详细内容（前10条）

1. ⭐ GSE331286 利用空间转录组学了解缺血性心脏重塑中βIV-spectrin/STAT3复合物的空间和时间调控。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Rebecca Shaheen ; Jhonny Rodriguez-Lopez ; Drew Nassal ; Xianyao xu ; Natalia Del Pilar Vanegas ; Ana Mora ; Mauricio Rojas ; Thomas HundSeries Type : OtherOrganism : Mus musculusAdverse fibrotic remodeling contributes to high morbidity and mortality in patients following myocardial infarction (MI). Healing after MI requires necrotic tissue to be cleared and replaced with fibrosis, which is driven by the coordinated effort of several distinct cardiac cell populations, including myocytes, immune cells, and cardiac fibroblasts (CFs). While a myriad of stimuli driving fibrotic remodeling post-MI have been identified, the contribution of specific cell populations to the signaling cascade and how these communication networks are tuned in response to chronic stress remains unclear. The cytoskeletal protein, βIV-spectrin, coordinates a signaling complex with the transcription factor, STAT3 to modulate CF activation and profibrotic signaling. Specifically, stress-induced loss of βIV-spectrin promotes subcellular redistribution and activation of STAT3 in CFs that increases secretion of profibrotic and proinflammatory factors. Mice expressing degradation-resistant βIV-spectrin (qv3J) show increased mortality and incidence of cardiac rupture within the first week after permanent occlusion of the left anterior descending (LAD) artery. Histology at 7 days post-MI shows improper scar formation with incomplete clearance compared to WT. Therefore, we hypothesized that stress-induced loss of βIV-spectrin in CFs coordinates spatial and temporal regulation of multiple cardiac cell populations to ensure proper healing. In this study, we subjected WT and qv3J mice to MI and assessed cardiac function and survival through 28 days and performed spatial transcriptomics at 7 days. Cell-type deconvolution from spatial transcriptomics analysis revealed dramatic differences in CF populations, with a decrease in the Cthrc1 CF population in qv3J hearts compared to WT. A STAT3-dependent fibroblast trajectory was identified that originates from vascular smooth muscle cells and progresses to Chtrc1 CF population in WT hearts, while qv3J fibroblast trajectory diverged into a more senescent-like state. The border zone in qv3J hearts showed a congregation of immune cells and fibroblasts that could not infiltrate the infarct zone, leading to high concentrations of MMPs at the location where rupture occurs in these mice. Aberrant CXCL12 signaling was observed in qv3J mice, explai…
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2. ⭐ GSE270300 N-糖基化抑制可阻碍免疫抑制性肿瘤微环境细胞，从而提高CAR T细胞的疗效[scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、T cell、scRNA
• 📝 描述：Contributors : Camilla Sirini ; Chiara Balestrieri ; Monica CasucciSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAdoptive transfer of CAR T cells demonstrated impressive results against B-cell malignancies, but still limited efficacy against solid tumors. In this context, multiple challenges need to be overcome, including poor tumor recognition and strong immunosuppression within the tumor microenvironment (TME). Our Unit has recently reported that pharmacological inhibition of N-glycan synthesis in cancer cells increases CAR T cell efficacy by improving tumor recognition and preventing T cell exhaustion. In this project, we investigated the role of N-glycosylation blockade on TME cells in the context of colorectal cancer (CRC) and pancreatic adenocarcinoma (PDAC)-derived liver metastases, exploiting CEA-specific CAR T cell therapy. Here, we evaluate the impact of N-glycosylation blockade on TME cells (both M2-like macrophages, M2-M and Hepatic stellate cells, HepSCs), analyzing phenotypic and transcriptional profile and performing in vitro functional assays. In vitro studies revealed that N-glycosylation inhibition abolishes the ability of both TME cells to restrain T cell proliferation and increases the elimination of cancer cell