详细内容（前10条）

1. ⭐ GSE302528 睡眠剥夺引起的HPA-肠道微生物轴失调：泪腺稳态的药理学和微生物学挽救

• ✍️ 作者：未知作者
• 🏷️ 关键词：regex:micro(b|be|bial|organism)、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Shenzhen Huang ; Zhijie LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSleep deprivation (SD) disrupts systemic homeostasis, yet its impact on lacrimal gland integrity through neuroendocrine–microbial pathways remains unclear. Using a male mice SD model, we show that chronic SD activates the hypothalamic-pituitary-adrenal (HPA) axis, elevates corticosterone, alters gut microbiota, and depletes short-chain fatty acids (SCFAs). These alterations coincide with lacrimal gland atrophy, reduced tear secretion, and increased CD4⁺/CD8⁺ T cell infiltration, accompanied by activation of IL-17-associated inflammatory pathways. Pharmacological inhibition of glucocorticoid synthesis with metyrapone preserves lacrimal gland structure and function while attenuating immune activation. Microbiome-directed interventions, including SCFA supplementation and fecal microbiota transplantation, rebalance gut communities, suppress proinflammatory T cell responses, and maintain lacrimal gland homeostasis. Transcriptomic and immunohistochemical analyses further reveal that all three interventions converge on downregulation of IL-17 signaling. Collectively, these findings establish an HPA-gut microbiome-lacrimal gland axis links neuroendocrine stress to microbial dysbiosis and ocular inflammation, and they suggest therapeutic strategies for SD-associated lacrimal gland dysfunction.
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2. ⭐ GSE294918 IFNγ 诱导的人类巨噬细胞记忆不是由表观遗传变化维持的，而是由细胞因子本身的持久性维持的 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、RNA-seq、epigenetic
• 📝 描述：Contributors : Vyas Koduvayur ; Noa Harriott ; Quen Cheng ; Aleksandr Gorin ; Alexander HoffmannSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMacrophages, as key sentinel cells of the innate immune system, can retain memory of prior stimulus exposure. Interferon gamma (IFNγ) plays a central role in maintaining trained immunity in vivo and can induce potent memory in macrophages. Such memory is associated with the formation of de novo enhancers that alter gene expression responses to subsequent stimuli. However, how such enhancers are maintained after cytokine exposure remains unclear. We report that durable IFNγ-induced enhancers can last for days after cytokine washout, yet the underlying persistence mechanism is not cell-intrinsic. IFNγ-treated macrophages continue to exhibit JAK/STAT signaling days after cytokine removal. Blocking IFNγ signaling with a JAK inhibitor or anti-IFNγ neutralizing antibodies after cytokine removal is sufficient to reverse IFNγ-induced enhancers and erase the potentiated state of the treated macrophages. Our findings suggest that epigenetic changes in macrophages do not inherently encode innate immune memory or a “potentiated” macrophage state, but that rather epigenetic changes are themselves dependent on ongoing cytokine signaling. These findings suggest new possibilities for pharmacologic interventions to reverse aberrantly trained immune states associated with pathology.
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3. ⭐ GSE294915 IFNγ 诱导的人类巨噬细胞记忆不是由表观遗传变化维持的，而是由细胞因子本身的持久性维持的 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、ATAC-seq、epigenetic
• 📝 描述：Contributors : Vyas Koduvayur ; Noa Harriott ; Quen Cheng ; Aleksandr Gorin ; Alexander HoffmannSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMacrophages, as key sentinel cells of the innate immune system, can retain memory of prior stimulus exposure. Interferon gamma (IFNγ) plays a central role in maintaining trained immunity in vivo and can induce potent memory in macrophages. Such memory is associated with the formation of de novo enhancers that alter gene expression responses to subsequent stimuli. However, how such enhancers are maintained after cytokine exposure remains unclear. We report that durable IFNγ-induced enhancers can last for days after cytokine washout, yet the underlying persistence mechanism is not cell-intrinsic. IFNγ-treated macrophages continue to exhibit JAK/STAT signaling days after cytokine removal. Blocking IFNγ signaling with a JAK inhibitor or anti-IFNγ neutralizing antibodies after cytokine removal is sufficient to reverse IFNγ-induced enhancers and erase the potentiated state of the treated macrophages. Our findings suggest that epigenetic changes in macrophages do not inherently encode innate immune memory or a “potentiated” macrophage state, but that rather epigenetic changes are themselves dependent on ongoing cytokine signaling. These findings suggest new possibilities for pharmacologic interventions to reverse aberrantly trained immune states associated with pathology.
