科研日报 2026-04-10
📅 Daily Report - 2026-04-10
今日筛选出 84 条内容,来自 3 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 单细胞测序技术揭示联合疗法(CDK4/6与PD-1阻断)在去分化脂肪肉瘤中的疗效预测生物标志物。空间转录组学技术进一步阐明了神经母细胞瘤与其免疫微环境的相互作用。
主要方向:
- 探索尼洛沙尼(Niclosamide)在克服肿瘤免疫逃逸中的治疗潜力。
- 鉴定驱动植物入侵性的B染色体作用机制。
- 揭示miR-21-5p在口咽鳞状细胞癌放疗抵抗中的作用。
- 研究三阴性乳腺癌卡铂耐药的克服策略。
- 阐明NF-κB信号通路在胰腺癌中的表观遗传调控。
技术亮点:
- 10x Genomics Xenium技术实现对胸膜间皮瘤的靶向空间转录组学分析。
- 整合RNA-seq、ChIP-seq、miRNA-seq、CUT&Tag等多种高通量测序技术,从不同层面深入解析癌症、免疫、发育等复杂生物学过程。
📊 学点生信
今日焦点: Bioconductor 与 R-universe 强强联合,共同开发通用基础设施,旨在提升 R 生物信息学生态系统的质量和可维护性。
主要方向:
- 整合 Bioconductor 的高质量、同行评审的生物信息学工具。
- 优化 R 包的构建、分发和管理流程。
技术亮点:
- 建立统一的开发和分发标准,促进 R 生物信息学工具的互操作性和复用性。
🧪 博客更新
今日焦点: 新型单细胞及时空测序技术首次绘制出人类毛囊衰老分子图谱,揭示了导致脱发和白发的细胞特异性变化。
主要方向:
- 揭示毛囊衰老过程中的细胞信号通路紊乱及干细胞功能下降机制。
- 探索脑内硫化氢(H₂S)生成蛋白CSE在阿尔茨海默病中的作用。
- 发现植物化合物协同增效机制,可将抗炎效果提升百倍。
技术亮点:
- 结合单细胞与时空测序,实现对毛囊衰老的精细分子解析。
- RNA测序与蛋白质分析联用,精确追踪免疫细胞活动和细胞因子动态。
📚 分类浏览
🧬 数据前沿 (79条)
详细内容(前10条)
1. ⭐ GSE320497 鉴定尼克酰胺在克服肿瘤微环境中 IFN-γ 依赖性癌症免疫逃逸方面的治疗潜力
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、cancer、immune、tumor microenvironment
- 📝 描述:Contributors : Yue Zhang ; En CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTumor cells frequently develop immune resistance through interferon-γ (IFN-γ)–induced PD-L1 expression, acquisition of cancer stem cell (CSC)–like features, and adaptation to hypoxia within the tumor microenvironment (TME). Although IFN-γ activates both STAT1 and STAT3, how these pathways interact to regulate immune evasion under hypoxia remains unclear. Using the MC38 murine colorectal cancer model and T cell–tumor spheroid co-culture assays, we examined how IFN-γ signaling through STAT1 and STAT3 regulates PD-L1 expression, CSC plasticity, and cytotoxic T cell function under normoxic and hypoxic conditions. Pharmacologic inhibitors and siRNA-mediated knockdown were used to dissect pathway function, and Niclosamide, an FDA-approved anthelmintic, was evaluated as a dual STAT1/STAT3 inhibitor. We found that IFN-γ primarily induced PD-L1 expression through STAT1 activation, whereas CSC plasticity was associated with STAT3 signaling. STAT1 and STAT3 displayed reciprocal regulation—blocking one enhanced activation of the other. Niclosamide effectively inhibited phosphorylation of both STAT1 and STAT3, resulting in suppressed PD-L1 upregulation and reduced CSC enrichment. In addition, it also partially inhibited hypoxia-induced HIF-1α expression. In co-culture assays, Niclosamide enhanced T cell infiltration and reduced exhaustion under hypoxic conditions, resulting in improved T cell killing. Our findings identified Niclosamide as a potent dual STAT1/3 inhibitor capable of reversing IFN-γ and hypoxia-driven immune evasion. Repurposing Niclosamide may represent a promising strategy to enhance the efficacy of immune checkpoint blockade in solid tumors.
