详细内容（前10条）

1. ⭐ GSE292017 SETD2 对组蛋白 3 赖氨酸 36 的三甲基化作用塑造肠道干细胞的表观遗传图谱，从而调控脂质代谢并防止细胞衰老 [ATAC-seq II]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ATAC-seq、epigenetic、histone、regex:intestin(e|al)
• 📝 描述：Contributors : Yue Xu ; Ziyi WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe self-renewal capacity of intestinal stem cells (ISCs) declines with aging, leading to a loss of homeostasis and an increased susceptibility to intestinal diseases. Despite the established significance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms that connect these processes to aging-related ISC dysfunction remain elusive. Here, we demonstrate that Histone 3 lysine 36 trimethylation (H3K36me3) caused by SETD2 is critical for ISC stemness. We found that H3K36me3 deficiency results in reduced ISC proliferation and differentiation, disrupts fatty acid oxidation (FAO) metabolism, and induces ISC senescence. Mechanistically, the loss of H3K36me3 triggers the activity of the SWI/SNF chromatin remodeling complex and leads to increased chromatin accessibility and enhancer activation, which alters FAO- and senescence-related gene expression. Importantly, we discover that metabolic intervention can prevent the senescence of ISC due to H3K36me3 deficiency. Our findings reveal a crucial role for H3K36me3 in maintaining the epigenetic landscape that orchestrates FAO metabolism and determines intestinal stem cell functions, emphasizing the role of FAO as a key modulator between H3K36me3 and ISC aging, suggesting that metabolic intervention may help mitigate age-related ISC dysfunction.
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2. ⭐ GSE292016 SETD2 对组蛋白 3 赖氨酸 36 的三甲基化作用塑造肠道干细胞的表观遗传图谱，从而调控脂质代谢并防止细胞衰老 [ATAC-seq I]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ATAC-seq、epigenetic、histone、regex:intestin(e|al)
• 📝 描述：Contributors : Yue Xu ; Ziyi WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe self-renewal capacity of intestinal stem cells (ISCs) declines with aging, leading to a loss of homeostasis and an increased susceptibility to intestinal diseases. Despite the established significance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms that connect these processes to aging-related ISC dysfunction remain elusive. Here, we demonstrate that Histone 3 lysine 36 trimethylation (H3K36me3) caused by SETD2 is critical for ISC stemness. We found that H3K36me3 deficiency results in reduced ISC proliferation and differentiation, disrupts fatty acid oxidation (FAO) metabolism, and induces ISC senescence. Mechanistically, the loss of H3K36me3 triggers the activity of the SWI/SNF chromatin remodeling complex and leads to increased chromatin accessibility and enhancer activation, which alters FAO- and senescence-related gene expression. Importantly, we discover that metabolic intervention can prevent the senescence of ISC due to H3K36me3 deficiency. Our findings reveal a crucial role for H3K36me3 in maintaining the epigenetic landscape that orchestrates FAO metabolism and determines intestinal stem cell functions, emphasizing the role of FAO as a key modulator between H3K36me3 and ISC aging, suggesting that metabolic intervention may help mitigate age-related ISC dysfunction.
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3. ⭐ GSE292892 SETD2 对组蛋白 3 赖氨酸 36 的三甲基化作用塑造了肠道干细胞的表观遗传景观，从而协调脂质代谢并防止细胞衰老。

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、epigenetic、histone、regex:intestin(e|al)
• 📝 描述：Contributors : Yue Xu ; Ziyi WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe self-renewal capacity of intestinal stem cells (ISCs) declines with aging, leading to a loss of homeostasis and an increased susceptibility to intestinal diseases. Despite the established significance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms that connect these processes to aging-related ISC dysfunction remain elusive. Here, we demonstrate that Histone 3 lysine 36 trimethylation (H3K36me3) caused by SETD2 is critical for ISC stemness. We found that H3K36me3 deficiency results in reduced ISC proliferation and differentiation, disrupts fatty acid oxidation (FAO) metabolism, and induces ISC senescence. Mechanistically, the loss of H3K36me3 triggers the activity of the SWI/SNF chromatin remodeling complex and leads to increased chromatin accessibility and enhancer activation, which alters FAO- and senescence-related gene expression. Importantly, we discover that metabolic intervention can prevent the senescence of ISC due to H3K36me3 deficiency. Our findings reveal a crucial role for H3K36me3 in maintaining the epigenetic landscape that orchestrates FAO metabolism and determines intestinal stem cell functions, emphasizing the role of FAO as a key modulator between H3K36me3 and ISC aging, suggesting that metabolic intervention may help mitigate age-related ISC dysfunction.
