详细内容（前10条）

1. ⭐ GSE308231 单细胞测序技术揭示胃癌及其腹膜转移瘤的肿瘤微环境特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、sequencing、single-cell
• 📝 描述：Contributors : Jun Zhang ; Qi WangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo analyze the tumor microenvironment characteristics of gastric cancer and its peritoneal metastases, we collected fresh surgical specimens pathologically confirmed as gastric cancer and peritoneal metastases, and performed single-cell sequencing.
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2. ⭐ GSE316190 靶向 HMGB2 通过增强 CD8+ T 细胞功能和抑制肝细胞癌肿瘤生长发挥双重免疫调节作用 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma、T cell、RNA-seq
• 📝 描述：Contributors : Weifeng Qu ; Guiqi Zhu ; Yinghong ShiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTranscriptional features were detected in NC versus HMGB2-knockout CD8+ T cells of C57BL/6J mice.
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3. ⭐ GSE304497 多区域空间转录组学揭示了阿尔茨海默病 (AD) 中淀粉样β蛋白 (Aβ) 斑块诱导变化的区域特异性差异

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Odmaa Bayaraa ; Michael Aksu ; Evon DeBose-Scarlett ; Emily Hocke ; Vaibhav Jain ; Shih-Hsiu J Wang ; Dianne Cruz ; Simon GregorySeries Type : OtherOrganism : Homo sapiensAlzheimer’s disease (AD) is the leading cause of dementia affecting 55 million people worldwide. The pathological hallmarks of AD, beta-amyloid (Aβ) plaques and neurofibrillary tangles (NFT), follow distinct stereotypical patterns of progression across brain regions and trigger a multicellular response that ultimately leads to neuronal loss and cognitive decline. Despite the uniform spread of Aβ plaque across the cortex during AD progression, different regions demonstrate varying levels of vulnerability and resilience to temporal Aβ plaque induced changes, such as NFT accumulation. There is a critical gap in our understanding of the cell types and molecular mechanisms that underlie these region-specific differences in resilience to Aβ plaque induced changes. In this study, we hypothesized that brain region and cell type specific transcriptional responses within the Aβ microenvironment, and more broadly within the grey matter, may contribute to this variation. We carried out matched multi-region spatial transcriptomics and Aβ immunofluorescence staining from the entorhinal, occipito-temporal, dorsolateral prefrontal and striate cortices from two individuals with Braak III and Thal 4 AD. Spatiotemporal comparisons of cell type proportions, gene expression, and cell-cell communication revealed differences in the vulnerability of somatostatin and somatostatin chondrolectin inhibitory neurons and the expression of endosomal and lysosomal trafficking and metallothionein genes within the Aβ plaque microenvironment. We also observed variations in blood-brain-barrier dysfunction, fibroblast growth factor signaling, and vascular impairment and repair related cell-cell communication networks within the grey matter. Our results demonstrate the value of simultaneously profiling AD-omic and spatial modalities in multiple regions to elucidate how cortical region-specific differences contribute to selective vulnerability and resilience during neurodegeneration.
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4. ⭐ GSE253667 通过整合单细胞和空间转录组学[H_scRNA-seq] 解析桑蚕飞行能力丧失的分子机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Rongpeng Liu ; Chen Zhao ; Jie Hu ; Yongbing Ba ; Yan Ma ; Yiting Ran ; Yuanyuan Mu ; Yinghao Li ; Xiaoqing Xu ; Yiyun Tang ; Qingjun Li ; Yuqin Chen ; Zhiming Zhang ; Kaiqi Guo ; Yuting Wang ; Zhiwei Li ; Keshu Dong ; Xiao Li ; Wei Tan ; Yumeng Zhu ; Zhonghuai Xiang ; Hanfu XuSeries Type : Expression profiling by high throughput sequencingOrganism : Helicoverpa armigeraLoss of flight is recurrently observed in flying species and markedly abates threats to human health and agricultural production posed by flying pests. However, our understanding of the flight organs involved remains limited. The silkworm Bombyx mori, a lepidopteran model insect, loses flight most recently, while the Bombyx mandarina capable of flight, therefore it is a good model for studying flight loss. Here, we represent the first description of the spatiotemporal architecture of Bombyx flight organs. We demonstrated that the weakened cellular function of NFDCs and FECs determining the flight energy and wing vein and flight muscle development largely result in flight loss in B. mori, and single-cell analyses of cotton bollworm flight organs and RNA interference (RNAi) of key genes validated these findings, and the cellular and molecular determinants of flight may be conserved across Lepidoptera. These findings will contribute to the understanding of flight loss encountered in flying species.
