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1. ⭐ GSE298142 m6A 甲基转移酶 METTL14 通过失调自噬促进致癌 Kras 诱导的幼年骨髓单核细胞白血病 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、regex:onco(logy|logist|gene|genic)、RNA-seq、KRAS
• 📝 描述：Contributors : Guangyao Kong ; Peihua ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe M6A modification plays an important role in the pathogenesis of various myeloid malignancies. However, its specific role in RAS mutant-induced myeloid malignancy is incompletely understood. In this study, we found that m6A methyltransferase METTL14 was highly expressed and associated with a shorter survival in a RAS-mutant myeloid malignancy, juvenile myelomonocytic leukemia (JMML). The knockout of METTL14 was revealed to significantly promote hematopoietic stem/progenitor cells (HSPCs) expansion and suppresses disease progression in a KrasG12D/+ mutant-induced mouse model of JMML. Moreover, knockout of METTL14 reduces hyperproliferation of KrasG12D/+ HSPCs and suppresses oncogenic KrasG12D/+-induced myeloid disease in a cell-autonomous manner. Mechanistically, we revealed that the knockout of METTL14 reduced the autophagy levels of HSPCs by suppressing the transcription and translation of autophagy-related genes, such as Atg5 and Atg9a, through m6A modification. Furthermore, we found that the autophagy inhibition through knockout of ATG5 in Kras mutant mice promoted the expansion of HSPCs and inhibited the progression of leukemia disease, consistent with the phenotypes of knockout of METTL14. Finally, we observed that combined treatment with an m6A inhibitor and a MEK inhibitor synergistically suppressed JMML growth. Collectively, these findings highlight the critical role of METTL14 in JMML tumorigenesis and suggest that m6A RNA modification represents a promising therapeutic target for this disease.
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2. ⭐ GSE311097 外周SARS-CoV-2感染后小鼠脑免疫细胞的单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、sequencing、single-cell
• 📝 描述：Contributors : Lu Tan ; Shea Lowery ; Andrew Thurman ; Stanley PerlmanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusNeurological and neuropsychiatric symptoms are among the most prevalent Post-Acute Sequelae of COVID-19 (PASC), collectively referred to as neuroPASC. Despite growing recognition, the mechanisms driving neuroPASC remain elusive, hindering therapeutic development. Brain immune cells - particularly microglia - have been implicated, yet current knowledge largely derives from post-mortem tissues with variable disease courses and comorbidities and limited spatial coverage. To address this, we established a PASC animal model by infecting C57BL/6 mice with a sublethal dose of mouse-adapted SARS-CoV-2. Infected mice exhibited persistent behavioural alterations and prolonged neuroinflammation in the absence of direct viral neuroinvasion. Single-cell RNA sequencing of brain immune cells collected at 0, 6, 30, and 100 days post-infection (dpi) revealed underlying dynamic, longitudinal immune responses. Microglia, the predominant brain-resident sentinel cells, displayed sustained expansion of subclusters characterized by inflammatory, stress response, and metabolic reprogramming signatures across all time points. Border-associated macrophages upregulated monocyte attractants during acute infection and were partially replaced by infiltrating monocytes. Concurrently, inflammatory monocytes and neutrophils showed maximal brain infiltration and antiviral activity at 6 dpi, potentially triggering long-term microglial activation. Together, these findings provide a high-resolution atlas of brain myeloid immune dynamics during neuroPASC and highlight a central role of microglia in sustaining chronic neuroinflammation, offering insight into potential therapeutic targets.
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3. ⭐ GSE298134 m6A甲基转移酶METTL14通过自噬失调促进致癌Kras诱导的幼年型骨髓单核细胞白血病

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、regex:onco(logy|logist|gene|genic)、KRAS
• 📝 描述：Contributors : Guangyao Kong ; Peihua ZhangSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusThe M6A modification plays an important role in the pathogenesis of various myeloid malignancies. However, its specific role in RAS mutant-induced myeloid malignancy is incompletely understood. In this study, we found that m6A methyltransferase METTL14 was highly expressed and associated with a shorter survival in a RAS-mutant myeloid malignancy, juvenile myelomonocytic leukemia (JMML). The knockout of METTL14 was revealed to significantly promote hematopoietic stem/progenitor cells (HSPCs) expansion and suppresses disease progression in a KrasG12D/+ mutant-induced mouse model of JMML. Moreover, knockout of METTL14 reduces hyperproliferation of KrasG12D/+ HSPCs and suppresses oncogenic KrasG12D/+-induced myeloid disease in a cell-autonomous manner. Mechanistically, we revealed that the knockout of METTL14 reduced the autophagy levels of HSPCs by suppressing the transcription and translation of autophagy-related genes, such as Atg5 and Atg9a, through m6A modification. Furthermore, we found that the autophagy inhibition through knockout of ATG5 in Kras mutant mice promoted the expansion of HSPCs and inhibited the progression of leukemia disease, consistent with the phenotypes of knockout of METTL14. Finally, we observed that combined treatment with an m6A inhibitor and a MEK inhibitor synergistically suppressed JMML growth. Collectively, these findings highlight the critical role of METTL14 in JMML tumorigenesis and suggest that m6A RNA modification represents a promising therapeutic target for this disease.
