详细内容（前10条）

1. ⭐ GSE315131 联合抑制 EZH2 和 KRAS 后胰腺癌免疫微环境变化的单细胞 RNA 测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、RNA-seq、single-cell、KRAS
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusOur study demonstrated that combined treatment with the EZH2 inhibitor tazemetostat and the KRAS inhibitor RMC-6236 significantly suppressed the growth of both subcutaneous and orthotopic tumors. To investigate changes in the tumor microenvironment following combined EZH2 and KRAS inhibition in pancreatic cancer, mice bearing subcutaneous KPC tumors were treated with vehicle, RMC-6236 alone, or RMC-6236 in combination with tazemetostat. CD45⁺ cells were isolated and subjected to 10× Genomics single-cell RNA sequencing.
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2. ⭐ GSE318080 血管STING激活促进NK细胞在小细胞肺癌中的抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、NK cell
• 📝 描述：Contributors : Marco Campisi ; Talal El Zarif ; Jacob E Berchuck ; Zhaorong Li ; Matthew Freedman ; Michael Y Tolstorukov ; David A Barbie ; Navin R MahadevanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensSmall cell lung cancer (SCLC) typically displays a “cold” tumor microenvironment with a paucity of immune infiltrate. Neuroendocrine SCLC cells also profoundly repress MHC-I expression, rendering them vulnerable to NK cell-mediated cytotoxicity. Here, we confirm that neuroendocrine SCLC cells are sensitive to NK cell mediated attack, yet quantitative spatial profiling of the SCLC immune microenvironment in patient samples reveals that effector immune cells, including NK cells, are excluded from MHC-Ilow/neg SCLC regions. To study this biology, we develop dynamic single cell RNA sequencing of microphysiological immune tumor environments (DynaMITE-seq) and integrate findings with spatial transcriptomics in patient tissue, unveiling the microvasculature as a major checkpoint restricting NK cell extravasation/recruitment. We demonstrate that activation of vascular Stimulator of Interferon Genes (STING) signaling restores NK cell infiltration and killing of neuroendocrine SCLC, suggesting a strategy to overcome this key SCLC immunologic barrier and prime therapeutic response to DLL3-targeted CAR-NK cell therapy.
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3. ⭐ GSE317381 spaTransfer：使用非负矩阵分解进行单细胞和空间转录组学数据的迁移学习 [DG]

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Cindy Fang ; Kelsey D Montgomery ; Sarah E Maguire ; Anthony D Ramnauth ; Boyi Guo ; Sarah E Maguire ; Ryan A Miller ; Annie B Nguyen ; Joel E Kleinman ; Thomas M Hyde ; Heena R Divecha ; Keri Martinowich ; Kristen R Maynard ; Stephanie C Page ; Stephanie C Page ; Stephanie C HicksSeries Type : OtherOrganism : Homo sapiensRecent advances in spatially-resolved transcriptomics have enabled profiling of gene expression in a spatial context, which has led to the generation of large-scale single-cell and spatial atlases with computationally-derived cell type or spatial domain labels. An increasingly important task with these data has become the transfer of cell type or spatial domain annotations from a given reference (or source) atlas into a new target tissue or sample. The reference and target datasets could be at different resolutions or measured on different experimental platforms. Here, we present a method to perform cross-platform transfer learning that takes as input single-cell or spatial domain labels from a reference atlas or dataset and transfers the labels to a target dataset at a similar or different resolution. Specifically, we use non-negative matrix factorization (NMF) on the reference data to identify factors associated with labels of interest and project these factors into the target dataset to label each new observation. We use a multinomial model with the factors as covariates and labels as the response to predict labels in the target dataset. In contrast to existing approaches, the advantage of our approach is interpretability, without compromising on accuracy. We demonstrate the performance of the method in two human brain tissues and show that our model identifies spatially coherent domains in the target datasets with concordance of marker gene expression. We implement spaTransfer in open-source software as an R package (github.com/cindyfang70/spaTransfer).