lines and patient-derived tumor organoids (PDOs from CRC-liver metastases and primary PDAC). Interestingly, these effects were associated with profound phenotypic and transcriptional changes in M2-M and HepSCs. Moreover, to evaluate the effect of N-glycosylation inhibition on TME cells in vivo, we exploited immunodeficient mice reconstituted with a human immune system (huSGM3), engrafted intra-liver with tumor cells and treated with CEA CAR T cells. Importantly, using these mice we observed that N-glycosylation inhibition, only with Tunicamycin, improves CEA CAR T cells fitness, increasing their antitumor activity in terms of survival. This effect is associated with the reduction of IL1B+ TAMs cluster and the absence of inhibitory interactions between TAMs and T cells in scRNAseq analysis. However, the combination of CAR with 2DG failed to enhance CEA CAR T cells efficacy. Indeed, by blocking also glycolysis it dampens lymphoid effector functions tuning down the immune response. Overall, these data suggest that blocking N-glycosylation can help overcome multiple barriers that currently limit CAR T cell efficacy in solid tumors, acting not only on tumor cells, but also on immunosuppressive…
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3. ⭐ GSE265950 N-糖基化抑制可阻碍免疫抑制性肿瘤微环境细胞，从而提高CAR T细胞的疗效[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、T cell、RNA-seq
• 📝 描述：Contributors : Camilla Sirini ; Chiara Balestrieri ; Monica CasucciSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAdoptive transfer of CAR T cells demonstrated impressive results against B-cell malignancies, but still limited efficacy against solid tumors. In this context, multiple challenges need to be overcome, including poor tumor recognition and strong immunosuppression within the tumor microenvironment (TME). Our Unit has recently reported that pharmacological inhibition of N-glycan synthesis in cancer cells increases CAR T cell efficacy by improving tumor recognition and preventing T cell exhaustion. In this project, we investigated the role of N-glycosylation blockade on TME cells in the context of colorectal cancer (CRC) and pancreatic adenocarcinoma (PDAC)-derived liver metastases, exploiting CEA-specific CAR T cell therapy.Here, we evaluate the impact of N-glycosylation blockade on TME cells (both M2-like macrophages, M2-M and Hepatic stellate cells, HepSCs), analyzing phenotypic and transcriptional profile and performing in vitro functional assays. In vitro studies revealed that N-glycosylation inhibition abolishes the ability of both TME cells to restrain T cell proliferation and increases the elimination of cancer cell lines and patient-derived tumor organoids (PDOs from CRC-liver metastases and primary PDAC). Interestingly, these effects were associated with profound phenotypic and transcriptional changes in M2-M and HepSCs. Moreover, to evaluate the effect of N-glycosylation inhibition on TME cells in vivo, we exploited immunodeficient mice reconstituted with a human immune system (huSGM3), engrafted intra-liver with tumor cells and treated with CEA CAR T cells. Importantly, using these mice we observed that N-glycosylation inhibition, only with Tunicamycin, improves CEA CAR T cells fitness, increasing their antitumor activity in terms of survival. This effect is associated with the reduction of IL1B+ TAMs cluster and the absence of inhibitory interactions between TAMs and T cells in scRNAseq analysis. However, the combination of CAR with 2DG failed to enhance CEA CAR T cells efficacy. Indeed, by blocking also glycolysis it dampens lymphoid effector functions tuning down the immune response. Overall, these data suggest that blocking N-glycosylation can help overcome multiple barriers that currently limit CAR T cell efficacy in solid tumors, acting not only on tumor cells, but also on immunosuppressive …
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4. ⭐ GSE335471 淋巴结收缩与中年时期性别偏向的初始CD8 T细胞减少和抗原识别受损有关

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、T cell、antigen、regex:lymph(o|atic)?
