详细内容（前10条）

1. ⭐ GSE287743 体外 PI3Kδ 抑制使 CD8 T 细胞分化向体内祖细胞耗竭方向偏移，并重编程肿瘤微环境代谢、免疫组成和炎症 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment、T cell、inflammation、metabolism、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Edward Usherwood ; Alexandrea Turnquist ; Owen WilkinsSeries Type : OtherOrganism : Mus musculusIn vitro PI3Kδ inhibition using Idelalisib (CAL-101) drives CD8 T cells toward a progenitor exhausted (Tpex) phenotype while resisting terminal exhaustion in vitro. We performed single-cell RNA sequencing and spatial transcriptomics on B16-melanoma tumors and show that CAL-101-treated T cells enhance oxidative phosphorylation, proliferation, and Ifnγ responsiveness. The CAL-101 treated cells deeply infiltrate tumors and upregulate the CXCR3-CXCL10 axis, coinciding with reduced tumor-associated macrophage signatures and increased pro-inflammatory signaling in the tumor microenvironment. CAL-101 reprograms T cell fate and remodels the TME, offering insight into how to improve immunotherapeutic efficacy for solid tumors.
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2. ⭐ GSE286925 体外 PI3Kδ 抑制使 CD8 T 细胞分化向体内祖细胞耗竭方向偏移，并重编程肿瘤微环境代谢、免疫组成和炎症 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、tumor microenvironment、T cell、inflammation、metabolism、scRNA
• 📝 描述：Contributors : Edward Usherwood ; Alexandrea Turnquist ; Owen WilkinsSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusIn vitro PI3Kδ inhibition using Idelalisib (CAL-101) drives CD8 T cells toward a progenitor exhausted (Tpex) phenotype while resisting terminal exhaustion in vitro. We performed single-cell RNA sequencing and spatial transcriptomics on B16-melanoma tumors and show that CAL-101-treated T cells enhance oxidative phosphorylation, proliferation, and Ifnγ responsiveness. The CAL-101 treated cells deeply infiltrate tumors and upregulate the CXCR3-CXCL10 axis, coinciding with reduced tumor-associated macrophage signatures and increased pro-inflammatory signaling in the tumor microenvironment. CAL-101 reprograms T cell fate and remodels the TME, offering insight into how to improve immunotherapeutic efficacy for solid tumors.
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3. ⭐ GSE316027 β-羟基丁酸驱动的组蛋白赖氨酸β-羟基丁酰化促进直肠癌中单核细胞来源巨噬细胞的免疫刺激活性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、monocyte、histone
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensOur previously reported phase II and phase III trials have demonstrated that short-course radiotherapy (SCRT) combined with neoadjuvant immunochemotherapy (SIC) has led to clinical benefits in locally advanced rectal cancer (LARC). Characterization of the molecular mechanisms underlying responses to SIC may lead to improved treatment strategies. Here, we prospectively collected and applied multi-omic analyses to paired pre- and post-treatment LARC specimens undergoing SIC.
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4. ⭐ GSE301047 早幼粒细胞白血病 PML 蛋白是三阴性乳腺癌中的关键免疫抑制剂 [RRBS]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、leukemia、immune
• 📝 描述：Contributors : Martina Uggè ; Cristina Fracassi ; Valentina Giansanti ; Rosa BernardiSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensTriple-negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options and frequent resistance to immunotherapy. Here, we identify the targetable protein PML as a key mediator of immune evasion in TNBC via independent and converging mechanisms. We demonstrate that PML promotes the establishment of an immunosuppressive tumor microenvironment while concurrently impairing antigen presentation by tumor cells. Mechanistically, we find that PML partakes to the chronic activation of inflammatory and interferon-γ-responsive signaling, leading to constitutive activation of immunosuppressive genes, including PD-L1. Additionally, PML collaborates with DNMT1 to repress HLA gene expression, thus limiting tumor recognition and killing by cytotoxic T cells. Analysis of human TNBC datasets links high PML expression to impaired immune activation and poor responses to chemotherapy. As PML-targeting therapies are already clinically available for leukemia, our findings position PML as a promising actionable target to enhance immune responses and improve outcomes for patients with TNBC.
