详细内容（前10条）

1. ⭐ GSE317661 CSN3促进胃癌侵袭，并通过激活NOD/TLR通路与免疫浸润相关

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、TLR
• 📝 描述：Contributors : Gang Wang ; Dalai Xu ; Lei Qiu ; Feng Lu ; Yongchang MiaoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe found that CSN3 is highly expressed in gastric cancer and is associated with advanced tumor stage, lymph node metastasis, and poor prognosis. Functional assays showed that CSN3 promotes proliferation and migration while inhibiting apoptosis in GC cells. RNA-sequencing revealed that CSN3 overexpression predominantly activates innate immune–related pathways, particularly the NOD-like receptor and Toll-like receptor signaling pathways, suggesting a role for CSN3 in inflammatory and immune remodeling of the tumor microenvironment. Consistently, CSN3 expression was positively correlated with B-cell and CD8⁺ T-cell infiltration, indicating that CSN3-driven transcriptional programs may link tumor aggressiveness with immune microenvironment alterations.
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2. ⭐ GSE313338 Xenium 空间转录组学研究 28 期胚胎和再生 3 厘米墨西哥钝口螈尾巴（3、7、10、14 天后），包括成熟的未截尾尾巴

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Vijayishwer S Jamwal ; Riley Grindle ; Ryan P Seam ; Fred Kolling ; Prayag Murawala ; Joel GraberSeries Type : OtherOrganism : Ambystoma mexicanum100 genes were selected, including cell-specific markers, transcription factors and signalling molecules, to understand tail patterning and gene oscillations in the embryo and in comparison to the tail.
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3. ⭐ GSE313080 microRNA-25 通过 Syndecan3 抑制先天性和体液免疫，从而驱动对免疫检查点疗法的初始耐药性。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、resistance
• 📝 描述：Series Type : Non-coding RNA profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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4. ⭐ GSE313005 microRNA-25 通过 Syndecan3 抑制先天性和体液免疫，从而驱动对免疫检查点疗法的初始耐药性 [single_clone_RNA_seq_B16]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、resistance
• 📝 描述：Contributors : Zhouting Zhu ; Zhaoyang Jia ; Tariq M RanaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmune Checkpoint Therapy (ICT) has demonstrated durable responses and long-lasting immunologic memory in cancer treatment. However, overcoming primary and acquired resistance remains a major challenge. Here, we show that CRISPR-Cas9-mediated deletion of miRNA-25 (miR-25) sensitizes tumors to ICT across three syngeneic mouse tumor models. Single-cell RNA sequencing (scRNA-seq) of the tumor microenvironment (TME) revealed that miR-25 deficiency induces innate immunity by upregulating major histocompatibility complex class II (MHC II) in antigen-presenting M1-like macrophages and enhances the classical complement cascade in cancer-associated fibroblasts (CAFs) to drive a humoral immune response. The complement activation polarizes CAFs from myofibroblastic CAFs (myCAFs) toward inflammatory CAFs (iCAFs) while simultaneously reduces immune-suppressive interactions between CAFs and tumor associated macrophages (TAMs). This shift results in a reduced macrophage population and fosters a pro-inflammatory, anti-tumor TME. Syndecan-3 (Sdc3), a membrane proteoglycan expressed in tumors, is repressed by miR-25 through miRISC (microRNA induced silencing complex) upon IFN-γ exposure. Using an adenine base editor (ABE8e) to mutate the miR-25 binding site in the 3’ untranslated region (3’ UTR) of Sdc3 effectively overcomes the resistance. The repression of SDC3 by miR-25 is further validated in five human cancer cell lines upon IFN-γ exposure but remains unaffected in non-cancerous cells. These findings identify miR-25 as a key driver of initial resistance through the repression of SDC3 and demonstrate that miR-25 deletion or stabilization of SDC3 could transform immune resistant “cold” tumors into immune responsive “hot” tumors, offering therapeutic avenues to enhance cancer immunotherapy.
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5. ⭐ GSE313004 microRNA-25 通过 Syndecan3 抑制先天性和体液免疫，从而驱动对免疫检查点疗法的初始耐药性 [single_cell_RNA_seq_MC38]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、resistance
• 📝 描述：Contributors : Zhouting Zhu ; Zhaoyang Jia ; Tariq M RanaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmune Checkpoint Therapy (ICT) has demonstrated durable responses and long-lasting immunologic memory in cancer treatment. However, overcoming primary and acquired resistance remains a major challenge. Here, we show that CRISPR-Cas9-mediated deletion of miRNA-25 (miR-25) sensitizes tumors to ICT across three syngeneic mouse tumor models. Single-cell RNA sequencing (scRNA-seq) of the tumor microenvironment (TME) revealed that miR-25 deficiency induces innate immunity by upregulating major histocompatibility complex class II (MHC II) in antigen-presenting M1-like macrophages and enhances the classical complement cascade in cancer-associated fibroblasts (CAFs) to drive a humoral immune response. The complement activation polarizes CAFs from myofibroblastic CAFs (myCAFs) toward inflammatory CAFs (iCAFs) while simultaneously reduces immune-suppressive interactions between CAFs and tumor associated macrophages (TAMs). This shift results in a reduced macrophage population and fosters a pro-inflammatory, anti-tumor TME. Syndecan-3 (Sdc3), a membrane proteoglycan expressed in tumors, is repressed by miR-25 through miRISC (microRNA induced silencing complex) upon IFN-γ exposure. Using an adenine base editor (ABE8e) to mutate the miR-25 binding site in the 3’ untranslated region (3’ UTR) of Sdc3 effectively overcomes the resistance. The repression of SDC3 by miR-25 is further validated in five human cancer cell lines upon IFN-γ exposure but remains unaffected in non-cancerous cells. These findings identify miR-25 as a key driver of initial resistance through the repression of SDC3 and demonstrate that miR-25 deletion or stabilization of SDC3 could transform immune resistant “cold” tumors into immune responsive “hot” tumors, offering therapeutic avenues to enhance cancer immunotherapy.
• 🔗 查看原文