• 📝 描述：Contributors : Lutz Menzel ; Maria Zschummel ; Timothy T PaderaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe numerical abundance of diverse naive CD8 T cell clones is essential to provide broad protection against infection and cancer. Here, we uncover a sex-biased mechanism of immune aging in which an early, male-biased depletion of naive CD8 T cells driven by accelerated, antigen-agnostic differentiation into virtual memory cells is combined with age-related thymic involution that limits naive CD8 T cell replenishment. These mechanisms lead to contraction of lymph nodes and reduced local naive T cell clone availability, limiting antigen recognition capacity. Therapeutic thymus regeneration via androgen ablation repopulates naive CD8 T cells in lymph nodes, which reinvigorates tumor-specific T cell responses and enhances responsiveness to immune checkpoint blockade. These findings reveal the crucial impact of sex and age on naive T cell clone abundance in lymph nodes and suggest strategies to restore immune competence in middle age males.
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5. ⭐ GSE298060 Smyca-FOXM1 核糖核蛋白复合物促进同源重组和肿瘤免疫逃逸，从而确定三阴性乳腺癌的治疗靶点

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune
• 📝 描述：Contributors : Hsin-Yi Chen ; Ruey-Hwa ChenSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTriple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with limited treatment options. We previously identified that the long noncoding RNA Smyca is highly expressed in TNBC to elicit multiple pro-tumor effects. Here, we show that Smyca is induced by DNA damage to enhance homologous recombination (HR) repair. Mechanistically, Smyca binds and guides FOXM1 to the promoters of a set of HR and nucleotide metabolism genes, thereby promoting their expression. Consequently, Smyca ablation induces BRCAness in HR-proficient TNBC, thereby sensitizing these tumors to platinum and PARP1 inhibitor (PARPi). Targeting Smyca/FOXM1 axis in combined with platinum or PARPi further activates cGAS/STING pathway and tumor immunogenicity to enhance anti-tumor immune surveillance. Clinically, Smyca expression in breast cancer patients correlates positively with therapy resistance and negatively with HR deficiency, interferon signature, and infiltration of anti-tumor immune cells. Our study identifies an unprecedented role of Smyca in HR repair to promote resistance to therapy and immune evasion during therapy and suggests Smyca as a potential target for sensitizing TNBC to chemotherapy, PARPi, or immune therapy.
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6. ⭐ GSE330488 CDCA4 通过激活 SESN2/mTOR/SREBP1 通路促进三阴性乳腺癌中的脂质代谢

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolism、pathway
• 📝 描述：Contributors : Jia Qi ; Xiaowen Wang ; Peng Zhang ; Jiani Wang ; Jiezhong Wu ; Zhirong Xuan ; Xiaoyuan Liang ; Kunpeng HuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by high metastatic potential, poor prognosis, and limited therapeutic options. However, the molecular mechanisms underlying TNBC progression and metabolic reprogramming remain incompletely understood. In this study, we identified cell division cycle-associated 4 (CDCA4) as a potential oncogenic driver in TNBC. Analysis of the TCGA-BRCA dataset revealed that CDCA4 was significantly upregulated in breast cancer tissues compared with normal tissues and was expressed at higher levels in TNBC than in non-TNBC. Elevated CDCA4 expression was also associated with poor overall survival in TNBC patients. Functional experiments demonstrated that CDCA4 knockdown suppressed TNBC cell proliferation, migration, invasion, and xenograft tumor growth, whereas CDCA4 overexpression exerted the opposite effects. RNA-sequencing analysis indicated that CDCA4-regulated genes were significantly enriched in lipid metabolism-related pathways and metabolism-associated signaling pathways, including PI3K/AKT and mTOR. Consistently, CDCA4 depletion reduced intracellular free fatty acids, total cholesterol, triglycerides, lipid accumulation, and the expression of lipogenic enzymes, including FASN and ACC1. Mechanistically, CDCA4 promoted mTOR activation and increased the level of the active nuclear form of SREBP1, thereby enhancing SREBP1 occupancy at the FASN and ACC1 promoter regions. Pharmacological inhibition of mTOR largely reversed CDCA4-induced malignant phenotypes and lipid metabolic alterations. Furthermore, we identified SESN2 as a critical mediator linking CDCA4 to mTOR activation, as SESN2 knockdown attenuated mTOR signaling and reversed the protumorigenic effects induced by CDCA4 overexpression. Collectively, these findings demonstrate that CDCA4 drives TNBC progression and lipid metabolic reprogramming through the SESN2/mTOR/SREBP1 axis, highlighting CDCA4 as a potential prognostic biomarker and therapeutic target in TNBC.
