详细内容（前10条）

1. ⭐ GSE317680 Single Cell and Spatial Transcriptomics Identify Novel Immune-Stromal Interactions in Cardiac Allograft Vasculopathy

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、cardiac、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Li Daniel Y ; Gu Wenduo ; Cheng Paul CSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCardiac allograft vasculopathy (CAV) is the leading cause of mortality in heart transplant recipients. Despite the prevalence of CAV, there are no targeted therapeutic options to prevent or reverse disease progression, and patients ultimately require retransplant. CAV is defined by progressive neointimal hyperplasia in donor heart coronary arteries, leading to luminal obliteration and ultimately allograft failure or sudden cardiac death. Although immune and stromal cell interactions are believed to play a key role in CAV pathogenesis, the specific cellular players and molecular signals driving disease remain undefined. In this study, we leverage single-cell RNA sequencing and spatial transcriptomics of human coronary arteries to transcriptionally characterize CAV and define the neointimal microenvironment. We compare arteries with CAV to atherosclerotic coronary artery disease and non-disease controls to identify a unique CAV transcriptional signature.
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2. ⭐ GSE322979 跨物种转录组整合揭示了一条保守的、MIRO1介导的巨噬细胞-T细胞信号通路驱动胶质瘤免疫抑制

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、macrophage、glioma、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Xinnan Wang ; Menghan Li ; Zehui DuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe generated bulk RNA sequencing (RNA-seq) data from human glioma surgical resections treated ex vivo with a MIRO1-binding compound (MR3) or vehicle control. Fresh tumor specimens were processed and cultured under controlled conditions prior to RNA extraction and high-throughput transcriptomic profiling to characterize treatment-associated gene expression changes within the tumor microenvironment (TME). The dataset captures global transcriptional programs from tumor tissue, reflecting contributions from malignant cells as well as stromal and immune components present in the resections. These data enable analysis of MIRO1-dependent transcriptional regulation in human glioma and facilitate cross-species integration with murine single-nucleus RNA-seq datasets. This resource supports investigation of mitochondrial-associated transcriptional programs and their impact on immune microenvironment remodeling in human glioma.
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3. ⭐ GSE261295 Gestational diabetes mellitus impairs metabolic homeostasis and cardiac development of offsprings by epigenetic regulation of H3K27 methylation to key pro-fibrosis transcription factor MEOX1

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、cardiac、epigenetic、methylation
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAs one of the most perinatal period metabolic disorders, gestational diabetes mellitus (GDM) has negative influence to the metabolic health as well as organ development of offsprings. The underlying mechanism(s) is not fully revealed.
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4. ⭐ GSE320101 研究发现，靶向 USP14 通过重编程结肠癌肿瘤相关巨噬细胞来增强免疫治疗反应。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCombining immunotherapy with other treatments improves survival in colorectal cancer, yet some patients remain unresponsive. Tumor-associated macrophages (TAMs) are a key immune cell population driving this immunotherapy resistance and fostering an immunosuppressive microenvironment. To overcome this, we screened a deubiquitinating enzyme (DUB) library targeting TAMs and identified USP14 as specifically upregulated in TAMs. Inhibiting USP14 reversed their pro-tumor functions, promoted M1 polarization, enhanced tumor cell killing, and activated effector T cells. USP14 inhibition also increased PD-L1 expression on tumor cells, alleviating T-cell suppression. In vivo, combining a USP14 inhibitor with an anti-PD-1 antibody synergistically enhanced immunotherapy efficacy, suppressed tumor progression, and improved survival in a mouse colon cancer model. Thus, USP14 is a promising target to overcome immunotherapy resistance in colorectal cancer.