• 🔗 查看原文

4. ⭐ GSE292018 SETD2 对组蛋白 3 赖氨酸 36 的三甲基化作用塑造肠道干细胞的表观遗传图谱，从而调控脂质代谢并防止细胞衰老 [CUT&Tag]

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、epigenetic、histone、regex:intestin(e|al)
• 📝 描述：Contributors : Yue Xu ; Ziyi WangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThe self-renewal capacity of intestinal stem cells (ISCs) declines with aging, leading to a loss of homeostasis and an increased susceptibility to intestinal diseases. Despite the established significance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms that connect these processes to aging-related ISC dysfunction remain elusive. Here, we demonstrate that Histone 3 lysine 36 trimethylation (H3K36me3) caused by SETD2 is critical for ISC stemness. We found that H3K36me3 deficiency results in reduced ISC proliferation and differentiation, disrupts fatty acid oxidation (FAO) metabolism, and induces ISC senescence. Mechanistically, the loss of H3K36me3 triggers the activity of the SWI/SNF chromatin remodeling complex and leads to increased chromatin accessibility and enhancer activation, which alters FAO- and senescence-related gene expression. Importantly, we discover that metabolic intervention can prevent the senescence of ISC due to H3K36me3 deficiency. Our findings reveal a crucial role for H3K36me3 in maintaining the epigenetic landscape that orchestrates FAO metabolism and determines intestinal stem cell functions, emphasizing the role of FAO as a key modulator between H3K36me3 and ISC aging, suggesting that metabolic intervention may help mitigate age-related ISC dysfunction.
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5. ⭐ GSE315510 线粒体潜能作为癌症免疫治疗中T细胞活力和功能的生物标志物

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Paul L Lindau ; Jeffrey C Rathmell ; Kathryn E BeckermannSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCheckpoint inhibitors have transformed cancer treatment, yet predicting responses remains challenging. Mitochondrial quality decreases in tumor infiltrating lymphocytes and correlates with impaired anti-tumor immunity in animal models. Mitochondrial membrane potential (MMP) increases with T cell activation but may also indicate cellular dysfunction. Here we assessed the MMP of tumor-associated T cells as an indicator of cell phenotypes and immunotherapy responses in Non-Small Cell Lung Carinoma and clear cell Renal Cell Carcinoma patients. Primary tumors were collected followed by analysis of peripheral blood mononuclear cells (PBMC) prior to and after three weeks on treatment with immune checkpoint inhibition (ICI). PBMC T cells were analyzed for MMP using tetramethylrhodamine ethyl ester (TMRE) and sorted into high and low populations. TCRβ and single cell RNA sequencing of primary tumors identified and characterized peripheral blood T cell clones associated with the tumor microenvironment. As anticipated, ICI therapy increased the frequency of effector T cells in patients who experienced clinical benefit. TMREhigh peripheral blood T cells with tumor-matching TCRβ sequences had elevated oxidative phosphorylation gene signatures. Gene signatures of stress and exhaustion, such as Tigit and Cmc1, were also elevated in the TMREhigh CD8 T cell populations while gene expression patterns in TMRElow cells suggested mitochondrial fitness and cell longevity. Importantly, clinical benefit from ICI was negatively correlated with the TMREhigh CD8 T cell gene expression signature. These findings highlight the presence of a T cell population of with elevated MMP that correlates with T cell exhaustion-like states and failed response to immunotherapy.