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7. ⭐ GSE325403 小鼠单细胞转录组学揭示皮肤和呼吸道化学致敏剂之间的免疫差异

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、single-cell、transcriptomics
• 📝 描述：Contributors : Mélanie Mourot-Bousquenaud ; Elsa Gratianne-Guillot ; Amélie Coiscaud ; Julianne Mathiot ; Samuel Muller ; Quentin Fort ; Fabrice BattaisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Chemical-induced sensitization is a major health concern. To date, no internationally accepted method is able to discriminate a skin from a respiratory sensitizer. The identification of an immune profile specific to skin or respiratory sensitizersation is therefore scientifically relevant. Methods: Female BALB/c mice were dermally exposed to a skin- (dinitrochlorobenzene, DNCB), or to a respiratory sensitizer (phthalic anhydride, PA) at day 0 (D0) and D5 to initiate allergic sensitization and at D10, D11 and D12 to induce elicitation. Auricular lymph nodes (LN) were collected at D0, D3, D7, D10 and D13. Single cell transcriptomic analyses were performed in order to identify immune cells proportions and markers expression. Results: Exposure to both sensitizers induced a strong immune reaction demonstrated by an increase of mature B cells and an evolution of the T cell subpopulations, with an increase of follicular and memory T cells. The proportion of NKT, Th2 and Th9 cells and the levels of IgE increased specifically during PA exposure. Follicular, memory and helper T cells showed distinct transcriptomic responses to DNCB or PA. The proportion of dendritic cells strongly increased starting from D10 in mice exposed to DNCB and those cells showed a specific genetic signature towards the skin sensitizer. Conclusion: A distinct transcriptomic signature was identified in immune cells during sensitization to DNCB or PA in this study.
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8. ⭐ GSE274468 ZMYM3 突变调节组蛋白乙酰化，并与 NOTCH1 突变在慢性淋巴细胞白血病中协同作用 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、RNA-seq、histone
• 📝 描述：Contributors : Alberto Rodríguez-Sánchez ; Claudia Pérez-Carretero ; Luis A Corchete-Sánchez ; Cristina Miguel-García ; Sandra Santos-Mínguez ; Ángela Villaverde Ramiro ; Julio Dávila ; Alfonso García Coca ; Josefina Galende ; Rocío Benito-Sánchez ; Ana E Rodríguez Vicente ; Miguel Quijada-Álamo ; Jesús M Hernández RivasSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRecent advances in next-generation sequencing (NGS) have significantly expanded our understanding of the mutational landscape of chronic lymphocytic leukemia (CLL), identifying over 200 potential genetic drivers. Nevertheless, the prognostic and functional impact of numerous mutations remains elusive. In this study, through the integration of clinical, in vitro and ex vivo data, we assessed the clinical and biological implications of ZMYM3 mutations in CLL, a gene recurrently mutated in 2-4% of patients. NGS analyses in a cohort of 487 CLL cases identified 32 ZMYM3 variants, with 75% (24/32) characterized as loss-of-function mutations. Notably, 70% of ZMYM3-mutated patients harbored mutations in the NOTCH signaling pathway, predominantly in NOTCH1 (60%). In terms of clinical impact, in both univariate and multivariate analysis ZMYM3 variants were significantly associated with a shorter time to first treatment compared to control cases (median: 35 vs 52 months; p=0.010) and stratified the clinical outcome of early-stage CLL cases (median: 48 vs 91 months; p=0.016). In parallel, using CRISPR/Cas9 editing, we demonstrated that ZMYM3 mutations exhibit cooperative effects with NOTCH1 mutations, evidenced by a profound transcriptional dysregulation. In line, our findings revealed that ZMYM3 mutations reduce global histone H4 acetylation and modulate chromatin accessibility. Furthermore, at the functional level, ZMYM3 mutations compromise DNA damage repair mechanisms and promote apoptosis evasion by caspases downregulation, correlating this anti-apoptotic phenotype with higher sensitivity to BCL-XL inhibition. Overall, this work underscores the significance of ZMYM3 mutations in chromatin modification and its relevance in CLL prognosis.