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4. ⭐ GSE317379 spaTransfer：利用非负矩阵分解进行单细胞和空间转录组学数据的迁移学习

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Cindy Fang ; Kelsey D Montgomery ; Sarah E Maguire ; Anthony D Ramnauth ; Boyi Guo ; Sarah E Maguire ; Ryan A Miller ; Annie B Nguyen ; Joel E Kleinman ; Thomas M Hyde ; Heena R Divecha ; Keri Martinowich ; Kristen R Maynard ; Stephanie C Page ; Stephanie C Page ; Stephanie C HicksSeries Type : OtherOrganism : Homo sapiensRecent advances in spatially-resolved transcriptomics have enabled profiling of gene expression in a spatial context, which has led to the generation of large-scale single-cell and spatial atlases with computationally-derived cell type or spatial domain labels. An increasingly important task with these data has become the transfer of cell type or spatial domain annotations from a given reference (or source) atlas into a new target tissue or sample. The reference and target datasets could be at different resolutions or measured on different experimental platforms. Here, we present a method to perform cross-platform transfer learning that takes as input single-cell or spatial domain labels from a reference atlas or dataset and transfers the labels to a target dataset at a similar or different resolution. Specifically, we use non-negative matrix factorization (NMF) on the reference data to identify factors associated with labels of interest and project these factors into the target dataset to label each new observation. We use a multinomial model with the factors as covariates and labels as the response to predict labels in the target dataset. In contrast to existing approaches, the advantage of our approach is interpretability, without compromising on accuracy. We demonstrate the performance of the method in two human brain tissues and show that our model identifies spatially coherent domains in the target datasets with concordance of marker gene expression. We implement spaTransfer in open-source software as an R package (github.com/cindyfang70/spaTransfer).
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5. ⭐ GSE283333 全面免疫分析揭示 IFN-γ 信号通路在 T 细胞介导啮齿动物疟疾模型中的寄生虫吞噬作用：空间转录组学数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Jingwen Lin ; Shasha Chen ; Qingxin YangSeries Type : OtherOrganism : Mus musculusMalaria-associated lung pathology, a severe and life-threatening manifestation of Plasmodium infection, involves complex immune remodeling within the pulmonary microenvironment. To resolve the spatial architecture of this immune response, we performed spatial transcriptomic analysis on lung tissues from a Plasmodium berghei NK65-induced rodent model. Our study identifies IFN-γ signaling in T cells as a pivotal regulator of the lung’s spatial immune landscape. By utilizing conditional knockout (cKO) mice lacking Ifngr1 specifically in T cells, we observed that the blockade of T cell-intrinsic IFN-γ signaling attenuates lung pathology. Spatially, this protection is characterized by an enriched colocalization and enhanced interaction between T cells and monocytes. This robust interaction drives the expansion of a unique proinflammatory monocyte subset defined by CD8 and Ly6C expression within specific pulmonary niches. These CD8+ Ly6C+ monocytes exhibit significantly enhanced phagocytic capacity and elevated MHCII expression in situ. Our spatially resolved findings illustrate that the T cell-IFN-γ signaling axis dictates the spatial organization of T cell-monocyte communication, highlighting this interaction as a potential therapeutic target for mitigating malaria-induced lung injury.
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6. ⭐ GSE305842 对免疫疗法反应不同的三阴性乳腺癌小鼠模型 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)、scRNA
• 📝 描述：Contributors : Thomas J Kalantzakos ; Yufan Zhou ; Xingyu Liu ; Joshua Proehl ; Cameron Durfee ; Ian Tamayo ; Nuri Temiz ; Benjamin Troness ; Anusha Soni ; Harshita B Gupta ; Reuben S HarrisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBreast cancer is the most common cancer diagnosis in women. Clinical studies with triple-negative breast cancer (TNBC) are encouraging for immunotherapy combined with chemotherapy (aPD-1 with paclitaxel and/or carboplatin). However, additional clinical advances may be pursued more rapidly with assistance from preclinical TNBC models including syngeneic mammary tumor cell lines. Here, we report two mammary tumor cell lines that exhibit differential responsiveness to immunotherapy in vivo. Spontaneous mammary tumors from C57BL/6J MMTV-Cre Trp53fl/+ animals were passaged serially in cell culture and in vivo in the mammary fat pad of fully wildtype animals. The resulting lines, MM001i and MM008i, lost Trp53 and formed 1000 mm3 tumors in the mammary fat pad within 21-28 days. Despite originating from the same genetic background, these lines exhibit differential responses to immunotherapy. For aPD-1 therapy, MM001i is poorly responsive and MM008i is strongly responsive with near-complete tumor regression. In comparison, both MM001i and MM008i respond rapidly to aCTLA-4 therapy. Both models express unique tumor antigens as evidenced by immunity to subsequent engraftments. Primary MM008i tumors exhibit greater T cell infiltration, and CD8-positive T lymphocytes are required for aPD-1 responses. These TNBC models are promising for further mechanistic studies and testing future single and combinatorial therapies.