6. ⭐ GSE313003 microRNA-25 通过 Syndecan3 抑制先天性和体液免疫，从而驱动对免疫检查点疗法的初始耐药性 [In_vitro_RNA_seq_B16]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、resistance
• 📝 描述：Contributors : Zhouting Zhu ; Zhaoyang Jia ; Tariq M RanaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmune Checkpoint Therapy (ICT) has demonstrated durable responses and long-lasting immunologic memory in cancer treatment. However, overcoming primary and acquired resistance remains a major challenge. Here, we show that CRISPR-Cas9-mediated deletion of miRNA-25 (miR-25) sensitizes tumors to ICT across three syngeneic mouse tumor models. Single-cell RNA sequencing (scRNA-seq) of the tumor microenvironment (TME) revealed that miR-25 deficiency induces innate immunity by upregulating major histocompatibility complex class II (MHC II) in antigen-presenting M1-like macrophages and enhances the classical complement cascade in cancer-associated fibroblasts (CAFs) to drive a humoral immune response. The complement activation polarizes CAFs from myofibroblastic CAFs (myCAFs) toward inflammatory CAFs (iCAFs) while simultaneously reduces immune-suppressive interactions between CAFs and tumor associated macrophages (TAMs). This shift results in a reduced macrophage population and fosters a pro-inflammatory, anti-tumor TME. Syndecan-3 (Sdc3), a membrane proteoglycan expressed in tumors, is repressed by miR-25 through miRISC (microRNA induced silencing complex) upon IFN-γ exposure. Using an adenine base editor (ABE8e) to mutate the miR-25 binding site in the 3’ untranslated region (3’ UTR) of Sdc3 effectively overcomes the resistance. The repression of SDC3 by miR-25 is further validated in five human cancer cell lines upon IFN-γ exposure but remains unaffected in non-cancerous cells. These findings identify miR-25 as a key driver of initial resistance through the repression of SDC3 and demonstrate that miR-25 deletion or stabilization of SDC3 could transform immune resistant “cold” tumors into immune responsive “hot” tumors, offering therapeutic avenues to enhance cancer immunotherapy.
• 🔗 查看原文

