详细内容（前10条）

1. ⭐ GSE228937 细菌来源的吲哚-3-乳酸通过调节信号传导和代谢途径影响肠道炎症期间上皮-巨噬细胞的相互作用 [EC]

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、macrophage、inflammation、regex:bacter(ia|ial|ium)、metabolic、regex:intestin(e|al)
• 📝 描述：Contributors : Kaiyuan Yu ; Qianqian Li ; Xuan SunSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo investigate the the effect of EC-TMU supernatant on on intestinal epithelial cells, SW480 cells were stimulated with EC-TMU supernatant.
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2. ⭐ GSE228409 细菌来源的吲哚-3-乳酸通过调节信号传导和代谢途径影响肠道炎症期间上皮细胞-巨噬细胞的相互作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、macrophage、inflammation、regex:bacter(ia|ial|ium)、metabolic、regex:intestin(e|al)
• 📝 描述：Contributor : Yu KaiyuanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo investigate the underlying molecular mechanism of ILA effect on CCL2/7 expression, we examined the gene expression profiles of SW480 cells treated by LPS and ILA using RNA sequencing
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3. ⭐ GSE181141 通过单核甲基化测序研究大脑衰老的表观遗传特征 [FC-9mo-m]

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、sequencing、epigenetic、methylation
• 📝 描述：Contributors : Wei Tian ; Anna Bartlett ; Jordan Altshul ; Rosa Gomez Castanon ; Joseph R Nery ; Jacinta D Lucero ; Julia K Osteen ; Huaming Chen ; M M Behrens ; Joseph R EckerSeries Type : Methylation profiling by high throughput sequencingOrganism : Mus musculusIllustrating aging effects on the epigenomic features of brain is critical to understand brain functional decline and neurodegeneration. Single nucleus methylation sequencing was applied to brain regions of both male and female mouse at the age of 2, 9 and 18 months. We use these data to identify the epigenomic changes with aging in mouse brains.
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4. ⭐ GSE311976 Piezo1敲低激活PI3K/AKT并增强SPP1以驱动M2巨噬细胞极化并减少心脏炎症

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、inflammation、cardiac
• 📝 描述：Contributors : Yunhan Zhang ; Ying Zhang ; Jiaoyan Song ; Ziwen Zhao ; Wenhao Ju ; Hao Zhang ; Shuang LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe have successfully established a mouse model with myeloid cell-specific knockdown of Piezo1. The intraperitoneal injection of lipopolysaccharide (LPS) resulted in a significant increase in cardiac macrophage infiltration, as well as an increase in the expression of inflammatory factors and the inflammatory response. However, myeloid cell-specific knockdown of Piezo1 impaired this response, leading to an increase in macrophage polarization towards the M2 type and the decreased inflammatory response. As a result, myocardial injury caused by sepsis was attenuated. We have also demonstrated that the PI3K/AKT pathway is significantly activated after Piezo1 knockdown, resulting in reduced myocardial dysfunction.
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5. ⭐ GSE249704 野生型与APOE-KO小鼠肿瘤引流淋巴结驻留CD11c+细胞的转录谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymph、regex:lymph(o|atic)?
• 📝 描述：Contributor : Benjamin N OstendorfSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHere, we analyze transcriptional profiles of CD11c+ enriched cells from the lymph nodes draining E0771-cOC tumors in either wildtype or APOE-KO mice.