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7. ⭐ GSE307584 组胺 N-甲基转移酶异常上调通过破坏 SAM/Frizzled-2/CaMKII 信号通路加剧病理性心脏肥大和心力衰竭 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、RNA-seq、pathway
• 📝 描述：Contributors : Jinyan Zhang ; Hao Jiang ; Liwei Liu ; Xin Li ; Jing Yang ; Junbo Ge ; Aijun SunSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMetabolites produced during the development of pathological cardiac hypertrophy and heart failure can influence disease progression. Methyl donor S-adenosyl methionine (SAM) levels are decreased in the hypertrophic heart, but related mechanisms and effects remain unknown. Histamine N-methyltransferase (HNMT) uses SAM as a substrate to deactivate histamine into N-methylhistamine. Here, we prove that HNMT was upregulated in cardiac tissues from patients with heart failure and post-transverse aortic constriction (TAC) mice as well as phenylephrine (PE)-treated neonatal mouse cardiomyocytes (NMCMs). N-methylhistamine, downstream metabolite of HNMT, was elevated in urine samples from heart failure patients. In mice, cardiomyocyte-specific Hnmt deletion ameliorated pathological cardiac hypertrophy and heart failure caused by TAC or Angiotensin-II infusion. Pharmacological inhibition of HNMT with amodiaquine ameliorated TAC-induced cardiac dysfunction. In contrast, cardiomyocyte-specific Hnmt overexpression caused cardiac dysfunction. Mechanistically, HNMT decreased intracellular SAM levels and interacted with enhancer of zeste homolog2 (EZH2). This interaction blocked EZH2 function and downregulated H3K27me3 modification at the Frizzled-2 (Fzd2) promoter, which increased Fzd2 expression. FZD2 upregulation activated the calcium/calcium–calmodulin (CaM)-dependent protein kinase II (CaMKII) pathway, which mediated the pro-hypertrophic effects of HNMT. This study identified HNMT as a promising therapeutic target for treating pathological cardiac hypertrophy and heart failure.
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8. ⭐ GSE317716 肠道菌群对口服药物吸收和代谢的影响

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Purna C Kashyap ; Krishna R Kalari ; Karunya K KandimallaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusGut microbiota are known to influence oral drug disposition, yet the specific host pathways they affect remain poorly characterized. This study provides a transcriptome-wide characterization of how physiological gut microbiota regulate the expression of intestinal transporters, phase I and phase II metabolic enzymes, and barrier machinery relevant to oral drug disposition. By identifying microbiota-responsive processes, this work defines the scope of inter-individual variability attributable to gut microbial effects.
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9. ⭐ GSE316867 静止胶质母细胞瘤活化和免疫逃逸的代谢许可通过星形胶质细胞-线粒体穿梭 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、metabolic、RNA-seq
• 📝 描述：Contributors : Hongrui Zhu ; Li Wang ; Qingsong HuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe reaction of quiescent tumor cell subpopulations at the invasive margin of glioblastoma (GBM) might be cleared by immune surveillance toward death or expand through immune escape, which can drive therapeutic resistance, tumor dissemination, and recurrence through phenotypic plasticity. However, the process and mechanisms underlying their activation remain largely unclear. This study revealed that astrocytes awaken quiescent GBM cells to cycling and immune-evasive phenotypes. Astrocytic mitochondria are indispensable in regulating the phenotypic changes. Specifically, the SHMT2 enzyme in astrocytic mitochondria catalyzes one-carbon metabolic products, which significantly promote synthetic metabolic activation and reactivation of quiescent GBM cells to immune evasion through intercellular mitochondrial transfer. Tumor cells that acquire astrocytic mitochondria enhanced one-carbon metabolism drives global hyperactive anabolic metabolism through YTHDC1-mediated transcriptional pause release of ribosomal and focal adhesion signaling genes, supporting rapid proliferation and conferring a potent immune-evasive phenotype. Therapeutically, pharmacologic or genetic inhibiting the astrocytic SHMT2 or blocking mitochondrial transfer markedly suppressed quiescent GBM cell activation and tumor progression. These findings elucidate a novel mechanism by which astrocytes in the tumor microenvironment drive GBM malignancy through metabolic symbiosis.