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5. ⭐ GSE277728 GSK3β介导的SOX4磷酸化及其与STAT6的相互作用调节MTHFD2表达、NADPH产生、癌症干细胞特性和肝细胞癌预后[ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、carcinoma、ChIP-seq
• 📝 描述：Contributors : Chia-Lung Tsai ; Ming-Chin Yu ; Chi-Neu TsaiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensSOX4 is associated with poor prognosis in various cancers, including hepatocellular carcinoma (HCC). SOX4 plays a crucial role in angiogenesis, cellular differentiation, and cell growth through interactions with transcription factors in response to stimuli. Despite its overexpression and link to poor prognosis, SOX4 remains an undruggable target. Therefore, targeting its interacting or regulatory proteins might disclose a therapeutic strategy in HCC. Our aim was to elucidate SOX4 regulation and interactions in HCC cells to provide further insights into its role in tumorigenesis. GSK3β phosphorylated SOX4 at serine residues 379, 383, 387, 391, and 395, as revealed by in vitro kinase assays, which stabilized SOX4 protein. Interactions between SOX4, STAT6, and GSK3β in HCC cells were confirmed by co-immunoprecipitation, immunofluorescence, and proximal-ligation assay. Knockout SOX4 or inhibition of STAT6 repressed cell growth, sphere formation, and NADPH production through modulating MTHFD2 expression, which in turn repressed expression of PD-L1 in HCC cells. The significant elevated NADPH was found in SOX4high HCC tumor specimen as compared with the SOX4low tumors. Positive correlations of GSK3β & SOX4, STAT6 & SOX4, and SOX4 & MTHFD2 proteins were observed in liver cancer specimens through western blot analysis. Furthermore, tumor lesion with elevated of SOX4, MTHFD2, or both SOX4 and MTHFD2 transcripts tend to have poor prognosis in patients with HCC using TCGA-LIHC database. Treatment with inhibitors targeting STAT6 or MTHFD2 reduced cell proliferation in vitro and attenuated tumor growth in an HCC patient-derived xenograft (PDX) mice model in vivo. The GSK3β/SOX4/STAT6/MTHFD2 regulatory axis played a critical role in modulating NADPH production and maintaining cancer stemness, associated with poor prognosis in HCC that might be a potential therapeutic target.
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6. ⭐ GSE315553 人类脉络丛空间转录组学数据

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributor : DiStasio MarcelloSeries Type : OtherOrganism : Homo sapiensThis study presents spatial transcriptomic data generated from postmortem human choroid plexus tissue. Spatially resolved gene expression profiles were obtained using the Curio Bioscience Seeker v1.1 platform, enabling in situ transcript capture across intact tissue sections. This dataset provides a resource for investigating spatial organization, cellular heterogeneity, and regional transcriptional programs within the human choroid plexus.
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7. ⭐ GSE316452 西方饮食和M​​C4R基因敲除诱导的MASH模型小鼠肠-肝轴微生物组和代谢组的跨器官多组学分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolome、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Mitsuharu Matsumoto ; Osamu Miura ; Takeo Moriya ; Hitomi Ogino ; Megumi Hirayama ; Akira Mitsui ; Takaharu Hirayama ; Yukihiko Ebisuno ; Manami Kaneko ; Yoshinori Satomi ; Yasunori NioSeries Type : OtherOrganism : Mus musculusBackground: Western diet (WD) fed Melanocortin 4 receptor-knockout (MC4R-KO) mice develop a phenotype resembling human metabolic dysfunction-associated steatohepatitis (MASH). Despite its clinical relevance, the role of the gut–liver axis in MASH pathogenesis remains unclear. This study investigated the gut-liver axis through microbiomic and metabolomic analyses of WD-fed MC4R-KO mice, and examined their association with MASH pathology. Methods: We performed an integrated microbiome and metabolome analysis of the liver, small intestinal contents, large intestinal contents, and plasma of wild-type (WT) and MC4R-KO mice fed either a normal diet or WD. Markers of hepatic inflammation, fibrosis, and steatosis measured in this study were used to assess MASH severity and to correlate microbiome and metabolite alterations. Results: WD-fed MC4R-KO mice exhibited significant hepatic steatosis, inflammation, and fibrosis. The abundance of certain microbiota, including Muribaculaceae and Allobaculum, negatively correlated with MASH severity, whereas increased levels of Desulfovibrionaceae and Bacteroides positively correlated with hepatic lipid accumulation, steatosis, and inflammation. Metabolomic profiling revealed increased triglyceride and diglyceride levels in the liver and a concomitant decrease in free fatty acids and monoglycerides in the intestines. Additionally, plasma taurine-conjugated bile acids were elevated in WD-fed MC4R-KO mice, which correlated with the reduced hepatic transport of bile salts from pathway enrichment analysis. These findings highlight substantial alterations in the gut microbiota and lipid and bile acid metabolism, indicating a mechanistic dysregulation of the gut–liver axis that may contribute to MASH progression. Conclusions: The observed gut microbial and metabolic alterations, particularly bile acid and lipid metabolism dysregulation, offer insights into potential therapeutic targets aimed at modulating the gut–liver axis to treat or prevent MASH.
