详细内容（前10条）

1. ⭐ GSE317527 整合的批量和单细胞转录组分析揭示了环磷酰胺对三阴性乳腺癌模型肿瘤微环境的影响 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、single-cell、scRNA、transcriptome
• 📝 描述：Contributors : Ling Zuo ; Jia Ge ; Xiaorong ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancer (TNBC) remains a formidable clinical challenge. Although preclinical investigations utilizing TNBC mouse models have demonstrated that intermittent cyclophosphamide (CTX) treatment yields superior anti-tumor effects, partly through immune stimulation, mechanisms by which CTX modulates the tumor microenvironment (TME) are not yet fully understood. In this study, we assessed the impact of optimal (140 mg/kg every 6 days, C140) and suboptimal (100 mg/kg every 6 days, C100) CTX treatment regimens on 4T1 tumors, a widely utilized orthotopic TNBC mouse model. While the C100 regimen was better tolerated than the C140 regimen, it was less effective in inhibiting tumor growth. Through integrated bulk and single-cell RNA sequencing of tumor tissues, we discovered that CTX treatment not only inhibited cancer cell proliferation and epithelial-mesenchymal transition but also remodeled the TME by recruiting and reprogramming various immune cells, thereby enhancing the anticancer immune response in a dose-dependent manner. Although the C140 regimen demonstrated significant tumor suppression, it also induced notable extracellular matrix remodeling and led to the accumulation of cancer-associated fibroblasts within the tumor microenvironment. Furthermore, the C140 regimen caused considerable exhaustion of CD8+ T cells and was linked to increased expression of various immune checkpoint molecules, including PD-L1/PD-L2, CD39, and CD200. These effects may compromise therapeutic efficacy and potentially contribute to the development of drug resistance. Overall, our findings elucidate both cancer-cell-intrinsic and tumor microenvironment-dependent mechanisms of CTX action at both local and systemic levels, highlighting potential targets for optimizing chemoimmunotherapy in TNBC.
• 🔗 查看原文

2. ⭐ GSE317281 整合的群体和单细胞转录组分析揭示了环磷酰胺对三阴性乳腺癌模型肿瘤微环境的影响

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、single-cell、transcriptome
• 📝 描述：Contributors : Ling Zuo ; Jia Ge ; Xiaorong ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancer (TNBC) remains a formidable clinical challenge. Although preclinical investigations utilizing TNBC mouse models have demonstrated that intermittent cyclophosphamide (CTX) treatment yields superior anti-tumor effects, partly through immune stimulation, mechanisms by which CTX modulates the tumor microenvironment (TME) are not yet fully understood. In this study, we assessed the impact of optimal (140 mg/kg every 6 days, C140) and suboptimal (100 mg/kg every 6 days, C100) CTX treatment regimens on 4T1 tumors, a widely utilized orthotopic TNBC mouse model. While the C100 regimen was better tolerated than the C140 regimen, it was less effective in inhibiting tumor growth. Through integrated bulk and single-cell RNA sequencing of tumor tissues, we discovered that CTX treatment not only inhibited cancer cell proliferation and epithelial-mesenchymal transition but also remodeled the TME by recruiting and reprogramming various immune cells, thereby enhancing the anticancer immune response in a dose-dependent manner. Although the C140 regimen demonstrated significant tumor suppression, it also induced notable extracellular matrix remodeling and led to the accumulation of cancer-associated fibroblasts within the tumor microenvironment. Furthermore, the C140 regimen caused considerable exhaustion of CD8+ T cells and was linked to increased expression of various immune checkpoint molecules, including PD-L1/PD-L2, CD39, and CD200. These effects may compromise therapeutic efficacy and potentially contribute to the development of drug resistance. Overall, our findings elucidate both cancer-cell-intrinsic and tumor microenvironment-dependent mechanisms of CTX action at both local and systemic levels, highlighting potential targets for optimizing chemoimmunotherapy in TNBC.
• 🔗 查看原文

3. ⭐ GSE337937 RASA3 通过限制 HCK 激酶抑制 Tc1 分化并减弱抗菌免疫力

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、bacteria、regex:bacter(ia|ial|ium)、kinase
• 📝 描述：Contributors : Jiayu Song ; Bing WuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusType I immunity is defined by IFN-γ secretion, with Tc1 cells as a key subset, yet their intrinsic negative regulators remain unclear. We identified RASA3 as a novel negative regulator of Tc1 cells. T cell-specific deletion of RASA3 enhanced Tc1 differentiation and antibacterial immunity. We further revealed the RASA3–HCK–STAT4 axis in the regulatoin of Tc1 cell generation.
• 🔗 查看原文

