详细内容（前10条）

1. ⭐ GSE320529 Eomes 维持 CD4⁺ T 辅助祖细胞，从而在免疫治疗期间促进抗肿瘤免疫。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、regex:immuno(logy|therapy|suppression)
• 📝 描述：Contributors : Arantxa Agesta ; Chloé Ferrand ; Anne-Louise Le Dorze ; Adeline Chaubet ; Margot Zahm ; Anne S DejeanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCD4⁺ T helper (Th) cells contribute to tumor immunity, yet the subsets and differentiation programs involved remain unclear. Here, we show that the transcription factor Eomesodermin (Eomes) is essential for Th–mediated anti-tumor immunity by orchestrating the differentiation and maintenance of an exhausted-like Th cell lineage, which is transcriptionally and functionally distinct from conventional effector or memory Th subsets. This Eomes-dependent program is further enhanced by 4-1BB stimulation, promoting effective Th cell–mediated tumor control. The precursor subset of this lineage (pTh) expresses stemness-associated transcription factors, displays self-renewal capacity, and can differentiate into effector cells capable of controlling tumor growth. At the transcriptional level, Eomes supports the survival, metabolic fitness, and apoptotic resistance of this lineage. Notably, Eomes⁺ pTh cells are directly relevant to human cancer, being detected across multiple tumor types, exhibiting conserved transcriptional features, and representing the most expanded Th cell population upon immune checkpoint blockade therapy.
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2. ⭐ GSE335282 通过双重靶向 PCSK9 和先天免疫检查点，增强巨噬细胞连接先天性和适应性抗肿瘤免疫的能力

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、macrophage
• 📝 描述：Contributors : Caili Xu ; Kaicheng Zhou ; Xiaozhi Hu ; Yanyang Nan ; Yun Sun ; Zihan Dou ; Rui Zhou ; Wenjing Xue ; Qinchao Hu ; Xiting Huang ; Xianxin Hua ; Dianwen Ju ; Xuyao ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMacrophage-directed immunotherapy has emerged as a promising strategy to eliminate tumors by unleashing phagocytosis, exemplified by blockade of the CD47-SIRPα “don’t eat me” axis. However, despite robust enhancement of phagocytosis, such approaches often fail to generate durable antitumor immunity in solid tumors, highlighting a critical disconnect between innate immune activation and effective T cell responses. Here, we identify PCSK9 as an adaptive resistance factor induced by macrophage immune checkpoint blockade. Tumor-derived PCSK9 promotes lysosomal degradation of MHC-I in macrophages, thereby impairing antigen cross-presentation and limiting CD8⁺ T cell priming. This previously unrecognized mechanism reveals how phagocytosis-targeted therapies can paradoxically suppress adaptive immunity. To overcome this resistance, we engineered bispecific fusion proteins that concurrently target the CD47-SIRPα phagocytosis checkpoint and the PCSK9–MHC-I antigen presentation axis, among which SIRPαD1-αPCSK9 emerged as the optimal format. Dual targeting synergistically enhances macrophage phagocytosis, preserves antigen cross-presentation capacity, and reprograms the tumor microenvironment toward an immunostimulatory state. Consequently, SIRPαD1-αPCSK9 elicits robust activation of both innate and adaptive antitumor immunity, leading to potent tumor control with improved safety. These findings uncover a novel mechanism of resistance to macrophage-centered immunotherapy and establish a rational dual-targeting strategy that bridges phagocytosis and T cell activation, offering a new paradigm for macrophage-driven cancer immunotherapy.