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8. ⭐ GSE226725 Next Generation Sequencing Facilitates Quantitative Analysis of Macrophage and Leukemia Cell Transcriptomes in Mouse Iron-overload MLL-AF9 Acute Myeloid Leukemia

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、macrophage、sequencing
• 📝 描述：Contributor : Feifei YangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe goals of this study aim to reveal functional and phenotypic diversity of Macrophage and Leukemia Cell in response to the Iron-overloaded microenvironmental cues in mouse acute myeloid leukemia
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9. GSE322498 CTNNB1 突变介导非小细胞肺癌对 EGFR 靶向治疗的耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Haura Eric ; Majumder AnurimaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCTNNB1 mutations, which cause activation of Wnt target genes, are found to co-occur in EGFR-mutant lung cancer. We hypothesize that these mutations enhance stability of β-catenin protein and upregulate Wnt signaling, thereby promoting resistance to targeted therapy. CTNNB1 mutation spectrum was analyzed in non-small cell lung cancer patients in The Cancer Genome Atlas (TCGA) and Moffitt Cancer Center patient databases to identify prevalent CTNNB1 mutations as well as frequency of co-occurring mutations. EGFR-mutant HCC827 cells were engineered to stably express most frequent CTNNB1 mutations to determine their ability to drive resistance to EGFR TKI. Western blotting and RNA sequencing were performed to assess the molecular differences between cells expressing wild-type and erlotinib resistant CTNNB1T41A. A viability screen was also performed in which these cells were treated with either with β-catenin siRNA or a panel of drugs with known targets, in combination with erlotinib, to identify new vulnerabilities in CTNNB1T41A cells. Our analysis shows that EGFR mutations co-occur in ~45% of CTNNB1 mutant patients. We show that CTNNB1 mutations cause stabilization and higher accumulation of active β-catenin but vary in their ability to cause erlotinib resistance, with T41A, S37F, S45C and D32H mutants being resistance inducers. Of the mutations tested, cells expressing CTNNB1T41A demonstrated the strongest resistance to erlotinib. Transcriptomics data reveals higher levels of β-catenin regulated proteins (axin2, TCF7 and survivin), EMT markers (vimentin and N-cadherin), and receptors/ligands of the FGFR signaling pathway, in HCC827 CTNNB1T41A cells when compared to CTNNB1WT. Pathway analysis of genes differentially expressed between the WT and T41A mutant cells reveal Wnt pathway to be the top upregulated pathway in the CTNNB1 mutant cells. CTNNB1T41A cells also showed sustained ERK, AKT, GSK3β and S6 signaling, and lower PARP cleavage compared to wild type. Combining erlotinib with PI3K/mTOR/MEK inhibitors or CTNNB1 knockdown can partially reverses erlotinib resistance in HCC827 CTNNB1T41A cells. Our data suggests that CTNNB1 may be an important co-occurring alteration in developing resistance to targeted EGFR therapy. We show that the ability of a CTNNB1 mutation to drive resistance to EGFR TKI relates with the activation of CTNN…
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10. GSE314155 BRD9 读取乳酸诱导的 H3K18 乳酸化驱动肝细胞癌中的致癌染色质重塑

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、regex:onco(logy|logist|gene|genic)