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6. GSE318600 银屑病样疾病通过中性粒细胞驱动的炎症反应阻止鳞状皮肤肿瘤的发生

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、inflammation
• 📝 描述：Contributors : Panagiota Tsokkou ; Martin Holcmann ; Katharina Rindler ; Kamil Mieczkowski ; Lisa Shaw ; Matthias Farlik ; Maria Sibilia ; Erwin F WagnerSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPsoriasis is a chronic inflammatory skin disease affecting millions of people worldwide. Although growing evidence links chronic inflammation with increased cancer risk, the association between psoriasis and cutaneous squamous cell carcinoma (cSCC) is still elusive. Using cell transplantation and chemical-induced models of cSCC combined with inducible genetically engineered mouse models (GEMMs) of psoriasis, we investigated how chronic skin and systemic inflammation affects squamous skin tumor initiation and progression. Here we show that in the context of severe psoriasis-like disease, neutrophil-dependent inflammation prevents squamous skin tumor development. Cellular and molecular analyses of psoriasis-like skin at the tumor initiation stage revealed a marked infiltration of CD54–expressing neutrophils, associated with the release of cytotoxic granules and neutrophil extracellular traps (NETs), as well as enhanced senescence and the expression of senescence-associated secretory phenotype (SASP) in keratinocytes. Furthermore, single-cell RNA sequencing demonstrated that inflammatory N1-like neutrophils mediate re-programming of the cell-cell communication networks, while keratinocytes displayed diminished responsiveness to mitogenic signals, including EGF and WNT. Importantly, neutrophil depletion ameliorated psoriasis-like inflammation, abolished the senescence-like phenotype in keratinocytes and restored tumor growth. We propose that the release of neutrophil granules and NETs in psoriasis-like skin eliminate tumor cells and/or mediate oxidative and inflammatory stress-induced senescence in keratinocytes, thereby preventing tumor growth. Taken together, we have defined an innate control of skin tumorigenesis in psoriasis-like disease, which will be relevant for developing cancer prevention strategies.
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7. GSE318413 Patient-derived orthotopic xenograft models recapitulate the peritoneal dissemination of pancreatic cancer and delineate its transcriptional and regulatory programs [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、scRNA
• 📝 描述：Contributors : Takaaki Furukawa ; Kohei Kumegawa ; Reo MaruyamaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBACKGROUND & AIMS: The mechanisms of peritoneal dissemination in pancreatic ductal adenocarcinoma (PDAC) remain unclear partly owing to the lack of patient-derived models that recapitulate this process. This study aimed to establish an orthotopic model of PDAC peritoneal dissemination and to uncover the transcriptional and regulatory programs underlying this process.METHODS: Organoids were established from primary pancreatic tumors and malignant effusions of patients with PDAC and orthotopically transplanted into the pancreas of immunodeficient mice to generate patient-derived orthotopic xenograft (PDOX) models. Subsequently, the organoids were rederived from pancreatic and peritoneal lesions of a representative model (PDOX12) and orthotopically reimplanted to assess the dissemination capacity. Single-nucleus RNA sequencing (snRNA-seq) and single-cell ATAC sequencing (scATAC-seq) were performed to analyze the tumors from these models.RESULTS: The organoids that were derived from malignant effusions reproducibly generated peritoneal metastases after orthotopic implantation. To dissect this process more precisely, we focused on one representative model (PDOX12) and rederived organoids from its pancreatic and peritoneal lesions. These organoids generated matched PDOX models that differed only in dissemination potential when reimplanted orthotopically. The results of snRNA-seq revealed a distinct subpopulation enriched in the high-dissemination model, which was characterized by the coordinated activation of genes involved in cytoskeletal dynamics, extracellular matrix remodeling, and plasticity-related signaling—suggesting a dissemination-primed state. Integration with scATAC-seq identified STAT3, SMAD3, and SOX2 as potential upstream regulators of this gene program.CONCLUSIONS: This study established PDOX models that isolate the peritoneal dissemination phenotype and reveal the transcriptional and regulatory programs driving this process.
