详细内容（前10条）

1. ⭐ GSE305110 GNL3 调控 AR 转录程序以驱动去势抵抗性前列腺癌和免疫逃逸 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、RNA-seq
• 📝 描述：Contributors : Edwin Cheung ; Cuiting Zhang ; Tin Long Cheong ; Nitin NarwadeSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAndrogen receptor (AR) signaling is a primary oncogenic driver of castration-resistant prostate cancer (CRPC), yet the mechanism remains incompletely understood. Through proteomic profiling of CRPC and primary PCa cells, we identify G Protein Nucleolar 3 (GNL3) as a novel AR coregulator. GNL3 physically interacts with AR, enhances its chromatin occupancy, and directly coactivates transcriptional programs that promote cell proliferation, including NEK2 and CDC20. Concurrently, GNL3 functions as a corepressor of immune-responsive genes such as CXCL10 and TAP1 via class I histone deacetylases (HDACs), thereby facilitating CD8+ T cell elimination and establishing an immunosuppressive tumor microenvironment. GNL3 expression and AR-GNL3 complex formation progressively increase from normal prostate to CRPC and correlate with poor clinical outcomes. Functionally, GNL3 knockdown sensitizes CRPC cells to AR antagonists and impairs tumor growth and metastasis. Furthermore, we demonstrate that combinatorial inhibition of NEK2, class I HDACs, and AR signaling can be a potential therapeutic strategy for CRPC. Overall, these findings establish GNL3 as a dual-function AR coregulator and therapeutic target, providing mechanistic insights into transcriptional regulation and immune evasion in advanced PCa.
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2. ⭐ GSE305109 GNL3 协调 AR 转录程序以驱动去势抵抗性前列腺癌和免疫逃逸 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、ChIP-seq
• 📝 描述：Contributors : Edwin Cheung ; Cuiting Zhang ; Tin Long Cheong ; Nitin NarwadeSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAndrogen receptor (AR) signaling is a primary oncogenic driver of castration-resistant prostate cancer (CRPC), yet the mechanism remains incompletely understood. Through proteomic profiling of CRPC and primary PCa cells, we identify G Protein Nucleolar 3 (GNL3) as a novel AR coregulator. GNL3 physically interacts with AR, enhances its chromatin occupancy, and directly coactivates transcriptional programs that promote cell proliferation, including NEK2 and CDC20. Concurrently, GNL3 functions as a corepressor of immune-responsive genes such as CXCL10 and TAP1 via class I histone deacetylases (HDACs), thereby facilitating CD8+ T cell elimination and establishing an immunosuppressive tumor microenvironment. GNL3 expression and AR-GNL3 complex formation progressively increase from normal prostate to CRPC and correlate with poor clinical outcomes. Functionally, GNL3 knockdown sensitizes CRPC cells to AR antagonists and impairs tumor growth and metastasis. Furthermore, we demonstrate that combinatorial inhibition of NEK2, class I HDACs, and AR signaling can be a potential therapeutic strategy for CRPC. Overall, these findings establish GNL3 as a dual-function AR coregulator and therapeutic target, providing mechanistic insights into transcriptional regulation and immune evasion in advanced PCa.
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3. ⭐ GSE297029 心理压力通过肠道菌群衍生的亚精胺消耗促进造血干细胞衰老

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Meng Zhao ; Xiaobin TianSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusinhibit mPFC and PAG brain region promote HSCs aging
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4. ⭐ GSE330032 患者来源类器官揭示KRAS突变型结直肠癌中抗表皮生长因子受体抗体敏感性的亚型特异性异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、antibody、KRAS
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAnti–epidermal growth factor receptor (anti-EGFR) antibodies are widely used in the treatment of colorectal cancer (CRC), and KRAS mutation status is commonly used as a predictive biomarker for therapeutic responsiveness. Nevertheless, emerging evidence suggests that drug sensitivity among KRAS-mutant CRC is heterogeneous and varies according to mutation subtype. In this study, we reevaluated the determinants of anti-EGFR antibody sensitivity using a patient-derived CRC organoid library. Eight organoid lines comprising KRAS wild-type, KRAS G12-mutant, and KRAS G13-mutant tumors were subjected to drug sensitivity assays. Although KRAS G12-mutant organoids generally exhibited reduced responsiveness to anti-EGFR antibodies, KRAS G13-mutant organoids demonstrated sensitivity comparable to that of KRAS wild-type organoids. Transcriptomic analysis of a KRAS G13-mutant organoid after anti-EGFR antibody treatment revealed significant alterations in gene expression, with enrichment of MYC-related signaling pathways. These results were supported by in silico analyses using public cancer cell line datasets, which showed relatively lower IC50 values for KRAS G13-mutant cells than for KRAS G12-mutant cells. Moreover, anti-EGFR antibody treatment induced the expression of apoptosis-related genes in KRAS G13-mutant organoids, and pharmacological inhibition of MYC signaling attenuated drug sensitivity, indicating a functional role for MYC activation in mediating therapeutic response. Altogether, our results demonstrate heterogeneity in anti-EGFR antibody sensitivity among KRAS-mutant CRCs and identify KRAS G13-mutant tumors as a subset with preserved responsiveness. These data provide mechanistic insights into subtype-specific differences in therapeutic vulnerability and suggest that downstream transcriptional programs, including MYC signaling, contribute to sensitivity to EGFR-targeted therapy.