4. ⭐ GSE337339 RNA 和 DNA 相互作用组的单细胞整合分析揭示了癌症中可靶向的染色质结构 [scBarcode 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing、single-cell
• 📝 描述：Contributor : Evgeny DeforzhSeries Type : OtherOrganism : Homo sapiensThe human genome is pervasively transcribed into protein-coding and regulatory non-coding RNAs whose functions are coordinated within higher-order nuclear architectures. However, direct mapping of RNA–RNA and DNA–DNA interaction networks in complex human tissues at single-cell resolution has remained a major challenge. Here, we present SCIENCE-seq, a multimodal single-cell interactomics platform enabling simultaneous detection of RNA–RNA interactions and chromatin DNA–DNA contacts within individual cells. Applied to primary glioma specimens, SCIENCE-seq reveals cancer-specific interactions organized by lncRNAs and centered on key oncogenic drivers, including EGFR, hTERT, SOX2, CDK6, CDC42, CD47, and HOX loci. These datasets uncover previously unrecognized molecular relationships between premature lncRNAs and pre-mRNAs that regulate transcription, alternative splicing, and polyadenylation. Notably, we identify a glioma-specific trans-chromosomal HOX hub driven by five interacting lncRNAs. Targeting these RNA and DNA interactions with steric antisense oligonucleotides (ASOs) or CRISPRi enables selective inhibition of oncogenic programs in malignant cells while sparing normal tissue, establishing chromatin interactomes as actionable therapeutic targets.
• 🔗 查看原文

5. ⭐ GSE337246 RNA 和 DNA 相互作用组的单细胞整合分析揭示了癌症中可靶向的染色质结构 [scRNA-Seq 类器官]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、single-cell、scRNA
• 📝 描述：Contributor : Evgeny DeforzhSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe human genome is pervasively transcribed into protein-coding and regulatory non-coding RNAs whose functions are coordinated within higher-order nuclear architectures. However, direct mapping of RNA–RNA and DNA–DNA interaction networks in complex human tissues at single-cell resolution has remained a major challenge. Here, we present SCIENCE-seq, a multimodal single-cell interactomics platform enabling simultaneous detection of RNA–RNA interactions and chromatin DNA–DNA contacts within individual cells. Applied to primary glioma specimens, SCIENCE-seq reveals cancer-specific interactions organized by lncRNAs and centered on key oncogenic drivers, including EGFR, hTERT, SOX2, CDK6, CDC42, CD47, and HOX loci. These datasets uncover previously unrecognized molecular relationships between premature lncRNAs and pre-mRNAs that regulate transcription, alternative splicing, and polyadenylation. Notably, we identify a glioma-specific trans-chromosomal HOX hub driven by five interacting lncRNAs. Targeting these RNA and DNA interactions with steric antisense oligonucleotides (ASOs) or CRISPRi enables selective inhibition of oncogenic programs in malignant cells while sparing normal tissue, establishing chromatin interactomes as actionable therapeutic targets.
• 🔗 查看原文

6. ⭐ GSE306578 肝细胞中致癌β-catenin的单细胞转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:onco(logy|logist|gene|genic)、single-cell、transcriptomics
• 📝 描述：Contributors : Abhinav Illendula ; Charles K Hewett ; Yuki Hayata ; Joan Font-BurgadaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis study analyzes hepatocytes recombined to express oncogenic β-catenin in the normal liver and chronically damaged liver background.
• 🔗 查看原文

7. ⭐ GSE337812 空间转录组学揭示慢性应激背侧纹状体中D2相关突触转录减弱

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Jinhee Bae ; Heh-In ImSeries Type : OtherOrganism : Mus musculusChronic stress alters striatal functions involved in motivation, action selection, and behavioral adaptation, yet cell-type-associated transcriptional organization in the dorsal striatum remains unclear. We used RNAscope-guided GeoMx spatial transcriptomics to compare D1- and D2-enriched neuronal compartments within anatomically matched dorsal striatal regions after chronic restraint stress. Chronic restraint stress engaged both populations and produced comparable numbers of differentially expressed genes. Pathway-level analysis revealed partially overlapping transcriptional attenuation in D1 and D2 neurons, whereas D2 responses showed more coherent organization around receptor-trafficking and synaptic signaling programs. CRS-downregulated D2 genes further resolved into synapse-centered functional categories, including glutamatergic synapse, postsynaptic organization, and dendritic spine.
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8. ⭐ GSE337578 小鼠脑组织空间转录组学分析（tMCAO后3天）