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10. ⭐ GSE315129 ChIP-seq 分析 EZH2 和 KRAS 抑制剂处理后的胰腺癌细胞中 H3K27ac 的变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq、KRAS
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensOur study demonstrates that combined treatment with the EZH2 inhibitor tazemetostat and the KRAS inhibitor RMC-6236 markedly activates the expression of senescence-associated secretory phenotype (SASP) genes in pancreatic cancer, thereby enhancing the therapeutic efficacy of RMC-6236 and potentially providing a strategy to overcome resistance to KRAS inhibition. To characterize the epigenetic features underlying SASP gene activation, H3K27ac ChIP-seq was performed in PSN1 cells treated with DMSO, tazemetostat, RMC-6236, or the combination of both inhibitors.
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详细内容（全部3条）

1. ⭐ RNA测序揭示阿尔茨海默病中的代谢和突触变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、Alzheimer、sequencing
• 📝 描述：RNA sequencing of blood samples reveals metabolic and synaptic gene expression changes linked to Alzheimer’s disease, highlighting the importance of studying diverse populations for inclusive biomarkers…
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2. RNA测序揭示了低剂量THC和塞来昔布如何改善阿尔茨海默病

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、sequencing
• 📝 描述：RNA sequencing shows that combining low-dose THC with celecoxib shifts inflammatory and synaptic gene expression toward healthier patterns while improving cognition in Alzheimer’s mouse models…
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3. 科学家发现胰腺癌扩散的隐秘途径

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have discovered how pancreatic cancer reprograms its surroundings to spread quickly and stealthily. By using a protein called periostin, the tumor remodels nearby tissue and invades nerves, which helps cancer cells travel and form metastases. This process also creates a tough, fibrous barrier that makes treatments less effective. Targeting periostin could help stop this invasion before it starts.
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• GSE312012 尼达尼布抑制人KRAS突变癌细胞中的VEGFR-ERK信号通路
• GSE285958 鉴定一种与双氢青蒿素相关的预后特征及其对胰腺癌肿瘤微环境的影响