- 🔗 查看原文
2. ⭐ GSE320212 鉴定预测去分化脂肪肉瘤联合 CDK4/6 和 PD-1 阻断疗法疗效的衰老和免疫生物标志物:连续肿瘤活检的单细胞 RNA 测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、immune、RNA-seq、single-cell
- 📝 描述:Contributors : Rosenbaum Evan ; Gularte Mérida Rodrigo ; D’Angelo SandraSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis dataset comes from an exploratory correlatives sub-study embedded within NCT04438824, a single-arm, open-label phase II trial evaluating the combination of the CDK4/6 inhibitor palbociclib and the PD-1 inhibitor INCMGA00012 in patients with advanced well-differentiated or dedifferentiated liposarcoma. The dbGaP submission is limited to the first 12 patients enrolled on the trial, for whom protocol-mandated tumor biopsies were collected for single-cell RNA sequencing. Single-cell RNASeq was performed to characterize cellular composition and transcriptional states within the tumor microenvironment in this pilot cohort. The dataset includes processed single-cell expression profiles and a restricted set of associated clinical variables such as demographics and response data abstracted from the parent study.
- 🔗 查看原文
3. ⭐ GSE295468 Single-cell and spatial transcriptomics uncover the role of B chromosomes in driving plant invasiveness
- ✍️ 作者:未知作者
- 🏷️ 关键词:single-cell、spatial、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Cui Wang ; James Ord ; Mengxiao Yan ; Yunfei Cai ; Hongjin Shao ; Lele Lin ; Jarkko Salojärvi ; Lele Liu ; Weihua GuoSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Phragmites australisInvasive plants can significantly disrupt native biodiversity, yet the genetic mechanisms driving their success remain poorly understood. This study investigates the genetic basis of invasiveness in the common reed (Phragmites australis), a resilient grass species that became invasive in North America following its introduction from Europe. By integrating whole-genome sequencing with bulk, single-cell, and spatial transcriptomics, we constructed a comprehensive single-cell atlas of the common reed’s shoot system. UMAP analysis revealed 19 distinct cell clusters within the shoot, which were annotated using Gene Ontology (GO) enrichment to identify key cell types, including mesophyll, epidermal, bundle sheath, differentiating vascular cells, shoot apical meristems, and a cell cycle-associated cluster. We inferred key genes involved in the specification of several tissues, such as epidermal cells and ground meristems. For gene expression analysis, shoot tissues from three individuals of the invasive North American population and three from the native European population were included. Comparative transcriptomic analysis revealed significant upregulation of genes associated with the light-harvesting components of photosynthesis in several tissues of the invasive population, while genes involved in the respiratory burst related to defense responses were notably downregulated.