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4. ⭐ GSE285346 线粒体代谢和信号传导直接调控树突状细胞在抗肿瘤免疫中的功能

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、dendritic cell、metabolism
• 📝 描述：Series Type : Expression profiling by array ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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5. ⭐ GSE302362 纳米颗粒诱导抗原呈递单核细胞来源的树突状细胞可抑制转移并缓解转移微环境中的免疫抑制

• ✍️ 作者：未知作者
• 🏷️ 关键词：monocyte、antigen、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Jeffrey A Ma ; Kate V Griffin ; Kathryn Kang ; Agustina Diener ; Ian A Schrack ; Elizabeth J Bealer ; Laila M Rad ; Rebecca S Pereles ; Jacqueline S Jeruss ; Lonnie D SheaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMyeloid immune cells play a major role in establishing a suitable microenvironment for metastatic tumor cells. Dysregulated myeloid cells suppress antigen-presentation pathways and effector T cell responses at distal organs, and reprogramming these cells may enhance anti-tumor cytotoxicity. Targeting myeloid cells with poly(lactide-co-glycolide) nanoparticles, which possess intrinsic immunomodulatory properties, can promote monocyte maturation to inhibit metastasis. Intravenously delivered nanoparticles made with polyvinyl alcohol, but not other surfactants, reduce the accumulation of neutrophils at the metastatic niche and induce the differentiation of monocytes into antigen-presenting monocyte-derived dendritic cells. The internalization of nanoparticles was linked to the upregulation of gene expression programs in monocyte-derived dendritic cells associated with antigen presentation and T cell stimulation, and ligand-receptor network modeling supports increased activation of Th1 cells by these monocyte-derived dendritic cells. Nanoparticle administration increased the proportion of CD4 cells with Th1 and Th17 phenotypes and did not inhibit metastasis in mice where monocytes or T cells were depleted, indicating that interactions between monocyte-derived dendritic cells and T cells are essential to the mechanism of action. Collectively, our findings demonstrate that nanoparticles can reprogram circulating monocytes into monocyte-derived dendritic cells to modulate the metastatic niche and enhance antigen presentation to stimulate intrinsic T cell responses.
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6. GSE313170 研究次黄素化途径在前列腺癌进展中的作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、pathway
• 📝 描述：Contributors : Michel Kahi ; Anne Vincent ; JeanJacques Diaz ; Frederic BostSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe studied the involvement of the hypusination pathway in prostate cancer progression using various models, including patient-derived tumor organoid cell lines and in vivo mouse models. We employed different omics techniques to identify the molecular mechanisms linking hypusination to the aggressiveness of prostate cancer.
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7. GSE306252 通过mRNA测序鉴定肝细胞癌中的诊断性外泌体miRNA和致病调控网络

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、sequencing
• 📝 描述：Contributors : Xiao Jingwen ; Ma Shiyue ; Tan Qiupei ; Xiao Jianlong ; Liu Shanshan ; Shi Qingfeng ; Yang JunSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensBackground/Objectives: Hepatocellular carcinoma (HCC) is the sixth most common malignancy worldwide and the third leading cause of cancer-related mortality. Prognosis is stage-dependent, but most patients are diagnosed at advanced stages when curative treatment is not feasible. Alpha-fetoprotein (AFP), the most widely used biomarker, has limited sensitivity and specificity for early detection. Serum-derived exosomal mi-croRNAs (miRNAs) are stable in circulation, tumor-specific, and actively involved in cancer biology, making them promising non-invasive biomarkers. This study aimed to identify, validate, and functionally characterize serum-derived exosomal miRNAs with diagnostic potential in HCC. Methods: Serum exosomes were isolated from 50 HCC pa-tients and 50 matched healthy controls, characterized by transmission electron micros-copy, nanoparticle tracking analysis, and CD9/CD63/CD81 flow cytometry. High-throughput small RNA sequencing of 3 HCC and 3 control samples identified dif-ferentially expressed miRNAs (DEMs). Target genes were predicted via multiple data-bases, integrated into STRING protein–protein interaction networks, and analyzed with cytoHubba. Gene Ontology (GO) and KEGG enrichment analyses were performed. Hub gene expression and survival relevance were evaluated using GEPIA2. Candidate miRNAs were validated by RT-qPCR, and diagnostic performance was assessed with receiver operating characteristic (ROC) analysis. Results: Seven DEMs were identified; FOXO1 and SRSF11 emerged as hub genes. hsa-miR-27a-3p targeted FOXO1, and hsa-miR-493-3p targeted SRSF11. RT-qPCR confirmed hsa-miR-27a-3p upregulation (P = 0.003) and hsa-miR-493-3p downregulation (P = 0.014) in HCC exosomes. ROC analysis showed high diagnostic accuracy for hsa-miR-493-3p (AUC = 0.840) and hsa-miR-27a-3p (AUC = 0.827), comparable to AFP (AUC = 0.828), with improved performance when combined. Conclusions: Serum-derived exosomal hsa-miR-27a-3p and hsa-miR-493-3p are promising non-invasive biomarkers for HCC, with diagnostic value comparable to AFP and mechanistic links to FOXO1 and SRSF11. Their integration into miRNA-based panels may improve early detection.