• 📝 描述：Contributors : Enwei Wei ; Donglei Ji ; Yanjie Jia ; Ze Sun ; Chunfeng Gao ; Caroline Zeng ; Chunyu Wang ; Miaomiao Yu ; Guanglei Shang ; Linying Xie ; Wenju Zhang ; Yameng Li ; Yingying Liang ; Bai Ji ; Yanzhu Yue ; Yahui Liu ; Ming-Ming Zhou ; Lei ZengSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensHistone lactylation bridges glycolytic metabolism to oncogenic transcription, but its mechanistic readers remain poorly defined. Here, we identify bromodomain-containing protein 9 (BRD9) as a lactyl-lysine reader that links lactate-driven H3K18 lactylation (H3K18la) to chromatin remodeling in hepatocellular carcinoma (HCC). Clinically, elevated H3K18la levels correlate with poor HCC prognosis. Structural (NMR) and biophysical analyses demonstrate BRD9’s bromodomain engages H3K18la through its acetyl-lysine pocket with weak, transient affinity, distinct from stable H3K18ac binding, enabling lactate-dependent chromatin interactions. Multi-omics profiling reveals H3K18la recruits BRD9 and the non-canonical BRG1-associated factor (ncBAF) complex to active enhancers and promoters, promoting chromatin accessibility and oncogenic transcription (SPARC, TMEM64, ANGEL1, SCARB1). Glycolytic inhibition or BRD9 targeting displaces BRD9 from chromatin, suppresses oncogenes, and impairs HCC proliferation. p300 or HDAC inhibition attenuates H3K18la-driven oncogenic transcription and tumor viability. Our findings establish BRD9 as a metabolic-epigenetic mediator that translates glycolytic flux into chromatin remodeling, offering actionable therapeutic targets for HCC.
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1. 北区医院推出先进的白血病检测

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia
• 📝 描述：A new hospital-based test uses RNA sequencing to detect leukemia gene fusions in days, helping physicians identify cancer subtypes and guide targeted treatment decisions more quickly…
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2. 解码香茅——首个单倍型解析基因组揭示香茅类化合物的生物合成

• ✍️ 作者：未知作者
• 🏷️ 关键词：genome
• 📝 描述：Researchers combine genome sequencing and RNA sequencing to identify genes and leaf cell types responsible for citronelloid biosynthesis in Cymbopogon, providing insight into terpene production in aromatic plants…
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3. Scientists discover the switch that revives exhausted cancer-fighting T cells

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have uncovered new genetic rules that determine whether the immune system’s “killer” T cells remain powerful long-term defenders or become worn out and ineffective. By building a detailed genetic atlas of CD8 T cell states, researchers identified key molecular switches that push these cells toward either resilience or exhaustion. Remarkably, disabling just two previously unknown genes restored the tumor-killing power of exhausted T cells while preserving their ability to provide lasting immune protection.
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• GSE277540 GSK3β-Mediated Phosphorylation of SOX4 and Its Interaction with STAT6 to Regulate MTHFD2 Expression, NADPH Production, Cancer Stemness, and Prognosis in Hepatocellular Carcinoma
• GSE276897 果蝇肠道特异性CrebB诱导后肠道转录组的变化
• GSE318848 奥加塔亚分支物种内的易位改变了局部亚端粒染色质，同时维持了整体基因组组织 [Hi-C]
• GSE318843 奥加塔亚分支物种内的易位改变了局部亚端粒染色质，同时维持了整体基因组组织 [RNA-Seq]
• GSE318721 奥加塔亚分支物种内的易位改变了局部亚端粒染色质，同时维持了整体基因组组织 [ChIP-Seq]
• GSE277262 库普弗细胞通过 VSIG4-CD5 相互作用校准 T 细胞反应，从而影响肿瘤免疫原性
• GSE322568 Integrated metabolome and transcriptome profiling demonstrates dynamic regulatory roles of hormones in direct-seeding rice
• GSE309057 PMEPA1 mediates resistance to mTOR inhibitors in triple-negative breast cancer via dual modulation of TGF-β signaling and PI3K/AKT activation
• GSE304864 Multiomics immune profiling of a patient-relevant orthotopic lung cancer model using SEPARATE-Seq.