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4. 利用 RNA 测序技术对 K562 伊马替尼耐药细胞中的 PLAG1 VC 和 KD 进行转录组学分析。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、transcriptomics
• 📝 描述：Contributors : Shashi Kumari ; Dr. Rukmini Govekar ; Dr. Rahul Mojidra ; Dr. Mythreyi NarasimhanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCML-CP Patients showing resistance to Imatinib, due to Bcr-Abl mechanisms of resistance are treated with 2nd and 3rd generation TKIs but some non-responders shown Bcr-Abl independant mechanism of resistance. We hypothesize that this could be due to activation of novel pathway, or activation of downstream molecules of Bcr-Abl pathway. In this study we have performed Transcriptomics and epigenomics analysis of K562 and KU812 CML-BC cell sensitive and resistant to imatinib, ITGB3 showed high transcript levels, and was also hypomethylated in K562/R cells as compared to sensitive counterparts and showed higher protein levels in both K562 and KU812 resistant cell lines. Previous studies in the lab also showed ITGB1 as a differentiator in proteomic analysis and further on-going studies indicate its role in resistance. ITGB1 was however not modulated at transcriptional level. The protein levels of ITGB3 were significantly increased in resistant cells (K562; KU812: while those of ITGB1 were significantly decreased in resistant cells (K562; KU812. With the known switching of integrins, whether higher expression of ITGB3 had a role in modulating the levels of transcriptionally non-regulated ITGB1 was investigated in K562/S cells with ITGB1 knocked down (KD) protein levels of ITGB3 were upregulated as compared to VC. Similarly, knock down of ITGB3 in K562/R resulted in increased level of ITGB1 protein. These striking results confirmed switching of integrins and explained reduced levels of ITGB1 despite no alteration at genomic or transcriptomic level in resistant cells.
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5. GSE295782 脉络丛巨噬细胞的多样性和免疫动力学受不同发育起源的影响 [scRNA-seq Tgfbr2_cKO]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Khai Nguyen ; Simone Brioschi ; Marco ColonnaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe choroid plexus (ChP) forms a critical interface between the central nervous system and systemic circulation. Despite its importance, the identity and dynamics of resident macrophages remain incompletely understood. Using single-cell RNA sequencing, flow cytometry, lineage tracing, and imaging, we identified three biologically distinct macrophage populations in the homeostatic ChP, defined by expression of CD163, MHCII, or CD9. These subsets arise from different combinations of primitive and definitive hematopoietic waves, occupy distinct anatomical niches, and differentially rely on CSF1 and IL34 for survival. TGFβ signaling is required to maintain their phenotype, and deletion of Tgfbr2 in these cells induces phenotypic reprogramming and disrupts the ChP epithelial barrier. During neuroinflammation, ChP macrophages initiate IFN-I responses and secrete chemokines for CD8 T cell recruitment, while microglia mainly express chemokines for B cells. Finally, we identify phenotypically conserved macrophage subsets in the human ChP, suggesting evolutionary preservation of their phenotypic and functional features.
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6. GSE294916 IFNγ 诱导的人类巨噬细胞记忆不是由表观遗传变化维持，而是由细胞因子本身的持久性维持 [CUT&Tag]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、epigenetic
• 📝 描述：Contributors : Vyas Koduvayur ; Noa Harriott ; Quen Cheng ; Aleksandr Gorin ; Alexander HoffmannSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMacrophages, as key sentinel cells of the innate immune system, can retain memory of prior stimulus exposure. Interferon gamma (IFNγ) plays a central role in maintaining trained immunity in vivo and can induce potent memory in macrophages. Such memory is associated with the formation of de novo enhancers that alter gene expression responses to subsequent stimuli. However, how such enhancers are maintained after cytokine exposure remains unclear. We report that durable IFNγ-induced enhancers can last for days after cytokine washout, yet the underlying persistence mechanism is not cell-intrinsic. IFNγ-treated macrophages continue to exhibit JAK/STAT signaling days after cytokine removal. Blocking IFNγ signaling with a JAK inhibitor or anti-IFNγ neutralizing antibodies after cytokine removal is sufficient to reverse IFNγ-induced enhancers and erase the potentiated state of the treated macrophages. Our findings suggest that epigenetic changes in macrophages do not inherently encode innate immune memory or a “potentiated” macrophage state, but that rather epigenetic changes are themselves dependent on ongoing cytokine signaling. These findings suggest new possibilities for pharmacologic interventions to reverse aberrantly trained immune states associated with pathology.