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6. ⭐ GSE315177 M2型肿瘤相关巨噬细胞衍生的CCL-18促进胶质瘤细胞增殖，但不介导胶质瘤放射抗性

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、macrophage、glioma
• 📝 描述：Contributor : Xiuping ZhouSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMost of glioma patients still experience relapse after radiotherapy owing to the formation of tumor immunosuppressive microenvironment. However, the comprehensive landscape of immune cell infiltration and the molecular mechanisms mediating glioma recurrence within the tumor microenvironment remains unclear. Bulk RNA-seq analysis revealed the significant changes in the immune system including increased total tumor-associated macrophages (TAMs) and elevated immune-suppressive M2 type TAMs in recurrent gliomas accepting radiotherapy. Meanwhile, C-C motif chemokine 18 (CCL-18) was the highest elevated molecule after radiotherapy. Consistently, the above results were confirmed in tissue microarray containing 23 pairs gliomas. Notably, low-dose fractionated radiation promoted TAM polarization into M2-TAMs accompanying CCL-18 secretion in vitro. Unexpectedly, CCL-18 promoted non-irradiated glioma cell proliferation, but did not mediate glioma radioresistance both in vivo and in vitro. Our findings indicate that the tumor microenvironment of recurrent gliomas accepting radiotherapy changes obviously, which exhibited the elevation of total TAM infiltration, M2-TAM polarization and CCL-18 expression. Remarkably, elevated CCL-18 promotes glioma cell proliferation, but does not mediate glioma radioresistance.
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7. ⭐ GSE315113 帕金森病环境毒素暴露的人类神经元模型中的染色质可及性和转录组 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、ATAC-seq、transcriptome
• 📝 描述：Contributors : Jingchao Hong ; Juanjuan HuangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensParkinson’s disease is a complex neurodegenerative disorder where environmental factors play a predominant role in sporadic cases. While environmental toxins are implicated in PD pathogenesis via epigenetic pathways, the specific alterations in chromatin accessibility induced by these toxins remain poorly characterized. To address this gap, we established in vitro models using the human neuroblastoma cell line SH SY5Y, a well established neuronal model, exposed to the PD associated environmental toxins rotenone and MPP+. We performed RNA sequencing to profile the transcriptome and Assay for Transposase-Accessible Chromatin sequencing to map genome-wide chromatin accessibility landscapes under toxin exposed conditions. This integrated dataset provides a comprehensive resource detailing both gene expression and chromatin accessibility dynamics in response to PD relevant environmental neurotoxins and will facilitate investigations into transcriptional regulation, biomarker discovery, and the epigenetic basis of environmentally linked sporadic PD.
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8. ⭐ GSE315111 帕金森病环境毒素暴露的人类神经元模型中的染色质可及性和转录组 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、RNA-seq、transcriptome
• 📝 描述：Contributors : Jingchao Hong ; Juanjuan HuangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensParkinson’s disease is a complex neurodegenerative disorder where environmental factors play a predominant role in sporadic cases. While environmental toxins are implicated in PD pathogenesis via epigenetic pathways, the specific alterations in chromatin accessibility induced by these toxins remain poorly characterized. To address this gap, we established in vitro models using the human neuroblastoma cell line SH SY5Y, a well established neuronal model, exposed to the PD associated environmental toxins rotenone and MPP+. We performed RNA sequencing to profile the transcriptome and Assay for Transposase-Accessible Chromatin sequencing to map genome-wide chromatin accessibility landscapes under toxin exposed conditions. This integrated dataset provides a comprehensive resource detailing both gene expression and chromatin accessibility dynamics in response to PD relevant environmental neurotoxins and will facilitate investigations into transcriptional regulation, biomarker discovery, and the epigenetic basis of environmentally linked sporadic PD.
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9. GSE285990 化疗通过促进肝转移中 LEPR+ Kupffer 细胞分化来触发免疫逃逸 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、RNA-seq
• 📝 描述：Contributors : Jun Qin ; Xuege Wang ; Qiang Pan ; Yaqi LiSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiens ; Mus musculusConventional chemotherapy achieves clinical efficacy beyond its cytotoxic effects by reactivating immune surveillance. However, whether chemotherapy promotes immune evasion by remodeling the tumor microenvironment (TME) remains largely unexplored. Here, we integrate cross-species single-cell and spatial transcriptomics to explore how chemotherapy reprograms immune cell dynamics and plasticity. Our findings reveal a central role for chemotherapy-educated, liver-resident Kupffer cells (KCs) in promoting immune tolerance and chemoresistance in liver metastases. These reprogrammed KCs, characterized by leptin receptor expression (LEPR+), originate from preexisting KCs and are differentiated via STING-ID1 signaling triggered by cGAMP released from chemotherapy-treated tumor cells. Unlike conventional KCs, LEPR+ KCs infiltrate tumors and engage in MerTK-dependent efferocytosis, which diminishes chemotherapy-induced immunogenic cell death (ICD) and suppresses antitumor immunity. Notably, targeting LEPR+ KCs enhances tumor immunogenicity and strengthens antitumor T-cell responses. Our study demonstrates that therapy-induced KC differentiation fosters immune evasion and suggests combining efferocytosis inhibitors with immunotherapy to overcome chemoresistance.
