详细内容（前10条）

1. ⭐ GSE277547 一种新型组蛋白 H3K27 阅读器 CBFA2T2 通过调节代谢基因和代谢物水平抑制 H3K27me3 去甲基化和肿瘤生长 [ChIP-seq II]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、metabolic、ChIP-seq、histone
• 📝 描述：Contributors : Shengfei He ; Rui GuoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHistone H3.1/3.2K27M and H3.3K27M mutation are driver mutations frequently identified in diffuse midline glioma (DMG). However, the precise mechanism by which H3K27M mediates tumorigenesis remains incompletely understood. By carrying out bait Protein-Protein Interaction followed by genome-wide screening (bPPI-seq) in H3.3WT and H3.3K27M mouse NSC models, we identified a novel histone reader CBFA2T2, which recognizes non-mutated or un-modified histone H3K27. Importantly, CBFA2T2 binding to H3K27, mediated by the NHR2 domain, is abrogated by the H3K27M oncogenic mutation. In H3.3 wildtype cells, CBFA2T2 represses transcription of genes involved in carbon metabolism and TCA cycle through its binding to H3K27. This alters the α-KG/Succinate (alpha-ketoglutarate/ Succinate) ratio and indirectly impacts H3K27me3 level, possibly through affecting the H3K27me3 demethylases. CBFA2T2 does not bind the H3.3K27M decorated chromatin in vivo, thus the K to M mutation, partially compromises the CBFA2T2 repressive function. However, over-expressing CBFA2T2 rescues the low H3K27me3 level in H3.3K27M mNSC and H3.3K27M DIPG cells, thus suppressing the H3.3K27M tumor growth. Our findings suggest a new mechanism, which may contribute to the low H3K27me3 level observed in the H3K27M cells, and provide a new strategy for H3K27M therapy through manipulation of CBFA2T2.
• 🔗 查看原文

2. ⭐ GSE277514 一种新型组蛋白 H3K27 阅读器 CBFA2T2 通过调节代谢基因和代谢物水平抑制 H3K27me3 去甲基化和肿瘤生长 [ChIP-seq I]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、metabolic、ChIP-seq、histone
• 📝 描述：Contributors : Shengfei He ; Wenyun Weng ; Yujie Tang ; Rui GuoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensHistone H3.1/3.2K27M and H3.3K27M mutation are driver mutations frequently identified in diffuse midline glioma (DMG). However, the precise mechanism by which H3K27M mediates tumorigenesis remains incompletely understood. By carrying out bait Protein-Protein Interaction followed by genome-wide screening (bPPI-seq) in H3.3WT and H3.3K27M mouse NSC models, we identified a novel histone reader CBFA2T2, which recognizes non-mutated or un-modified histone H3K27. Importantly, CBFA2T2 binding to H3K27, mediated by the NHR2 domain, is abrogated by the H3K27M oncogenic mutation. In H3.3 wildtype cells, CBFA2T2 represses transcription of genes involved in carbon metabolism and TCA cycle through its binding to H3K27. This alters the α-KG/Succinate (alpha-ketoglutarate/ Succinate) ratio and indirectly impacts H3K27me3 level, possibly through affecting the H3K27me3 demethylases. CBFA2T2 does not bind the H3.3K27M decorated chromatin in vivo, thus the K to M mutation, partially compromises the CBFA2T2 repressive function. However, over-expressing CBFA2T2 rescues the low H3K27me3 level in H3.3K27M mNSC and H3.3K27M DIPG cells, thus suppressing the H3.3K27M tumor growth. Our findings suggest a new mechanism, which may contribute to the low H3K27me3 level observed in the H3K27M cells, and provide a new strategy for H3K27M therapy through manipulation of CBFA2T2.
• 🔗 查看原文

