详细内容（前10条）

1. GSE319269 阻断 NKp46-CCR6-ILC3 自噬通过恢复能量代谢平衡缓解坏死性小肠结肠炎 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ATAC-seq
• 📝 描述：Contributors : Junyu He ; Yumei He ; Yuxiong Guo ; Kai Wu ; Laiqin Peng ; Qiqiong WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusGroup 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.
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2. GSE317911 GPR56 作为前列腺癌细胞中雄激素反应转录组的关键调节因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、transcriptome
• 📝 描述：Contributors : Gargi Bagchi* ; Versha Dahiya ; Ravi SharmaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo investigate the role of GPR56 in androgen-mediated gene regulation, RNA sequencing was performed in LNCaP (prostate cancer cells) wild-type or GPR56-knockdown (LNCaP cells transfected with GPR56 siRNA, GPR56-KD), following testosterone stimulation. Transcriptomic analysis revealed extensive androgen-responsive gene expression in LNCaP-WT cells, including established androgen target genes, which was markedly reduced upon GPR56 knockdown. These findings suggest that GPR56 is required for optimal androgen response of androgen-dependent transcriptome in prostate cancer cells.
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3. GSE306522 阻断 NKp46-CCR6-ILC3 自噬通过恢复能量代谢平衡缓解坏死性小肠结肠炎 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、scRNA
• 📝 描述：Contributors : Junyu He ; Yumei He ; Yuxiong Guo ; Kai Wu ; Laiqin Peng ; Qiqiong Wang ; Xinyao LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusGroup 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.
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4. GSE306398 阻断 NKp46-CCR6-ILC3 自噬通过恢复能量代谢平衡缓解坏死性小肠结肠炎 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、RNA-seq
• 📝 描述：Contributors : Junyu He ; Yumei He ; Yuxiong Guo ; Kai Wu ; Laiqin Peng ; Qiqiong Wang ; Xinyao LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusGroup 3 innate lymphoid cells (ILC3s) play a crucial role in intestinal inflammatory disorders such as necrotizing enterocolitis (NEC) in neonates; however, the mechanisms by which ILC3s contribute to NEC remain unclear. In this study, single-cell transcriptomics, in vivo experiments on T cell-deficient mice, and targeted cell interventions demonstrated that NKp46−CCR6− (double-negative, DN) ILC3 autophagy significantly impacts NEC development by regulating intracellular metabolism. Mice lacking ATG5 or treated with autophagy inhibitors exhibited reduced ILC3 abundance and impaired ILC3 function, alleviating NEC. Mechanistically, ATG5 deficiency enhanced fatty acid metabolism while reducing glycolysis. Conversely, inhibiting fatty acid oxidation or supplementing with lactate restored the quantity and functionality of ATG5-deficient DN ILC3s, exacerbating NEC. Lipid metabolism analyses combined with a mouse model of NEC indicated that phosphatidylcholine supplementation alleviated intestinal inflammation by inhibiting DN ILC3 autophagy. Clinically, patients with NEC showed elevated ILC3 levels and significant enrichment of autophagy genes. These findings highlight the importance of DN ILC3 autophagy in metabolic adaptation, suggesting potential strategies for managing NEC.
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5. GSE294085 SIRT6 过表达可对抗染色质老化 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、ChIP-seq
• 📝 描述：Contributors : Ron Nagar ; Zacharia Scwartz ; Haim Y CohenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusAging is associated with detrimental changes in chromatin structure and gene expression, contributing to inflammation, metabolic decline and tissue dysfunction. SIRT6, a histone deacetylase, plays a key role in maintaining chromatin integrity and promoting longevity. Here, we show that aging leads to increased chromatin accessibility in the murine liver, accompanied by upregulation of inflammation and downregulation of metabolic pathways. Remarkably, SIRT6 overexpression reversed these changes, reducing inflammation and enhancing metabolic function. Notably, ETS family members were enriched in regions with increased accessibility during aging, while liver-enriched transcription factors (LETFs) were enriched in regions with reduced accessibility. ChIP-seq analyses of H3K9ac and H3K56ac binding showed that H3K9ac, but not H3K56ac, is associated with increased accessibility during aging, and that SIRT6 can reverse this effect. Furthermore, AAV-mediated SIRT6 overexpression in aged mice demonstrated that SIRT6 not only slows age-related chromatin changes but can also reverse them, rejuvenating chromatin accessibility to a youthful state.
