详细内容（前10条）

1. ⭐ GSE304429 DMAP1 通过维持复制叉稳定性并抑制 IFN 信号介导的抗肿瘤免疫来促进肺癌进展 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、scRNA
• 📝 描述：Contributors : Kan Huang ; Xi Dai ; Shuaihu Li ; Yingxue Chen ; Yaxin Yu ; Lin Wang ; Kun Liu ; Chongyang Li ; Yihua Sun ; Fei LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDespite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression. Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1’s function in lung cancer development and offer a scientific basis for designing novel treatment approaches.
• 🔗 查看原文

2. ⭐ GSE304428 DMAP1 通过维持复制叉稳定性并抑制 IFN 信号介导的抗肿瘤免疫来促进肺癌进展 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity、RNA-seq
• 📝 描述：Contributors : Kan Huang ; Xi Dai ; Shuaihu Li ; Yingxue Chen ; Yaxin Yu ; Lin Wang ; Kun Liu ; Chongyang Li ; Yihua Sun ; Fei LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusDespite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression. Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1’s function in lung cancer development and offer a scientific basis for designing novel treatment approaches.
• 🔗 查看原文

3. ⭐ GSE302611 布氏锥虫染色质中 DNA G-四链体的全基因组定位揭示了编码区和转录起始位点的富集 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、genome、enrichment
• 📝 描述：Contributors : Ludovica Monti ; Genta Firth ; Joana R Correia Faria ; John M Kelly ; Gem Flint ; Silvia Galli ; Thomas E Maher ; Htay Mon Aye ; Marco Di AntonioSeries Type : Expression profiling by high throughput sequencingOrganism : Trypanosoma bruceiG-quadruplexes (G4s) are non-canonical DNA structures formed in guanine-rich sequences that are proposed to act as regulatory elements in trypanosomatid parasites, including Trypanosoma brucei, the causative agent of African sleeping sickness. However, their functional roles remain poorly understood, largely due to limited knowledge of their genomic distribution. Herein, we performed in silico analyses across 64 trypanosomatid species uncovering high degree of variability in G4 prevalence and species-specific patterns. We generated the first chromatin-based, genome-wide G4 map in T. brucei using G4 chromatin immunoprecipitation followed by sequencing (G4 ChIP-Seq), revealing enrichment within gene-associated regions, including coding DNA sequences (CDSs), and transcription boundaries such as transcription start sites (TSSs) and transcription termination sites (TTSs). This pattern diverges markedly from previous genome-wide G4 maps in humans, suggesting that G4s may play roles unique to trypanosome biology. To investigate their functional relevance, we profiled the transcriptome of T. brucei upon treatment with the G4-stabilizing ligand PhenDC3. PhenDC3 induced targeted transcriptional perturbation of genes bearing G4s, particularly those located within CDSs and TSSs. Altogether, our findings highlight a distinctive role for G4s in regulating gene expression in T. brucei and support their potential as therapeutic targets in the treatment of African sleeping sickness.
• 🔗 查看原文