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8. GSE285347 IgA肾病表观遗传生物标志物的发现：利用ATAC-Seq分析循环CD8+ T细胞的染色质开放性

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq、epigenetic
• 📝 描述：Contributors : Gwanghun Kim ; Soojin Lee ; Ik Soo Kim ; Hyun Mu Shin ; Hang-Rae Kim ; Dong Ki KimSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensChromatin openess plays a critical role in understanding epigenetic regulation in disease states. Using ATAC-seq, we profiled circulating CD8+ T cells from IgA nephropathy (IgAN) patients to identify biomarkers distinguishing early and late disease stages. A total of 279 differential ATAC peaks were identified, with 122 selected as biomarkers based on fold change (>2) and statistical significance (P < 0.05). These biomarkers exhibited distinct chromatin accessibility patterns, highlighting differential regulatory mechanisms. Combining multiple biomarkers through weighted scoring enhanced predictive accuracy, with ROC analysis confirming their diagnostic potential. Our findings demonstrate that chromatin openness in circulating CD8+ T cells provides valuable insights into disease progression and serves as a robust platform for biomarker discovery in IgAN.
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9. GSE277903 γδ T 细胞的先天组织免疫监视对 T 细胞受体具有实时依赖性 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、RNA-seq
• 📝 描述：Contributors : Miguel Munoz-Ruiz ; Nicolas Veland ; Adrian HaydaySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWith clonotypic potential to engage different ligands, T cell receptor (TCR) γδ fulfils a key tenet of adaptive immunity. Nonetheless, many γδ repertoires are non-circulating, display limited diversity, and are commonly classified as innate-like, questioning any requirement for the TCR beyond the cells’ development. Addressing this long-standing issue, we now show that the steady-state phenotypes of different tissue-intrinsic γδ T cell compartments share a dependence on constitutive TCR expression. Deprived of this, cells rapidly become dysregulated, losing their capacity to respond to wide-ranging tissue insults, including imiquimod, an innate inducer of psoriasis-like pathology, u.v. irradiation, and melanoma. Thus, beyond any developmental requirements, the TCR is required in real time to regulate the cells’ innate-like tissue immunosurveillance. Biologically, this clearly distinguishes intrinsic γδ T cells from NK and other innate lymphoid cells, while clinically it stresses the importance of the TCR in delivering gd T cell-based immunotherapies.
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10. GSE277902 γδ T 细胞的先天组织免疫监视对 T 细胞受体具有实时依赖性 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、ATAC-seq
• 📝 描述：Contributors : Miguel Munoz-Ruiz ; Nicolas Veland ; Adrian HaydaySeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusWith clonotypic potential to engage different ligands, T cell receptor (TCR) γδ fulfils a key tenet of adaptive immunity. Nonetheless, many γδ repertoires are non-circulating, display limited diversity, and are commonly classified as innate-like, questioning any requirement for the TCR beyond the cells’ development. Addressing this long-standing issue, we now show that the steady-state phenotypes of different tissue-intrinsic γδ T cell compartments share a dependence on constitutive TCR expression. Deprived of this, cells rapidly become dysregulated, losing their capacity to respond to wide-ranging tissue insults, including imiquimod, an innate inducer of psoriasis-like pathology, u.v. irradiation, and melanoma. Thus, beyond any developmental requirements, the TCR is required in real time to regulate the cells’ innate-like tissue immunosurveillance. Biologically, this clearly distinguishes intrinsic γδ T cells from NK and other innate lymphoid cells, while clinically it stresses the importance of the TCR in delivering gd T cell-based immunotherapies.