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5. ⭐ GSE253666 通过整合单细胞和空间转录组学来解析桑蚕飞行能力丧失的分子机制 [B_scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Rongpeng Liu ; Chen Zhao ; Jie Hu ; Yongbing Ba ; Yan Ma ; Yiting Ran ; Yuanyuan Mu ; Yinghao Li ; Xiaoqing Xu ; Yiyun Tang ; Qingjun Li ; Yuqin Chen ; Zhiming Zhang ; Kaiqi Guo ; Yuting Wang ; Zhiwei Li ; Keshu Dong ; Xiao Li ; Wei Tan ; Yumeng Zhu ; Zhonghuai Xiang ; Hanfu XuSeries Type : Expression profiling by high throughput sequencingOrganism : Bombyx mandarina ; Bombyx moriLoss of flight is recurrently observed in flying species and markedly abates threats to human health and agricultural production posed by flying pests. However, our understanding of the flight organs involved remains limited. The silkworm Bombyx mori, a lepidopteran model insect, loses flight most recently, while the Bombyx mandarina capable of flight, therefore it is a good model for studying flight loss. Here, we represent the first description of the spatiotemporal architecture of Bombyx flight organs. We demonstrated that the weakened cellular function of NFDCs and FECs determining the flight energy and wing vein and flight muscle development largely result in flight loss in B. mori, and single-cell analyses of cotton bollworm flight organs and RNA interference (RNAi) of key genes validated these findings, and the cellular and molecular determinants of flight may be conserved across Lepidoptera. These findings will contribute to the understanding of flight loss encountered in flying species.
• 🔗 查看原文

6. ⭐ GSE253665 通过整合单细胞和空间转录组学 [stRNA-seq] 来解析桑蚕飞行能力丧失的分子机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Rongpeng Liu ; Chen Zhao ; Jie Hu ; Yongbing Ba ; Yan Ma ; Yiting Ran ; Yuanyuan Mu ; Yinghao Li ; Xiaoqing Xu ; Yiyun Tang ; Qingjun Li ; Yuqin Chen ; Zhiming Zhang ; Kaiqi Guo ; Yuting Wang ; Zhiwei Li ; Keshu Dong ; Xiao Li ; Wei Tan ; Yumeng Zhu ; Zhonghuai Xiang ; Hanfu XuSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Bombyx mandarina ; Bombyx moriLoss of flight is recurrently observed in flying species and markedly abates threats to human health and agricultural production posed by flying pests. However, our understanding of the flight organs involved remains limited. The silkworm Bombyx mori, a lepidopteran model insect, loses flight most recently, while the Bombyx mandarina capable of flight, therefore it is a good model for studying flight loss. Here, we represent the first description of the spatiotemporal architecture of Bombyx flight organs. We demonstrated that the weakened cellular function of NFDCs and FECs determining the flight energy and wing vein and flight muscle development largely result in flight loss in B. mori, and single-cell analyses of cotton bollworm flight organs and RNA interference (RNAi) of key genes validated these findings, and the cellular and molecular determinants of flight may be conserved across Lepidoptera. These findings will contribute to the understanding of flight loss encountered in flying species.
• 🔗 查看原文

7. ⭐ GSE284108 小鼠肠壁（纵肌和肌间神经丛）衰老转录组分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、transcriptome、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Jared Slosberg ; Subhash Kulkarni ; Loyal A GoffSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThese data represent the changing transcriptal profiles of the longitudinal muscle and myenteric plexus (LMMP) of the murine ileum with age. Tissues from 1-month, 6-month, and 17-month old mice were characterized.