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6. GSE294084 SIRT6 过表达可对抗染色质老化 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、ATAC-seq
• 📝 描述：Contributors : Ron Nagar ; Zacharia Scwartz ; Haim Y CohenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusAging is associated with detrimental changes in chromatin structure and gene expression, contributing to inflammation, metabolic decline and tissue dysfunction. SIRT6, a histone deacetylase, plays a key role in maintaining chromatin integrity and promoting longevity. Here, we show that aging leads to increased chromatin accessibility in the murine liver, accompanied by upregulation of inflammation and downregulation of metabolic pathways. Remarkably, SIRT6 overexpression reversed these changes, reducing inflammation and enhancing metabolic function. Notably, ETS family members were enriched in regions with increased accessibility during aging, while liver-enriched transcription factors (LETFs) were enriched in regions with reduced accessibility. ChIP-seq analyses of H3K9ac and H3K56ac binding showed that H3K9ac, but not H3K56ac, is associated with increased accessibility during aging, and that SIRT6 can reverse this effect. Furthermore, AAV-mediated SIRT6 overexpression in aged mice demonstrated that SIRT6 not only slows age-related chromatin changes but can also reverse them, rejuvenating chromatin accessibility to a youthful state.
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7. GSE294067 SIRT6 过表达可对抗染色质老化 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、RNA-seq
• 📝 描述：Contributors : Ron Nagar ; Zacharia Scwartz ; Haim Y CohenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAging is associated with detrimental changes in chromatin structure and gene expression, contributing to inflammation, metabolic decline and tissue dysfunction. SIRT6, a histone deacetylase, plays a key role in maintaining chromatin integrity and promoting longevity. Here, we show that aging leads to increased chromatin accessibility in the murine liver, accompanied by upregulation of inflammation and downregulation of metabolic pathways. Remarkably, SIRT6 overexpression reversed these changes, reducing inflammation and enhancing metabolic function. Notably, ETS family members were enriched in regions with increased accessibility during aging, while liver-enriched transcription factors (LETFs) were enriched in regions with reduced accessibility. ChIP-seq analyses of H3K9ac and H3K56ac binding showed that H3K9ac, but not H3K56ac, is associated with increased accessibility during aging, and that SIRT6 can reverse this effect. Furthermore, AAV-mediated SIRT6 overexpression in aged mice demonstrated that SIRT6 not only slows age-related chromatin changes but can also reverse them, rejuvenating chromatin accessibility to a youthful state.
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8. GSE305530 METTL3 驱动的 RNA 修饰：小鼠胰腺腺泡细胞癌的关键机制和潜在治疗靶点 [scRNA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、scRNA
• 📝 描述：Contributors : Shotaro Tatekawa ; Tomoaki Hara ; Sikun Meng ; Tetsuya Sato ; Hideshi IhiiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPancreatic acinar cell carcinoma (ACC) represents a rare and aggressive malignancy with poorly understood molecular mechanisms. N6-methyladenosine (m6A) RNA modification, particularly through the methyltransferase METTL3, has emerged as a critical regulator in various cancers. This study investigates the role of METTL3-mediated RNA methylation in ACC development and progression. We utilized transgenic mouse models over-expressing Mettl3 and SV40 large T antigen under the pancreatic Elastase I promoter. Comprehensive analyses included m6A-methylated RNA immunoprecipitation sequencing (MeRIP-seq), single-cell RNA sequencing (scRNA-seq), and functional studies with the METTL3 inhibitor STM2457. SAM-binding domain deletion mutants were generated to assess functional requirements. Mettl3 overexpression significantly accelerated ACC development and enhanced tumor aggressiveness. The SAM-binding domain proved essential for tumor formation, as deletion mutants failed to promote carcinogenesis. MeRIP-seq revealed preferential methylation of cell cycle and DNA replication genes in Mettl3-overexpressing tumors. scRNA-seq analysis demonstrated enhanced malignancy signatures, including epithelial-to-mesenchymal transition and TGF-β signaling. METTL3 promoted PRSS1-mediated signaling from ACC cells to inflammatory cancer-associated fibroblasts, creating a feed-forward loop involving IGF1 that amplifies tumor growth. Conditional Mettl3 deletion induced rapid tumor apoptosis. Pharmacological inhibition with STM2457 similarly triggered caspase-3/7-dependent apoptosis in pancreatic tumors. METTL3-mediated RNA methylation drives ACC pathogenesis through tumor-intrinsic cell cycle regulation and tumor-extrinsic stromal interactions. These findings establish METTL3 as a promising therapeutic target and provide mechanistic insights supporting clinical development of METTL3 inhibitors for pancreatic cancer treatment.