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Yueman Zhang ; Yonghui Chen ; Yue ChengSeries Type : OtherOrganism : Mus musculusThis study employed spatial transcriptomics to profile the expression and spatial distribution of Htr2b, P2ry12, Mrc1, and Ms4a7 in mouse brains 3 days after transient middle cerebral artery occlusion (tMCAO). By capturing genome‑wide transcriptional data with spatial coordinates, we aimed to map the regional expression patterns of these genes across the ischemic core, penumbra, and remote areas, and to delineate their co‑localization relationships with distinct immune and glial cell populations. This spatially resolved approach will provide insights into the topographic organization of serotonergic signaling and neuroimmune interactions during the acute phase of ischemic stroke.
• 🔗 查看原文

9. ⭐ GSE327645 BACH1 作为先锋抑制因子，能够使巨噬细胞在不同组织和炎症环境中表现出可塑性和适应性 [RNA-seq/ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、RNA-seq、ATAC-seq
• 📝 描述：Contributors : Laszlo Nagy ; Dora Bojcsuk ; Petros TzerposSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTranscriptional master regulators of the myeloid lineage (like PU.1, Cebpa/b, etc.) are believed to be the main drivers of chromatin reprogramming during differentiation and polarization. Such developmental transcription factors act via their pioneer ability to open chromatin de novo and bookmark genomic regulatory sites (enhancers and promoters) to later recruit signal-dependent TFs, co-factors, and the basal transcriptional machinery. However, recent studies by us and others challenged this “developmental TF-centric” mode as they suggested that signal-dependent TFs, particularly repressors, can also have a pioneer and thus safeguarding role in the MF epigenome at baseline and during acute inflammation. Such an expanded model predicts that active transcriptional repression and chromatin bookmarking by signal-dependent master regulators are key mechanisms for safeguarding the enhancer repertoire and proper priming, deployment, and resolution of an inflammatory response. Here, we show that BACH1, a heme-sensitive transcriptional repressor, acts as such a pervasive epigenomic safeguard to regulate tissue macrophage identity. We show that BACH1 is part of the core hardwired transcriptional program of ground-state macrophages shaping the chromatin accessibility of thousands of distal regulatory elements. Furthermore, BACH1 cistrome is extensive, not static but dynamic, and expanding upon different inflammatory stimuli and correlates with pre-formed and de novo formed enhancer-promoter networks. We further show that myeloid BACH1 is indispensable in vivo for tissue regeneration upon injury as it regulates the kinetics of Ly6C+ to Ly6C- transition of inflammatory macrophages and regulates the onset, the kinetics and magnitude of expression of critical inflammatory and repair-related genes. Finally, BACH1 was found to be required in vivo for competitive fitness and tissue adaptation of several tissue-resident macrophage populations (eg. lung, peritoneal macrophages), further supporting its pervasive role in acquiring and maintaining the functional specificity and diversity of tissue macrophages. Taken together, our data suggest that BACH1 acts as a signal-dependent master regulator that directly controls key transcriptional circuits during tissue macropha…
• 🔗 查看原文

10. GSE337464 RNA 和 DNA 相互作用组的单细胞整合分析揭示了癌症中可靶向的染色质结构 [RNA SCIENCE]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、single-cell
• 📝 描述：Contributor : Evgeny DeforzhSeries Type : OtherOrganism : Homo sapiensThe human genome is pervasively transcribed into protein-coding and regulatory non-coding RNAs whose functions are coordinated within higher-order nuclear architectures. However, direct mapping of RNA–RNA and DNA–DNA interaction networks in complex human tissues at single-cell resolution has remained a major challenge. Here, we present SCIENCE-seq, a multimodal single-cell interactomics platform enabling simultaneous detection of RNA–RNA interactions and chromatin DNA–DNA contacts within individual cells. Applied to primary glioma specimens, SCIENCE-seq reveals cancer-specific interactions organized by lncRNAs and centered on key oncogenic drivers, including EGFR, hTERT, SOX2, CDK6, CDC42, CD47, and HOX loci. These datasets uncover previously unrecognized molecular relationships between premature lncRNAs and pre-mRNAs that regulate transcription, alternative splicing, and polyadenylation. Notably, we identify a glioma-specific trans-chromosomal HOX hub driven by five interacting lncRNAs. Targeting these RNA and DNA interactions with steric antisense oligonucleotides (ASOs) or CRISPRi enables selective inhibition of oncogenic programs in malignant cells while sparing normal tissue, establishing chromatin interactomes as actionable therapeutic targets.
• 🔗 查看原文