7. ⭐ GSE313002 microRNA-25 通过 Syndecan3 抑制先天性和体液免疫，从而驱动对免疫检查点疗法的初始耐药性 [Bulk_tumor_RNA_seq_B16]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、resistance
• 📝 描述：Contributors : Zhouting Zhu ; Zhaoyang Jia ; Lingling Wang ; Hui Hui ; Tariq M RanaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmune Checkpoint Therapy (ICT) has demonstrated durable responses and long-lasting immunologic memory in cancer treatment. However, overcoming primary and acquired resistance remains a major challenge. Here, we show that CRISPR-Cas9-mediated deletion of miRNA-25 (miR-25) sensitizes tumors to ICT across three syngeneic mouse tumor models. Single-cell RNA sequencing (scRNA-seq) of the tumor microenvironment (TME) revealed that miR-25 deficiency induces innate immunity by upregulating major histocompatibility complex class II (MHC II) in antigen-presenting M1-like macrophages and enhances the classical complement cascade in cancer-associated fibroblasts (CAFs) to drive a humoral immune response. The complement activation polarizes CAFs from myofibroblastic CAFs (myCAFs) toward inflammatory CAFs (iCAFs) while simultaneously reduces immune-suppressive interactions between CAFs and tumor associated macrophages (TAMs). This shift results in a reduced macrophage population and fosters a pro-inflammatory, anti-tumor TME. Syndecan-3 (Sdc3), a membrane proteoglycan expressed in tumors, is repressed by miR-25 through miRISC (microRNA induced silencing complex) upon IFN-γ exposure. Using an adenine base editor (ABE8e) to mutate the miR-25 binding site in the 3’ untranslated region (3’ UTR) of Sdc3 effectively overcomes the resistance. The repression of SDC3 by miR-25 is further validated in five human cancer cell lines upon IFN-γ exposure but remains unaffected in non-cancerous cells. These findings identify miR-25 as a key driver of initial resistance through the repression of SDC3 and demonstrate that miR-25 deletion or stabilization of SDC3 could transform immune resistant “cold” tumors into immune responsive “hot” tumors, offering therapeutic avenues to enhance cancer immunotherapy.
• 🔗 查看原文

8. ⭐ GSE313001 microRNA-25 通过 Syndecan3 抑制先天性和体液免疫，从而驱动对免疫检查点疗法的初始耐药性 [small_RNA_seq_B16]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、resistance
• 📝 描述：Contributors : Zhouting Zhu ; Zhaoyang Jia ; Gulshanbir Baidwan ; Hui Hui ; Tariq M RanaSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Mus musculusImmune Checkpoint Therapy (ICT) has demonstrated durable responses and long-lasting immunologic memory in cancer treatment. However, overcoming primary and acquired resistance remains a major challenge. Here, we show that CRISPR-Cas9-mediated deletion of miRNA-25 (miR-25) sensitizes tumors to ICT across three syngeneic mouse tumor models. Single-cell RNA sequencing (scRNA-seq) of the tumor microenvironment (TME) revealed that miR-25 deficiency induces innate immunity by upregulating major histocompatibility complex class II (MHC II) in antigen-presenting M1-like macrophages and enhances the classical complement cascade in cancer-associated fibroblasts (CAFs) to drive a humoral immune response. The complement activation polarizes CAFs from myofibroblastic CAFs (myCAFs) toward inflammatory CAFs (iCAFs) while simultaneously reduces immune-suppressive interactions between CAFs and tumor associated macrophages (TAMs). This shift results in a reduced macrophage population and fosters a pro-inflammatory, anti-tumor TME. Syndecan-3 (Sdc3), a membrane proteoglycan expressed in tumors, is repressed by miR-25 through miRISC (microRNA induced silencing complex) upon IFN-γ exposure. Using an adenine base editor (ABE8e) to mutate the miR-25 binding site in the 3’ untranslated region (3’ UTR) of Sdc3 effectively overcomes the resistance. The repression of SDC3 by miR-25 is further validated in five human cancer cell lines upon IFN-γ exposure but remains unaffected in non-cancerous cells. These findings identify miR-25 as a key driver of initial resistance through the repression of SDC3 and demonstrate that miR-25 deletion or stabilization of SDC3 could transform immune resistant “cold” tumors into immune responsive “hot” tumors, offering therapeutic avenues to enhance cancer immunotherapy.
• 🔗 查看原文