- 🔗 查看原文
4. ⭐ GSE304579 miR-21-5p 激活替代末端连接赋予口腔鳞状细胞癌放射抗性 [SUGH-OSCC 患者肿瘤的 RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:carcinoma、resistance、RNA-seq
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMarked heterogeneity in radiosensitivity is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), often resulting in poor outcomes for radioresistant tumors. The underlying molecular drivers of this resistance remain elusive. Here, we identify a novel mechanism in which miR-21-5p promotes radiation resistance by selectively activating the error-prone DNA double-strand break (DSB) repair pathway alternative end-joining (Alt-EJ). Integrative miRNA profiling, multi-omic analyses, and functional assays demonstrate that miR-21-5p upregulation coupled with suppression of its target gene signature increases Alt-EJ dependence for DSB repair. This Alt-EJ reliance enhances genomic instability, increases tumor mutational burden and microhomology-mediated indels, and confers pronounced radiation resistance in OSCC models, while correlating with poor radiotherapy response in patients. Importantly, pharmacological or genetic inhibition of Alt-EJ components, including PARP1 and POLQ, restores radiosensitivity in vitro and in vivo, with PARP1 inhibition specifically reversing miR-21-5p-mediated resistance in a syngeneic mouse model. Further RNA-seq analyses of these mice tumors confirmed that PARP inhibitor induced selective radiosensitization effects for miR-21-5p-overexpressing tumors were accompanied by a pronounced reduction in alt-EJ expression. Collectively, these findings establish the miR-21-5p/Alt-EJ axis as a key driver of radiation resistance in OSCC and support Alt-EJ targeting as a promising approach for precision radiosensitization.
- 🔗 查看原文
5. ⭐ GSE304277 miR-21-5p 激活替代末端连接赋予口腔鳞状细胞癌放射抗性 [SCC7 小鼠肿瘤的 RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:carcinoma、resistance、RNA-seq
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMarked heterogeneity in radiosensitivity is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), often resulting in poor outcomes for radioresistant tumors. The underlying molecular drivers of this resistance remain elusive. Here, we identify a novel mechanism in which miR-21-5p promotes radiation resistance by selectively activating the error-prone DNA double-strand break (DSB) repair pathway alternative end-joining (Alt-EJ). Integrative miRNA profiling, multi-omic analyses, and functional assays demonstrate that miR-21-5p upregulation coupled with suppression of its target gene signature increases Alt-EJ dependence for DSB repair. This Alt-EJ reliance enhances genomic instability, increases tumor mutational burden and microhomology-mediated indels, and confers pronounced radiation resistance in OSCC models, while correlating with poor radiotherapy response in patients. Importantly, pharmacological or genetic inhibition of Alt-EJ components, including PARP1 and POLQ, restores radiosensitivity in vitro and in vivo, with PARP1 inhibition specifically reversing miR-21-5p-mediated resistance in a syngeneic mouse model. Further RNA-seq analyses of these mice tumors confirmed that PARP inhibitor induced selective radiosensitization effects for miR-21-5p-overexpressing tumors were accompanied by a pronounced reduction in alt-EJ expression. Collectively, these findings establish the miR-21-5p/Alt-EJ axis as a key driver of radiation resistance in OSCC and support Alt-EJ targeting as a promising approach for precision radiosensitization.
- 🔗 查看原文
6. ⭐ GSE327347 利用 10x Genomics Xenium 对胸膜间皮瘤进行靶向空间转录组分析
- ✍️ 作者:未知作者
- 🏷️ 关键词:10x、spatial、genomics
- 📝 描述:Contributors : David T Severson ; Sam Freyaldenhoven ; Ben Wadowski ; William G Richards ; Raphael Bueno ; Matthew B CougarSeries Type : OtherOrganism : Homo sapiensTargeted spatial transcriptomic profiling was performed on seven formalin-fixed paraffin-embedded pleural mesothelioma tumor samples from four cases using the 10x Genomics Xenium platform. The Xenium Human Immuno-Oncology panel supplemented with 100 additional custom genes selected from known pleural mesothelioma biomarkers and single-cell RNA-seq-derived marker genes was used. Raw and processed Xenium files are provided for each sample. To ensure data integrity with downloaded Xenium files, md5 checksums are provided in ‘Xenium_GEO.md5’. This dataset is part of a multi-modality study including matched scRNA-seq, bulk RNA-seq, and Xenium spatial transcriptomics generated from overlapping pleural mesothelioma samples. Related controlled-access sequencing data are available in dbGaP under accession phs004285.