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8. ⭐ GSE316491 靶向 YAP/TEAD 信号通路干扰 RNA 聚合酶 II 活性，并通过激活胞质 DNA 感应通路增强胃食管癌的免疫治疗反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)、pathway
• 📝 描述：Contributors : Yan-ting Y Zhang ; Ayna Mammedova ; Dipti Athavale ; Curt Balch ; Mikel Ghelfi ; Xiaodan Yao ; Gennaro Calendo ; Songjie Liu ; David N Pulipati ; Yahui Li ; Xiaoxin Chen ; Francis Spitz ; Generosa Grana ; Vladimir Khazak ; Shumei SongSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGastroesophageal adenocarcinoma (GEAC) accounts for a significant global cancer burden. Our previous studies demonstrated that YAP1/TEAD are highly expressed in GEAC, and play a critical role in tumor progression, therapy resistance and metastasis. Thus, targeting YAP/TEAD signaling presents a promising therapeutic strategy. Here, we developed a novel YAP/TEAD inhibitor VT00278 based on the structure of CA3 and showed that VT00278 strongly downregulated YAP/TEAD transcriptional activity, and potently suppress tumor-promoting phenotypes, including proliferation, invasion, tumor sphere formation; induce apoptosis and inhibit tumor growth in vivo especially in radiation resistant FLO-1 XTR GEAC cells. Mechanistically, in addition to impairing YAP1/TEAD signaling, VT00278 or YAP1 depletion repressed RNA polymerase II transcriptional regulators, reduced RNAPII S2 phosphorylation and decreased anti-apoptosis MCL-1 expression. More interestingly, we revealed that VT00278 strongly induced DNA damage, activated cytosolic DNA sensing pathway, upregulation of innate immune genes (e.g.INFβ) and increased PDL-1 expression. In a syngeneic mouse model, combining VT00278 with anti-PD-1 therapy synergistically inhibited tumor growth and increased CD3+ and CD8+ T cell infiltration and induced the production of INFγ from CD3 and CD8 cells in the combination treatment. These findings support VT00278 as a promising candidate for GEAC treatment, either alone or in combination with immunotherapy.
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9. ⭐ GSE274639 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性 [scATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、scATAC
• 📝 描述：Contributors : Yun Wei ; Luis A Sanchez ; Shuze Wang ; Esther Rheinbay ; David M LangenauSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRhabdomyosarcoma (RMS) is a common pediatric soft tissue sarcoma of skeletal muscle. Worse outcomes are associated with specific subtypes of RMS, including the 10% of fusion-negative tumors that harbor point mutations in the DNA binding domain of MYOD1 (myogenic differentiation 1) transcription factor. Due to the rarity of these patient samples and dearth of cell lines/animal models, the molecular function of MYOD1L122R remains unknown. Here, we create the first animal model of this disease showing that MYOD1L122R is not oncogenic but collaborates with RAS activation to create highly aggressive RMS in transgenic zebrafish, akin to what is reported in human disease. Limiting dilution cell transplantation revealed that MYOD1L122R also elevated the overall frequency of tumor propagating cells in the zebrafish model. We next generated isogenic knock-in MYOD1L122R human cell line models and showed that these cells were refractory to standard of care vincristine, actinomycin, and cyclophosphamide while also elevating the overall frequency of tumor propagating cells. Indeed, single-cell RNA transcriptional profiling and single-cell assay for transposase-accessible chromatin with sequencing (ATAC-Seq) of patient and patient-derived xenografts confirmed the elevation of cancer stem cell programs within MYOD1L122R tumors. Using unbiased whole-genome ChIP and RNA sequencing, we next identified the shared and differential genomic binding regions by MYOD1L122R as compared to wildtype MYOD1. Most notably, MYOD1L122R bound uniquely to and transcriptionally upregulated mesenchymal pathway enriched genes that are known to correlate with RMS cancer stemness. Finally, mechanistic studies uncovered that MYOD1L122R binds to the regulatory element of ROR2 (receptor tyrosine kinase like orphan receptor 2), upregulating its expression, which then turns on a novel WNT11-ROR2-VANGL2 axis to induce non-canonical WNT signaling and elevate cancer stemness.