4. ⭐ GSE302610 布氏锥虫染色质中 DNA G-四链体的全基因组定位揭示了编码区和转录起始位点的富集 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome、enrichment
• 📝 描述：Contributors : Ludovica Monti ; Genta Firth ; Joana R Correia Faria ; John M Kelly ; Gem Flint ; Silvia Galli ; Thomas E Maher ; Htay Mon Aye ; Marco Di AntonioSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Trypanosoma bruceiG-quadruplexes (G4s) are non-canonical DNA structures formed in guanine-rich sequences that are proposed to act as regulatory elements in trypanosomatid parasites, including Trypanosoma brucei, the causative agent of African sleeping sickness. However, their functional roles remain poorly understood, largely due to limited knowledge of their genomic distribution. Herein, we performed in silico analyses across 64 trypanosomatid species uncovering high degree of variability in G4 prevalence and species-specific patterns. We generated the first chromatin-based, genome-wide G4 map in T. brucei using G4 chromatin immunoprecipitation followed by sequencing (G4 ChIP-Seq), revealing enrichment within gene-associated regions, including coding DNA sequences (CDSs), and transcription boundaries such as transcription start sites (TSSs) and transcription termination sites (TTSs). This pattern diverges markedly from previous genome-wide G4 maps in humans, suggesting that G4s may play roles unique to trypanosome biology. To investigate their functional relevance, we profiled the transcriptome of T. brucei upon treatment with the G4-stabilizing ligand PhenDC3. PhenDC3 induced targeted transcriptional perturbation of genes bearing G4s, particularly those located within CDSs and TSSs. Altogether, our findings highlight a distinctive role for G4s in regulating gene expression in T. brucei and support their potential as therapeutic targets in the treatment of African sleeping sickness.
• 🔗 查看原文

5. ⭐ GSE335257 训练免疫将造血干细胞衰老与衰老相关炎症联系起来

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、aging、inflammation
• 📝 描述：Contributors : Marine Barthez ; Danica ChenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusSIRT3 is a mitochondrial NAD+-dependent deacetylase. To investigate the role of SIRT3 in hematopoietic stem cell aging, we generated and characterized mouse models overexpressing SIRT3.
• 🔗 查看原文

6. ⭐ GSE304430 DMAP1 通过维持复制叉稳定性并抑制 IFN 信号介导的抗肿瘤免疫来促进肺癌进展 [CUT&Tag]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity
• 📝 描述：Contributors : Kan Huang ; Xi Dai ; Shuaihu Li ; Yingxue Chen ; Yaxin Yu ; Lin Wang ; Kun Liu ; Chongyang Li ; Yihua Sun ; Fei LiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusDespite substantial progress in targeted and immune therapies, lung cancer remains the leading cause of cancer-related mortality, highlighting the urgent need for novel therapeutic strategies. Through a CRISPR-based knock-out screen, we identified the DNA methyltransferase 1-associated protein 1 (DMAP1) as a critical regulator of tumor progression. Functional studies showed that loss of DMAP1 exerts its anti-tumor effects through attenuating tumor cell proliferation and activating T cell-mediated adaptive anti-tumor effects. Mechanistically, loss of DMAP1 causes replication fork retardance, disturbs genome stability, and induces endogenous DNA damage, thereby activating tumor-intrinsic immune signaling and enhancing anti-tumor immune response during cancer cell growth. Clinical data analyses revealed that high DMAP1 expression is associated with reduced immune infiltration, a “cold” tumor microenvironment, and poorer overall survival in lung cancer. These findings significantly advance our knowledge of DMAP1’s function in lung cancer development and offer a scientific basis for designing novel treatment approaches.
• 🔗 查看原文