3. ⭐ GSE277513 一种新型组蛋白 H3K27 阅读器 CBFA2T2 通过调节代谢基因和代谢物水平抑制 H3K27me3 去甲基化和肿瘤生长 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、metabolic、RNA-seq、histone
• 📝 描述：Contributors : Shengfei He ; Rui GuoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHistone H3.1/3.2K27M and H3.3K27M mutation are driver mutations frequently identified in diffuse midline glioma (DMG). However, the precise mechanism by which H3K27M mediates tumorigenesis remains incompletely understood. By carrying out bait Protein-Protein Interaction followed by genome-wide screening (bPPI-seq) in H3.3WT and H3.3K27M mouse NSC models, we identified a novel histone reader CBFA2T2, which recognizes non-mutated or un-modified histone H3K27. Importantly, CBFA2T2 binding to H3K27, mediated by the NHR2 domain, is abrogated by the H3K27M oncogenic mutation. In H3.3 wildtype cells, CBFA2T2 represses transcription of genes involved in carbon metabolism and TCA cycle through its binding to H3K27. This alters the α-KG/Succinate (alpha-ketoglutarate/ Succinate) ratio and indirectly impacts H3K27me3 level, possibly through affecting the H3K27me3 demethylases. CBFA2T2 does not bind the H3.3K27M decorated chromatin in vivo, thus the K to M mutation, partially compromises the CBFA2T2 repressive function. However, over-expressing CBFA2T2 rescues the low H3K27me3 level in H3.3K27M mNSC and H3.3K27M DIPG cells, thus suppressing the H3.3K27M tumor growth. Our findings suggest a new mechanism, which may contribute to the low H3K27me3 level observed in the H3K27M cells, and provide a new strategy for H3K27M therapy through manipulation of CBFA2T2.
• 🔗 查看原文

4. ⭐ GSE285766 单细胞多组学测序揭示肠道微生物代谢产物丁酸在疼痛调节中细胞特异性的转录组和染色质可及性特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Ran Tao ; Feng TaoSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusPain is a predominant symptom of temporomandibular joint (TMJ) disorders, presenting significant clinical challenges due to their complexity and limited treatment options. This study investigated the therapeutic potential of butyrate, a gut microbiome metabolite, in a complete Freund’s adjuvant (CFA)-induced mouse model of TMJ inflammatory pain. Butyrate administration significantly alleviated TMJ pain and restored butyrate levels in mouse feces, plasma, and the spinal trigeminal nucleus caudalis (Sp5C). Additionally, it reversed TMJ pain-induced reductions in acetylation within Sp5C neurons, a critical epigenetic mechanism linked to pain states. Utilizing single-nucleus RNA sequencing (snRNA-seq) and single-nucleus ATAC sequencing (snATAC-seq), we profiled transcriptional and chromatin accessibility changes at the single-cell level.
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5. ⭐ GSE320157 卵巢肿瘤 FAK 抑制释放 Omega-3 脂肪酸刺激 GATA6 腹膜巨噬细胞 CXCL13 产生，增强免疫疗法 II

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、macrophage、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Dwayne Stupack ; Xiao L Chen ; David SchlaepferSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSupernatants from murine KMF tumors lacking or expressing focal adhesion kinases were added to macrophage to determine the impact of each tumor line on macrophage gene expression.
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6. ⭐ GSE299693 全基因组 CRISPR 筛选鉴定出 DTX4 调节肺泡蛋白沉积症中肺泡巨噬细胞胆固醇外流 [RNA-seq II]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、RNA-seq、genome
• 📝 描述：Contributors : Xinmei Huang ; Zimu Wang ; Jingwei Shi ; Yonglong Xiao ; Mengshu Cao ; Yingwei Zhang ; Xinye XiaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPulmonary alveolar proteinosis (PAP) is a rare pulmonary syndrome characterized by impaired surfactant clearance, driven by dysfunctional cholesterol efflux in alveolar macrophages (AMs). However, the molecular determinants governing AM cholesterol homeostasis remain largely elusive. Here, through a genome-wide CRISPR activation screen in foamy macrophages and bulk RNA sequencing of AMs from PAP patients, we identify Deltex E3 Ubiquitin Ligase 4 (DTX4) as a pivotal regulator of cholesterol efflux in AMs. Adeno-associated virus (AAV) -mediated silencing of DTX4 led to excessive lipid accumulation in AMs, exacerbated alveolar proteinosis, increased lung opacities on imaging, and significantly deteriorated pulmonary function in mice. Similarly, DTX4 depletion in primary AMs impaired cholesterol efflux and promoted intracellular lipid deposition. In contrast, AM-specific overexpression of DTX4 markedly alleviated lipid accumulation, mitigated alveolar proteinosis, restored lung densities on computed tomography, and rescued pulmonary function in Csf2ra-/-mice, a model of PAP. Mechanistically, DTX4 deficiency downregulated PPAR-γ expression, driving foamy AM formation. Notably, the regulatory function of DTX4 in lipid homeostasis was partially mediated by PPAR-γ but independent of its canonical E3 ubiquitin ligase activity. Collectively, our findings establish DTX4 as a central orchestrator of AM cholesterol efflux and surfactant homeostasis, positioning it as a promising therapeutic target for PAP and a potential paradigm for cholesterol dysregulation in related disorders.
• 🔗 查看原文