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5. GSE330842 GALNT3 缺失通过抑制 TNF-α/NF-κB/MAPK 信号通路来抑制炎症相关纤维化，从而改善慢性肾脏病

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、pathway
• 📝 描述：Contributor : Meng YangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChronic kidney disease (CKD) seriously degrades the life quality of human beings, but the molecular mechanisms that drive CKD pathogenesis have not been fully delineated.
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6. GSE313114 STC-15 对 METTL3 的抑制诱导 RNA 错误加工，导致 dsRNA 形成并激活先天免疫 [RNA-Seq 剂量反应]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、RNA-seq
• 📝 描述：Contributor : Harry FischlSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe RNA methyltransferase METTL3 is responsible for the generation of m6A, the most abundant modification mark on mRNA and long non-coding RNA. Accumulating evidence suggests numerous roles of METTL3 in cancer initiation and progression and highlights the potential for targeting this enzyme in oncology. STC-15 is a potent and selective METTL3 inhibitor and the first RNA modifying enzyme inhibitor to enter human clinical development. It is structurally related to the previously published tool inhibitors STM2457 and STM3675. We previously identified the induction of a cancer cell-intrinsic interferon response following pharmacological inhibition of METTL3, leading to activation of T-cell-mediated anti-tumour response. Here, we profiled m6A levels at nucleotide resolution using GLORI and characterised RNA changes following METTL3 inhibition with STC-15 or STM3675. Following loss of m6A, we uncovered aberrant mRNA transcripts arising from intron retention (IR) and transcriptional run-on (RO) events downstream of m6A-enriched exons in human cancer cells and in tumour samples in vivo. We found that these IR and RO events produce double-stranded RNA and are bound by the cytoplasmic dsRNA sensor MDA5.Using preclinical in vitro and in vivo models, we characterised in detail the anti-tumour immune responses induced by STC-15. Our study reveals how METTL3 inhibition leads to dsRNA accumulation, which triggers a type I interferon response and induces anti-tumour immunity. Together, these findings provide a mechanistic rationale for STC-15 as a novel anti-cancer drug both as monotherapy and in combination with anti-PD1 checkpoint inhibitors.
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7. GSE294156 PFF 诱导 LRRK2 介导的 Rab5 磷酸化触发溶酶体功能障碍和神经元衰老 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、ATAC-seq
• 📝 描述：Contributors : Xinxin Zuo ; Zeyu Chen ; William MobleySeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusWhile there is significant progress in characterizing the pathogenesis of Parkinson’s disease (PD), underlying cell biological events are less well-defined. Increasing evidence suggests that endolysosomal dysfunction is a critical driver of PD pathogenesis. In this study, we explored the impact of preformed α-synuclein fibrils (PFF) on endolysosomal function and downstream events, including activation of cellular senescence pathways. We found that PFF treatment of primary cultures of mouse cortical neurons caused widespread endolysosomal dysfunction. PFF treatment also induced changes in transcriptional reprogramming and chromatin accessibility. To define underlying mechanisms we explored the status of LRRK2, finding that PFF treatment activated LRRK2 on early endosomes where it phosphorylated Rab5. PFF also induced phosphorylation of Rab7. LRRK2 activation was necessary for endolysosomal dysfunction and transcriptional changes as these changes were prevented by pharmacological inhibition of LRRK2 with MLi-2. In addition, Rab5 changes mediated by PFF treatment contributed to changes in chromatin remodeling. These cell biological insights point to a critical role in PD pathogenesis for LRRK2 activation and its engagement of the endolysosomal network and to a novel role for the LRRK2-Rab5 axis in mediating its manifestations.