- 🔗 查看原文
7. ⭐ GSE309617 治疗协同作用克服三阴性乳腺癌的卡铂耐药性 [批量 RNA 测序]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、resistance、RNA-seq
- 📝 描述:Contributors : Julia E Altman ; Emily K Zboril ; Aaron Valentine ; Nina Dashti-Gibson ; David C Boyd ; Rachel K Myrick ; Amy L Olex ; Mikhail G Dozmorov ; Joshua C HarrellSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapeutic options, where platinum-based chemotherapy such as carboplatin serves as a cornerstone of treatment. Despite initial responses, the rapid emergence of acquired resistance remains a major clinical barrier. Understanding the molecular adaptations that drive platinum resistance is essential to develop strategies to restore sensitivity and identify alternative vulnerabilities. Methods: We generated four isogenic patient-derived xenograft (PDX) pairs (WHIM30, BCM‑2147, BCM‑3887, BCM‑7482) through serial carboplatin exposure to model acquired resistance in TNBC. Bulk RNA sequencing, immunohistochemistry, and histopathological analyses were performed to define transcriptomic and phenotypic changes associated with resistance. Synergistic therapeutic combinations were identified using high-throughput drug screening in carboplatin-resistant (CR) PDX-derived models, followed by in vivo validation in NSG mice. Tumor growth and survival were assessed using mixed-effects modeling, two-way ANOVA, and Welch’s student t-test. Results: The resulting isogenic PDX pairs captured both convergent and model-specific adaptations to carboplatin. CR tumors demonstrated heterogeneous activation of DNA damage repair pathways, including restoration of BRCA1-dependent homologous recombination (BCM‑2147, WHIM30) and compensatory upregulation of mismatch repair (BCM‑3887). In the BRCA1-mutant BCM‑7482 model, resistance correlated with HORMAD1 upregulation, suggesting an alternative HRD-associated mechanism. Morphologically, BCM‑7482CR tumors exhibited a significant increase in nuclear size compared to their sensitive counterpart (p < 0.0001). Drug screening identified mTOR pathway inhibition as a recurrent vulnerability across CR models. Sacituzumab govitecan (SG) combined with Everolimus produced robust synergy in vitro and superior tumor control in vivo compared to single agents in both WHIM30CR and BCM‑2147CR. A second combination, Everolimus + Selinexor (KPT‑330), also reduced tumor burden, achieving statistical significance in an expanded WHIM30CR cohort and suppressing metastatic progression in the intrinsically resistant WHIM2…
- 🔗 查看原文
8. ⭐ GSE309616 治疗协同作用克服三阴性乳腺癌的卡铂耐药性 [scRNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、resistance、scRNA
- 📝 描述:Contributors : Julia E Altman ; Emily K Zboril ; Aaron Valentine ; Nina Dashti-Gibson ; David C Boyd ; Rachel K Myrick ; Amy L Olex ; Mikhail G Dozmorov ; Joshua C HarrellSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapeutic options, where platinum-based chemotherapy such as carboplatin serves as a cornerstone of treatment. Despite initial responses, the rapid emergence of acquired resistance remains a major clinical barrier. Understanding the molecular adaptations that drive platinum resistance is essential to develop strategies to restore sensitivity and identify alternative vulnerabilities. Methods: We generated four isogenic patient-derived xenograft (PDX) pairs (WHIM30, BCM‑2147, BCM‑3887, BCM‑7482) through serial carboplatin exposure to model acquired resistance in TNBC. Bulk RNA sequencing, immunohistochemistry, and histopathological analyses were