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5. ⭐ GSE296217 早幼粒细胞白血病PML蛋白是三阴性乳腺癌中的关键免疫抑制因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、leukemia、immune
• 📝 描述：Contributors : Martina Uggè ; Cristina Fracassi ; Anna S Tascini ; Matteo Dugo ; Francesca GianneseSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options and frequent resistance to immunotherapy. Here, we identify the targetable protein PML as a key mediator of immune evasion in TNBC via independent and converging mechanisms. We demonstrate that PML promotes the establishment of an immunosuppressive tumor microenvironment while concurrently impairing antigen presentation by tumor cells. Mechanistically, we find that PML partakes to the chronic activation of inflammatory and interferon-γ-responsive signaling, leading to constitutive activation of immunosuppressive genes, including PD-L1. Additionally, PML collaborates with DNMT1 to repress HLA gene expression, thus limiting tumor recognition and killing by cytotoxic T cells. Analysis of human TNBC datasets links high PML expression to impaired immune activation and poor responses to chemotherapy. As PML-targeting therapies are already clinically available for leukemia, our findings position PML as a promising actionable target to enhance immune responses and improve outcomes for patients with TNBC.
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6. GSE327115 Treg衍生的IFN-γ支持肿瘤免疫和自身免疫中Th1-Treg的分化

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity
• 📝 描述：Contributors : Ayumi Kuratani ; Masahiro YamamotoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTregs in tumors are functionally heterogeneous, and Th1-Tregs represent a highly suppressive subset. This study identifies Tregs themselves as a source of IFN-γ, which promotes Th1-Treg differentiation. Treg-derived IFN-γ acts in an autocrine manner to sustain T-bet expression and the Th1-Treg phenotype, while PF4 from Arg1(+) TAMs further amplifies this pathway by inducing Ifng expression in Tregs. Conditional deletion of Ifng in Foxp3(+) cells impaired Th1-Treg differentiation in both tumors and spleen, and a similar mechanism was observed in EAE. Overall, Treg-derived IFN-γ forms a positive feedback loop with other IFN-γ sources and TAM-derived PF4, driving the maintenance and accumulation of Th1-Tregs and reinforcing immunosuppression.
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7. GSE326575 雌性小鼠深静脉血栓形成静脉壁的单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Huan Yang ; Ting Zhou ; Bo LiuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDeep vein thrombosis (DVT) is a common clinical problem, but its cellular and molecular mechanisms remain incompletely understood. We performed single-cell RNA sequencing (scRNA-seq) on the vein wall of female C57BL/6J mice. Using the inferior vena cava (IVC) ligation model of DVT, we profiled the cellular heterogeneity and gene expression shifts occurring within the vein wall during the acute phase of thrombosis. This dataset provides a high-resolution map of the vascular response to acute venous thromboembolism.
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8. GSE322615 研究 C4-2B 前列腺癌细胞对 PARP 抑制剂和雄激素受体通路抑制剂的反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、pathway
• 📝 描述：Contributors : Alan P Lombard ; Bryan Correa Gonzalez ; Akshaya KarthikeyanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensUse of PARP inhibitors (PARPi) has been shown effective in the management of selected patients with advanced prostate cancer. Still, it is incompletely understood how PARPi work and what mechanisms may enable adaptation and progression. This study utilized RNA-sequencing to understand response to PARP inhibition (olaparib) in regard to both intensity and duration of treatment. PARPi have also been shown to be effective when combined with androgen receptor (AR) pathway inhibitors (ARPi), but much remains unknown regarding the utility of combination regimens. We additionally performed RNA-sequencing to better define transcriptomic changes associated with either monotherapy PARPi (olaparib or talazoparib), monotherapy ARPi (abiraterone or enzalutamide), or combinations (abiraterone + olaparib, enzalutamide + talazoparib).
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9. GSE315635 ChIP-Seq 分析胰腺癌细胞系中的 SIRT6 和 KDM5C

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq
• 📝 描述：Contributors : Shuai Leng ; Wenqian YuSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensPancreatic cancer is among the deadliest malignant tumours, characterized by rapid progression, poor prognosis, and high mortality.SIRT6 and KDM5C plays an important role in tumorigenesis, development, and drug resistance .However, the precise molecular mechanisms through which SIRT6 and KDM5C inhibit tumorigenesis and metastasis in pancreatic cancer, as well as its role in cancer stem cells (CSCs), remain unclear.Collectively, our findings identify SIRT6 and KDM5C as key regulators of pancreatic cancer progression and suggest that they represent potential targets for early diagnosis and therapeutic intervention.
