详细内容（前10条）

1. ⭐ GSE329470 黑色素瘤干细胞驱动巨噬细胞重编程为混合表型，调节黑色素瘤干性并损害NK细胞介导的免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、macrophage、NK cell
• 📝 描述：Contributors : Michela Francesconi ; Tiziana Triulzi ; Michele SommarivaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMelanoma stem cells may contribute to tumor progression not only through intrinsic plasticity, but also by shaping the immune microenvironment. However, their interaction with the monocyte-macrophage compartment remains poorly understood. Melanosphere cultures derived from A375 and WM115 melanoma cell line were used as an in vitro model enriched for stemness-associated features. THP-1 monocytes were differentiated under a standardized low-dose PMA protocol and exposed to stem cell-conditioned media (SC-CM). Monocyte migration, macrophage transcriptomic and secretory profiling, effect of macrophage CM on NK cytotoxicity, melanoma stem cell phenotype and exploratory clinical relevance in the TCGA melanoma cohort were assessed. Both melanosphere models were enriched for stemness-associated programs and secreted high levels of CCL2. SC-CM promoted THP-1 migration, which was reduced by CCR2 inhibition. RNA-seq showed that SC-CM induced a shared but non-canonical macrophage phenotype enriched for inflammatory, interferon-related, pro-angiogenic, and immune-regulatory programs. Conditioned media from SC-educated macrophages impaired NK-cell cytotoxicity through heat-labile soluble mediators and induced cell line-dependent changes in melanoma stemness-associated transcriptional regulators. In TCGA, a high A375-educated macrophage score was associated with shorter overall survival, whereas the WM115-derived score showed a similar but non-significant trend. Melanoma stem cells actively shape the monocyte-macrophage compartment by promoting monocyte recruitment and inducing an inflammatory and immunomodulatory macrophage program with downstream effects on NK-cell function and melanoma cell-state regulation. These findings support a bidirectional melanoma stem cell-macrophage axis that warrants validation in more physiological systems.
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2. GSE327430 系统研究揭示了 Epstein-Barr 病毒对人类基因组的广泛转录调控 [ChIP-Seq ZTA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Matthew Weirauch ; Leah KottyanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV’s functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.
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3. GSE327427 系统研究揭示了 Epstein-Barr 病毒对人类基因组的广泛转录调控 [ChIP-seq YY1]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Matthew Weirauch ; Leah KottyanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV’s functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.
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4. GSE327426 系统研究揭示了 Epstein-Barr 病毒对人类基因组的广泛转录调控 [ChIP-Seq EBNA2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Matthew Weirauch ; Leah KottyanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV’s functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.
• 🔗 查看原文

5. GSE307072 Rbm5 通过与 Myc 网络协同调节白血病转录程序来维持白血病干细胞 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、ChIP-seq
• 📝 描述：Contributors : Fields Shaela ; Qiong Zhang ; Beisi Xu ; Chunliang LiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAcute myeloid leukemia (AML) represents a type of malignant hematological disease that is caused by the dysregulated developmental program of leukemia stem cells (LSCs). Compared to other hematological malignancies, AML often predicts poor prognosis and unfavorable treatment outcomes in the clinic, urging the need for complex mechanism studies. Rbm5 was recently reported as a key regulator in maintaining the survival of human AML cell lines via non-canonical transcriptional activation of Hoxa9. However, its function in LSCs and the broad genome-wide transcriptional targets remain elusive. Here, using genetic mouse models, ex vivo AML culture, and patient-derived xenografts, we report that Rbm5 is required for murine leukemogenesis and maintains self-renewal of LSCs in vivo but is dispensable for normal hematopoiesis. Rbm5 is highly expressed in LSCs, and its deficiency results in specifically defective LSC function, along with the inhibition of self-renewal gene expression and the induction of a myeloid differentiation program. Multi-disciplinary mechanistic investigations targeting gene expression at both the single-cell level and in bulk populations, together with an acute RBM5 degradation system, further identified the direct transcriptional targets of Rbm5 in primary leukemia cells, including stemness genes, such as Hoxa9 and Myc. Moreover, RBM5 not only interacts with MYC but also maintains its protein levels, thereby sustaining the Myc downstream transcriptional network through its proper genome-wide occupancy. Forced expression of Myc sufficiently rescued the Rbm5-depleted defects both in vitro and in vivo. Thus, our study demonstrates that Rbm5 regulates the AML LSC program through non-canonical transcriptional mechanisms, providing a strong rationale for therapeutically targeting Rbm5 in the treatment of myeloid leukemia.
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6. GSE303908 靶向髓系细胞的癌症免疫疗法需要内体模式识别