7. ⭐ GSE299689 全基因组 CRISPR 筛选鉴定出 DTX4 调节肺泡蛋白沉积症中肺泡巨噬细胞胆固醇外流 [RNA-seq 1]

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、RNA-seq、genome
• 📝 描述：Contributors : Xinmei Huang ; Zimu Wang ; Jingwei Shi ; Yonglong Xiao ; Mengshu Cao ; Yingwei Zhang ; Xinye XiaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPulmonary alveolar proteinosis (PAP) is a rare pulmonary syndrome characterized by impaired surfactant clearance, driven by dysfunctional cholesterol efflux in alveolar macrophages (AMs). However, the molecular determinants governing AM cholesterol homeostasis remain largely elusive. Here, through a genome-wide CRISPR activation screen in foamy macrophages and bulk RNA sequencing of AMs from PAP patients, we identify Deltex E3 Ubiquitin Ligase 4 (DTX4) as a pivotal regulator of cholesterol efflux in AMs. Adeno-associated virus (AAV) -mediated silencing of DTX4 led to excessive lipid accumulation in AMs, exacerbated alveolar proteinosis, increased lung opacities on imaging, and significantly deteriorated pulmonary function in mice. Similarly, DTX4 depletion in primary AMs impaired cholesterol efflux and promoted intracellular lipid deposition. In contrast, AM-specific overexpression of DTX4 markedly alleviated lipid accumulation, mitigated alveolar proteinosis, restored lung densities on computed tomography, and rescued pulmonary function in Csf2ra-/-mice, a model of PAP. Mechanistically, DTX4 deficiency downregulated PPAR-γ expression, driving foamy AM formation. Notably, the regulatory function of DTX4 in lipid homeostasis was partially mediated by PPAR-γ but independent of its canonical E3 ubiquitin ligase activity. Collectively, our findings establish DTX4 as a central orchestrator of AM cholesterol efflux and surfactant homeostasis, positioning it as a promising therapeutic target for PAP and a potential paradigm for cholesterol dysregulation in related disorders.
• 🔗 查看原文