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3. ⭐ GSE334547 ACKR2 有助于调节骨髓嗜酸性粒细胞，从而促进单核细胞分化和抗菌免疫。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、monocyte、regex:bacter(ia|ial|ium)
• 📝 描述：Contributors : Gillian J Wilson ; Lily Koumbas Foley ; Zuzanna Pocalun ; Elise Pitmon ; Ayumi Fukuoka ; Kit M Lee ; Lauren Fernandez ; Heather Mathie ; Robin Bartolini ; Laura Medina-Ruiz ; John J Cole ; Gerard J GrahamSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChemokine receptors control cell migration within the body. Here we reveal interactions between eosinophils and monocytes in the bone marrow, indirectly controlled by the atypical chemokine receptor ACKR2. In the absence of ACKR2, there are decreased numbers of eosinophils in the bone marrow. As a result, eosinophil and monocyte interactions are reduced within the bone marrow niche, and are associated with changes in monocyte gene expression. Monocytes from ACKR2-/- mice are recruited to the tissues but are fundamentally altered in their ability to differentiate into macrophages, in the lung, peritoneal cavity and cavity wall. Bacterial elimination is impaired in ACKR2-/- mice during peritoneal infection. ACKR2 is therefore a key regulator of eosinophil-driven monocyte education in the bone marrow, required for full monocyte differentiation and macrophage function within the tissues.
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4. GSE335490 小鼠模型中4-NQO诱导的口腔鳞状细胞癌的单细胞转录组分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、single-cell
• 📝 描述：Contributors : Xing Liu ; Yalun Li ; Lanlan Gao ; Rihui Lu ; Yongjin Fang ; Xiao YangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo investigate the cellular heterogeneity and molecular drivers of oral squamous cell carcinoma (OSCC), we performed single-cell RNA sequencing (scRNA-seq) on tongue tissues from a 4-nitroquinoline 1-oxide (4-NQO)-induced mouse model. This dataset revealed eight distinct cell populations, with a significant reduction in epithelial cells and an increase in fibroblasts in OSCC compared to controls. Notably, a distinct Col1a1⁺ epithelial subpopulation was identified that exhibited the highest epithelial-mesenchymal transition (EMT) signature and was significantly expanded in OSCC. This study provides a valuable resource for understanding the transcriptional landscape and cellular dynamics underlying OSCC progression.
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5. GSE310314 ACSS2 通过调节 AIF1 介导的炎症加剧代谢功能障碍相关性脂肪性肝炎 (MASH)

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、metabolic
• 📝 描述：Contributor : Xiao WenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMetabolic dysfunction associated steatohepatitis (MASH) is one of the most common types of liver disease, which is caused by hepatotoxicity caused by metabolic disorder. The incidence rate and mortality are very high, but the current treatment drugs are still limited. The role of ACSS2 in regulating inflammation in MASH is unclear. This study aims to explore the role and potential mechanisms of ACSS2 in the progression of MASH.
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6. GSE295919 胎儿特异性基因 LIN28B 对人类胎儿 B 淋巴细胞生成和 KMT2A::AFF1 婴儿白血病的发生至关重要 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、RNA-seq
• 📝 描述：Contributors : Rebecca Ling ; Thomas Jackson ; Thomas Milne ; Anindita RoySeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensInfant ALL (iALL) is initiated in utero, most often by rearrangement of the KMT2A gene (KMT2Ar). It carries a very poor prognosis despite a lack of additional oncogenic driver mutations common in childhood ALL. Here, we aimed to identify specific properties of human fetal hematopoietic stem/progenitor cells (HSPC) that promote leukemic transformation in KMT2Ar iALL using molecular, functional and in vivo assays. First, by comparing transcriptomes of human fetal HSPC with adult HSPC we derived a fetal-specific gene signature and identified the fetal oncogene LIN28B and its downstream effectors among the top hits. These genes were also expressed in iALL. Functional assays revealed that LIN28B was essential in human fetal liver (FL) CD34+ cells to maintain proliferation and stemness, and support B- and NK-lymphopoiesis. To interrogate the role of LIN28B in iALL, we utilised a human FL-derived CRISPR-Cas9 KMT2A::AFF1 model. In this CRISPRKMT2A::AFF1 model, human FL CD34+ cells fail to transform upon induction of KMT2A::AFF1 translocation in the absence of LIN28B. In addition, LIN28B-expressing CRISPRKMT2A::AFF1 leukemias were more proliferative in vitro and in vivo, with this advantage being lost upon LIN28B knockdown. Mechanistic studies showed that LIN28B acts by stabilizing key early B-lymphoid genes, epigenetic regulators, and cell cycle and anti-apoptotic genes. Thus, LIN28B has an essential role in normal human fetal B-lymphopoiesis, and is necessary for the initiation of KMT2A::AFF1 iALL in fetal cells in the absence of co-operating mutations. LIN28B activity may help explain why KMT2A::AFF1 leukemias are so aggressive, making it a potential target in LIN28B-expressing leukemias.