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💡 该来源还有 66 条内容，详见 文末

• GSE272538 EZH2 和 E2F1 的新关联通过染色质重塑促进乳腺癌细胞增殖 [RNA-Seq]
• GSE272537 EZH2 和 E2F1 的新关联通过染色质重塑促进乳腺癌细胞增殖 [CHIP-Seq]
• GSE272536 EZH2 和 E2F1 的新关联通过染色质重塑促进乳腺癌细胞增殖 [ATAC-Seq]
• GSE305891 ATF4 的基础水平促进 T 细胞活化诱导增殖的准备状态 [ATAC-seq]
• GSE288143 ATF4 基础水平促进 T 细胞活化诱导增殖的准备状态 [RNA-seq]
• GSE288073 ARTS 通过 Livin-MDM2-p53 通路诱导凋亡依赖性自噬，从而赋予乳腺癌细胞化疗耐药性。
• GSE283719 EGR1依赖级联调节CSF1R基因座的基因组结构[Hi-C]
• GSE283718 EGR1依赖级联调节CSF1R基因座的基因组结构[ChIP-seq]
• GSE283663 EGR1依赖级联调节CSF1R基因座的基因组结构[RNA-Seq]
• GSE255626 原发性胶质母细胞瘤患者组织的下一代测序（总RNA测序）
• GSE208745 肿瘤特异性lncRNA IGF1R-AS1反式调控与致癌MYC信号相关的染色质相互作用
• GSE298483 诱导肾脏发育细胞状态与预后良好型肾母细胞瘤的化疗耐药性相关
• GSE230838 肝脏中顺式磷酸转移酶功能的丧失促进了一种高外显率的脂肪肝疾病，该疾病迅速转变为肝细胞癌 [RNA-seq]
• GSE230616 肝脏中顺式磷酸转移酶功能的丧失促进了一种高外显率的脂肪肝疾病，该疾病迅速转变为肝细胞癌 [scRNA-seq]
• GSE289395 pTα 增强 mRNA 翻译并增强 CAR T 细胞对实体瘤的根除作用 [scRNA-seq]
• GSE289390 pTα 增强 mRNA 翻译并增强 CAR T 细胞对实体瘤的根除作用 [批量 RNA 测序]
• GSE315268 高能脉冲电子束 (HEPE) 诱导链霉菌 lividans 1326 菌株基因表达的全基因组分析
• GSE299892 MSC-exo 处理的 HUVEC 的转录组分析研究
• GSE299879 N-乙酰-L-半胱氨酸乙酯 (NACET) 可诱导视网膜中的转录因子 NRF2，并防止视网膜老化和糖尿病视网膜病变。[IV]
• GSE299877 N-乙酰-L-半胱氨酸乙酯 (NACET) 可诱导视网膜中的转录因子 NRF2，并防止视网膜老化和糖尿病视网膜病变。[III]
• GSE299876 N-乙酰-L-半胱氨酸乙酯 (NACET) 可诱导视网膜中的转录因子 NRF2，并防止视网膜老化和糖尿病视网膜病变。[II]
• GSE299875 N-乙酰-L-半胱氨酸乙酯 (NACET) 可诱导视网膜中转录因子 NRF2 的表达，并预防视网膜衰老和糖尿病视网膜病变。[I]
• GSE297705 甲基红杆菌 AM1 野生型和甲醇适应菌株的 RNA-seq 数据 [RNA-seq]
• GSE294020 U2AF2 缺陷对卵巢癌细胞基因表达的影响
• GSE293681 靶向长链非编码RNA lnc-Megacluster对肥胖症的代谢有益作用
• GSE290701 抗氧化纳米技术介导的太空神经元损伤防护（PROMETEO，抗氧化保护）
• GSE289379 DNA甲基化可预测囊性纤维化患者痰液样本中的肺功能和肺部急性加重情况
• GSE285335 IgAN患者外周血单核细胞的单细胞转录组分析
• GSE285114 LOXL2 缺失在创伤后损伤中会扰乱膝关节稳态，并促进疼痛敏感性、炎症和骨关节炎
• GSE262416 睾丸间质综合图谱揭示 Cd34+/Sox4+ 间充质细胞是潜在的 Leydig 细胞祖细胞 [scRNA-Seq]
• GSE247323 母体补充吲哚可通过改变肠道菌群和芳烃受体介导的神经酰胺代谢来保护后代免受非酒精性脂肪性肝病 (NAFLD) 的侵害
• GSE316529 JAK1 功能丧失导致 G2/M 细胞周期缺陷，易受 KIF18A 抑制的影响 [Detroit562 RNAseq]