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Yueyun Pan ; Shengduo Pei ; Heng Liang ; Mikael KarlssonSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmunotherapy is now an established and efficient treatment option for many cancer patients, but unfortunately, a proportion of the patients still experience poor outcomes due to resistance to treatment. Thus, there is a need to both understand key mechanisms of resistance as well as to develop new treatments. Herein, we explore an immunotherapeutic approach that targets tumor associated macrophages (TAMs) as an alternative to direct T cell targeting. We demonstrate that TAMs need to have a functional endosomal pattern recognition machinery for immunotherapy to be efficient. This is true for TAM targeting using both anti-PD-L1 (αPD-L1) or anti-MARCO (αMARCO) antibodies, and we determine that the absence of endosomal Toll-like receptors (TLRs) makes the TAMs unresponsive to treatment while retaining an immunosuppressive phenotype. For αMARCO treatment, we also find that TLR9 activation to express components of the inflammasome is specifically needed to render TAMs responsive to treatment. This key feature of immunotherapy efficacy, with TAMs being sensitized by the tumor microenvironment via endosomal TLRs, could be exploited to improve immunotherapeutic outcomes.
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7. GSE303389 系统研究揭示了 Epstein-Barr 病毒对人类基因组的广泛转录调控 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、genome
• 📝 描述：Contributors : Matthew Weirauch ; Leah KottyanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV’s functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.
• 🔗 查看原文

8. GSE303331 系统研究揭示了 Epstein-Barr 病毒对人类基因组的广泛转录调控 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Matthew Weirauch ; Leah KottyanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV’s functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.
• 🔗 查看原文

9. GSE303329 系统研究揭示了 Epstein-Barr 病毒对人类基因组的广泛转录调控 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq、genome
• 📝 描述：Contributors : Matthew Weirauch ; Leah KottyanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV’s functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.
• 🔗 查看原文

10. GSE301116 RBM5 通过与 MYC 协同调节白血病转录程序，对维持白血病干细胞至关重要 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、scRNA
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute myeloid leukemia (AML) represents a type of malignant hematological disease that is caused by the dysregulated developmental program of leukemia stem cells (LSCs). RBM5 was recently reported as a key regulator in maintaining the survival of human leukemia cells via non-canonical transcriptional activation of HOXA9. However, its function in LSCs and the broad genome-wide transcriptional targets remain elusive. Here, we report that RBM5 is required for murine leukemogenesis and maintains self-renewal of LSCs in vivo, but dispensable for normal hematopoiesis. RBM5 is highly expressed in LSCs, and its deficiency results in specifically defective LSC function with the inhibition of self-renewal gene expression and induction of myeloid differentiation program. Gene expression, chromatin accessibility, and direct genome-wide RBM5 binding further identify the direct transcriptional targets of RBM5 in primary leukemia cells including several stemness genes Hoxa9 and Myc. Forced expression of both HOXA9 and MYC rescued the RBM5 depletion effects on colony formation and self-renewal gene expression program. Thus, our study shows that RBM5 regulates the AML LSC program through transcriptional regulation and provides a rationale to therapeutically target RBM5 in myeloid leukemia.
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详细内容（全部2条）

1. 新电子书 | RNA测序：窥探转录组内部

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、transcriptome
• 📝 描述：This collection highlights how RNA sequencing is advancing transcriptomics research, from single-cell analysis and disease mechanisms to nanopore sequencing and AI-driven data interpretation… The post New eBook | RNA-seq: A peek inside the transcriptome appeared first on RNA-Seq Blog.
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2. 科学家发现了一种新的阿尔茨海默病诱因，以及一种可以阻止这种诱因的药物。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers have identified a new Alzheimer’s target and created an experimental compound that blocks a damaging process inside brain cells. In mice, the treatment slowed nerve cell loss, reduced Alzheimer’s-related changes, and even appeared to promote healthier aging.
• 🔗 查看原文

