA测序）
• GSE330557 蛋白质组学筛选发现 CTCF 是一种关键的 G-四链体结合蛋白 [Hi-C]
• GSE330215 子宫内膜癌中肥胖相关基因表达程序的空间转录组学特征
• GSE320140 通过比较单细胞分辨率下的转录谱来了解衰老对肠道上皮细胞的影响。
• GSE312913 SARS-CoV-2 Omicron重症患者支气管肺泡灌洗液单细胞转录组分析
• GSE308087：皮质性白内障患者血液的RNA测序和生物信息学分析
• GSE302661 单核 RNA-seq 分析解析了纤维板层癌的染色质和转录特征
• GSE302568 单核 ATAC-seq 分析解析了纤维板层癌的染色质和转录特征
• GSE294607 通过转录组测序分析鉴定与主动脉夹层中程序性细胞死亡相关的生物标志物
• GSE288430 蛋白质组学筛选发现 CTCF 是一种关键的 G-四链体结合蛋白 [RNA-seq]
• GSE287919 人类晶状体稳态和衰老的单细胞转录组图谱
• GSE285838 组蛋白伴侣 ASF1B 在胎儿和成人红细胞生成过程中通过招募不同的表观遗传因子来调控组蛋白变体 H3.3 II
• GSE215076 组蛋白伴侣 ASF1B 在胎儿和成人红细胞生成过程中招募不同的表观遗传因子来调控组蛋白变体 H3.3。
• GSE214528 组蛋白伴侣 ASF1B 在胎儿和成人红细胞生成过程中招募不同的表观遗传因子来调控组蛋白变体 H3.3
• GSE330642 一种靶向人类 ENPP1（一种在患病人类肾脏中表达的外核苷酸酶）的人源化单克隆抗体可增强肾小管增殖和肾脏修复，并且在非人灵长类动物中安全 [scRNA-seq]
• GSE330470 人类 HCC 细胞系 HCCLM3 中 YAP/TAZ-TEAD 和 SMAD3 基因组结合的 ChIP-seq 和 CUT&Tag 分析 [ChIP-seq]
• GSE330469 ChIP-seq 和 CUT&Tag 分析 YAP/TAZ-TEAD 和 SMAD3 在人类 HCC 细胞系 HCCLM3 中的基因组结合情况 [CUT&Tag]
• GSE331078 CMPK2 限制结核分枝杆菌复制并调节巨噬细胞基因表达
• GSE330560 蛋白质组学筛选揭示 CTCF 是一种关键的 G-四链体结合蛋白
• GSE327120 miR-712-3p干预后HT22的转录组表达
• GSE327067 FTO促进膀胱癌进展和干细胞相关表型
• GSE320366 短期 HIPEC 模拟暴露于米索霉素 A 可诱导 HT-29 结直肠癌细胞发生结构化转录重编程
• GSE319107 APC/C 亚基 APC7 通过介导 LATS1/2 的泛素化和降解来激活 YAP/TAZ，从而促进肝细胞癌的进展。
• GSE318175 一氧化氮依赖性波形蛋白稳定作用赋予卵巢癌化疗耐药性
• GSE315612 益气活血养阴汤通过METTL3-m6A-mTOR通路激活自噬，减轻足细胞损伤，从而缓解糖尿病肾病
• GSE314724 通过从半胱氨酸中分配细胞内硫来独特地控制 T 细胞增殖和效应功能
• GSE312448 CS2164 与放射治疗联合使用，可通过干扰 DNA 损伤修复和改变肿瘤微环境来抑制肿瘤生长。
• GSE309360：牛窦前卵泡早期卵泡发育过程中的转录组分析
• GSE306271 敲除 MSLN 基因的 NOMO-1 细胞转录组分析
• GSE305183 结直肠癌转移进展过程中肝脏的基因表达
• GSE301181 利用新一代测序技术鉴定肺组织来源成纤维细胞表达的特发性肺纤维化特异性基因
• GSE299580 TCOF1沉默对肾癌细胞的影响
• GSE293647 人类iPSC衍生GABA能中间神经元移植可挽救阿尔茨海默病模型中的回路功能障碍和tau蛋白病理
• GSE292718 超级增强子驱动的 SOX4/SMAD3 通过膜磷脂重塑增强 AXL 信号传导，加速白血病进展 [CUT&Tag]
• GSE292560 RBFOX1 缺陷诱导 APOE4 人类脑类器官中固有小胶质细胞生成并加剧阿尔茨海默病病理
• GSE288290 幼鼠和老年鼠的结肠上皮细胞和免疫细胞
• GSE277546 胆管细胞癌成分 (CLC) 预测了肝内胆管癌 (MF-iCC) 的一个在遗传和生物学上不同的亚组。
• GSE237434 巴西素在乳腺癌细胞中的转录效应
• GSE330619 CRISPR干扰筛选在ALK+间变性大细胞淋巴瘤细胞培养物（SU-DHL-1）中进行，该细胞培养物接受外周T细胞淋巴瘤治疗中使用的疗法处理。
• GSE328954：两种新型分枝杆菌（卡氏分枝杆菌和蓬卡分枝杆菌）的转录组分析
• GSE328953 感染分枝杆菌的THP-1来源巨噬细胞的转录组学
• GSE325086 神经酰胺诱导的内质网应激作为内分泌治疗耐药乳腺癌的可靶向脆弱性