performed to define transcriptomic and phenotypic changes associated with resistance. Synergistic therapeutic combinations were identified using high-throughput drug screening in carboplatin-resistant (CR) PDX-derived models, followed by in vivo validation in NSG mice. Tumor growth and survival were assessed using mixed-effects modeling, two-way ANOVA, and Welch’s student t-test. Results: The resulting isogenic PDX pairs captured both convergent and model-specific adaptations to carboplatin. CR tumors demonstrated heterogeneous activation of DNA damage repair pathways, including restoration of BRCA1-dependent homologous recombination (BCM‑2147, WHIM30) and compensatory upregulation of mismatch repair (BCM‑3887). In the BRCA1-mutant BCM‑7482 model, resistance correlated with HORMAD1 upregulation, suggesting an alternative HRD-associated mechanism. Morphologically, BCM‑7482CR tumors exhibited a significant increase in nuclear size compared to their sensitive counterpart (p < 0.0001). Drug screening identified mTOR pathway inhibition as a recurrent vulnerability across CR models. Sacituzumab govitecan (SG) combined with Everolimus produced robust synergy in vitro and superior tumor control in vivo compared to single agents in both WHIM30CR and BCM‑2147CR. A second combination, Everolimus + Selinexor (KPT‑330), also reduced tumor burden, achieving statistical significance in an expanded WHIM30CR cohort and suppressing metastatic progression in the intrinsically resistant WHIM2…
- 🔗 查看原文
9. ⭐ GSE296832 表观遗传背景定义了胰腺癌中经典和非经典 NF-κB 信号通路的转录活性 [RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、RNA-seq、epigenetic
- 📝 描述:Contributors : Joana E Aggrey-Fynn ; Steven A JohnsenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensNF-κB signaling in pancreatic ductal adenocarcinoma (PDAC) operates through canonical and noncanonical pathways mediated by RELA and RELB, respectively. We show that TNFα selectively activates the canonical RELA pathway, while TWEAK induces noncanonical signaling through RELB. Through integrated transcriptomic, epigenomic, and transcription factor binding analyses, we reveal distinct temporal dynamics and binding patterns, with RELB preferentially occupying AP1-rich, epigenetically active regions. Single-cell RNA-seq and tissue staining highlight pathway-specific crosstalk with the tumor microenvironment. These findings uncover fundamental differences in RELA and RELB regulatory mechanisms and their distinct contributions to PDAC gene regulation.
- 🔗 查看原文
10. ⭐ GSE296831 表观遗传背景定义了胰腺癌中经典和非经典 NF-κB 信号通路的转录活性 [ChIP-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、ChIP-seq、epigenetic
- 📝 描述:Contributors : Joana E Aggrey-Fynn ; Steven A JohnsenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensNF-κB signaling in pancreatic ductal adenocarcinoma (PDAC) operates through canonical and noncanonical pathways mediated by RELA and RELB, respectively. We show that TNFα selectively activates the canonical RELA pathway, while TWEAK induces noncanonical signaling through RELB. Through integrated transcriptomic, epigenomic, and transcription factor binding analyses, we reveal distinct temporal dynamics and binding patterns, with RELB preferentially occupying AP1-rich, epigenetically active regions. Single-cell RNA-seq and tissue staining highlight pathway-specific crosstalk with the tumor microenvironment. These findings uncover fundamental differences in RELA and RELB regulatory mechanisms and their distinct contributions to PDAC gene regulation.