• GSE312457 RNA-Seq 数据来自 Pdgfra-Cre 介导的 Esr1 条件性敲除小鼠的输卵管基质细胞
• GSE310469 RNA-seq 数据用于研究输卵管间质细胞和/或雌激素治疗对输卵管上皮细胞的影响
• GSE307602 DKK3 最初通过 MEK-Fos 信号通路维持腺泡完整性，但随后在胰腺导管腺癌中转变为致癌作用。
• GSE306878 肿瘤抑制因子REST对雌激素受体（ESR1）表达和子宫肌瘤病理生理学的调控作用
• GSE305975 ATF4 的基础水平促进 T 细胞活化诱导增殖的准备状态
• GSE305890 ATF4 的基础水平促进 T 细胞活化诱导增殖的准备状态 [CUT&Run]
• GSE303595 Leo1 缺失揭示 Set1 依赖性转录激活 [ChIP-Seq]
• GSE298999 ANCA相关性血管炎中免疫相关基因的肾脏转录组分析
• GSE298852 NSMF 减轻过度复制压力以促进结直肠癌进展
• 胸腺 iNKT 细胞的 GSE298293 单细胞 RNA 测序
• GSE298292 全胸腺细胞和纯化的 CD4+CD8+TCRlow DP 胸腺细胞的 RNA 测序
• GSE298291 DP胸腺细胞的ATAC-seq
• GSE297499：患有神经精神性长新冠的女性脑脊液免疫细胞改变
• GSE297480 BRG1/BRM 抑制剂与 BET 抑制剂或地西他滨联合治疗高危 MECOM 重排 AML 的高效疗效 [RNA-seq]
• GSE297477 BRG1/BRM 抑制剂与 BET 抑制剂或地西他滨联合治疗高危 MECOM 重排 AML 的高效疗效 [ChIP-Seq]
• GSE297475 BRG1/BRM 抑制剂与 BET 抑制剂或地西他滨联合治疗高危 MECOM 重排 AML 的高效疗效 [ATAC-seq]
• GSE296003 组蛋白3赖氨酸56乙酰化（H3K56ac）调控染色体外DNA（ecDNA）枢纽的生物合成
• GSE293519 雄激素信号在 2 型固有淋巴细胞中驱动幽门螺杆菌感染引起的胃炎症和萎缩的性别差异
• GSE283672 EGR1依赖级联调节CSF1R基因座的基因组结构[CUT&Run]
• GSE283670 EGR1依赖级联调节CSF1R基因座的基因组结构[Capture-C]
• GSE283238 DKK3 最初通过 MEK-Fos 信号传导来维持腺泡完整性，但后来在 PDAC 中转变为致癌作用。
• GSE279659 CD40L靶向工程化调节性T细胞作为一种治疗T细胞介导的炎症性疾病的新型细胞疗法
• GSE315410 肝脏中顺式磷酸转移酶功能的丧失促进了一种高外显率的脂肪肝疾病，该疾病迅速转变为肝细胞癌 [RNAseq_ChowDiet_NgBR_Liver]
• GSE288778 MYRF 控制间皮细胞分化、信号传导和可塑性 [scRNA-Seq]
• GSE288777 MYRF 控制间皮细胞分化、信号传导和可塑性 [RNA-Seq]
• GSE287422 MYCN 和 ALK 共表达诱导人 iPS 细胞衍生的颅神经嵴细胞发生神经母细胞瘤样肿瘤 [RNA-seq]
• GSE230972 研究发现，肝脏中顺式磷酸转移酶（cisPTase）功能的丧失会促进一种高外显率的脂肪肝疾病的发生，该疾病会迅速发展为肝细胞癌。
• GSE316672 利用 GeoMx DSP 对细支气管进行空间转录组分析
• 利用单克罗他林（MCT）诱导的肺动脉高压（PH）大鼠模型，通过RNA测序分析鉴定了右心房组织中的基因表达变化（GSE316596）。
• GSE308540 RORγ通过上调NGF信号通路驱动非小细胞肺癌进展
• GSE304796 pTα 增强 mRNA 翻译并增强 CAR T 细胞对实体瘤的根除作用 [Ribo-seq]
• GSE304795 pTα 增强 mRNA 翻译并增强 CAR T 细胞对实体瘤的根除作用 [eCLIP-seq]
• GSE302228 下一代测序有助于对经化合物 20 处理或未处理的白色念珠菌 SC5314 进行转录谱定量分析。
• GSE248722 Cyfip2 敲除小鼠前脑单细胞转录组分析