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9. ⭐ GSE274467 ZMYM3 突变调节组蛋白乙酰化，并与 NOTCH1 突变在慢性淋巴细胞白血病中协同作用 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、ATAC-seq、histone
• 📝 描述：Contributors : Alberto Rodríguez-Sánchez ; Claudia Pérez-Carretero ; Luis A Corchete-Sánchez ; Cristina Miguel-García ; Sandra Santos-Mínguez ; Ángela Villaverde Ramiro ; Julio Dávila ; Alfonso García Coca ; Josefina Galende ; Rocío Benito-Sánchez ; Ana E Rodríguez Vicente ; Miguel Quijada-Álamo ; Jesús M Hernández RivasSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRecent advances in next-generation sequencing (NGS) have significantly expanded our understanding of the mutational landscape of chronic lymphocytic leukemia (CLL), identifying over 200 potential genetic drivers. Nevertheless, the prognostic and functional impact of numerous mutations remains elusive. In this study, through the integration of clinical, in vitro and ex vivo data, we assessed the clinical and biological implications of ZMYM3 mutations in CLL, a gene recurrently mutated in 2-4% of patients. NGS analyses in a cohort of 487 CLL cases identified 32 ZMYM3 variants, with 75% (24/32) characterized as loss-of-function mutations. Notably, 70% of ZMYM3-mutated patients harbored mutations in the NOTCH signaling pathway, predominantly in NOTCH1 (60%). In terms of clinical impact, in both univariate and multivariate analysis ZMYM3 variants were significantly associated with a shorter time to first treatment compared to control cases (median: 35 vs 52 months; p=0.010) and stratified the clinical outcome of early-stage CLL cases (median: 48 vs 91 months; p=0.016). In parallel, using CRISPR/Cas9 editing, we demonstrated that ZMYM3 mutations exhibit cooperative effects with NOTCH1 mutations, evidenced by a profound transcriptional dysregulation. In line, our findings revealed that ZMYM3 mutations reduce global histone H4 acetylation and modulate chromatin accessibility. Furthermore, at the functional level, ZMYM3 mutations compromise DNA damage repair mechanisms and promote apoptosis evasion by caspases downregulation, correlating this anti-apoptotic phenotype with higher sensitivity to BCL-XL inhibition. Overall, this work underscores the significance of ZMYM3 mutations in chromatin modification and its relevance in CLL prognosis.
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10. ⭐ GSE270301 N-糖基化抑制可阻碍免疫抑制性肿瘤微环境细胞，从而提高CAR-T细胞疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、T cell
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis SuperSeries is composed of the SubSeries listed below.
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1. ⭐ 科学家将益生菌转化为治疗胰腺癌的微型药物工厂

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Engineered probiotic bacteria were able to infiltrate pancreatic tumors, stimulate cancer-fighting immune cells, and slow tumor growth in animal studies. Even more strikingly, the treatment worked better when combined with chemotherapy, radiation, or immunotherapy.
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2. 微型光能机器人可以追踪并收集细菌

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Researchers have built microscopic, light-driven robots that can rapidly navigate through liquid, collect bacteria, and deposit them in chosen locations. These tiny “cleaners” could open new possibilities for manipulating cells and microbes with remarkable precision.