• 🔗 查看原文

10. ⭐ GSE274638 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、scRNA
• 📝 描述：Contributors : Yun Wei ; Luis A Sanchez ; Shuze Wang ; Esther Rheinbay ; David M LangenauSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRhabdomyosarcoma (RMS) is a common pediatric soft tissue sarcoma of skeletal muscle. Worse outcomes are associated with specific subtypes of RMS, including the 10% of fusion-negative tumors that harbor point mutations in the DNA binding domain of MYOD1 (myogenic differentiation 1) transcription factor. Due to the rarity of these patient samples and dearth of cell lines/animal models, the molecular function of MYOD1L122R remains unknown. Here, we create the first animal model of this disease showing that MYOD1L122R is not oncogenic but collaborates with RAS activation to create highly aggressive RMS in transgenic zebrafish, akin to what is reported in human disease. Limiting dilution cell transplantation revealed that MYOD1L122R also elevated the overall frequency of tumor propagating cells in the zebrafish model. We next generated isogenic knock-in MYOD1L122R human cell line models and showed that these cells were refractory to standard of care vincristine, actinomycin, and cyclophosphamide while also elevating the overall frequency of tumor propagating cells. Indeed, single-cell RNA transcriptional profiling and single-cell assay for transposase-accessible chromatin with sequencing (ATAC-Seq) of patient and patient-derived xenografts confirmed the elevation of cancer stem cell programs within MYOD1L122R tumors. Using unbiased whole-genome ChIP and RNA sequencing, we next identified the shared and differential genomic binding regions by MYOD1L122R as compared to wildtype MYOD1. Most notably, MYOD1L122R bound uniquely to and transcriptionally upregulated mesenchymal pathway enriched genes that are known to correlate with RMS cancer stemness. Finally, mechanistic studies uncovered that MYOD1L122R binds to the regulatory element of ROR2 (receptor tyrosine kinase like orphan receptor 2), upregulating its expression, which then turns on a novel WNT11-ROR2-VANGL2 axis to induce non-canonical WNT signaling and elevate cancer stemness.
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详细内容（全部3条）

1. RNA测序揭示了OTULIN如何调控tau蛋白和大脑衰老

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、sequencing
• 📝 描述：Researchers show OTULIN regulates tau production and brain aging, using CRISPR and RNA sequencing to reveal widespread effects on RNA metabolism and inflammatory gene pathways in neurons…
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2. 科学家在温泉细菌中发现了一种天然防晒霜