• GSE315590：KLF1​​5介导的心力衰竭心脏保护作用的单细胞转录组分析
• GSE306294 RNA聚合酶III组织和肿瘤图谱揭示了与3D表观基因组调控机制相关的特定环境活性
• GSE306220 RNA聚合酶III组织和肿瘤图谱揭示了与3D表观基因组调控机制相关的特定情境活性
• GSE305800 小鼠三阴性乳腺癌模型对免疫疗法的反应存在差异
• GSE307583 组胺 N-甲基转移酶异常上调通过破坏 SAM/Frizzled-2/CaMKII 信号通路加剧病理性心脏肥大和心力衰竭 [CUT&Tag]
• GSE318153 用IL-7和放射疗法治疗的放射抗性TC-1小鼠模型中的肿瘤细胞因子谱
• GSE317416 局部早期前列腺癌的转录组癌症免疫通路
• GSE316331 S-腺苷高半胱氨酸水解酶缺乏通过表观遗传调控炎症加剧克隆1造血和动脉粥样硬化[亚硫酸氢盐测序]
• GSE316282 S-腺苷高半胱氨酸水解酶缺乏症通过表观遗传调控炎症加剧克隆1型造血和动脉粥样硬化
• GSE311057 Müller 胶质细胞-小胶质细胞交叉对话重编程 Müller 胶质细胞转录组，以参与视网膜再生过程中的细胞分裂相关过程 [scRNA-Seq]
• GSE310499 前列腺癌中乙二醛酶 1 表达与甲基乙二醛诱导的致癌应激之间的机制联系
• GSE310100 多组学分析揭示了三阴性乳腺癌小鼠模型中具有不同化疗-免疫治疗脆弱性的免疫分子簇
• GSE309839 侵袭性变异型前列腺癌活检的RNA测序
• GSE304711 增生性和轻度发育不良性口腔白斑的基因组规模甲基化数据
• GSE291866 LSECs通过巨噬细胞来源的IL-1β诱导IL-1R1介导的趋化因子产生促进MASH进展
• GSE288413 灯刷藻染色体的 3D 基因组学突显了活性转录在染色质组织中的作用 [scRNA-seq]
• GSE287437 早期剥夺性近视豚鼠的单细胞RNA测序
• GSE283289 多组学测序揭示了与未经治疗的儿童溃疡性结肠炎原发性硬化性胆管炎发展相关的独特基因表达和表观遗传改变
• GSE282932 预先存在的记忆B细胞表型决定了疫苗加强针的B细胞反应质量
• GSE254688 整合转录组学和代谢组学为紫竹变种‘黄花竹’的叶片着色提供了新的见解
• GSE80686 III类HD-ZIP转录因子的全基因组靶标分析[ChIP-Seq]
• GSE80571 III类HD-ZIP转录因子的全基因组靶标分析[RNA-Seq]
• GSE317901 利用 APHRODYTHE（一种多组学患者来源的异种移植平台）揭示西妥昔单抗在头颈癌中的疗效
• GSE312918 异染色质的转录调控是三维基因组接触中遗传变异的基础
• GSE312897 异染色质的转录调控是三维基因组接触遗传变异的基础 IV
• GSE312895 异染色质的转录调控是三维基因组接触遗传变异的基础 III
• GSE312893 异染色质的转录调控是三维基因组接触遗传变异的基础 II
• GSE312889 异染色质的转录调控是三维基因组接触遗传变异的基础 I
• GSE290045 结直肠癌来源的骨桥蛋白通过PI3K/AKT/CSF1-CSF1R轴将巨噬细胞重塑为促转移的M2状态
• GSE273827 核酸酶缺陷型 Cas9VPR 恢复内源性转录因子活性可预防应激性心力衰竭 II
• GSE273656 核酸酶缺陷型 Cas9VPR 恢复内源性转录因子活性可预防应激性心力衰竭
• GSE249915 FABP7 前体细胞是 BRCA1 乳腺癌中可靶向的代谢根源
• GSE317054 野生型和TIGAR缺陷型小鼠组织中Parkin基因的DNA甲基化分析[EM-seq]
• GSE317052 野生型和TIGAR缺陷型小鼠组织中Parkin基因的DNA甲基化分析[亚硫酸氢盐测序]
• GSE317050 RNA-seq 分析野生型和 TKO 小鼠心脏在正常饲料和高脂饮食下 Parkin (Prkn) 的表达 [RNA-Seq]
• GSE317048 野生型和 TigarKO 小鼠心脏的转录组分析 [RNA-Seq]
• GSE314943 单细胞多组学揭示内皮细胞机械敏感性 PIEZO1-IL-33 轴驱动肺纤维化
• GSE314709 单细胞多组学揭示内皮细胞机械敏感性 PIEZO1-IL-33 轴驱动肺纤维化
• GSE302314 PHGDH 的 RNA 结合活性驱动散发性阿尔茨海默病人脑类器官模型中淀粉样蛋白β的产生
• GSE277881 Th1 和 Th2 分化过程中 PI3K-delta 过度活跃 [RNA-seq]
• GSE314702 双靶向 TOP1/G4 抑制剂 ZBH-01 处理的结直肠癌细胞的转录组分析
• GSE307184 猕猴大脑终生单细胞、多区域分析
• GSE318248 纵向多组学图谱揭示耐药性黑色素瘤中空间组织免疫抑制生态系统的出现 [DSP 蛋白]