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10. GSE315634 RNA-Seq 分析 SIRT6 或 KDM5C 敲低对胰腺癌细胞系的影响

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Shuai Leng ; Wenqian YuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPancreatic cancer is among the deadliest malignant tumours, characterized by rapid progression, poor prognosis, and high mortality.SIRT6 and KDM5C plays an important role in tumorigenesis, development, and drug resistance .However, the precise molecular mechanisms through which SIRT6 and KDM5C inhibit tumorigenesis and metastasis in pancreatic cancer, as well as its role in cancer stem cells (CSCs), remain unclear.Collectively, our findings identify SIRT6 and KDM5C as key regulators of pancreatic cancer progression and suggest that they represent potential targets for early diagnosis and therapeutic intervention.
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1. RNA测序揭示了基孔肯雅病毒感染为何会转为慢性感染

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Single-cell RNA sequencing revealed that chikungunya virus persists within joint-associated macrophages, providing new insights into chronic inflammation and long-term disease following infection…. The post RNA-sequencing reveals why chikungunya virus infections can turn chronic appeared first on RNA-Seq Blog.
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2. 癌症最常用的逃脱技巧或许反而更容易杀死癌症患者。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have uncovered a surprising new way the immune system fights cancer, overturning a core belief that has guided immunology for decades. The research found that when cancer cells shut down a key immune-recognition molecule called MHC I—a common trick used to hide from “killer” T cells—they can actually become more vulnerable to attack by a different group of immune cells known as CD4+ “helper” T cells.
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• GSE311284 RNAseq 来自“细胞非自主性血红素获取途径使红细胞血红蛋白化在应激条件下得以实现”
• GSE309866 弥漫性中线胶质瘤中的小胶质细胞促进细胞外基质重塑和癌细胞侵袭
• GSE296380 心脏长链非编码 RNA Charme 缺失对心脏成纤维细胞成熟和旁分泌信号传导的影响 [RNA-Seq 2]