• 🔗 查看原文

7. GSE271592 脉络丛巨噬细胞的多样性和免疫动力学受不同发育起源的影响 [scRNA-seq 稳态]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Siling Du ; Alina Ulezko Antonova ; Marco Colonna ; Simone BrioschiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe choroid plexus, responsible for cerebrospinal fluid production, is vital for brain functions. This organ serves as a crucial interface between the central nervous system and systemic circulation and thus faces constant immunological challenges. While resident macrophages within the choroid plexus provide immunosurveillance, their biological characteristics and immune dynamics remain poorly understood. In this study, we extensively examined the phenotype of choroid plexus macrophages using high-throughput single-cell RNA sequencing, flow cytometry, and imaging techniques. Our data unveiled three distinct macrophage populations within the homeostatic choroid plexus expressing either CD163, MHCII, or CD9. These macrophage subsets exhibited differential input from primitive and definitive hematopoietic waves, different spatial location and relied on distinct factors for survival. Upon neuroinflammation, these cells orchestrated IFN responses producing chemokines for effector CD8 T cells, while microglia predominantly expressed chemokines for B cells. Finally, we present evidence of phenotypically conserved macrophage subsets in the human choroid plexus.
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8. GSE271590 脉络丛巨噬细胞的多样性和免疫动力学受不同发育起源的影响 [bulk RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、RNA-seq
• 📝 描述：Contributors : Siling Du ; Alina Ulezko Antonova ; Marco Colonna ; Simone BrioschiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe choroid plexus, responsible for cerebrospinal fluid production, is vital for brain functions. This organ serves as a crucial interface between the central nervous system and systemic circulation and thus faces constant immunological challenges. While resident macrophages within the choroid plexus provide immunosurveillance, their biological characteristics and immune dynamics remain poorly understood. In this study, we extensively examined the phenotype of choroid plexus macrophages using high-throughput single-cell RNA sequencing, flow cytometry, and imaging techniques. Our data unveiled three distinct macrophage populations within the homeostatic choroid plexus expressing either CD163, MHCII, or CD9. These macrophage subsets exhibited differential input from primitive and definitive hematopoietic waves, different spatial location and relied on distinct factors for survival. Upon neuroinflammation, these cells orchestrated IFN responses producing chemokines for effector CD8 T cells, while microglia predominantly expressed chemokines for B cells. Finally, we present evidence of phenotypically conserved macrophage subsets in the human choroid plexus.
• 🔗 查看原文

9. GSE271316 脉络丛巨噬细胞的多样性和免疫动力学受不同发育起源的影响 [scRNA-seq LCMV]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Siling Du ; Alina Ulezko Antonova ; Marco Colonna ; Simone BrioschiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe choroid plexus, responsible for cerebrospinal fluid production, is vital for brain functions. This organ serves as a crucial interface between the central nervous system and systemic circulation and thus faces constant immunological challenges. While resident macrophages within the choroid plexus provide immunosurveillance, their biological characteristics and immune dynamics remain poorly understood. In this study, we extensively examined the phenotype of choroid plexus macrophages using high-throughput single-cell RNA sequencing, flow cytometry, and imaging techniques. Our data unveiled three distinct macrophage populations within the homeostatic choroid plexus expressing either CD163, MHCII, or CD9. These macrophage subsets exhibited differential input from primitive and definitive hematopoietic waves, different spatial location and relied on distinct factors for survival. Upon neuroinflammation, these cells orchestrated IFN responses producing chemokines for effector CD8 T cells, while microglia predominantly expressed chemokines for B cells. Finally, we present evidence of phenotypically conserved macrophage subsets in the human choroid plexus.