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8. GSE294140 PFF 诱导 LRRK2 介导的 Rab5 磷酸化触发溶酶体功能障碍和神经元衰老 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、RNA-seq
• 📝 描述：Contributors : Xinxin Zuo ; Zeyu Chen ; William MobleySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWhile there is significant progress in characterizing the pathogenesis of Parkinson’s disease (PD), underlying cell biological events are less well-defined. Increasing evidence suggests that endolysosomal dysfunction is a critical driver of PD pathogenesis. In this study, we explored the impact of preformed α-synuclein fibrils (PFF) on endolysosomal function and on transcriptional reprogramming.
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9. GSE288925 小肠内皮细胞单细胞RNA测序[WT_EC]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNAseq、regex:intestin(e|al)
• 📝 描述：Contributors : Irena Roci ; Jeremiah Berner-Latmani ; Tatiana V Petrova ; Tania WyssSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe investigated the transcriptomic diversity of endothelial cells of the mouse small intestine using single-cell RNA sequencing.
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10. GSE288670 小肠内皮细胞单细胞RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNAseq、regex:intestin(e|al)
• 📝 描述：Contributors : Silvia Arroz Madeira ; Tatiana V Petrova ; Tania WyssSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe investigated the transcriptomic diversity of endothelial cells of the mouse small intestine using single-cell RNA sequencing.
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1. SCSEQ——用于分析单细胞RNA测序数据的Web工具

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、single-cell
• 📝 描述：SCSEQ makes single-cell RNA sequencing analysis more accessible through a web-based platform that supports preprocessing, clustering, cell type identification, and downstream biological interpretation. By reducing the need for programming expertise, the tool helps researchers explore complex…
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2. 从microRNA发现到分子机制：构建稳健的miRNA工作流程以用于癌症研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Integrated miRNA workflows connect sequencing, dPCR validation, and pathway analysis to improve cancer biomarker discovery and biological interpretation from challenging samples like FFPE tissue and exosomes…
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• GSE329396 用铜(I)双膦配合物（配合物1）处理的A549肺癌细胞的RNA测序
• GSE283159 SPTEdU-seq：并行无光学新生儿细胞追踪和空间全转录组学解析跨组织和物种的时空动态
• GSE330850 人类肿瘤细胞系中体细胞向原始生殖细胞样转化的谱系追踪
• GSE310531 线粒体驱动的质量控制通路消除错位的过氧化物酶体膜蛋白
• GSE297338 ZC3H7A 和 ZC3H7B RNA 结合蛋白对 mRNA 翻译和稳定性的密码子依赖性调控 [RNA-seq]
• GSE319947 组蛋白调节剂小分子库筛选揭示 Kdm5b 是 CM 中细胞周期基因表达的主要表观遗传调控因子
• GSE314414 溶细胞性鼠γ疱疹病毒68 (MHV-68) 感染期间宿主转录重塑的时间序列RNA测序分析
• GSE243165 信号响应转录因子协同作用建立肺泡巨噬细胞特性
• GSE243162 使用 CD11c-Cre+ 小鼠模型 (ATAC-Seq) 研究 RXRαβ 缺陷型和野生型肺泡巨噬细胞的染色质可及性差异
• GSE243160 利用 CD11c-Cre+ 小鼠模型 (RNA-Seq) 分析 RXRαβ 缺陷型和野生型肺泡巨噬细胞的转录组差异
• GSE330548 多组学整合鉴定小细胞肺癌 II 中的关键分子驱动因素和可变剪接事件
• GSE315316 促排卵日使用 hCG 对 DNA 甲基化改变的影响
• GSE326742 TENT5 蛋白的 C 端区域通过 FNDC3 相互作用驱动 ER 相关 mRNA 多聚腺苷酸化 [RNA-seq]
• GSE326057 靶向 KRAS G12V 降解在体内引起高效且持久的肺腺癌消退 [dTAG_expt3_RNAseq]
• GSE301620 靶向 KRAS G12V 降解可有效且持久地在体内抑制肺腺癌 [R_invivo_invitro]
• GSE301303 靶向 KRAS G12V 降解可在体内诱导高效且持久的肺腺癌消退
• GSE301302 靶向 KRAS G12V 降解在体内引起高效且持久的肺腺癌消退 [dTAG_expt2_RNAseq]
• GSE301301 靶向 KRAS G12V 降解在体内引起高效且持久的肺腺癌消退 [dTAG_expt1_RNAseq]
• GSE284808：来自拉伸介导皮肤扩张小鼠模型的成纤维细胞分选的批量RNA测序