• GSE324253 RNA-seq 在用黄连碱处理的 HCT116 细胞中进行
• GSE324248 小分子破坏 G4-STAT1 相互作用并与奥拉帕尼协同作用以驱动癌细胞死亡
• GSE320421 羟氯喹通过减弱颗粒细胞衰老和调节 mtDNA-cGAS 通路缓解环磷酰胺诱导的卵巢早衰
• GSE316626 Th17过继转移介导的实验性自身免疫性脑脊髓炎期间的免疫细胞动力学
• GSE315376 线粒体原位释放的科罗索酸通过激活线粒体自噬增强去势抵抗性前列腺癌的抗肿瘤作用
• GSE314864 区室化的炎症环境和巨噬细胞可塑性调节 Tet2+/- 介导的克隆性造血
• GSE314387 复发性 ZC3H18 突变稳定致癌内源性逆转录病毒 RNA [SW480_pA]
• GSE314385 复发性 ZC3H18 突变稳定致癌内源性逆转录病毒 RNA [A375_ribominus]
• GSE314384 复发性 ZC3H18 突变稳定致癌内源性逆转录病毒 RNA [A375_polyA]
• GSE311396 NELFA介导的启动子近端暂停抑制YAP驱动的转录并影响乳腺癌中与上下文相关的结果
• GSE311235 RNA-seq 分析 WT 和 ZBP-KO 小鼠在普瑞斯坦诱导的狼疮样小鼠肾脏中的表达谱
• GSE307329 持续的基于 NRTI 的抗逆转录病毒疗法诱导肺泡巨噬细胞进行性衰老样重编程 [ChIP-seq]
• GSE306684 E 蛋白驱动的 iNKT 亚群调节塑造甲型流感病毒感染期间的早期免疫反应。
• GSE305096 DNAJ-PKAc诱导纤维板层型肝细胞癌的代谢重编程和谷氨酰胺依赖性
• GSE303530 抑制 HIF1 信号传导作为转移性去势抵抗性前列腺癌的治疗选择。
• GSE302790 下一代测序分析 Eurotium cristatum JLU 与不同人参属物种相互作用过程中的转录组。
• GSE296751 特发性肺纤维化患者FFPE肺组织单细胞RNA测序数据
• GSE295779 全基因组复制是小鼠成纤维细胞诱导多能干细胞重编程的障碍
• GSE295652 抗氧化纳米技术介导的保护作用对抗太空中的神经元损伤 2 (PROMETEO 2，纳米保护)
• GSE292685 Fpr2缺失对脾脏转录组的影响
• GSE290548转录组分析和实验验证揭示了PI3K/AKT信号通路参与高海拔认知功能障碍
• GSE289817 多发性硬化症小鼠模型中性别依赖性结肠微生物组和宿主转录组谱
• GSE289384 细胞表面 TMPRSS11E 与 CD98 相互作用，介导 SARS-CoV-2 有效进入 M1 型巨噬细胞
• GSE288516 蛋白质组学筛选发现 CTCF 是一种关键的 G-四链体结合蛋白 [CUT&Tag]
• GSE285154 普通豆根单核转录组图谱
• GSE278862 GNE肌病中的自噬缺陷可通过抑制补充性mTOR激活而逆转[细胞RNA测序]
• GSE277395 肢体发育过程中 En1 的时间性错误表达导致不同的表型 [ATAC-seq]
• GSE277394 肢体发育过程中 En1 的时间性错误表达导致不同的表型 [Capture Hi-C]
• GSE277393 肢体发育过程中 En1 的时间性错误表达导致不同的表型 [RNA-seq]
• GSE276335 Gadd45b 敲除小鼠造血干细胞的年龄样甲基化变化
• GSE275370 多细胞来源的 S100A8/A9 在免疫性血小板减少症中维持巨核细胞处于未成熟状态。
• GSE271491 复发性致癌 ZC3H18 突变稳定内源性逆转录病毒 RNA [zfmelanoma_ribominus_RNAseq]
• GSE271490 复发性致癌 ZC3H18 突变稳定内源性逆转录病毒 RNA [zfmelanoma_pAselected_RNAseq]
• GSE271489 复发性致癌 ZC3H18 突变稳定内源性逆转录病毒 RNA [hs_pAselected_RNAseq]
• GSE271488 复发性致癌 ZC3H18 突变稳定内源性逆转录病毒 RNA [hs_PARCLIP_ribominus_RNAseq]
• GSE262268 CDK12缺陷通过重塑核心转录机制促进表观遗传可塑性（MeDIP-seq）
• GSE207859 SN-011给药后Trex1基因敲除小鼠多种组织中的转录组变化
• GSE143826：Trex1基因敲除小鼠BMDM细胞在STING拮抗剂治疗前后的转录组变化
• GSE331034 疣状塔拉霉TS63-9果胶降解碳水化合物活性酶的转录组研究
• GSE330634 BMP8B调控滋养层细胞功能的分子机制研究：基于RNA-seq的转录组分析
• GSE330629 一种靶向人ENPP1（一种在患病人肾脏中表达的外核苷酸酶）的人源化单克隆抗体，可增强肾小管增殖和肾脏修复，且在非人灵长类动物中安全。