• GSE273609 Chemogenomic dissection of the role of Class I Histone Deacetylases as therapeutically relevant dependencies in H3K27M-glioma
• GSE319538 用多菌株乳杆菌/双歧杆菌衍生的后生元 (IBM) 治疗的小鼠的直肠 RNA 测序
• GSE318701 肺成纤维细胞促进血清淀粉样蛋白 A 的释放，作为小鼠肺纤维化加重的潜在生物标志物 [RNA-seq]
• GSE318150 肺成纤维细胞促进血清淀粉样蛋白 A 的释放，作为小鼠肺纤维化加重的潜在生物标志物 [scRNA-seq]
• GSE314557 PyMT小鼠乳腺肿瘤内皮细胞的单细胞RNA测序
• GSE310974 Hypatia：单细胞RNA异构体数据分析的统计框架
• GSE303671 混合谱系白血病细胞在中枢神经系统微环境中经历独特的适应性变化
• GSE284212 刺胞动物免疫相关细胞的功能表征
• GSE324005 利用 Domino Signal 从单细胞数据中推断细胞间通讯的差异细胞信号传导测试
• GSE318849 一个Ogataea分支物种内的易位改变了局部亚端粒染色质，同时维持了整体基因组结构
• GSE317314 RNA-seq 分析了与 DU-145 细胞共培养的人类 NK 细胞，这些 DU-145 细胞预先用 hIgG1 同型抗体、7C6-hIgG1 或 7C6-GAALIE 处理。
• GSE315551 人类脉络丛单核 RNA 测序数据 [snRNA-Seq]
• GSE314566 一个患者来源的异种移植模型库，捕捉了大B细胞淋巴瘤的临床和分子异质性
• GSE313889 过敏原诱导的上皮细胞衰老通过 AhR-c-Myc 轴驱动气道炎症
• GSE310560 利用单细胞RNA测序对多种小鼠肿瘤微环境进行深度分析
• GSE305769 用或不用酪氨酸激酶抑制剂处理HCV感染的Huh-7.5细胞的基因表达
• GSE298781 H3K27M 儿童高级别胶质瘤向神经元样状态的细胞重编程
• GSE295556 CBPWTp53-floxed、CBPAAp53-floxed、CBPWTp53ΔIEC 和 CBPAAp53ΔIEC 肠道隐孢子虫的基因表达谱
• GSE323321 snATAC-seq from activated CD4-positive, alpha-beta memory T cell (ENCSR810IIV)
• GSE323320 snATAC-seq from activated naive CD4-positive, alpha-beta T cell (ENCSR600UDB)
• GSE323319 snATAC-seq from activated CD4-positive, alpha-beta T cell (ENCSR569ZMI)
• GSE323318 snATAC-seq from activated CD8-positive, alpha-beta T cell (ENCSR472HFJ)
• GSE323316 snATAC-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR196EOO)
• GSE323315 snATAC-seq from activated naive CD8-positive, alpha-beta T cell (ENCSR110IID)
• GSE322954 DNase-seq from activated B cell (ENCSR992GTE)
• GSE322945 DNase-seq from stimulated activated CD4-positive, alpha-beta T cell (ENCSR915DCW)
• GSE322944 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR853IHW)
• GSE322939 DNase-seq from CD4-positive, alpha-beta T cell (ENCSR840FLY)
• GSE322938 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR834HNG)
• GSE322935 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR792ZWJ)
• GSE322934 DNase-seq from inflammatory macrophage (ENCSR773SWT)
• GSE322933 DNase-seq from stimulated activated CD4-positive, alpha-beta T cell (ENCSR762ZVI)
• GSE322928 DNase-seq from stimulated activated CD4-positive, alpha-beta T cell (ENCSR582SEN)
• GSE322927 DNase-seq from stimulated activated CD4-positive, alpha-beta T cell (ENCSR573JCI)
• GSE322925 long read RNA-seq from dorsolateral prefrontal cortex (ENCSR872GND)
• GSE322924 long read RNA-seq from dorsolateral prefrontal cortex (ENCSR697CSS)
• GSE322922 long read RNA-seq from dorsolateral prefrontal cortex (ENCSR543NWW)
• GSE322921 DNase-seq from stimulated activated CD4-positive, alpha-beta T cell (ENCSR552PGF)
• GSE322912 DNase-seq from activated CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR497BYS)
• GSE322911 DNase-seq from activated B cell (ENCSR441WRS)
• GSE322910 long read RNA-seq from C2C12 (ENCSR160HKZ)
• GSE322908 DNase-seq from activated B cell (ENCSR418YUJ)
• GSE322905 long read RNA-seq from dorsolateral prefrontal cortex (ENCSR111GJE)
• GSE322904 DNase-seq from activated CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR383EMG)
• GSE322901 DNase-seq from suppressor macrophage (ENCSR361JSG)