7. ⭐ GSE298450 SEMA6A 通过阻断 ISG15/TGFβ 轴抑制结直肠癌中的肿瘤进展并增强抗肿瘤免疫力

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity
• 📝 描述：Contributors : Rixin Zhang ; Fang Zhang ; Min YangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSemaphorin is an axon-guiding factor regulating nervous system development. A growing body of evidence shows that semaphorin could regulate tumor progress and immune responses. The research found that Semaphorin 6A (SEMA6A) may play a dual role in the occurrence and development of tumors. Nevertheless, the regulatory role of SEMA6A in colorectal cancer (CRC) remains unclear. This study aimed to investigate the prognostic value, expression pattern, clinical significance, and immune effects of SEMA6A in CRC. Through multi-database analyses and validation with clinical specimens and tissue microarray, we identified reduced SEMA6A expression in CRC tissues, establishing it as an independent prognostic factor. Functional enrichment and immune infiltration analyses revealed SEMA6A’s protective role through tumor immune microenvironment modulation, with elevated expression correlating with enhanced immune cell infiltration. Cellular experiments including CCK8, Transwell, and immunofluorescence assay demonstrated SEMA6A can suppress the proliferation, migration, and invasion ability of CRC. Integrated RNA-seq and proteomic analyses, we identified ISG15 as a downstream effector of SEMA6A. Functional validation confirmed that ISG15 promotes malignant progression and counteracts SEMA6A-mediated tumor suppression. Coculture experiments revealed that SEMA6A can activate the CD8+ T cells and inhibit the expression of TGF-β1 by reducing the expression level of ISG15. Moreover, SEMA6A could induce the response of CRC to PD-1 monoclonal antibody by up-regulating immunostimulatory factors, thus playing an anti-tumor role in a subcutaneous CRC model. Our findings indicate that SEMA6A can stratify the risk of CRC patients and serve as a novel biomarker to predict response to immunotherapy, providing novel insights into precision medicine and immunotherapeutic strategies for CRC.
• 🔗 查看原文

8. GSE335924 RNA-seq 鉴定出 FOS 为潜在的治疗靶点，可通过 miR-21/SOX2 通路激活高血压性脑出血中的神经干细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、pathway
• 📝 描述：Contributors : Wei Dai ; Jiarui Du ; Gang Shen ; Zuopeng Su ; Fulin XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensObjective: Intracerebral hemorrhage (ICH) is a severely devastating neurological disorder. At present, there is no specific effective therapy for ICH, and its pathophysiological mechanism remains incompletely elucidated. Herein, we attempted to identify blood mRNA biomarkers, potential therapeutic targets and pathways associated with ICH via RNA sequencing.Results: Biological analysis of RNA-seq data screened numerous differentially expressed genes involved in various biological processes including inflammation, immunity and regeneration, which were systematically summarized in this study. Through bioinformatic analysis and experimental validation, we found that the expression level of FOS gene was upregulated after ICH, with the potential to participate in the proliferation and differentiation of neural stem cells and promote neural recovery. Our research further indicated that Fos may be involved in the regulation of biological behaviors of neural stem cells via the miR-21/SOX2 signaling pathway, although its exact mode of action requires further investigation.Conclusion: Collectively, RNA-seq delineated the precise transcriptional alterations in peripheral blood between patients with hypertensive intracerebral hemorrhage and hypertensive control subjects. These findings establish a potential therapeutic target centered on the FOS gene, which is aimed at activating neural stem cells following intracerebral hemorrhage.
• 🔗 查看原文

9. GSE329370 Caspase-11介导的过度炎症反应会损害重症SARS-CoV-2感染中的CD8⁺ T细胞免疫和病毒清除能力

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、T cell
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
• 🔗 查看原文

10. GSE329369 Caspase-11 介导的过度炎症会损害严重 SARS-CoV-2 感染中的 CD8⁺ T 细胞免疫和病毒清除 [Casp11WT]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、T cell
• 📝 描述：Contributors : Amal O Amer ; Amy Webb ; Mostafa Eltobgy ; Mohamed ShamseldinSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSevere SARS-CoV-2 infection is characterized by lung hyperinflammation, impaired interferon responses, and defective T-cell activation, yet the molecular drivers of these immune dysregulations remain incompletely understood. Caspase-11 (CASP11), a key mediator of the non-canonical inflammasome, has been shown to mediate an innate hyperinflammatory response and cytokine release in a non-severe, non-lethal SARS-CoV-2 infection model. However, the role played by CASP11 in severe SARS-CoV-2 disease and how it impacts adaptive immunity is not identified. Here, we discover that CASP11 exacerbates severe SARS-CoV-2 pathogenesis by amplifying early innate immune responses while concurrently impairing antiviral CD8 T cell immunity. Using global knockouts, reciprocal bone marrow chimeras, and Cx3cr1-expressing mononuclear phagocyte system (MPS) cell-specific CASP11 deletion models, we show that targeting reduces lung inflammation, promotes early Natural Killer (NK) cell-mediated interferon-γ (IFN-γ) production, and enhances robust virus-specific effector CD8⁺ T cell responses. This was associated with enhanced viral clearance and improved survival, even under lethal infection conditions. Importantly, CASP11 KO mice also exhibited faster resolution of post-viral inflammation, suggesting a role in long-term immune remodeling. These findings position CASP11 as a promising immunomodulatory target for acute and delayed manifestations of severe SARS-CoV-2 infection.
• 🔗 查看原文