• GSE301020 RBM5 通过与 MYC 合作调节白血病转录程序，对维持白血病干细胞至关重要 [bulk RNA-seq]
• GSE288196 单细胞多组学揭示控制不同 EMT 肿瘤状态的转录网络 [bulk RNA-seq]
• GSE140893 果蝇肠道干细胞（ISCs）衰老过程中的单细胞分析
• GSE334763 肺癌中细胞毒性 CD39+ 肿瘤相关 NK 细胞对 NKG2A 阻断的反应
• GSE306673 Akkermansia muciniphila 通过诱导小肠上皮细胞的表观遗传和转录变化，促进禁食介导的辐射防护
• GSE306576 禁食通过微生物组-代谢物-染色质轴促进小肠损伤后的再生 [RNA-seq]
• GSE334500 人类 iPSC 衍生的心脏和视网膜类器官的精神药物和神经递质扰动 RNA 测序 (ToxiPred)
• GSE334497 TROP2/claudin 程序介导免疫排斥，从而阻碍乳腺癌中的检查点阻断
• GSE334369 纤维肌痛中性粒细胞的矛盾表型：基础炎症水平升高但对刺激的反应减弱
• GSE325894 人类结肠炎芯片模型揭示丁酸盐在抵抗白色念珠菌组织侵袭的上皮细胞和巨噬细胞防御中的双重作用
• GSE303478 系统性研究揭示了 Epstein-Barr 病毒对人类基因组广泛的转录调控
• GSE288220 单细胞多组学揭示控制不同 EMT 肿瘤状态的转录网络 [多组学]
• GSE190886 PA14 处理的对照组和 roX2 耗竭的 ISC（PA14 处理）的单细胞分析
• GSE334710 系统性硬化症或局限性硬皮病皮肤组织的空间转录组数据
• GSE334588 成人皮肌炎、皮肤红斑狼疮和健康皮肤的单细胞转录组图谱
• GSE334192 磺基转移酶信号传导维持成纤维细胞特性并拮抗治疗性心脏重编程
• GSE311457 利用沼泽红假单胞菌（Rhodopseudomonas palustris）作为模式细菌研究褐腐菌（Rhodonia placenta）腐烂木材中的真菌-细菌相互作用
• GSE309123 人类发育增强子在从原始多能性向启动多能性转变过程中的定位和连接性 - RNA-seq
• GSE309054 人类发育增强子在从原始多能性向启动多能性转变过程中的定位和连接性 - ChIP-seq
• GSE306671 禁食通过微生物组-代谢物-染色质轴促进小肠损伤后的再生
• GSE306577 禁食通过微生物组-代谢物-染色质轴促进小肠损伤后的再生 [Cut & Tag]
• GSE298763 野生型和GRA敲入小鼠海马中糖皮质激素转录组
• GSE298420 使用靶向 Claudin-1 的人源化单克隆抗体治疗胆管癌（HuCC-A1 CDX 肿瘤短期治疗的 RNA-Seq）
• GSE334545 通过 ATAC-seq 分析染色质可及性变化，以确定 HNSCC 细胞中持续暴露于生理相关的色氨酸代谢物如何重塑染色质。
• GSE334138 眼镜蛇毒素激活NLRP3/Caspase-1/GSDMD细胞焦亡通路诱导皮肤组织损伤
• GSE333925 31个RAS/RAF野生型结直肠癌（CRC）干细胞（SC）球体和7个FGFR抑制剂耐药的CSC-SC球体的基因表达谱
• GSE299449 工程化构建具有非典型钙晶体结构的脂质纳米颗粒以增强IFNβ介导的免疫疗法
• GSE299286 通过血清药理化学、网络药理学和转录组学相结合的方法，探索半夏泻心汤对DSS诱导的溃疡性结肠炎的抑制机制。
• GSE286012 杨树生根性状差异及WUSCHEL相关同源异型盒（WOX）基因家族的全基因组鉴定与分析
• GSE283820 依赖于 Eomes 和 Myb 的辅助性 T 细胞干细胞样前体在慢性感染期间维持 CD4+ T 细胞反应
• GSE291616：小鼠肝细胞经PBS、50nm聚苯乙烯或500nm聚苯乙烯每周处理12周后，进行单核（sn）RNA测序分析。