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1. ScPanKD——新型人工智能框架改进了单细胞RNA测序中T细胞亚型的识别

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、sequencing
• 📝 描述：RNA sequencing combined with knowledge distillation improves identification of fine grained T cell subtypes, increasing the accuracy of cancer single cell transcriptomics analyses..
• 🔗 查看原文

2. 嵌合RNA拓展了RNA测序在疾病检测方面的潜力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing combined with the ChiTaRS platform improves detection of disease associated chimeric RNAs, supporting biomarker discovery, liquid biopsy, and precision medicine…
• 🔗 查看原文

3. 新英格兰生物实验室®推出用于牛津纳米孔技术®直接RNA测序的NEBNext®配套模块

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：New England Biolabs introduces a new RNA sequencing companion module that simplifies direct native RNA sequencing with Oxford Nanopore for transcriptomics and RNA…
• 🔗 查看原文

4. 科学家终于破解了自然界制造更有效抗癌药物的秘密

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Researchers have cracked the code behind bacteria’s ability to naturally manufacture multiple versions of powerful anti-cancer drugs. The discovery could make it much easier to engineer new cancer treatments inspired by nature, including improved versions of existing medicines.
• 🔗 查看原文

5. 微小的二氧化硅颗粒能清除小鼠体内侵袭性前列腺癌。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Tiny silica nanoparticles engineered to seek out prostate cancer caused tumor cells to self-destruct and supercharged the immune system in preclinical mouse studies. Combined with immunotherapy, the treatment produced complete remissions in multiple mice, raising hopes for a powerful new approach to prostate cancer.
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• GSE336545 RNA 和 DNA 相互作用组的单细胞整合分析揭示了癌症中可靶向的染色质结构 [GRO-Seq]
• GSE336543 RNA 和 DNA 相互作用组的单细胞整合分析揭示了癌症中可靶向的染色质结构 [DNA SCIENCE]
• GSE336541 RNA 和 DNA 相互作用组的整合单细胞分析揭示了癌症中可靶向的染色质结构 [4C-Seq]
• GSE334406 RNA转录组学研究：MUP+HFD肿瘤中致癌β-catenin的表达
• GSE318306：对经RTX或5FdUR处理后DNA修复能力发生改变的HCT116细胞进行全转录组测序
• GSE315794 非剥脱性点阵激光 1940nm 治疗系列调节表观遗传通路和皮肤衰老迹象：一项半脸研究
• GSE308391 MDI1228，一种局部泛JAK抑制剂，通过破坏真皮成纤维细胞-T细胞趋化因子相互作用来缓解自身免疫性皮肤病