8. GSE319257 2,3-二磷酸甘油酸变位酶 (BPGM) 定义了透明细胞肾细胞癌中的一种应激抵抗代谢状态

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、metabolic
• 📝 描述：Contributors : Robert Labes ; Michael Faehling ; Philipp N BeckerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: Clear cell renal cell carcinoma (ccRCC) is characterized by profound metabolic reprogramming and limited responsiveness to diverse therapeutic stressors, including epigenetic modulation. How glycolytic enzymes contribute to metabolic stress tolerance in ccRCC remains incompletely understood. Methods: We investigated the role of the glycolytic enzyme 2,3-bisphosphoglycerate mutase (BPGM) in ccRCC using human tumor specimens, siRNA-mediated gene silencing, functional cell-based assays, and transcriptomic profiling. Epigenetic stress was induced using the histone deacetylase inhibitor Vorinostat as a tool compound. Results: BPGM expression was consistently elevated in human ccRCC tissue compared with adjacent normal kidney. ccRCC A498 cells exhibited high basal BPGM levels and limited sensitivity to Vorinostat, whereas BPGM depletion increased cellular stress responses and reduced proliferative capacity. Despite inducing similar phenotypic outcomes, BPGM silencing and Vorinostat treatment triggered markedly distinct transcriptional programs. While HDAC inhibition caused broad, unspecific gene deregulation, BPGM loss elicited a focused stress-associated response, including activation of unfolded protein response and ferroptosis-related gene signatures. Conclusions: Our data identify BPGM as a determinant of metabolic stress resilience in ccRCC. By shaping selective transcriptional stress responses rather than global epigenetic reprogramming, BPGM may contribute to the intrinsic robustness of renal cancer cells. Targeting metabolic stress adaptation pathways may therefore complement epigenetic strategies in ccRCC.
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9. GSE314272 PDS5 蛋白通过限制粘连蛋白-NIPBL 复合物的寿命来控制基因组结构 [Hi-C]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Hi-C、genome
• 📝 描述：Contributors : Roman R Stocsits ; Gordana Wutz ; Jan-Michael Peters ; Wen TangSeries Type : OtherOrganism : Gallus gallus ; Homo sapiensCohesin-NIPBL complexes extrude genomic DNA into loops that are constrained by CTCF boundaries. This process has important regulatory functions and weakens the separation between euchromatic and heterochromatic compartments. Cohesin can also bind PDS5A or PDS5B, which do not support loop extrusion but are required for the formation of CTCF boundaries. How PDS5 proteins perform this function is unknown. Here we show by in vitro single-molecule imaging that PDS5 proteins stop loop extrusion by facilitating the dissociation of NIPBL from cohesin. Hi-C experiments suggest that this function is required for the establishment of CTCF boundaries in cells. In silico modelling indicates that PDS5 proteins enable the separation between compartments by limiting cohesin’s velocity and chromatin-residence time. The degree of this compartmentalization depends on the frequency with which chromatin is extruded relative to the time it takes for compartments to form. These results identify PDS5 proteins as key regulators of genome organization.
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10. GSE314270 PDS5 蛋白通过限制黏连蛋白-NIPBL 复合物的寿命来控制基因组结构 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Wen Tang ; Roman R Stocsits ; Gordana Wutz ; Jan-Michael PetersSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensCohesin-NIPBL complexes extrude genomic DNA into loops that are constrained by CTCF boundaries. This process has important regulatory functions and weakens the separation between euchromatic and heterochromatic compartments. Cohesin can also bind PDS5A or PDS5B, which do not support loop extrusion but are required for the formation of CTCF boundaries. How PDS5 proteins perform this function is unknown. Here we show by in vitro single-molecule imaging that PDS5 proteins stop loop extrusion by facilitating the dissociation of NIPBL from cohesin. Hi-C experiments suggest that this function is required for the establishment of CTCF boundaries in cells. In silico modelling indicates that PDS5 proteins enable the separation between compartments by limiting cohesin’s velocity and chromatin-residence time. The degree of this compartmentalization depends on the frequency with which chromatin is extruded relative to the time it takes for compartments to form. These results identify PDS5 proteins as key regulators of genome organization.
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1. ⭐ 肠道内隐藏的病毒可能与结肠癌有关

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、gut、regex:gut(-?microbiome)?
• 📝 描述：A newly discovered virus hiding inside a common gut bacterium could help explain one of medicine’s long-standing mysteries: why a microbe found in both healthy people and cancer patients is linked to colorectal cancer. The research suggests that the interaction between bacteria and the viruses they carry may be key to understanding disease risk. It may even lead to future screening tests that detect cancer risk earlier.
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2. 简单的“肠道重置”或许可以阻止服用 Ozempic 或 Wegovy 后体重增加。