- 🔗 查看原文
💡 该来源还有 69 条内容,详见 文末
📊 学点生信 (1条)
详细内容(全部1条)
1. Bioconductor 和 R-universe 在通用基础设施开发方面开展合作
- ✍️ 作者:未知作者
- 🏷️ 关键词:Bioconductor
- 📝 描述:For more than two decades, the Bioconductor project has been a cornerstone of the R ecosystem, providing high-quality, peer-reviewed tools for bioinformatics and computational biology. Its curated repository model, rigorous review standards, and tight… Continue reading: Collaborating between Bioconductor and R-universe on Development of Common Infrastructure
- 🔗 查看原文
🧪 博客更新 (4条)
详细内容(全部4条)
1. ⭐ 揭示毛发衰老的奥秘:利用单细胞和时空测序技术绘制人类毛囊衰老的分子图谱
- ✍️ 作者:未知作者
- 🏷️ 关键词:aging、sequencing、single-cell
- 📝 描述:RNA sequencing reveals cell-specific changes in hair follicle aging, identifying disrupted signaling and stem cell decline that contribute to hair loss and graying…
- 🔗 查看原文
2. 新的测序方法揭示了免疫信号传导中隐藏的缺口
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、sequencing
- 📝 描述:RNA sequencing combined with protein analysis enables detailed tracking of immune cell activity, revealing cytokine dynamics and improving understanding of cancer and immune response timing…
- 🔗 查看原文
3. 科学家发现香料协同作用可将抗炎效果提升100倍。
- ✍️ 作者:未知作者
- 🏷️ 关键词:inflammation
- 📝 描述:Chronic inflammation often works quietly in the background but can fuel serious diseases like diabetes, heart disease, and cancer. New research reveals that everyday plant compounds—like menthol from mint, cineole from eucalyptus, and capsaicin from chili peppers—can team up inside immune cells to dramatically boost their anti-inflammatory power. While individual compounds showed modest effects, certain combinations amplified results hundreds of times over by activating different cellular pathways at once.
- 🔗 查看原文
4. 这种“臭鸡蛋”状脑气体可能是对抗阿尔茨海默病的关键。
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer
- 📝 描述:Scientists have uncovered a surprising new player in Alzheimer’s disease: a protein called CSE that helps produce tiny amounts of hydrogen sulfide gas in the brain. In experiments with genetically engineered mice, removing this protein led to memory loss, brain damage, and other hallmarks of Alzheimer’s, including weakened blood-brain barriers and reduced formation of new neurons. The findings suggest that this “rotten egg” gas, when carefully regulated, may actually protect brain cells and support memory.