💡 该来源还有 47 条内容，详见 文末

详细内容（全部2条）

1. 一种利用单细胞RNA测序数据重建细胞进化的新方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：RNA sequencing data analyzed with SCITE-RNA enabled reconstruction of cell lineage trees and linked cancer cell evolution to gene expression profiles… The post New method reconstructs cell evolution from single-cell RNA sequencing data appeared first on RNA-Seq Blog.
• 🔗 查看原文

2. ZINB-GRAN——一种基于ZINB先验的图对抗框架，用于从单细胞RNA测序数据中推断基因调控网络。

• ✍️ 作者：未知作者
• 🏷️ 关键词：scRNA
• 📝 描述：RNA sequencing combined with graph adversarial learning improved reconstruction of gene regulatory networks and identified cell type-specific regulators in immune and cancer datasets… The post ZINB-GRAN – A ZINB-prior graph adversarial framework for gene regulatory network inference from scRNA-seq data appeared first on RNA-Seq Blog.
• 🔗 查看原文

• GSE329366 Caspase-11 介导的过度炎症会损害严重 SARS-CoV-2 感染中的 CD8⁺ T 细胞免疫和病毒清除 [FLOX]
• GSE329365 Caspase-11 介导的过度炎症会损害重症 SARS-CoV-2 感染中的 CD8⁺ T 细胞免疫和病毒清除 [Lung4Day]
• GSE322599 一种mRNA疫苗通过I型干扰素依赖性途径增强对单纯疱疹病毒的保护作用
• GSE327924 基于 CRISPR 的基因依赖性筛选揭示了间变性甲状腺癌中 BRAF 抑制剂耐药的机制
• GSE308594 单细胞RNA测序揭示A型肉毒杆菌毒素调节海马小胶质细胞吞噬活性
• GSE307434 SIRT3 调控造血干细胞衰老 [RNA-Seq，腓肠肌]
• GSE307126 SIRT3 调控造血干细胞衰老 [RNA-Seq]
• GSE307123 SIRT3 调控造血干细胞衰老 [ATAC-Seq]
• GSE306336 衰老通过线粒体ROS诱导的胶原蛋白生成损害巨噬细胞的吞噬作用
• GSE300742 基底细胞特异性 Mettl3 条件性敲除小鼠气管上皮的单细胞转录组分析
• GSE336404 F-肌动蛋白动力学将鞘脂代谢与慢性结肠炎上皮屏障完整性联系起来
• 利用靶向氧化还原响应纳米凝胶表达PGC1α可在体内预防前列腺癌（GSE335925）。
• GSE328412 RNA-seq 对经 BRD9 PROTAC 降解剂 WA-68 处理的 HS-SY-II 滑膜肉瘤细胞进行了时间序列分析
• GSE328411 ChIP-seq 分析了经 BRD9 PROTAC 降解剂 WA-68 处理的 HS-SY-II 滑膜肉瘤细胞中 GLTSCR1 和 SS18::SSX 融合基因的表达情况，并进行了时间序列分析。
• GSE328410 滑膜肉瘤细胞系经 BRD9 PROTAC 降解剂 WA-68 处理的 ATAC-seq