• GSE296379 心脏长链非编码 RNA Charme 缺失对心脏成纤维细胞成熟和旁分泌信号传导的影响 [RNA-Seq 1]
• GSE294425 组蛋白赖氨酸特异性去甲基化酶抑制剂 JIB-04 通过诱导铁死亡使 AML 细胞对维奈托克敏感 [RNA-seq]
• GSE282301 组蛋白 H3 表观遗传修饰 ChIPseq [男性]
• GSE276723 T细胞耗竭是由动态3D基因组重组控制的
• GSE275892 RNA编辑酶ADAR1的缺失增强NK细胞的抗肿瘤免疫力
• GSE260699 利用光驱动组合条形码技术对组织中的分子进行空间可调多组学测序
• GSE260698 利用光驱动组合条形码技术对组织中的分子进行空间可调多组学测序 / RNA_LCM
• GSE260696 利用光驱动组合条形码技术对组织/悬垂筛选中的分子进行空间可调多组学测序
• GSE260695 利用光驱动组合条形码技术对组织中的分子进行空间可调多组学测序 / RNA_BALI
• GSE260694 利用光驱动组合条形码技术对组织中的分子进行空间可调多组学测序 / 多组学
• GSE260688 利用光驱动组合条形码技术对组织中的分子进行空间可调多组学测序 / ATAC
• GSE334273 性腺单细胞 RNA-seq 分析揭示了对海七鳃鳗 (Petromyzon marinus) 生殖细胞发育和性分化至关重要的基因
• GSE320131 脊椎动物雄性生殖细胞三维基因组结构的差异 [scRNA-seq]
• GSE320128 脊椎动物雄性生殖细胞三维基因组结构的差异 [Hi-C]
• GSE318405 NK2R信号通路调控肠道脂质动员和黏膜炎症
• GSE296818 靶向胰腺癌中促增殖程序的转录依赖性 [scATAC 类器官]
• GSE296813 靶向胰腺癌中促增殖程序的转录依赖性 [scRNA 类器官]
• GSE296811 靶向胰腺癌中促增殖程序的转录依赖性 [scRNA 小鼠]
• GSE334172 靶向转移瘤的一碳代谢脆弱性及其治疗潜力
• GSE329380 一项针对污染校正的组织血小板生成框架研究揭示了非小细胞肺癌中具有临床意义的CAF-髓系微环境：一项配对转录组学和生存分析研究
• GSE328630 单细胞RNA测序分析揭示脊椎动物物种间少突胶质细胞分化的共有和差异性转录程序
• GSE327957 诱导痰液转录组分析发现感染后闭塞性细支气管炎中 TNF-α/NF-κB 信号通路上调和线粒体呼吸链功能下调
• GSE327221 RNA测序分析Long-Evans大鼠前扣带回皮层和伏隔核，揭示了性别特异性发育变化以及产前和青春期酒精暴露对雌性的持续影响（仅II）。
• GSE327217 RNA测序分析Long-Evans大鼠前扣带回皮层和伏隔核，揭示了性别特异性发育变化以及产前和青春期酒精暴露对雌性的持续影响 I
• GSE326694 用炎症巨噬细胞条件培养基处理的小鼠原代主动脉平滑肌细胞的转录组分析
• GSE326523 潜伏感染HSV-1的小鼠脑干在神经炎症和衰老方面表现出性别特异性效应
• GSE325102 CXCL6 通过抑制肝细胞中 LPIN1 介导的脂肪酸氧化加剧代谢功能障碍相关的脂肪性肝炎
• GSE320192 拟南芥根结线虫感染后14天诱发的根结线虫的转录组分析
• GSE319281 CELF2依赖的RNA调控在早期脑发育过程中支持皮层结构和突触稳定性[RNA测序]
• GSE316549 母源 PADI6 的缺失会破坏晚期植入前小鼠胚胎的 DNA 甲基化和基因组印记维持。
• GSE316341 母源PADI6缺失破坏小鼠植入前晚期胚胎的DNA甲基化和基因组印记维持
• GSE316326 通过 GSK-126 抑制 EZH2 可减轻糖尿病中的 EndMT 和动脉粥样硬化：转化表观遗传学方法。
• GSE312231 海洋细菌斯氏斯氏单胞菌通过调节铁死亡减轻秀丽隐杆线虫的帕金森病病理
• GSE312197 MEK抑制剂通过mTOR介导的蛋白质合成抑制诱导结直肠癌中AXIN1的丢失
• GSE312196 MEK 抑制通过 mTOR 相关抑制蛋白质合成诱导结直肠癌中 AXIN1 丢失 [RiboSeq_HCT116]
• GSE312195 MEK 抑制通过 mTOR 相关抑制蛋白质合成诱导结直肠癌中 AXIN1 丢失 [RNASeq_SW480]
• GSE312194 MEK 抑制通过 mTOR 相关抑制蛋白质合成诱导结直肠癌中 AXIN1 丢失 [RNASeq_HCT116]
• GSE312010 碘酸钠诱导小鼠神经视网膜单细胞转录组变化
• GSE311281 细胞非自主性血红素获取途径在应激条件下促进红系血红蛋白化
• GSE310754 研究显示，接受醋酸格拉替雷治疗的多发性硬化症患者外周血单核细胞 (PBMC) 中 DNA 甲基化发生改变。