- 🔗 查看原文
📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| RNA-seq | 22 |
| cancer | 9 |
| resistance | 8 |
| transcriptome | 6 |
| metabolic | 6 |
| immune | 5 |
| metabolism | 5 |
| ATAC-seq | 5 |
| sequencing | 4 |
| single-cell | 4 |
| carcinoma | 4 |
| spatial | 4 |
| tumor | 3 |
| pathway | 3 |
| leukemia | 3 |
| epigenetic | 3 |
| scRNA | 3 |
| ChIP-seq | 3 |
| transcriptomics | 2 |
| Alzheimer | 2 |
📎 更多内容
🧬 数据前沿 其他内容 (69条)
- GSE282603 谷氨酰胺促进肿瘤增殖的新见解:线粒体代谢通路——Gln/GGCT/GSH/ROS轴
- GSE294373 定量蛋白质组学揭示赖氨酸乳酸化在多发性骨髓瘤细胞来那度胺耐药性中的作用 [RNA-Seq]
- GSE304815 miR-21-5p 激活替代末端连接赋予口腔鳞状细胞癌放射抗性[放射抗性或敏感性 OSCC 细胞的 miRNA-seq]
- GSE322823 IFNγ诱导嵌合抗原受体(CAR)-T细胞疗法中的抗原丢失
- GSE288396 受损滋养层细胞和蜕膜 XCR1+PMN-MDSC 相互作用驱动的代谢重编程控制高龄产妇的不良结局 [RNA-Seq]
- GSE280195 白血病侵袭性是由染色质重塑和核心调控因子的表达变化驱动的[ChIP-seq]
- GSE280194 白血病侵袭性由染色质重塑和核心调控因子的表达变化驱动 [RNA-seq]
- GSE270234 空间多组学揭示神经母细胞瘤与其免疫环境之间的相互作用
- GSE247783 靶向干细胞样 T 细胞中的一碳代谢以防止慢性移植排斥反应 [ChIP-seq]
- GSE247781 靶向干细胞样 T 细胞中的一碳代谢以预防慢性移植排斥反应 [RNA-seq]
- GSE294374 定量蛋白质组学揭示赖氨酸乳酸化在多发性骨髓瘤细胞来那度胺耐药性中的作用 [CUT&Tag]
- GSE294137 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
- GSE279112 基于全长转录组测序筛选田间蒺藜(Cenchrus pauciflorus Benth.)蒺藜木质化发育相关基因
- GSE327357 病毒样颗粒可实现原代人类髓系细胞的靶向基因工程和混合 CRISPR 筛选 [RNA-Seq Exp1]
- GSE327354 病毒样颗粒可实现原代人类髓系细胞的靶向基因工程和混合 CRISPR 筛选 [RNA-seq Exp3]
- GSE327352 病毒样颗粒可实现原代人类髓系细胞的靶向基因工程和混合 CRISPR 筛选 [RNA-seq Exp2]
- GSE325101 人参皂苷Rg3通过转录组学缓解小鼠过敏性哮喘
- GSE319656 再生障碍性贫血的骨髓微环境:来自Nestin/CXCL12免疫组织化学和RNA测序的启示
- GSE317101 造血干细胞保护机制用于急性髓系白血病(AML)定向免疫治疗
- GSE313989 范可尼贫血症中视黄酸代谢的差异性调节
- GSE307597 NAT10 依赖的 R 环上的 N4-乙酰胞苷 (ac4C) 驱动胶质母细胞瘤的肿瘤发生和干性 [RNA-Seq]
- GSE290215 体外多替拉韦暴露对少突胶质细胞前体细胞和少突胶质细胞转录组的影响
- GSE275659 B型核纤层蛋白通过与核纤层和核斑点的关联来组织3D染色质结构[RNA-seq]
- GSE261506 具有时间分辨率的成年C57BL/6小鼠萘棒状细胞损伤后肺上皮细胞的单细胞转录组分析
- GSE324826 全反式维甲酸通过TGF-β2/Smad2/3通路调节绒山羊次级毛囊-真皮乳头细胞的增殖和凋亡
- GSE319842 TOP2B驱动的蒽环类药物诱导的小鼠心脏毒性的空间转录组分析
- GSE317172 对前额叶皮层的转录组分析鉴定出与多发性硬化症模型认知障碍相关的炎症基因
- GSE316006 TCR 信号诱导 Kdm6b 拮抗 Ezh2 以维持组织调节性 T 细胞 [ATAC-seq]
- GSE315121 NAT10 介导的 ac4C RNA 乙酰化稳定 CXCL5/DEK mRNA 以驱动肺腺癌的增殖和转移 [RNA-Seq]
- GSE314157 通过单碳代谢调控靶向 Mapk13-Tcf1-Slc7a5 轴预防慢性同种异体移植血管病变