• GSE327507 Hnrnpa1 对斑马鱼早期发育和脂质代谢至关重要
• GSE319513 DNA-PKcs抑制剂KU-57788与铁死亡在间变性甲状腺癌细胞中具有协同作用
• GSE309105 ZMAT3 驱动范可尼贫血的代谢适应，通过鞘脂重编程创造白血病前期微环境。
• GSE304832 大鼠真皮成纤维细胞共培养条件下软骨细胞的测序
• GSE304724 大鼠滑膜成纤维细胞测序
• GSE297509 LINC01857 调控人类抗原呈递细胞的活力和抗菌防御
• GSE288448 ISX9 处理对 RBPJ 靶基因的影响表征。[ChIP-Seq]
• GSE288439 ISX9 处理对 RBPJ 靶基因的影响特征分析。[ATAC-Seq]
• GSE288438 ISX9 处理对 RBPJ 靶基因影响的特征分析。[RNA-Seq]
• GSE285091 SGLT2抑制剂通过抑制mTOR/p70S6K/cyclin D1信号通路，在肥胖相关肾病模型中改善足细胞肥大应激和疾病进展。
• GSE235578 移植的人类细胞和鸡邻近细胞的转录组时间分析
• GSE235576：不同方案下由不同hPSC衍生的NEC的转录组分析
• GSE235573 iTeO、TeO 和 NCC 的转录组分析
• GSE327228 RNA末端尿苷酰转移酶是AML中的可药物靶向的脆弱点，但对正常造血作用并非必需[RNA-seq]
• GSE326338 单细胞转录组分析揭示了鸡沙门氏菌感染期间先天样细胞毒性上皮内淋巴细胞的扩增
• GSE307908 SIRT3调控造血干细胞衰老
• GSE307432 SIRT3 调控造血干细胞衰老 [Cut & Tag]
• GSE306732 GADD45A在自闭症病因学中的新作用：通过TET1/R环依赖性KCNQ5调节来调节神经元兴奋性
• GSE300264 拟南芥单细胞RNA测序样本处理策略的性能评估
• GSE296546 糖尿病与类鼻疽和结核病患者共同的过度炎症免疫反应相关：一项观察性病例对照研究
• GSE214011 仓鼠（Phodopus sungorus）自发性每日蛰伏觉醒期间下丘脑核心区域视交叉上核和室旁核的转录组学研究。
• GSE181298 利用转录组从头组装方法，对短光周期适应的准噶尔仓鼠在自发进入每日蛰伏期和正常体温期间下丘脑核心区域视交叉上核和室旁核的转录组进行分析
• GSE336019 利用 QuantSeq 3’ mRNA-seq 对 HepG2 肝癌细胞中 NAT10 敲低进行基因表达谱分析
• GSE311287 RNA-Seq analysis of Leptospira interrogans serogroup Icterohaemorrhagiae and Pomona strains
• GSE296848 Hep3B 细胞中 NR1D1 的 ChIP-Seq 数据
• GSE295749 髓系细胞中的 CD44 是酒精相关肝病中肝脏炎症和损伤的主要驱动因素 [CD44_Myelo_KO_Ethanol]
• GSE295747 髓系细胞中的 CD44 是酒精相关肝病中肝脏炎症和损伤的主要驱动因素 [CD44_KO_Ethanol]
• GSE270684 EZH2 和 EZH1 抑制剂 valemetostat 可解除 p16INK4a 的抑制，从而诱导巨核细胞早期内有丝分裂退出 [scATAC-Seq]
• GSE270683 EZH2 和 EZH1 抑制剂 valemetostat 可解除 p16INK4a 的抑制，从而诱导巨核细胞早期内有丝分裂退出 [RNA-Seq]
• GSE330097 STING诱导免疫的突变图谱
• GSE324246 3-(4-羟基-3-甲氧基苯基)丙酸可预防腺嘌呤诱导的慢性肾病小鼠的肾纤维化和炎症
• GSE308873 ZMAT3 通过调节鞘脂代谢减轻范可尼贫血中的细胞死亡