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Researchers studying cyanobacteria from hot springs in Thailand have discovered a new natural UV-blocking compound with impressive antioxidant power. Unlike conventional sunscreens, it’s biocompatible and potentially safer for both people and the environment. The molecule is produced only under UV and salt stress and uses a unique biosynthetic pathway never seen before. This could help drive a new generation of eco-friendly sunscreens and skincare products.
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3. RNA测序揭示病毒感染如何提高海洋生产力

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Using RNA sequencing, researchers show viral infection of ocean cyanobacteria boosts microbial productivity and nutrient recycling, helping drive a recurring subsurface oxygen maximum in the Sargasso Sea…
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• GSE274637 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性 [ChIP-seq]
• GSE246491 HLA-A2限制性免疫优势SARS-CoV-2特异性CD8+ T细胞受体库对抗原漂移的抵抗潜力
• GSE292417 通过 SREBP1-PCSK9 靶向脂质代谢重编程增强胰腺癌对免疫化疗的敏感性 [CUT&Tag]
• GSE249906 Calhm6：巨噬细胞可塑性和免疫反应的守门人
• GSE249905 Calhm6：巨噬细胞可塑性和免疫反应的守门人 [Raw264.7-OE]
• GSE249904 Calhm6：巨噬细胞可塑性和免疫反应的守门人 [BMDM]
• GSE310301 精氨酸缺乏重塑肿瘤和免疫转录程序，并增强 4T1 小鼠乳腺肿瘤中的 IFNγ–JAK–STAT 信号传导
• GSE308019 RNA-seq 分析对照组和 PARylator 敲低组 TE13 人食管鳞状细胞癌细胞
• GSE305642 TIMP1介导的M2巨噬细胞极化促进结直肠癌肝转移
• GSE299958 LXRβ/NF-κB轴重编程CAR-T细胞以抵抗肿瘤微环境中的耗竭
• GSE298471 用于免疫细胞重编程的组合转录因子筛选平台 [scRNA-seq]
• GSE298271 小胶质细胞转录组系统评分，用于评估人类脐带间充质干细胞治疗方案在炎症相关早产儿脑损伤大鼠模型中的疗效。
• GSE297682 BRRIAR lncRNA 通过 BHLHE40 和 RIG-I 顺式和反式调节干扰素信号传导来改变乳腺癌风险 [RNA-Seq]
• GSE289585 累积发育扰动改变成年雄性行为，与C57BL/6小鼠血液和大脑中的表观遗传、核糖体和免疫失调有关
• GSE274640 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性。
• GSE274636 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性 [RNAseq_Ruch2oe]
• GSE274635 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性 [RNAseq_Rdoe]
• GSE274634 MYOD1L122R 诱导癌症干细胞通路，使侵袭性横纹肌肉瘤产生化疗和放射抗性 [RNA-seq_HDR]
• GSE252521 利用CUT&Tag分析对人类衰老细胞的染色质特征进行全基因组研究并表征基因组-转录组相互作用
• GSE313671 前列腺素 I₂ 受体激活通过 JUN/p53 通路促进肺泡再生 [scRNA-seq]
• GSE316213 氧化应激诱导的免疫原性细胞死亡增强了同源胰腺癌模型中全细胞疫苗的疗效
• GSE312445 单细胞多组学研究揭示了神经元激活的背景依赖性遗传控制机制，揭示了脑部疾病的发生机制
• GSE303512 野生型和/或 Dazl 突变小鼠卵巢细胞在胚胎发育阶段的单细胞 RNA 测序（E10.5（野生型）、E11.5（野生型和 Dazl-/-）、E12.5（Dazl-/-）、E15.5（野生型））
• GSE287241 抑制鞘氨醇代谢可抑制铁死亡并使衰老的造血干细胞恢复活力，从而促进认知和延长寿命 [scRNA-seq]
• GSE287181 抑制鞘氨醇代谢可抑制铁死亡并使衰老的造血干细胞恢复活力，从而促进认知和延长寿命 [低投入 RNA-seq]
• GSE287104 抑制鞘氨醇代谢可抑制铁死亡并使衰老的造血干细胞恢复活力，从而促进认知和延长寿命 [RNA-seq]
• GSE286217 体外扩增的造血干细胞及其T细胞祖细胞子代的转录和表观遗传程序
• GSE285884 黄连解毒汤通过调节肠道菌群来调控胃抑制多肽的释放，从而改善肥胖小鼠的脂质代谢紊乱。