- GSE313096 白血病侵袭性是由染色质重塑和核心调控因子的表达变化驱动的
- GSE311442 PI3Kδ 和 PPARα 双重靶向通过 FoxO1 激活增强滤泡性淋巴瘤的抗肿瘤活性
- GSE311047 一个保守的增强子簇控制脊椎动物背视网膜中 efnb2 的表达 [Tetraodon RNA-Seq]
- GSE310896 一个保守的增强子簇控制脊椎动物背视网膜中 efnb2 的表达 [RNA-Seq]
- GSE310895 一个保守的增强子簇控制脊椎动物背视网膜中 efnb2 的表达 [ATAC-seq-Tn]
- GSE310894 一个保守的增强子簇控制脊椎动物背视网膜中 efnb2 的表达 [ATAC-Seq-Aa]
- GSE310598 镍暴露破坏小鼠胚胎干细胞中发育基因的表观遗传抑制
- GSE310480 犬内脏血管肉瘤诊断生物标志物的microRNA差异表达分析
- GSE307343 Pum2 缺失通过破坏巨噬细胞-上皮细胞间的相互作用并促进上皮细胞坏死而加剧结肠炎
- GSE301700 自噬激活剂可使异常的 Tau 蛋白稳态正常化,并挽救人类家族性阿尔茨海默病 iPSC 衍生皮质类器官中的突触
- GSE298617 多重类器官诱变揭示了驱动卵巢癌转化、病理和化疗敏感性的基因组合
- GSE298120 琥珀酸调节作为间歇性禁食对饮食诱导肥胖的脑功能和代谢影响的新机制
- GSE296738 Hes1通过抑制NFATc2介导的炎症来调节骨髓间充质基质细胞功能
- GSE291446 TCR 信号诱导 Kdm6b 拮抗 Ezh2 以维持组织调节性 T 细胞 [RNA-seq]
- GSE290182 基于微阵列的UBA3髓系敲除小鼠和对照小鼠BMDM转录组分析
- GSE289975 受损滋养层细胞和蜕膜 XCR1+PMN-MDSC 相互作用驱动的代谢重编程控制高龄产妇的不良妊娠结局
- GSE288405 受损滋养层细胞和蜕膜 XCR1+PMN-MDSC 相互作用驱动的代谢重编程控制高龄产妇的不良结局 [CUT&Tag]
- GSE275827 免疫调节因子Fgl2的缺失影响小鼠脾脏免疫谱
- GSE270840 超级增强子重组控制奥沙利铂耐药FBXW7突变型结直肠癌的再敏感性
- GSE256148 IL-17信号通路和NMDAR1抗体影响NMDAR脑炎
- GSE247784 靶向干细胞样T细胞中的一碳代谢以预防慢性移植排斥反应
- GSE227622 神经元MCT2通过增加乳酸促进星形胶质细胞HIF1α-VEGFa信号传导,从而促进活动诱导的血管形成
- GSE327361 BCL11B 的基序导向染色质抑制塑造异位靶向和谱系决定 [RNA-seq]
- GSE327360 BCL11B 的基序导向染色质抑制塑造异位靶向和谱系决定 [ATAC-seq]
- GSE327047 乳腺癌细胞中LRG1诱导的差异表达基因(DEG)中心谱的鉴定和整合
- GSE326864 FLASH 和常规放射疗法对关键代谢器官(白色脂肪组织)的不同影响
- GSE325752 JAX 研究 12 - 五种不同转录因子纯合缺失的雄性 KOLF2.2J hiPSC 衍生滋养层细胞系的 RNA 测序
- GSE317501 SPOP 和 CHD1 在 ACSL4 调控中的不同作用揭示了前列腺癌中铁死亡靶向治疗的背景依赖性脆弱性
- GSE295945 基于拉马苏的抗病毒免疫的结构基础及其从DNA修复机制的进化
- GSE294240 m6a 和 NuRD 复合物调控 AML 中的单核细胞分化和对 BCL2/BCL2L1 抑制剂的耐药性
- GSE293976 组蛋白乳酸化驱动幽门螺杆菌感染后胃癌发生过程中 HAS2 的表达
- GSE293851 偶然发现的脑膜瘤的DNA甲基化谱分析
- GSE292212 物种特异性氧感知控制脊椎动物肢体再生的启动 [scRNA-seq]
- GSE315030 变形链球菌的细菌胞外囊泡通过β-catenin信号通路驱动口腔鳞状细胞癌的进展
- GSE312138 重编程胰腺导管腺癌微环境:一种新型的整合素靶向细胞毒素 ProAgio 可增强化疗效果 [scRNA-seq]
- GSE312137 重编程胰腺导管腺癌微环境:一种新型的整合素靶向细胞毒素 ProAgio 可增强化疗效果 [RNA-seq]
- GSE310514 A circuit of mechanically regulated transcription factors balances regenerative and fibrotic memory of mesenchymal stromal cells [RNA-seq]
- GSE310502 机械调控转录因子回路平衡间充质基质细胞的再生记忆和纤维化记忆 [ATAC-Seq]
- GSE304564 不同温度下拟南芥天然种质Col-0和IP-Svi-0的转录组分析
📅 报告生成时间:2026-04-09 22:01
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