9. ⭐ GSE309890 抗抑郁药舍曲林通过应激驱动的磷酸戊糖途径重编程导致耐药性产生：tktA 使代谢回滚

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、resistance、pathway
• 📝 描述：Contributors : Yueting Cui ; Shiyuan Xue ; Jianhua Guo ; Chengdong ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Escherichia coli str. K-12 substr. MG1655Selective serotonin reuptake inhibitors (SSRIs) may accelerate antibiotic resistance, but the metabolic changes behind this process—and how to restore susceptibility—are still not well understood. We demonstrated that sertraline led to a biased resistance profile in Escherichia coli, characterized by early accumulation of mutations targeting rifampicin and ciprofloxacin. These genetic alterations were linked to a compensatory respiratory mechanism dependent on Complex I, leading to reduced nicotinamide adenine dinucleotide and superoxide/hydrogen peroxide buildup. They also caused a rapid shift of glucose from glycolysis to the pentose-phosphate pathway (PPP) to produce reduced nicotinamide adenine dinucleotide phosphate during oxidative stress, similar to paraquat-like redox stress. Inhibiting the non-oxidative PPP, especially transketolase A (tktA), eliminated the sertraline-primed advantage and brought back antibiotic susceptibility, decreasing survival by approximately 10,000 times during antibiotic challenge, even with rpoBC and gyrAB mutations fixed. These findings uncover an electron transfer chain/PPP–coupled redox module as the hidden driver behind sertraline-induced resistance, highlighting mutation-agnostic ways to restore bacterial sensitivity. By reframing SSRI-induced resistance as a modifiable metabolic trait, we provide a basis for using metabolic adjuvants to shield the millions of SSRI users from the unintended risk of antibiotic resistance—transforming a pharmacological challenge into a manageable, reversible target
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10. ⭐ GSE266852 利用单细胞转录组测序分析比较健康对照者、类风湿性关节炎患者和狼疮患者血液 PBMC 中的差异基因表达。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、transcriptome
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSingle-cell transcriptome sequencing was used to detect and compare differentially expressed genes in PBMCs from healthy controls in patients with rheumatoid arthritis, systemic lupus erythematosus patients.
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💡 该来源还有 64 条内容，详见 文末