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8. GSE318412 患者来源的原位异种移植模型重现了胰腺癌的腹膜播散，并阐明了其转录和调控程序 [scATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、scATAC
• 📝 描述：Contributors : Takaaki Furukawa ; Kohei Kumegawa ; Reo MaruyamaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensBACKGROUND & AIMS: The mechanisms of peritoneal dissemination in pancreatic ductal adenocarcinoma (PDAC) remain unclear partly owing to the lack of patient-derived models that recapitulate this process. This study aimed to establish an orthotopic model of PDAC peritoneal dissemination and to uncover the transcriptional and regulatory programs underlying this process.METHODS: Organoids were established from primary pancreatic tumors and malignant effusions of patients with PDAC and orthotopically transplanted into the pancreas of immunodeficient mice to generate patient-derived orthotopic xenograft (PDOX) models. Subsequently, the organoids were rederived from pancreatic and peritoneal lesions of a representative model (PDOX12) and orthotopically reimplanted to assess the dissemination capacity. Single-nucleus RNA sequencing (snRNA-seq) and single-cell ATAC sequencing (scATAC-seq) were performed to analyze the tumors from these models.RESULTS: The organoids that were derived from malignant effusions reproducibly generated peritoneal metastases after orthotopic implantation. To dissect this process more precisely, we focused on one representative model (PDOX12) and rederived organoids from its pancreatic and peritoneal lesions. These organoids generated matched PDOX models that differed only in dissemination potential when reimplanted orthotopically. The results of snRNA-seq revealed a distinct subpopulation enriched in the high-dissemination model, which was characterized by the coordinated activation of genes involved in cytoskeletal dynamics, extracellular matrix remodeling, and plasticity-related signaling—suggesting a dissemination-primed state. Integration with scATAC-seq identified STAT3, SMAD3, and SOX2 as potential upstream regulators of this gene program.CONCLUSIONS: This study established PDOX models that isolate the peritoneal dissemination phenotype and reveal the transcriptional and regulatory programs driving this process.
• 🔗 查看原文

9. GSE318411 患者来源的原位异种移植模型重现了胰腺癌的腹膜播散，并阐明了其转录和调控程序 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Takaaki Furukawa ; Kohei Kumegawa ; Reo MaruyamaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBACKGROUND & AIMS: The mechanisms of peritoneal dissemination in pancreatic ductal adenocarcinoma (PDAC) remain unclear partly owing to the lack of patient-derived models that recapitulate this process. This study aimed to establish an orthotopic model of PDAC peritoneal dissemination and to uncover the transcriptional and regulatory programs underlying this process.METHODS: Organoids were established from primary pancreatic tumors and malignant effusions of patients with PDAC and orthotopically transplanted into the pancreas of immunodeficient mice to generate patient-derived orthotopic xenograft (PDOX) models. Subsequently, the organoids were rederived from pancreatic and peritoneal lesions of a representative model (PDOX12) and orthotopically reimplanted to assess the dissemination capacity. Single-nucleus RNA sequencing (snRNA-seq) and single-cell ATAC sequencing (scATAC-seq) were performed to analyze the tumors from these models.RESULTS: The organoids that were derived from malignant effusions reproducibly generated peritoneal metastases after orthotopic implantation. To dissect this process more precisely, we focused on one representative model (PDOX12) and rederived organoids from its pancreatic and peritoneal lesions. These organoids generated matched PDOX models that differed only in dissemination potential when reimplanted orthotopically. The results of snRNA-seq revealed a distinct subpopulation enriched in the high-dissemination model, which was characterized by the coordinated activation of genes involved in cytoskeletal dynamics, extracellular matrix remodeling, and plasticity-related signaling—suggesting a dissemination-primed state. Integration with scATAC-seq identified STAT3, SMAD3, and SOX2 as potential upstream regulators of this gene program.CONCLUSIONS: This study established PDOX models that isolate the peritoneal dissemination phenotype and reveal the transcriptional and regulatory programs driving this process.