• GSE308643 前扣带回皮层到外侧缰核的通路控制雄性小鼠慢性疼痛诱导的抑郁症
• GSE306288 人类主动脉瓣膜的空间转录组分析揭示了钙化部位附近的细胞性别差异
• GSE305664 TUT1 催化的 U6 snRNA 3’ 端成熟是 mRNA 剪接维持胚胎发生过程中干细胞库所必需的 [纳米孔长读长 RNA 测序]
• GSE305663 TUT1 催化的 U6 snRNA 3’ 端成熟是 mRNA 剪接维持胚胎发生过程中干细胞库所必需的 [RNA-Seq]
• GSE304587 单核多组学分析揭示肺腺癌中的细胞状态转变和表观遗传程序
• GSE303294 骨肉瘤类器官中阿霉素耐药性的转录组学特征
• GSE300518 心外膜衍生细胞分泌细胞外囊泡，调节心脏对缺血再灌注损伤反应中的基因表达 [BW mRNAseq]
• GSE300517 心外膜衍生细胞分泌细胞外囊泡，调节心脏对缺血再灌注损伤反应中的基因表达 [EV miRNAseq]
• GSE299969 对受小鼠 DNA 污染的人类 DNA 样本进行 DNA 甲基化微阵列分析。
• GSE297636 WAT-BAT 通讯促进 BAT 在寒冷暴露期间持续激活产热 [RNA-Seq]
• GSE296583 小鼠子宫蜕膜化过程中的基因表达[scRNA-seq]
• GSE296581 小鼠子宫蜕膜化过程中的基因表达 [Visium]
• GSE296019 用重组CTSC处理的RSV感染的THP-1细胞的RNA测序
• GSE294417 组蛋白赖氨酸特异性去甲基化酶抑制剂 JIB-04 通过诱导铁死亡使 AML 细胞对维奈托克敏感。
• GSE287727 胆汁酸代谢失调加剧了 HuR 缺陷雄性小鼠肝脏中饮食诱导的 MASLD 发展。
• GSE277839 TUT1 和 USB1 是 U6 snRNA 3’ 末端 2’,3’-环磷酸修饰的生物合成酶，在哺乳动物发育中发挥着不同的作用 [scRNA-seq]
• GSE277835 TUT1 和 USB1 是 U6 snRNA 3’ 末端 2’,3’-环磷酸修饰的生物合成酶，在哺乳动物发育中发挥着不同的作用 [RNA-seq]
• GSE255483 SARS-CoV-2先天免疫反应的多层拮抗作用
• 对 Prdm16 平滑肌特异性敲除小鼠和对照小鼠的主动脉组织进行 GSE227692 RNA 测序
• GSE213426 TAp63 在肌生成中的作用 [ChIP-Seq]
• GSE213423 TAp63 在肌生成中的作用 [RNA-Seq]
• GSE316088 RNA-seq 分析，比较了 shRNA 介导的 Npc1 基因敲低的 bEnd.3 细胞与对照组细胞的差异
• GSE314574 脂质-肽聚糖相互作用介导的外膜重塑使缺乏脂寡糖的细菌能够产生粘菌素耐药性
• GSE309939 调节 MyoD1 剂量可激活肌源性分化以外的其他细胞命运 [RNA-seq]
• GSE309864 调节 MyoD1 剂量可激活肌源性分化以外的其他细胞命运 [ATAC-seq]
• GSE309395：来自接受抗逆转录病毒疗法（cART）的HIV感染孕妇的细胞外囊泡来源的环状RNA谱分析揭示了与炎症和病毒潜伏相关的关键相互作用网络
• GSE299920 先锋因子 Ascl1/E12a 与核小体之间的独特相互作用驱动细胞命运转变 [ChIP-seq]
• GSE264078 糖基化通过 Wnt-Muc13 信号通路调控造血干细胞的巨核细胞命运 [scRNA]
• GSE334279 RPL27 通过 FMC1 增强氧化磷酸化促进胃癌进展
• GSE333874 小 RNA 测序揭示胎盘 miRNA 与克氏锥虫先天性传播相关
• GSE333851 空间糖编码定义人类肝脏病理和进展
• GSE299030 慢性应激对晚期阿尔茨海默病病理的悖论性保护作用
• GSE298572 从降解到破译：在降解条件下将ATAC-seq应用于法医分子诊断
• GSE234567 用于分离人类传导系统样心肌细胞的双报告基因模型 [scRNA-seq]
• GSE234562 用于分离人类传导系统样心肌细胞的双报告基因模型 [批量 RNA 测序]
• GSE296820 靶向胰腺癌中促增殖程序的转录依赖性
• GSE296819 靶向胰腺癌中促增殖程序的转录依赖性 [ChIPmentation]
• GSE296816 靶向胰腺癌中促增殖程序的转录依赖性 [ChIPmentation organoid]
• GSE296809 靶向胰腺癌中促增殖程序的转录依赖性 [scATAC_Mice]
• GSE296808 靶向胰腺癌中促增殖程序的转录依赖性 [RNAKD]
• GSE255090 丁酸盐阻断特定组蛋白乙酰化