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7. GSE295009 对结直肠癌腹膜转移灶类器官的表观基因组分析揭示了阿霉素耐药机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Tara L Hogenson ; Martin E Fernandez-ZapicoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensIn this study, we generated patient-derived organoids (PDOs) from patients with colorectal cancer peritoneal mestasis and performed RNA- and ATAC-sequencing to study mechanisms for doxorubicin response.
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8. GSE294934 对结直肠癌腹膜和肝转移灶类器官的表观基因组分析揭示了阿霉素耐药机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Tara L Hogenson ; Martin E Fernandez-ZapicoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensIn this study, we generated patient-derived organoids (PDOs) from patients with colorectal cancer peritoneal and liver mestases and performed RNA- and ATAC-sequencing to study mechanisms for doxorubicin response.
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9. GSE335126 10x Genomics Xenium 分析成年和老年小鼠脑对照组和热应激组

• ✍️ 作者：未知作者
• 🏷️ 关键词：10x、genomics
• 📝 描述：Contributors : Roy Subhajit ; Trivedi Ayushi ; Sarkar Subham ; Kumar Ram ; Chatterjee SaurabhSeries Type : OtherOrganism : Mus musculus10x Genomics Xenium in situ targeted gene expression was performed on FFPE mouse brain tissue using the Xenium Mouse Brain Gene Expression panel (mBrain_v1.1). The staged dataset contains adult and aged cohorts with control and heat-stress sample annotations. Heat-stress mice received periodic heat exposure at approximately 40 deg C for 3 hours/day for 14-15 days. Raw files include high-resolution morphology images and decoded transcripts; processed files include transcript count matrices, cell summaries, and cell and nucleus segmentation boundaries.
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10. GSE335058 进化引导的转录因子设计程序新的 T 细胞状态 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、ChIP-seq
• 📝 描述：Contributors : Oliver Takacsi-Nagy ; Sivakanthan Kasinathan ; Austin Hartman ; Theo L Roth ; Ansuman T SatpathySeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensHuman protein-coding genes evolved via modular rearrangement of domains from ancestral genes. Here, we develop a scalable, evolutionarily guided method to assemble novel protein-coding genes from constituent domains within a protein family, termed DESynR (Domain Engineered via Synthesis and Recombination) genes. Using primary human chimeric antigen receptor T cells as a model, we find that the expression of DESynR Activator Protein-1 (AP-1) transcription factors (TFs) significantly outperforms the overexpression of natural AP-1 TFs in multiple functional assays in vitro and in vivo. Top DESynR AP-1 TFs exhibit non-intuitive domain architectures, including from TFs not canonically expressed in T cells. DESynR AP-1 TFs induce broad transcriptional and epigenetic reprogramming and establish non-natural T cell states that optimize features of exhaustion, effector and cytotoxic function, and persistence— in some cases co-opting gene expression modules from disparate cell types. We show that this reprogramming is primarily driven by differential regulation of established AP-1-bound regulatory elements, rather than unique binding. Finally, we extend the DESynR methodology to Erythroblast Transformation Specific (ETS) and Forkhead box (FOX) TFs to support the generalizability across protein families. Overall, we demonstrate that novel configurations of existing protein domains may uncover non-evolved genes that program cell states with therapeutic relevance.