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10. GSE285989 化疗通过促进肝转移中 LEPR+ Kupffer 细胞分化来触发免疫逃逸 [CUT&Tag, ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、ATAC-seq
• 📝 描述：Contributors : Jun Qin ; Xuege Wang ; Qiang Pan ; Yaqi LiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusConventional chemotherapy achieves clinical efficacy beyond its cytotoxic effects by reactivating immune surveillance. However, whether chemotherapy promotes immune evasion by remodeling the tumor microenvironment (TME) remains largely unexplored. Here, we integrate cross-species single-cell and spatial transcriptomics to explore how chemotherapy reprograms immune cell dynamics and plasticity. Our findings reveal a central role for chemotherapy-educated, liver-resident Kupffer cells (KCs) in promoting immune tolerance and chemoresistance in liver metastases. These reprogrammed KCs, characterized by leptin receptor expression (LEPR+), originate from preexisting KCs and are differentiated via STING-ID1 signaling triggered by cGAMP released from chemotherapy-treated tumor cells. Unlike conventional KCs, LEPR+ KCs infiltrate tumors and engage in MerTK-dependent efferocytosis, which diminishes chemotherapy-induced immunogenic cell death (ICD) and suppresses antitumor immunity. Notably, targeting LEPR+ KCs enhances tumor immunogenicity and strengthens antitumor T-cell responses. Our study demonstrates that therapy-induced KC differentiation fosters immune evasion and suggests combining efferocytosis inhibitors with immunotherapy to overcome chemoresistance.
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1. RNA测序揭示了妊娠期糖尿病如何影响后代的新线索

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：RNA sequencing reveals that gestational diabetes disrupts placental RNA splicing, altering metabolic gene regulation and implicating SRSF10 as a key molecular driver of pregnancy-related complications…
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2. 麻省理工学院的科学家们找到了一种方法，可以帮助我们随着年龄的增长恢复免疫系统的活力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：As the immune system weakens with age, scientists have found a way to restore some of its lost strength. By delivering mRNA to the liver, they created a temporary source of immune-boosting signals that normally come from the thymus. Older mice treated this way produced more effective T cells and responded far better to vaccines and cancer treatments. The strategy could one day help extend healthy years of life.