• GSE314553 利用患者来源细胞构建晚发性散发性阿尔茨海默病模型：综述
• GSE306978 衰老肿瘤细胞来源的纳米囊泡直接激活脾脏T细胞以增强放射治疗
• GSE306883 表达 Postn 的成纤维细胞中的 Runx1 会加剧心肌梗死后的不良心脏重塑
• GSE305410 批量 RNA 测序顶骨 PND9 同型与 aCSF1R 比较
• GSE226507 对脑细胞间通讯的系统性表征揭示了 SEMA6D 在阿尔茨海默病中 TREM2 相关小胶质细胞功能中的新作用
• GSE316401 CD8 immgenT 框架作为小鼠 CD8 T 细胞分化状态的通用参考
• GSE315721 对不同遗传背景下经雷帕霉素处理的酵母菌株进行测序，包括有无 U18 的情况
• GSE315211 诱导型Δ133p53α突变的早衰症小鼠LmnaG609G多器官的批量RNA测序
• GSE307729 小细胞外囊泡 microRNA-302f 在子宫内膜异位症相关卵巢癌中的作用
• GSE306823 RNA-seq 分析柠檬酸合酶 (CS) 敲低细胞
• GSE306126 MSLN介导的EGFR-ERK1/2信号激活驱动乳腺癌肝转移[HCC1806-HM3]
• GSE306125 MSLN介导的EGFR-ERK1/2信号通路激活驱动乳腺癌肝转移
• GSE305661 研究发现，靶向 CHD1L 通过 FOXO3-PUMA 轴抑制前列腺癌进展
• GSE305211 碳酸酐酶 12 是高危滤泡性甲状腺癌的新型预后生物标志物和治疗靶点
• GSE300824 人工整理以改进功能性灭绝的北方白犀牛（Ceratotherium simum cottoni）的基因组注释
• GSE298487 用于免疫细胞重编程的组合转录因子筛选平台 [bulkRNA-seq]
• GSE295508 MT靶向MT1/2调控线粒体融合动力学介导的WNT/β-catenin信号通路，促进人iPS细胞DA神经元分化和PD小鼠神经再生
• GSE294726 利用人原代肺上皮细胞的离体转录组学研究甲型流感病毒对肺炎链球菌感染的调控 [AEIC 和 AHFJ]
• GSE293583 小鼠胰腺导管腺癌中肿瘤浸润免疫细胞的基因表达谱
• GSE291454 EZH2-PRC2 在抑制原始内胚层细胞命运中的保守功能 [RNA-Seq - 小鼠]
• GSE291367 EZH2-PRC2 在抑制原始内胚层细胞命运中的保守功能 [RNA-Seq - 人类]
• GSE291070 人类前列腺转录组图谱与死后间隔时间的关系
• GSE288774 揭示 TCF7L2 在滋养层干细胞 (TSC) 自我更新和分化中的作用 [ChIP-Seq]
• GSE288773 揭示 TCF7L2 在滋养层干细胞 (TSC) 自我更新和分化中的作用 [RNA-Seq]
• GSE288585 Jk DNA GAGA 基序是局部核小体重塑和 Vk-Jk 重组所必需的 [ATAC-Seq]
• GSE288584 Jk DNA GAGA 基序是局部核小体重塑和 Vk-Jk 重组所必需的 [RNA-Seq]
• GSE288092 过敏性气道炎症急性及慢性模型中组织重塑的不同机制
• GSE277963 金属硫蛋白 1 调控 DNMT3A;NPM1 突变型急性髓系白血病的生长和存活
• GSE259327 基于血液的早期胰腺导管腺癌microRNA生物标志物特征及其在诊断前样本中的前瞻性轨迹
• GSE242941 皮肤癌 NK 细胞的转录谱分析揭示了糖皮质激素受体活性的升高改变了其促炎特性。
• GSE242112 组蛋白H1.5敲低导致着丝粒转录丧失
• GSE239301 衰老导致的RNA输出下降通过诱导R环损伤造血干细胞
• GSE239300 衰老导致的RNA输出下降通过诱导R环路损害造血干细胞
• GSE239299 衰老导致的RNA输出下降通过诱导R环损伤造血干细胞
• GSE239298 衰老导致的RNA输出下降通过诱导R环损伤造血干细胞
• GSE193429 治疗诱导衰老过程中人类基质细胞染色体结构的空间重组
• GSE313673 前列腺素 I₂ 受体激活通过 JUN/p53 通路促进肺泡再生 [CUT&Tag]
• GSE313672 前列腺素 I₂ 受体激活通过 JUN/p53 通路促进肺泡再生 [多组测序]
• GSE285476 解码介导肝移植排斥反应的中间单核细胞中的 Retn-Cap1 通路
• GSE282985 Schlafen 5 (SLFN5) 是一种细胞内免疫检查点，可控制胰腺导管腺癌 (PDAC) 中的干扰素 (IFN) 反应。
• GSE316183 通过病毒递送工程化TnpB实现高效的无转基因多重基因组编辑
• GSE316172 小鼠脑外伤后NeuroD1-星形胶质细胞治疗的单细胞RNA测序
• GSE315991：高脂饮食和福莫特罗治疗雄性小鼠肝脏组织中大量RNA的转录组学分析
• GSE315974 对暴露于游离脂肪酸（油酸和棕榈酸）、福莫特罗或两者的 HepaRG 细胞的大量 RNA 进行转录组学分析
• GSE315850 Toll信号通​​路控制果蝇肠道再生
• GSE313430 CTCF介导的顺式调控染色质绝缘强化了B细胞耐受性检查点[RNA-seq]
• GSE313428 CTCF 介导的顺式调控染色质绝缘强化了 B 细胞耐受性检查点 [ATAC-seq]
• GSE312328 高效 CRISPR 基因敲入实验表明 TCF1 不足以逆转 T 细胞耗竭
• GSE302841 是分别用 BSA（牛血清白蛋白）或 NEFA（非酯化脂肪酸）混合物培养的颗粒细胞的 mRNA 转录组数据。
• GSE287103 抑制鞘氨醇代谢可抑制铁死亡并使衰老的造血干细胞恢复活力，从而促进认知和延长寿命 [CUT&TAG]
• GSE287059 细胞静止期表现出与细胞衰老相似的转录炎症表型 [scRNA-seq]
• GSE287058 细胞静止期表现出与细胞衰老相似的转录炎症表型 [bulk RNA-seq]
• GSE214255 新型miR-7974调控轴对结直肠癌发生和转移能力的功能动态调控