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1. 铜制剂能清除阿尔茨海默病产生的有毒蛋白质，并恢复记忆力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：A copper-based compound restored the brain’s ability to clear toxic Alzheimer’s proteins, dramatically reducing amyloid buildup and improving memory in laboratory experiments. The findings point to a potentially fast-tracked new treatment strategy because the drug has already been tested in humans for other neurological conditions.
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• GSE306036 前列腺癌中参与EMT和免疫抑制的临床FOXA1突变靶点的鉴定
• GSE335464 人类胰岛单细胞多组学整合分析鉴定出与 1 型糖尿病相关的基因和调控信号 [单细胞]
• GSE331527 工程化心脏组织有助于对与肥厚型和扩张型心肌病相关的非编码变异进行功能表征 [批量 RNA-Seq]
• GSE331444 工程化心脏组织有助于对与肥厚型和扩张型心肌病相关的非编码变异进行功能表征 [ATAC-seq]
• GSE329414 星形胶质细胞氧化还原失衡是癫痫患者前边缘神经元活动减弱和情感行为的基础
• GSE328106 星形胶质细胞氧化还原失衡是癫痫患者前边缘神经元活动减弱和情感行为的基础 [星形胶质细胞_MACS]
• GSE319933：在TNFα和IFNγ刺激下，AdvCre介导的ELF3缺失后小鼠原代肾小管上皮细胞的批量RNA测序分析
• GSE318686 婴儿回肠肠道类器官对混合人乳外泌体的转录反应
• GSE306738 儿童期逆境、异质性负荷和表观遗传特征与儿童和成人发病的多发性硬化症
• GSE335644 梭杆菌和IFNγ协同激活牙龈成纤维细胞是通过自分泌机制驱动的，并增强免疫细胞的炎症反应
• GSE335103 全基因组筛选鉴定出针对 SARS-CoV-2 的独特宿主靶向药物和促病毒信号通路
• GSE328671 4T1 ATAC-seq
• GSE327926 PBRM1 RNA-seq [4T1]
• GSE310185 NMuMG PBRM1 ChIP-seq
• GSE302547 真皮抗原呈递细胞亚群在伤口愈合中的相反功能
• GSE298752 NMuMG PBRM1 ATAC-seq
• GSE295391 胎儿特异性基因 LIN28B 对人类胎儿 B 淋巴细胞生成和 KMT2A::AFF1 婴儿白血病的发生至关重要 [RIP-Seq]
• GSE269428 PBRM1 RNA-seq
• GSE335569 研究发现，靶向翻译复合物 eIF4F 可破坏 BCR::ABL1 翻译并克服慢性粒细胞白血病 (CML) 的耐药性。
• GSE335427 雄性小鼠内皮细胞经载体或LPS刺激后的批量RNA测序
• GSE335040 进化引导的转录因子设计程序新的 T 细胞状态 [RNAseq_Paired]
• GSE335026 进化引导的转录因子设计程序新的 T 细胞状态 [RNAseq_HA]
• GSE335017 肺部 mRNA-LNP 疫苗可快速持久地预防细菌感染
• GSE334999 间充质干细胞来源的 miR-143-3p 通过 TLR3/NF-κB/p53 信号通路对多巴胺能神经元发挥神经保护作用
• GSE329112 衰老会破坏小鼠卵巢周期的时空协调性
• GSE300090 从传统汤剂到精制制剂：网络药理学揭示青黛汤的抗肿瘤网络并实现分子相容性中药设计
• GSE298987 UVRAG-ITCH-ESCRT通路通过K27连接的泛素化对NOTCH进行检查点调控
• GSE281758 RNA-seq 测序结果显示，在皮肤 tbx20 基因敲除小鼠的颊部注射模型中，bnp 基因被敲除。