• GSE307186 解码生长素诱导蛋白降解中的新型获得性抗性机制 [ChIP-Seq]
• GSE298447 模拟肿瘤微环境的生物打印3D肺球体模型的转录组分析
• GSE298141 AT/RT 的治疗耐药性是由上皮-间质转化、细胞外基质变化和 CD1A+ CD207+ 树突状细胞的富集驱动的 [RNA-seq_cell_lines]
• GSE298140 AT/RT 的治疗耐药性是由上皮-间质转化、细胞外基质变化和 CD1A+ CD207+ 树突状细胞的富集驱动的 [RNA-seq_FFPE]
• GSE298139 AT/RT 的治疗耐药性是由上皮-间质转化、细胞外基质变化和 CD1A+ CD207+ 树突状细胞的富集驱动的 [snRNA-seq]
• GSE293752 IL4Ra阻断抑制恶性淋巴细胞增殖和蕈样肉芽肿的免疫抑制性肿瘤微环境
• GSE290119 解码生长素诱导蛋白降解中的新型获得性抗性机制 [RNA-Seq]
• GSE287042 合成人类着丝粒的表观遗传景观：常染色质修饰在 CENP-A 密集区域相互依存，并阻止其他修饰的入侵 [ChIP-seq]
• GSE287041 合成人类着丝粒的表观遗传景观：常染色质修饰在 CENP-A 密集区域相互依存，并阻止其他修饰的入侵 [RNA-seq]
• GSE287040 合成人类着丝粒的表观遗传景观：常染色质修饰在 CENP-A 密集区域相互依存，并阻止其他修饰的入侵 [DNA-seq]
• GSE335245 强制 Notch2 信号传导指导 B 细胞中的 TLR 和 BCR 反应性 [RNA-Seq]
• GSE310707 结肠特异性 Pten 单倍体不足模型模拟 PI3K 通路驱动的人类结直肠癌侵袭
• GSE309102 纤维蛋白依赖的 2′-O-甲基化调节 RPS28 核糖体掺入和致癌翻译
• GSE273078 纤维蛋白调节三阴性乳腺癌中的致癌蛋白池和核糖体蛋白组成
• GSE245591 干扰素γ处理的IEC 4.1细胞转录组谱的RNA-Seq分析
• GSE317884 通过调节 NRF2/HSF1/HO-1 信号通路增强藤黄酸在顺铂耐药肺癌细胞中的治疗效果
• GSE314455 支原体感染通过非小细胞肺癌中趋同的转录组重编程驱动EGFR-TKI耐药性
• GSE328371 KMT2D 缺失促进 KRAS 诱导的胰腺癌发生，且该过程独立于 TP53。
• GSE327657 非人灵长类动物气道上皮细胞反复暴露于木材烟雾后持续的转录组变化 [RNA-Seq]
• GSE318789 通过功能性 CRISPR-dCas9 干扰筛选鉴定参与急性髓系白血病白血病发生和维奈托克反应的长链非编码 RNA
• GSE318530 通过功能性 CRISPR-dCas9 干扰筛选鉴定参与急性髓系白血病白血病发生和维奈托克反应的长链非编码 RNA
• GSE317847 脐带血来源的功能性巨核细胞的生成和单细胞表征
• GSE317489 BCKDK 通过调节线粒体 ROS 驱动的 JNK/p38 MAPK 信号通路来抵抗肥胖引起的心脏重塑和功能障碍
• GSE312659 重复激活 TLR7 可增加小鼠的酒精摄入量并诱导细胞类型特异性转录组变化
• GSE309543 自然杀伤细胞衍生的细胞外囊泡重编程人类免疫系统以增强肿瘤细胞毒性
• GSE308250 Dek 缺失导致小鼠出现性别依赖性、任务特异性认知缺陷并重编程海马转录组
• GSE307188 解码生长素诱导蛋白降解中的新型获得性抗性机制
• GSE302144 AML 细胞中 H1.3 的耗竭导致 H1.2 的重新分布，引起染色质重塑和细胞周期失调 [RNA-Seq]
• GSE302143 AML 细胞中 H1.3 的耗竭导致 H1.2 的重新分布，引起染色质重塑和细胞周期失调 [ChIP-Seq]
• GSE302140 AML 细胞中 H1.3 的耗竭导致 H1.2 的重新分布，引起染色质重塑和细胞周期失调 [ATAC-Seq]
• GSE301192 XRCC1 缺陷驱动癌细胞端粒染色质渗漏、炎症信号传导和衰老
• GSE282805 炎症消退可增加造血干细胞数量和红细胞生成
• GSE280028 开发一种诱导分化的治疗策略用于肉瘤样肾细胞癌
• GSE275046 Ezh2 和细胞内 Ca2+ 信号相互依赖地协调 GVHD 和 CAR T 细胞反应 [RNA-seq_2]
• GSE275045 Ezh2 和细胞内 Ca2+ 信号相互依赖地协调 GVHD 和 CAR T 细胞反应 [RNA-seq_1]
• GSE337837 巨噬细胞来源的IL-18通过IFN-γ/JAK1-STAT1轴驱动M1极化，从而促进暴发性心肌炎中的心肌损伤
• GSE337359 RAI1 保障人类神经发育基因表达的保真度和节奏 [scRNA-Seq]