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：A new minimally invasive procedure may help people keep weight off after stopping popular drugs like Ozempic and semaglutide—something most patients struggle with. In a clinical trial, those who underwent a technique called duodenal mucosal resurfacing regained far less weight compared to others after discontinuing the medication. The procedure works by renewing the lining of the upper small intestine, potentially “resetting” metabolism and preserving the benefits of weight loss.
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3. 高质量的腺泡细胞分离技术能够对健康和受损的胰腺进行单细胞分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：RNA sequencing reveals improved recovery and analysis of pancreatic acinar cells, enabling clearer insights into cell states in healthy tissue and disease conditions…
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4. 简单的血液检测就能在数年前揭示阿尔茨海默病的风险。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：A routine blood marker tied to inflammation may reveal Alzheimer’s risk years in advance. Scientists found that higher neutrophil levels—part of the body’s first immune response—were linked to a greater chance of developing dementia. The discovery suggests this common lab value could help flag at-risk individuals before symptoms appear. It also raises the possibility that immune cells themselves may be fueling the disease.
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• GSE309138 肺部微生物群通过 SCFA-FFAR2 轴协调肺泡巨噬细胞和 γδ T 细胞活化以对抗肺炎克雷伯菌
• GSE307524 NUTM1重排白血病的综合分子和功能分析 [ChIP-Seq]
• GSE307522 NUTM1重排白血病的综合分子和功能分析[甲基化芯片]
• GSE276679 NUTM1重排白血病的综合分子和功能分析 [白血病-RNA-seq]
• GSE276675 NUTM1重排白血病的综合分子和功能分析 [ATAC-Seq]
• GSE328721 Azacytidine 对 DNA 甲基化的调节可以恢复 AML 中的 T 细胞功能和衰竭。
• GSE316631 空间分辨亚型进展揭示胰腺导管腺癌的代谢脆弱性。
• GSE314771 H4K5 乳酸化对糖酵解的正反馈调节促进肝细胞癌的恶性进展 [RNA-seq]
• GSE314769 H4K5 乳酸化对糖酵解的正反馈调节促进肝细胞癌的恶性进展 [ChIP-seq]
• GSE312491 单细胞分析揭示复发型和进展型多发性硬化症小鼠模型中免疫血管串扰的介质
• GSE309739 空间分辨亚型进展揭示胰腺导管腺癌 II 的代谢脆弱性
• GSE309669 空间分辨亚型进展揭示胰腺导管腺癌的代谢脆弱性
• GSE300851 DGAT：一种用于从转录组学推断空间蛋白质景观的双图注意力网络
• GSE298347 斑马鱼pde6c突变体眼部小胶质细胞/巨噬细胞的单细胞RNA测序
• GSE278614 人类肾脏发育的单细胞空间映射揭示细胞微环境和谱系动态 [CosMx]
• GSE277893 人类肾脏发育的单细胞空间图谱揭示了细胞微环境和谱系动态
• GSE328637 GET通路通过丝状真菌中的甾醇代谢重塑和蛋白质运输调节唑类药物敏感性
• GSE328515 RNA-seq 分析皮下 HCC 小鼠模型中对乐伐替尼敏感和耐药的肿瘤组织
• GSE328508 用T-oligo处理的卵巢癌细胞的高通量测序