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3. 从实验室到数据：RNA测序数据分析实用指南

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：A practical guide helps molecular biologists understand RNA sequencing data analysis, from quality control and normalization to differential expression and biological interpretation…
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4. RNA测序可解析线粒体疾病中的隐匿性致病变异

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Mitochondrial diseases are a diverse group of inherited disorders that interfere with the ability of cells to produce and use energy. Because mitochondria are important in nearly every tissue, these disorders can affect the brain, muscles, heart, liver, and other organs. Symptoms and severity can also vary considerably from one patient to another. Finding …
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5. 亚裔美国女性乳腺癌发病率激增——科学家们却不知其原因。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Breast cancer is rising rapidly among Asian American women, with some of the most alarming increases occurring in younger women and in aggressive or advanced cancers. Researchers say screening alone can’t explain the surge, suggesting important risk factors may still be undiscovered.
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6. 人工智能设计的“体内抗体”有望为阿尔茨海默病、帕金森病和运动神经元疾病带来新的治疗方法。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers have developed a new way to turn ordinary antibodies into tiny disease-fighting molecules that can work inside human cells, potentially opening new paths for treating Alzheimer’s, Parkinson’s, Huntington’s disease, and motor neurone disease.
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• GSE242319 新型转录因子 BTNL9 通过细胞周期调控增强非小细胞肺癌的肿瘤抑制和药物敏感性 [RNA-seq]
• GSE242317 新型转录因子 BTNL9 通过细胞周期调控增强非小细胞肺癌的肿瘤抑制和药物敏感性 [ChIP-seq]
• GSE319163 肿瘤细胞内在应激状态驱动胰腺癌对 CAR-T 细胞疗法的敏感性
• GSE309280 小鼠破骨细胞分化的转录组分析（单细胞RNA测序）
• GSE344032 Ptpn1 缺失导致 B 细胞急性淋巴细胞白血病
• GSE341121 通过 ChIP-seq 对 Flo8 结合区域进行全基因组鉴定。
• GSE339453：对携带 EGFR/RB1/TP53 突变的 LUAD 细胞系进行单细胞 RNA 测序，以评估 PHOX2B 过表达与否对神经内分泌表型诱导的影响
• GSE334010 人类肺成纤维细胞的转录和空间分析突显了 CTHRC1+ 细胞作为纤维化中的成纤维信号枢纽 [scRNA-seq 培养]
• GSE318117 Hsa_circ_0000231 通过 CACNA1H 加速宫颈癌细胞增殖、侵袭和 MAPK 通路激活
• GSE337871 SELENOF 在皮肤癌中发挥抑癌基因的作用