• GSE322900 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR361EAQ)
• GSE322899 DNase-seq from inflammatory macrophage (ENCSR358FCI)
• GSE322886 DNase-seq from activated B cell (ENCSR321YPI)
• GSE322882 DNase-seq from activated CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR298SHM)
• GSE322881 long read RNA-seq from technical sample (ENCSR731MFY)
• GSE322875 DNase-seq from inflammatory macrophage (ENCSR227ODJ)
• GSE322872 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR208RXB)
• GSE322871 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR188VGU)
• GSE322870 DNase-seq from activated CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR182ZRL)
• GSE322868 DNase-seq from inflammatory macrophage (ENCSR168WGF)
• GSE322867 DNase-seq from suppressor macrophage (ENCSR166BXN)
• GSE322865 DNase-seq from activated B cell (ENCSR161LOZ)
• GSE322864 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR145ORS)
• GSE322861 DNase-seq from activated CD8-positive, alpha-beta memory T cell (ENCSR121AEC)
• GSE322859 DNase-seq from activated CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR105LXZ)
• GSE322858 DNase-seq from activated CD4-positive, CD25-positive, alpha-beta regulatory T cell (ENCSR101OTC)
• GSE322856 DNase-seq from stimulated activated CD4-positive, alpha-beta T cell (ENCSR033HUY)
• GSE322850 total RNA-seq from dorsolateral prefrontal cortex (ENCSR944UJZ)
• GSE322848 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR905NAN)
• GSE322847 DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR905BAW)
• GSE322845 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR793FAY)
• GSE322843 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR719DJX)
• GSE322842 DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR641HZO)
• GSE322840 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR610YUT)
• GSE322839 DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR530ZCQ)
• GSE322837 DNase-seq from CD4-positive, alpha-beta memory T cell (ENCSR509BPF)
• GSE322835 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR453ZWK)
• GSE322832 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR436ASB)
• GSE322830 DNase-seq from naive thymus-derived CD4-positive, alpha-beta T cell (ENCSR353SYG)
• GSE322829 DNase-seq from naive thymus-derived CD8-positive, alpha-beta T cell (ENCSR308XZY)
• GSE322595 A Bioorthogonal Nanoconcentrisome System for Epigenetic and Immunometabolic Reprogramming in Aged Bone Repair
• GSE322519 Cancerformer: A CRISPR Screen-benchmarked Multimodal AI Platform for Predication of Cancer Dependencies in Patient-derived Organoids
• GSE291258 Autocrine Activity of Engineered IL-33 mRNA Enhances Adoptive T Cell Therapy for Peritoneal Carcinomatosis and Synergizes with IL-12 mRNA
• GSE291176 Gene expression profile at single cell level of intestinal epithelial cells from the distal colon
• GSE235721 The functional role of Musashi-2 uncovers targetable metabolic vulnerabilities of MLL-rearranged infant ALL
• GSE235720 The functional role of Musashi-2 uncovers targetable metabolic vulnerabilities of MLL-rearranged infant ALL [RIPchip]
• GSE235719 The functional role of Musashi-2 uncovers targetable metabolic vulnerabilities of MLL-rearranged infant ALL [GEP]