• GSE324158 灵长类松果体的单细胞多组学和空间图谱揭示了昼夜节律和褪黑激素的调控结构
• GSE306092 患者来源的淋巴瘤球体揭示了复发/难治性 B 细胞非霍奇金单抗耐药的预测标志物
• GSE303444 错配修复缺陷型结直肠癌的转录组和免疫组库分析
• GSE299696 全基因组 CRISPR 筛选发现 DTX4 调节肺泡蛋白沉积症中的肺泡巨噬细胞胆固醇外流 [CRISPR]
• GSE326873 组蛋白H4乙酰甲基赖氨酸标记可及染色质，使其不易压缩
• GSE325634 HP1B 和 H3K9me3 调控嗅觉受体选择和 2 转录特性 [RNA-Seq]
• GSE324864 HP1B 和 H3K9me3 调控嗅觉受体选择和 2 转录特性 [ChIP-seq]
• GSE324834 HP1B 和 H3K9me3 调控嗅觉受体选择和 2 转录同一性 [ATAC-seq]
• GSE320151 转录组分析揭示了人小肠上皮细胞成熟依赖于底物和剪切应力
• GSE318992 雷公藤内酯醇外泌体制剂对 A549 肺癌细胞的疗效研究
• GSE316442 新型驱动基因 MDC1 导致化疗耐药复发性卵巢癌的同源重组修复缺陷和基因组不稳定性
• GSE315390 截短侧耳素类抗生素抑制肝细胞癌生长
• GSE312875 IL-33促进组织驻留Th2细胞的转录和代谢适应
• GSE311559 Caspase-6 控制饮食诱导肥胖中的脂质和能量代谢
• GSE311159 通过无动物源生产工艺增强人诱导多能干细胞来源的巨噬细胞的免疫反应
• GSE310305 特定 HDAC3 抑制剂与 5-氮杂胞苷联合治疗弥漫性大 B 细胞淋巴瘤的疗效增强 [OCI_ly7_RNAseq_Day5]
• GSE307525 NUTM1重排白血病的综合分子和功能分析 [iLS-bulkRNA]
• GSE307387 乳腺癌患者活检肿瘤和放疗后手术切除肿瘤的靶向基因表达谱
• GSE305461 miR-4711-5p抑制胰腺癌的干性、增殖和侵袭活性
• GSE303132 circTGFBR2(3-6) 作为 IGF2BP3 蛋白和 TGFBR1 mRNA 的组装平台，增强乳腺癌细胞可塑性
• GSE299278 脑病相关UFM1变异体阻碍神经元蛋白翻译、发育和功能
• GSE298810 Huh7 和 HLF 肝细胞癌细胞在二维和三维培养条件下的转录组谱
• GSE287959 由于 RPA 复合物对 RNAseH1 的加载缺陷导致 R 环加工减慢，这是癌基因诱导的过早衰老的特征。
• GSE286109 人类原代成骨细胞单细胞转录组分析
• GSE279005 MIEN1基肽LA3IK对EGF诱导的PC3前列腺癌细胞在0小时、30分钟、1小时和6小时时间点的基因表达的影响
• GSE276680 NUTM1重排白血病的综合分子和功能分析
• GSE276676 NUTM1重排白血病的综合分子和功能分析 [cKitChIP-seq]
• GSE246165 RNA-seq for NK-92, and NK-IL-7R-IM cells
• GSE328432 HEK-293 细胞在长时间轻度酸化 (pH 6.6) 和 SR 蛋白激酶抑制剂 (SRPIN340) 处理下的转录组分析
• GSE325788 妊娠会加剧线粒体心肌病动物模型的代谢失衡并加速其死亡
• GSE325546 可生物降解聚合物的免疫反应及相应的胶原蛋白再生
• GSE314030 不同 pClik 5 质粒变体（天然型与高拷贝型）对基因组简化谷氨酸棒状杆菌 CR099 中 mCherry 表达的影响
• GSE311622 干细胞转录组的微环境依赖性模块化调控区分了细胞身份和潜能
• GSE308712 HKDC1 过表达对两种结肠癌细胞基因表达的影响。
• GSE307832 绒毛外滋养层细胞分化过程中的发育标志和细胞转变 [scRNA-Seq]
• GSE303469 ANXA2P1敲低后AGS中蛋白质编码RNA的转录组分析
• GSE303348 胃癌细胞中RNA结合蛋白的RIP-seq分析
• GSE303312 葡萄糖剥夺后人胃癌细胞的表达谱分析
• GSE299738 牙周肉芽组织和牙周炎症牙龈的单细胞RNA测序
• GSE284246 利用新方法（高通量转录组学）研究纳米农用化学品——商业氯氧化铜的毒性机制
• GSE261942：PLXNC1作为结直肠癌共识分子亚型4的新型生物标志物的鉴定
• GSE328573 光敏剂 DTP 与他汀类药物联合使用，通过调节胆固醇增强 PDT 来增强肾癌治疗。
• GSE328424 导管上皮 MXD3 通过 Wnt/β-catenin 介导的炎症和损伤促进急性胰腺炎的疾病进展
• GSE328279 CD74 缺陷后小鼠骨髓来源巨噬细胞的批量 RNA 测序
• GSE326423 补体调节的稳态增殖控制记忆B细胞的寿命和库组成
• GSE303838 MECP2 突变重塑人类 ESC 命运并偏向皮质谱系定向 [RNA-Seq]
• GSE295411 Numb-Ifi204抑制LPS诱导的小胶质细胞活化和海马炎症
• GSE303217 突变型 TP53 劫持 RNA 剪接因子 RBM28 以抑制双链 RNA 触发的抗肿瘤免疫
• GSE299896 微肽 UEIS 减弱 cGAS-STING-I 型干扰素信号传导以抑制抗肿瘤免疫
• GSE218624 睡眠剥夺和反弹睡眠小鼠下丘脑视前区的单细胞RNA测序