• GSE318201 接受标准疗法和表达 HER2 的李斯特菌疫苗治疗的骨肉瘤犬的免疫反应和临床结果
• GSE317937 纵向多组学图谱揭示耐药性黑色素瘤中空间组织化的免疫抑制生态系统的出现 [nCounter RNA]
• GSE317936 纵向多组学图谱揭示耐药性黑色素瘤中空间组织化的免疫抑制生态系统的出现 [nCounter 蛋白]
• GSE317918 纵向多组学图谱揭示耐药性黑色素瘤中空间组织免疫抑制生态系统的出现 [SNV]
• GSE317912 纵向多组学图谱揭示耐药性黑色素瘤中空间有序的免疫抑制生态系统的出现
• GSE317695 通过高通量测序鉴定 HaCaT 细胞中的祖细胞角质形成细胞亚群
• GSE317583 在标准含血清条件下对 11 株人类胶质母细胞瘤细胞系进行 RNA 测序
• GSE317455 局部早期前列腺癌的转录通路
• GSE317424 局部早期前列腺癌的转录组泛癌通路
• GSE317392 灵芝酸A通过靶向RORA抑制IL-17信号通路，从而缓解溃疡性结肠炎
• GSE315529 RB 缺失通过调节黏连蛋白依赖性环和增强子-启动子相互作用来调节染色质组织 [ChIP-seq]
• GSE315528 RB 缺失通过调节黏连蛋白依赖性环和增强子-启动子相互作用来调节染色质组织 [scRNA-seq]
• GSE315508 高温下花烛属植物的转录组
• GSE315138 单细胞 RNA 测序揭示乳糜泻十二指肠活检中独特的细胞动力学
• GSE315130 DMSO、tazemetostat、RMC-6236 或联合治疗后多种人类和小鼠胰腺癌细胞和肿瘤的差异 mRNA 表达分析。
• GSE314995 二硫键导向的多环肽用于靶向实体瘤的嵌合抗原受体
• GSE313788 活性转录基因与绝缘元件之间的功能重叠 [ChIP-seq]
• GSE313787 活性转录基因与绝缘子元件之间的功能重叠 [ATAC-seq]
• GSE313785 活性转录基因与绝缘元件之间的功能重叠 [RNA-seq]
• GSE313539 C1QBP 与 Dectin-1 信号通路相互作用，通过表观遗传沉默抑制念珠菌感染中的 IL-1β 表达
• GSE313205 脂滴巨噬细胞中染色质可及性分析（SLC27A1 沉默或未沉默）(ATAC-seq)
• GSE312994 tRF3019a敲低后H1299肺腺癌细胞的转录组分析
• GSE312726 长链非编码 RNA H19 在阿扎胞苷耐药的 K562 细胞中过表达，但不调节药物敏感性 [RNA-Seq]
• GSE309855 转移性前列腺癌样本基因表达谱的重新分析
• GSE309847 前列腺癌类器官的建立和表征 II
• GSE305420 RHOV 是一种对脱离有反应的 Rho GTP 酶，是卵巢癌早期转移重编程所必需的
• GSE305375 卵巢癌中脱离反应转录本的鉴定
• GSE299935 穆勒胶质细胞-小胶质细胞相互作用重编程穆勒胶质细胞转录组，以参与视网膜再生过程中的细胞分裂相关过程
• GSE288415 灯刷藻染色体的三维基因组学研究突显了活性转录在染色质组织中的作用
• GSE288411 灯刷藻染色体的 3D 基因组学突显了活性转录在染色质组织中的作用 [scNOME-seq]
• GSE288409 灯刷染色体的 3D 基因组学突显了活性转录在染色质组织中的作用 [scHi-C]
• GSE287069 结核分枝杆菌中 VapC36 过表达的转录组分析
• GSE285993 VRK1 是宫颈小细胞神经内分泌癌的新型治疗靶点
• GSE285931 两种胸苷酸合成酶抑制剂在 HCT116 结肠癌细胞中诱导明显不同的基因组尿嘧啶模式、诱变过程和细胞反应 [GSE126822 的重新分析]
• GSE281561 QKI失调诱导T细胞急性淋巴细胞白血病（T-ALL）中广泛的剪接变化
• GSE278468 Single cell mRNA sequencing of Peyer’s patch LysoDCs and cDC2s and blood CD45+CD115hi cells
• GSE274897 受体酪氨酸激酶 EphB2 促进小鼠 MASH 纤维化。
• GSE261697 人类原代、骨髓来源和 iPSC 来源的单核细胞和巨噬细胞的染色质可及性特征 [ATAC-Seq]
• GSE261696 人类原代、骨髓来源和 iPSC 来源的单核细胞和巨噬细胞的转录特征 [RNA-Seq]
• GSE254752 神经元与化生腺泡细胞之间的相互激活作用促进胰腺癌的发生和发展
• GSE254750 RNA-Seq 分析 Axonopus compressus 根系对铝毒性的响应
• GSE225024 Terc 缺乏对衰老过程中破骨细胞分化和成熟的影响[培养皿]
• GSE99682 CD11b 缺乏导致成熟小肠巨噬细胞基因表达变化的分析
• GSE99672 分析 CX3CR1 缺陷导致成熟小肠巨噬细胞基因表达变化
• GSE80687 III类HD-ZIP转录因子的全基因组靶标分析