• 🔗 查看原文

10. GSE180559 KDM2A 和 KDM2B 协同保护一部分 CpG 岛免受 DNA 甲基化 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、methylation
• 📝 描述：Contributors : Yuan Liu ; Ying Liu ; Yunji Zhu ; Yali Xie ; Hu NieSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusIn the mammalian genome, most CpGs are methylated, however, regions of the genome known as CpG islands (CGIs) are largely unmethylated, which are closely associated with modulating gene expression. The KDM2 proteins (KDM2A and KDM2B) are recruited via their ZF-CxxC domains to CGIs and mediate demethylation of H3K36me2 at these regions. However, the mechanism whether and how KDM2 proteins protect CGIs from DNA methylation remains unknown. Here, we report that depletion of each or both KDM2 proteins, or mutation JmjC domains of KDM2 proteins, leads to a modest increase of DNA methylation at CGIs, but a significant increase at CGI shores. Depletion of both KDM2 proteins shows most obvious increase of DNA methylation, indicating that KDM2A and KDM2B cooperatively regulate DNA methylation at CGIs. We further show that DNA methylation in the absence of KDM2 proteins show more obvious increase at a subset of CpG Islands such as non-marked and H3K27me3-only CGIs than other CpG Islands like bivalent and H3K4me3-only CGIs. Taken together, our finding reveals the role for KDM2 proteins in regulating DNA methylation at CGIs, and uncovers the mechanism by which complex chromatin state including histone modifications and CGI binding proteins synergistically protect CGIs from DNA methylation.
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1. 一种新工具正在揭示癌症内部的隐形网络

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Spanish researchers have created a powerful new open-source tool that helps uncover the hidden genetic networks driving cancer. Called RNACOREX, the software can analyze thousands of molecular interactions at once, revealing how genes communicate inside tumors and how those signals relate to patient survival. Tested across 13 different cancer types using international data, the tool matches the predictive power of advanced AI systems—while offering something rare in modern analytics: clear, interpretable explanations that help scientists understand why tumors behave the way they do.
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• GSE290558 绘制多种癌细胞系的断裂组图谱
• GSE313748 吉西他滨联合白蛋白紫杉醇，加或不加维生素D受体激动剂帕立骨化醇治疗转移性胰腺癌：一项随机、多臂、I期试验
• GSE300321 3D分形地形可减轻炎症并赋予肾小球足细胞韧性
• GSE307218 戈梅辛肽的细胞毒性是由糖鞘脂途径和脂质-胆固醇相互作用介导的
• GSE305670 对嵌入不同基质中的离体微肿瘤模型进行 RNA 测序，这些模型由对照细胞或 Arpc4 敲除细胞构建而成。
• GSE284423 对包含对照组或 Arpc4 敲除 (KO) PDAC 细胞的离体微肿瘤模型进行 RNA-seq 分析
• GSE277650：鉴定JAK/STAT/miR155HG正反馈环路在调控NK细胞增殖和效应功能中的作用
• GSE277631 NFκB1缺陷与Flt3髓系白血病相关，并通过RelA:p52和SOD2表达失调增强细胞自我更新能力
• GSE314298 NKG2A+ NK 细胞对 Epstein-Barr 病毒感染的 B 细胞的细胞毒性是通过 NKG2D 和 NKp30 激活受体介导的
• GSE313825 母系缺失 UBE3A 基因的猪的批量 RNA 测序 [Pig_CSC_bulkRNAseq]
• GSE313824 母系缺失 UBE3A 基因的猪的批量 RNA 测序 [Pig_Cortex_bulkRNAseq]
• GSE312561 肽酰-tRNA水解酶2是围产期心肌病伴母体心力衰竭的重要负调控因子（人和小鼠RNA测序）
• GSE311823 成年绵羊尾部胚胎位置身份程序的维持：来自 HOXB13 空间 RNA 表达梯度的证据
• GSE311725 GWAS 研究结果的功能表征凸显了 REST 在内皮可塑性和动脉粥样硬化中的作用 [RNA-seq]
• GSE306207 RNA-seq 分析了单独使用 I-BET726 以及 I-BET726 和奥沙利铂序贯联合处理的 A375 细胞。
• GSE295783 脉络丛巨噬细胞的多样性和免疫动力学受不同发育起源的影响 [CD45_TotalSeq_ICV_injection]
• GSE285259 SlMBD5 通过表观遗传抑制番茄赤霉素分解代谢基因 SlGA2ox4 促进种子萌发 [RNA-Seq]
• GSE285255 SlMBD5 通过表观遗传抑制番茄赤霉素分解代谢基因 SlGA2ox4 促进种子萌发 [ChIP-Seq]
• GSE271630 脉络丛巨噬细胞的多样性和免疫动力学受不同发育起源的影响
• GSE180570 非人灵长类动物植入前胚胎基因组印记的研究 [RNA-seq]
• GSE180560 KDM2A 和 KDM2B 协同保护一部分 CpG 岛免受 DNA 甲基化影响
• GSE180558 KDM2A 和 KDM2B 协同保护一部分 CpG 岛免受 DNA 甲基化 [RRBS]