• GSE302731 家袋狸三层脐侧膜的微量RNA测序研究胎盘细胞因子信号传导
• GSE318164 分子异质性和免疫浸润驱动上尿路尿路上皮癌的临床结局
• GSE317599 抑制NEDDylation可通过线粒体自噬延长寿命并在衰老过程中维持心脏功能
• GSE316764 结肠炎的克隆记忆积累并促进肿瘤生长 [ATAC-Seq]
• GSE316618 结肠炎的克隆记忆积累并促进肿瘤生长 [Visium]
• GSE316616 结肠炎克隆记忆积累并促进肿瘤生长 [ATAC-seq]
• GSE314758 同时测量翻译速率和转录组揭示了活跃细菌细胞群体内的关联调控。
• GSE313713 NSD2 通过 Hippo 信号通路的表观遗传调控驱动糖尿病肾病中的足细胞损伤 [RNA-Seq]
• GSE313573 变形虫样间质转化和癌症侵袭可塑性的蛋白水解控制 [RNA-Seq]
• GSE313572 变形虫样间质转化和癌症侵袭可塑性的蛋白水解控制 [scRNA-seq]
• GSE308747 TCR-SUB1-DOCK2 信号轴通过调节 CD4+ T 细胞迁移能力来控制自身免疫 [ATAC-Seq]
• GSE308746 TCR-SUB1-DOCK2 信号轴通过调节 CD4+ T 细胞迁移能力来控制自身免疫 [RNA-Seq]
• GSE305438 NUDT21 在急性 T 淋巴细胞白血病中的作用机制研究 [RNA-Seq]
• GSE302132 单细胞转录组学揭示小鼠单次臭氧暴露模型中肺泡巨噬细胞的特异性反应
• GSE290624 通府平川汤治疗或不治疗败血症大鼠盲肠组织的转录组测序
• GSE290518 靶向MET酪氨酸激酶和NRF2之间新型相互作用可增强三阴性乳腺癌对紫杉醇的敏感性
• GSE289009 粒细胞来源的抵抗素诱导CMML中经典单核细胞重新分布和免疫抑制
• GSE288741 通过 CRISPR/Cas9 基因编辑技术连续敲入表皮生长因子受体配体结合域，可改变其在宫颈癌细胞中的亚细胞定位和磷酸化水平。
• GSE288679 RNase H1 依赖性 R 环清除是小鼠卵子发生过程中基因组沉默的先决条件 [RNA-Seq]
• GSE287246 干扰T细胞记忆可改善体重波动引起的过度代谢反应
• GSE287025 BCAA代谢通过胆固醇合成修饰促进肺癌的肿瘤发生
• GSE275500 TEX 细胞命运和分化受 3D 基因组重组和染色质结构完整性的影响 [Hi-C]
• GSE275499 TEX 细胞命运和分化受 3D 基因组重组和染色质结构完整性的影响 [RNA-seq]
• GSE275497 TEX 细胞命运和分化受 3D 基因组重组和染色质结构完整性的影响 [ATAC-seq]
• GSE270215：贝利木单抗治疗系统性红斑狼疮患者血液外周血单核细胞基因表达的单细胞转录组测序分析
• GSE263903 单细胞转录组学研究发现，暴露于烟草味电子烟的小鼠肺部中性粒细胞动力学发生改变，T细胞细胞毒性增强。
• GSE255094 PRC2 启动二价靶基因的转录诱导，且不依赖于组蛋白甲基转移酶活性 [RNA-seq]
• GSE255093 PRC2 启动二价靶基因的转录诱导，且不依赖于组蛋白甲基转移酶活性 [ChIP-seq]
• GSE225634 来自 M2 巨噬细胞来源的外泌体处理的 MDA-MB-231 乳腺癌细胞的表达数据
• GSE274080 RORγt+ APC 需要独特的顺式调控元件来指导对膳食抗原的耐受性 [RNA-seq]
• GSE317817 多巴胺神经元特异性 RNA 测序揭示脑啡肽酶 1 在黏连蛋白复合物下游发挥作用，抑制学习
• GSE317753 扁豆（Lens culinaris Medik.）中microRNA的全基因组鉴定和组织特异性分析
• GSE317276 整合多平台代谢组学揭示胫前黏液性水肿中脂肪酸介导的炎症特征
• GSE316763 结肠炎的克隆记忆积累并促进肿瘤生长 [IVFP]
• GSE316762 结肠炎的克隆记忆积累并促进肿瘤生长[组织 EM-seq]
• GSE316761 结肠炎的克隆记忆积累并促进肿瘤生长[类器官 EM-seq]
• GSE316724 CHD2 的深度突变扫描，用于神经发育障碍的变异解读 [RNA-seq]
• GSE316617 结肠炎的克隆记忆积累并促进肿瘤生长 [CUT&Tag]
• GSE316581 HOXB2敲低后MCF-7乳腺癌细胞的转录组分析
• GSE316113 Ly6C+Sca-1+虚拟记忆CD8+ T细胞响应IL-15/Rα复合物促进慢性肝脏炎症
• GSE315645 白细胞介素-4:STAT6信号通路通过拮抗IL-18感知延迟保护性CD8 T细胞的旁观者激活
• GSE311118 NSD2 通过 Hippo 信号通路的表观遗传调控驱动糖尿病肾病中的足细胞损伤 [Cut & Run]
• GSE311115 NSD2通过表观遗传调控Hippo信号通路驱动糖尿病肾病中的足细胞损伤
• GSE310466 表观遗传持续时间的种内变异
• GSE310074 ΔNp73 亚型定义了急性髓系白血病中一种类似 TP53 突变的预后不良亚组。
• GSE310000 人类背根神经节的 snRNA 测序
• GSE309052 TCR-SUB1-DOCK2信号轴通过调节CD4+ T细胞迁移能力来调控自身免疫
• GSE307402 ADAR1沉默对人单核细胞来源巨噬细胞的影响
• GSE307015 雄性野生型和IRF8敲除型小胶质细胞的转录组谱
• GSE305852 NUDT21 在急性 T 淋巴细胞白血病中的作用机制研究 [CUT&Tag]
• GSE305851 NUDT21 在急性 T 淋巴细胞白血病中的作用机制研究 [eCLIP-seq]
• GSE305770 全转录组分析揭示了患有疼痛性糖尿病周围神经病变的大鼠背根神经节的关键调控网络和潜在治疗靶点
• GSE305544 基底尿路上皮细胞作为膀胱癌起源细胞，其内在分化为中间细胞和伞状细胞的能力更强
• GSE305440 NUDT21 在急性 T 淋巴细胞白血病中的作用机制研究 [PAS-seq]
• GSE289271 衰老相关的UFMylation调控阻碍秀丽隐杆线虫的蛋白质稳态
• GSE288680 RNase H1 依赖性 R 环清除是小鼠卵子发生过程中基因组沉默的先决条件 [Stacc-seq]
• GSE288634 RNase H1依赖的R环清除是小鼠卵子发生过程中基因组沉默的先决条件
• GSE286918 卵巢储备功能减退患者颗粒细胞中发生的代谢重编程和铁死亡
• GSE275498 TEX 细胞命运和分化受 3D 基因组重组和染色质结构完整性的影响 [CUT&RUN]
• GSE259315 蜂王浆酸在溃疡性结肠炎治疗中的应用：通过 miRNA 表达和 NLRP3 炎症小体调节 miR-210-3P/Gbp3 通路和细胞焦亡（miRNA-Seq）
• GSE256425 蜂王浆酸在溃疡性结肠炎治疗中的应用：通过 miRNA 表达和 NLRP3 炎症小体调节 miR-210-3P/Gbp3 通路和细胞焦亡
• GSE246725 TPX2 作为 MYCN 驱动的神经母细胞瘤中 eIF4A 控制的翻译程序的关键下游靶点[RNA-Seq]
• GSE225870 基于转录组学的成年斑马鱼（Danio rerio）长期暴露于双酚AF后肝毒性性别差异机制分析
• GSE117956 神经视网膜的细胞环境影响补体免疫调节 [Hs]