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9. GSE302399 三阴性乳腺癌来源外泌体诱导的T细胞反应的多模态转录组分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell
• 📝 描述：Contributors : Reza Shahbazi ; Samaneh Maleknia ; Sanam Rezaei Benam ; Kent Williams ; Lionel ApetohSeries Type : Expression profiling by high throughput sequencing ; Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensTriple-negative breast cancer (TNBC) is a highly aggressive and immunogenic subtype that lacks effective targeted therapies. Although tumor-derived exosomes are known to influence immune responses, their direct role in shaping human T cell plasticity and antigen specificity remains insufficiently characterized. In this study, we performed an integrative single-cell multiomic analysis of primary human T cells following exposure to exosomes isolated from 17 genomically distinct TNBC cell lines. By combining single-cell transcriptomics, T cell receptor (TCR) V(D)J sequencing, non-coding RNA profiling, and both bulk and single-cell cytokine analyses, we identified conserved and subtype-specific immunoregulatory programs elicited by TNBC-derived exosomes.
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10. GSE307226 hnRNPC 在中期与成熟 RNA 结合：proTAME 阻滞的 HeLa/HeLa S3 细胞的 RNA-seq 和 fCLIP 分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Liat Lev-Ari ; Sandra Laster ; Andrea Atzmon ; Daniel Blumenkrants ; Daniel Benhalevy ; Orna Elroy-SteinSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensProper progression through mitosis requires coordinated changes in RNA metabolism, but the specific contributions of individual RNA-binding proteins remain unclear. Heterogeneous nuclear ribonucleoprotein C (hnRNPC) is a ubiquitous RBP that normally binds uridine-rich sequences to influence pre-mRNA processing and stability. Here we investigated the role of hnRNPC in mitotic cells by profiling both global RNA abundance and hnRNPC–RNA interactions during metaphase arrest. To this end, we combined bulk RNA-seq with fluorescent crosslinking and immunoprecipitation (fCLIP) in proTAME-arrested HeLa S3 cells. This dataset enables the characterization of hnRNPC binding to mature RNAs during mitosis, the evaluation of biochemical fractionation (low-density vs high-density complexes), and the assessment of binding site resolution across distinct RNase digestion conditions. Together, the study provides a resource for exploring how hnRNPC contributes to RNA stability and gene expression control during cell division
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1. 侵袭性乳腺癌如何关闭免疫系统

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Researchers are launching a new project to crack the mystery of aggressive breast cancer, where predicting disease progression remains a major hurdle. By studying how tumors interact with and suppress the immune system, scientists aim to identify new biomarkers that reveal how the cancer evolves. Using real patient samples, the team hopes to turn earlier discoveries into practical clinical tools. The goal: more precise, personalized treatments that can outsmart even the most dangerous tumors.
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• GSE294103 SIRT6 过表达可对抗染色质老化 [ATAC-Seq_tg]
• GSE283791 一项针对晚期低级别浆液性癌女性患者的新辅助氟维司群联合阿贝西利治疗的II期试点研究
• GSE308719 PAK4 缺陷对肝星状细胞转录组的影响
• GSE305529 METTL3-Driven RNA Modifications: A Key Mechanism and Potential Therapeutic Target in Pancreatic Acinar Cell Carcinoma in Mice [MeRIP]
• GSE298918 PurR 嘌呤转录抑制因子和 Rae1 核糖核酸内切酶在耐甲氧西林金黄色葡萄球菌中 Erm 介导的大环内酯类耐药性中的作用。