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10. GSE317930 PD-1 信号传导和抗 PD-1 抗体介导的肿瘤控制在微绒毛 T 细胞接触处建立。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、antibody
• 📝 描述：Contributors : Sumana Sharma ; Yuan Lui ; Martin Fellermeyer ; Edward JenkinsSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo investigate the differences between nivolumab_mIgG1 and nivolumab_mIgG1_D265A, and to identify the context in which antibody agonism might impact therapy, we employed a single-cell RNA sequencing approach using 10x Genomics to study the immune populations of tumors, and draining lymph nodes (dLN), and non-draining lymph nodes (non-dLN).
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1. 二甲双胍的隐秘脑通路在60年后被揭示

• ✍️ 作者：未知作者
• 🏷️ 关键词：pathway
• 📝 描述：A major discovery reveals that metformin works not just in the body, but in the brain. By switching off a key protein and activating specific neurons, the drug lowers blood sugar through a previously hidden pathway, opening new doors for diabetes treatment.
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2. 科学家发现这种致命肺癌为何会反复复发。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have discovered that losing a key protein in small cell lung cancer triggers inflammation that actually helps tumors grow and spread. Even more surprising, it pushes cancer cells into a more aggressive, neuron-like state linked to relapse.
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• GSE303323 长期 KRAS-MAPK 抑制诱导干扰素介导的上皮间质转化，并揭示治疗机会 [RNA-Seq]
• GSE302632 小鼠造血干细胞和祖细胞的单细胞转录组分析
• GSE261484 高水平的干扰素-γ诱导蛋白30可阻断PD-L1介导的溶酶体降解，并增加CD8+免疫细胞浸润，从而改善免疫治疗反应。
• GSE322956 ADAMTS9-AS2 作为一种表观遗传刹车，限制了 DNMT3B 介导的 CADM2 沉默在食管鳞状细胞癌转移中的作用
• GSE307565 通过捕获键工程克服T细胞对肿瘤自身抗原的耐受性 - TCR156wt 和 S32M
• GSE307528 通过捕获键工程克服T细胞对肿瘤自身抗原的耐受性
• GSE294096 整合扰动测序和计算建模鉴定 KAT6A-Menin-DOT1L 协同作用及相关基因程序为急性髓系白血病的治疗靶点 [RNA-Seq]
• GSE277561 INHBA激活胃癌细胞系MKN45中的PI3K/AKT通路
• GSE169383 TGFβ1 和 BMP2 处理的小鼠关节软骨细胞转录组的下一代测序 [RNA-seq]
• GSE325617 MAF 将代谢状态转化为骨髓瘤中的超级增强子结构和依赖性 [RPMI8226 p300 ChIP-seq]
• GSE325615 MAF 将代谢状态转化为骨髓瘤中的超级增强子结构和依赖性 [shscr ChIP-Seq]