• GSE336167 RAI1 保障人类神经发育基因表达的保真度和节奏 [RNA-seq]
• GSE335246 滤泡B细胞、边缘区B细胞和新生浆细胞的染色质可及性差异。[ATAC-Seq]
• GSE334407 生理相关培养基与原代人肝细胞和Huh7细胞的重叠代谢反应相关
• GSE331323 肾脏中 lncRNA 的表达图谱和昼夜节律调控 [RNA-Seq]
• GSE328722 Mettl14 KO 小鼠胰岛单核 RNA 测序
• GSE328602 转染Yy1过表达构建体的aTC6细胞转录组
• GSE324037 适应性免疫塑造基线 pImmunity Shapes Baseline Physology of M. Tuberculosis in High-Dose Versus Low-Dose I in high-Dose versus low-Dose infection BALB/c mouse drug treatment mMouse Drug Treatment Models
• GSE320260：CLRN1基因敲除兔视网膜单核转录组学揭示Müller胶质细胞驱动的视网膜退化机制
• GSE318297 Integrator 和 NELF 中触手系带微区之间的动态相互作用调节启动子近端暂停检查点 [RNA-Seq]
• GSE316662 小鼠出生后子宫发育的空间转录组图谱
• GSE315495 SARS-CoV-2 刺突蛋白通过调控 A549 细胞中的 MEG3 和 BCYRN1 发挥抗癌作用
• GSE310589 Rho效应蛋白ARHGAP18通过YAP和Merlin协调Hippo通路反馈回路，以调节细胞骨架和上皮细胞极性。
• GSE305236 BUI1 是一种肌动蛋白细胞骨架蛋白，可赋予水稻持久且广谱的抗性。
• GSE303509 生物标志物指导的患者来源类器官反应可预测乳腺癌的有效疗法
• GSE279020 m6A-eCLIP 测序在小鼠α细胞系aTC1-6细胞中进行，使用Scramble或Mettl14 KD。
• 在小鼠α aTC1-6细胞中，使用Scramble、Mettl3 KD或Mettl14 KD进行GSE278831 mRNA测序
• GSE276535 通过调节其液-液相分离倾向来调控 p53 转录激活和肿瘤抑制活性
• GSE337529 寄生蜂 Nasonia vitripennis 的转录组图谱（涵盖倍性、性别和组织）[RNA-seq WPL]
• GSE337528 寄生蜂 Nasonia vitripennis 的转录组图谱（涵盖倍性、性别和组织）[RNA-seq WOM]
• GSE337527 寄生蜂 Nasonia vitripennis 的转录组图谱（涵盖倍性、性别和组织）[RNA-seq WGDL]
• GSE337526 寄生蜂 Nasonia vitripennis 的转录组图谱（涵盖倍性、性别和组织）[RNA-seq TRA]
• GSE337350 脑感应 synNotch-CAR T 细胞能够在多种临床前模型中实现对弥漫性中线胶质瘤的精准靶向和清除
• GSE337340 抑制 H3K27M 增强的 ATM 信号传导可提高弥漫性中线胶质瘤的放射治疗疗效
• GSE337335 靛玉红抑制RSL3诱导的铁死亡，并通过激活Wnt/β-catenin信号通路改善急性肺损伤
• GSE302951 肠道微生物群对潘氏细胞染色质可及性的影响
• GSE302293 过氧化物酶体增殖激活受体γ调节侵袭性滋养层细胞分化和血绒毛膜胎盘形成 [RNA-seq]
• GSE302291 过氧化物酶体增殖激活受体γ调控侵袭性滋养层细胞分化和血绒毛膜胎盘形成 [ChIP-seq]
• GSE301987 无菌小鼠和SPF小鼠潘氏细胞中的DNA甲基化和羟甲基化谱
• GSE237108 足底电击刺激下 Grin2b-C456Y 突变小鼠的转录组变化
• GSE338002 基于 RNA-seq 的生产细胞与 STV-C8 的相关性分析
• GSE335500 APOE3 和 APOE4 人类星形胶质细胞对嵌合小鼠阿尔茨海默病病理和微胶质细胞反应的差异性调节
• GSE307201 TET2 通过 AGO2 调控驱动髓系细胞命运的获得 [RNA-seq，TET2 KD 转分化]
• GSE305029 TET2 通过 AGO2 调控驱动髓系细胞命运的获得 [RNA-seq，AGO2 KD 转分化]
• GSE304947 TET2 通过 AGO2 调控驱动髓系细胞命运的获得 [DNA 甲基化阵列]
• GSE304943 TET2 通过 AGO2 调控驱动髓系细胞命运的获得 [ChIP-seq, TET2]
• GSE245651 BACH1 作为一种先锋抑制因子，能够促进巨噬细胞在不同组织和炎症环境下的可塑性和适应性。