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• GSE310954 通过颗粒介导的 STING/IL-6/PD-L1 轴调节重塑抑制性黑色素瘤微环境可改善肿瘤免疫和存活率
• GSE292026 2p增益驱动的REL过表达赋予慢性淋巴细胞白血病对BTK抑制剂的耐药性
• GSE315010 RAS(ON)抑制剂双药阻断致癌RAS信号通路，使免疫难治性KRASG12C突变型非小细胞肺癌对免疫检查点阻断疗法产生免疫反应
• GSE288563 锌缺乏期间 KAT7 依赖性组蛋白 H3K14 乙酰化受损的病理生理意义 [RNA-seq]
• GSE277238 ICAM1 mRNA通过dsRNA-ILF2/ILF3通路抑制肺癌中的翻译，其功能独立于蛋白质编码。
• GSE315059 细胞因子受体Fn14是神经元活动的分子刹车，介导体内昼夜节律功能。
• GSE315057 单细胞转录组学揭示乳腺癌肉瘤的组织结构
• GSE315048 RNA测序：16D前列腺癌细胞系中OGDHL基因敲除和恢复的RNA测序
• GSE315014 DOT1L介导的CDK9甲基化对DNA双链断裂修复至关重要[RNA-seq]
• GSE300387 鼻内混合疗法（含基于dNS1的病毒和STFKB疫苗）可诱导全身和黏膜体液免疫。
• GSE299617 体外全能细胞模型的 3D 基因组景观分析 [RNA-seq]
• GSE299616 体外全能细胞模型的 3D 基因组景观 [Hi-C]
• GSE299615 体外全能细胞模型的 3D 基因组景观分析 [ATAC-Seq]
• GSE291085 激酶抑制剂处理的癌细胞系转录组分析揭示了药物反应机制的见解
• GSE286357 人类神经发生和神经元成熟过程中时间动态的转录调控 [scRNA-seq]
• GSE285570 人类神经发生和神经元成熟过程中时间动态的转录调控 [RNA-seq]
• GSE285531 人类神经发生和神经元成熟过程中时间动态的转录调控 [ATAC-seq]
• GSE218861 惰性原发性皮肤B细胞淋巴瘤类似于持续性抗原反应，但无去分化迹象
• GSE312951 急性髓系白血病促进3型固有淋巴细胞的发育和功能
• GSE303423 LXR激动剂在初始CD8+ T细胞中引发效应前状态[ATAC-seq]
• GSE249709 LXR激动剂增强交叉呈递后的T细胞活化。
• GSE249707 LXR激动剂促进树突状细胞交叉启动后T细胞效应染色质景观的形成。
• GSE315139 小胶质细胞 CLEC7A 抑制阿尔茨海默病小鼠模型中的β-淀粉样蛋白斑块病理
• GSE307132 Dox诱导的Cas13表达在稳定细胞系中对小鼠转录组和共培养的人类PSC的影响
• GSE288565 锌缺乏期间 KAT7 依赖性组蛋白 H3K14 乙酰化受损的病理生理意义 [ChIP-seq_Hela]
• GSE288564 锌缺乏期间 KAT7 依赖性组蛋白 H3K14 乙酰化受损的病理生理意义 [ChIP-seq_小鼠]
• GSE280372 ETC-501 是一种可穿透血脑屏障的 MNK 激酶抑制剂，它能增强替莫唑胺 (TMZ) 诱导的细胞衰老，并使胶质母细胞瘤细胞对衰老细胞清除疗法更加敏感。
• GSE315038 真核翻译起始因子3B通过与RAB14相互作用调控胰腺癌细胞增殖
• GSE313238 利用脊索细胞再生潜能的生物活性水凝胶可作为髓核修复的指导性细胞载体 [scRNA-seq dog]
• GSE313236 一种利用脊索细胞再生潜能的生物活性水凝胶可作为髓核修复的指导性细胞载体 [scRNA-seq human]
• GSE303905 KNSTRN基因敲低会损害自噬通量，并通过ROS介导的溶酶体功能障碍抑制膀胱癌的进展。
• GSE303320染色质可及性动态变化提示维生素D3在体内具有免疫调节作用
• GSE299942 CBX7，一种多梳抑制因子，在淋巴细胞中发挥甲基化依赖性转录激活因子和胞质信号调节因子的作用。
• GSE299619 体外全能细胞模型的 3D 基因组景观分析 [CUT&Tag]
• GSE299582：与恰加斯病易感性和慢性恰加斯心肌病严重程度相关的循环microRNA转录组分析
• GSE289089 睡眠剥夺小鼠小肠隐窝细胞亚群及基因表达
• GSE285532 人类神经发生和神经元成熟过程中时间动态的转录调控 [CUT&Tag]
• GSE263483 基于胎盘转录组学的妊娠期糖尿病宫内高血糖对子代发育的影响
• GSE189685 外泌体Nm23-H1水平升高通过改变下游信号级联抑制乳腺癌细胞来源外泌体的促迁移潜能