• GSE325614 MAF 将代谢状态转化为骨髓瘤中的超级增强子结构和依赖性 [RPMI8226 ChIP-Seq]
• GSE325612 MAF 将代谢状态转化为骨髓瘤中的超级增强子结构和依赖性 [ChIP-Seq]
• GSE325936 全基因组组合基因融合产生用于高级微生物性状发育的新基因
• GSE325832 RNA-seq 分析来自对照组 (Cre) 和 Terf2 敲除 (KO) 小鼠的腓肠肌-跖肌-比目鱼肌 (GPS) 和胫前肌 (TA) 骨骼肌
• GSE313527 血浆细胞外囊泡调节急性心肌梗死后的免疫细胞转录反应
• GSE312237 空间转录组分析揭示了干燥综合征中泪腺上皮细胞驱动的自身免疫机制
• GSE306887 FABP4 通过扰乱脂质代谢和诱导滋养层细胞线粒体氧化应激促进先兆子痫的发生
• GSE304941 野生型小鼠和NEU4突变体小鼠P7期耳蜗的RNA测序分析
• GSE303106 长期 KRAS-MAPK 抑制诱导干扰素介导的上皮间质转化并揭示治疗机会 [cut and run-ChipSeq]
• GSE303105 长期 KRAS-MAPK 抑制诱导干扰素介导的上皮间质转化，并揭示治疗机会 [scRNAseq-RMC-6236]
• GSE303104 长期 KRAS-MAPK 抑制诱导干扰素介导的上皮间质转化，并揭示治疗机会 [scRNAseq-Ulixertinib]
• GSE303051 长期 KRAS-MAPK 抑制诱导干扰素介导的上皮间质转化，揭示治疗机会。
• GSE302981 长期抑制KRAS-MAPK可诱导干扰素介导的上皮间质转化，并揭示治疗机会
• GSE298050 复制体与 Pol II 之间的冲突解决 [RNA-seq]
• GSE293644 染色体臂获得和丢失的蛋白质组耐受性存在差异
• GSE281011 粪肠球菌诱导的旁观者效应驱动组蛋白乙酰化，进而通过TGF-β信号通路导致上皮-间质转化
• GSE263352 树突状细胞通过嵌合突触加速 CAR T 细胞在受辐射肿瘤中的增殖 [RNA-seq]
• GSE324976 精氨酸代谢支持嘧啶从头合成，从而阻断DNA损伤并维持EB病毒潜伏状态
• GSE314803 显性恶性克隆利用谱系限制性表观基因组程序驱动室管膜瘤发展 [10X Multiome]
• GSE314057 全基因组关联分析发现 Shroom3 与心肌细胞倍性有关，并导致超多倍体和心室扩张 [bulkRNA-Seq]
• GSE307551 全基因组关联分析揭示心肌细胞倍性与 Shroom3 基因相关，该基因与超多倍体和心室扩张有关
• GSE294098 整合扰动测序和计算建模鉴定 KAT6A-Menin-DOT1L 协同作用及相关基因程序为急性髓系白血病的治疗靶点 [扰动测序]
• GSE278367 与转铁蛋白受体 1 结合的双环肽偶联可增强 ASO 和 siRNA 在骨骼肌和心肌中的效力
• GSE232734 滑膜 Th17 转分化为 exTh17 可维持慢性 IL-17 非依赖性炎症性关节炎 [Visium]
• GSE188327：TGFβ1和BMP2处理的小鼠关节软骨细胞转录组的下一代测序
• GSE188326 TGFβ1 和 BMP2 处理的小鼠关节软骨细胞转录组的下一代测序 [MRE-seq]
• GSE169380 TGFβ1 和 BMP2 处理的小鼠关节软骨细胞的 ATAC 测序
• GSE325727 葡聚糖包覆的氧化铁纳米颗粒会损害斑马鱼幼体的心脏功能
• GSE325611 RNA-seq 分析 HD11 细胞对新城疫病毒感染的宿主反应
• GSE312715 骨髓来源巨噬细胞在Ptpn6或Rraga基因缺失后对CSF1R刺激或饥饿的反应
• GSE312503 利用单细胞RNA测序表征海马中Ptpn6 (SHP-1) cKO的细胞反应
• GSE310324 肥胖会增强中风的免疫反应
• GSE309545 炎症信号通路对人和小鼠帕金森病相关激酶LRRK2的染色质可及性和基因表达的影响存在差异
• GSE309355 炎症信号对人类和小鼠帕金森病相关激酶 LRRK2 的染色质可及性和基因表达产生不同的影响 [snRNA-Seq 人类]
• GSE309354 炎症信号对人类和小鼠 PD 相关激酶 LRRK2 的染色质可及性和基因表达产生不同的影响 [多组学]
• GSE309352 炎症信号通路对人和小鼠帕金森病相关激酶LRRK2的染色质可及性和基因表达产生不同的影响
• GSE293052 母体微生物组来源的丙酸：通过组蛋白乳化介导的cGMP-PKG激活，成为子代髓鞘形成的关键调节因子
• GSE293010 生育状况对未来健康风险表观遗传指标的影响
• GSE284562 运输应激诱导免疫失调并加剧小鼠结核分枝杆菌感染
• GSE290393 从内皮特异性 RiboTag 小鼠中纯化的心脏内皮细胞核糖体相关 RNA