• GSE337803 发育调控祖细胞衰老塑造果蝇肠道长期稳态
• GSE337532 RNA-seq 分析 C2C12 肺癌相关疲劳细胞模型经 elesclomol 和索拉非尼治疗
• GSE334349 未经处理和经骨髓移植的小鼠肝脏 CD45+ 免疫细胞的 ATAC-seq 分析
• GSE333856 EZH1/2 抑制剂通过抑制干细胞特性和增殖选择性地靶向 SMARCA4/2 共缺陷的肺癌细胞 [ATAC-seq]
• GSE317641 单核 RNA 测序揭示犬棘皮瘤性成釉细胞瘤的特征是存在一群独特的神经元样上皮细胞
• GSE306476 细胞因子基因组合在 iPS 细胞衍生的 T 细胞中协同改善实体瘤的迁移、增殖和记忆形成 [ATAC-seq]
• GSE293401 ZMYM3 突变调节组蛋白乙酰化，并与 NOTCH1 突变在慢性淋巴细胞白血病中协同作用
• GSE242320 新型转录因子 BTNL9 通过细胞周期调控增强非小细胞肺癌的肿瘤抑制作用和药物敏感性
• GSE217934 神经球单细胞 RNA 测序
• GSE343985 对感染 PPRV 的山羊子宫内膜上皮细胞进行转录组测序分析，并揭示 STING 信号通路在 PPRV 感染中的关键作用
• GSE343966 亲代和 EMP1 缺陷型 MB49 膀胱肿瘤免疫细胞的单细胞转录组分析。
• GSE343708 小鼠骨髓细胞 CNP 信号改变的单细胞 RNA 测序。
• GSE343667 Lgr4 维持 Lgr5+ 隐窝基底柱状细胞的特性，这是肠道稳态和再生所必需的 [RNA-Seq]
• GSE343665 Lgr4 维持 Lgr5+ 隐窝基底柱状细胞的特性，这是肠道稳态和再生所必需的 [scRNA-seq]
• GSE314307 急性降解介导的 RUNX1 丢失重编程增强子活性，与上皮不稳定和癌症标志的启动有关 [ChIP-seq]
• GSE314305 急性降解介导的 RUNX1 丢失重编程增强子活性与上皮不稳定和癌症标志的启动有关 [RNA-seq]
• GSE314301 急性降解介导的 RUNX1 丢失重编程增强子活性与上皮不稳定和癌症标志的启动有关 [ATAC-seq]
• GSE306019 KRASG12D-p53 缺失驱动的小鼠肺癌中 Usp22 的基因缺失 [Visium]
• GSE306017 KRASG12D-p53 null 驱动的肺癌中 Usp22 基因缺失 [RNA-Seq]
• GSE343567 棘阿米巴 Neff 株包囊形成时间进程的 RNA-seq 分析
• GSE342403 裂殖酵母中Swi1缺失后Rad52与全基因组染色质的关联
• GSE342402 裂殖酵母Swi1基因缺失后的转录组分析
• GSE339246 RNA-seq 分析表达对照 shRNA 或 Timeless shRNA 的 U-2 OS 骨肉瘤细胞。
• GSE337104 m6A 阅读器 IGF2BP1 对铁死亡的抑制是胰腺导管腺癌吉西他滨耐药的基础 [shRNA-Seq]
• GSE337103 m6A 阅读器 IGF2BP1 对铁死亡的抑制是胰腺导管腺癌吉西他滨耐药的基础 [RIP-Seq]
• GSE337101 m6A 阅读器 IGF2BP1 对铁死亡的抑制是胰腺导管腺癌吉西他滨耐药的基础 [MeRIP-Seq]
• GSE325471 CDK4/6抑制剂dalpiciclib通过抑制MCM4介导的DNA复制，增强恩扎卢胺在去势抵抗性前列腺癌临床前模型中的抗肿瘤疗效。
• GSE316878 鼻细胞衍生的肺泡类器官-巨噬细胞共培养
• GSE315704 拟南芥中DCP2依赖的5’端帽足迹的全基因组定位
• GSE313515 小胶质细胞中胆固醇晶体-STING通路失调驱动缺血性卒中后的神经炎症
• GSE308838 三阴性乳腺癌相关蛋白γKlotho和miRNA作为犬乳腺癌的潜在预后标志物和治疗靶点
• GSE306038 肿瘤内浆细胞是原发性恶性周围神经鞘瘤免疫检查点阻断疗法所必需的
• GSE301649 肺动脉平滑肌细胞中HMGB1驱动的增殖和迁移的RNA测序
• GSE344335 放射后6小时GPC3野生型和敲除型HepG2和Hep3B肝细胞癌细胞的比较转录组分析
• GSE341884 研究SOX9诱导和敲除对原代人肠道干细胞单层的影响
• GSE341376 肺孢子菌感染期间细胞内巨噬细胞的存活
• GSE337298 用 miR-374b-5p 和 miR-374a-5p 转染的 MCF7 乳腺癌细胞的基因表达谱分析
• GSE336862 AI驱动发现尼克酰胺作为VTRNA1-1模拟物靶向急性髓系白血病中的p62 ZZ结构域
• GSE335697 氟维司群处理的 MCF7 乳腺癌细胞的 miRNA 表达谱分析
• GSE334350：来自未经处理和Mr BMT小鼠的肝脏巨噬细胞的批量RNA测序
• GSE334348 在稳态和炎症条件下，对未接受任何处理的小鼠、接受tBMT和MrBMT的小鼠的外周器官进行批量RNA测序
• GSE333828 EZH1/2抑制剂通过抑制干细胞特性和增殖，选择性地靶向SMARCA4/2共缺陷的肺癌细胞。
• GSE329964 鼻咽拭子转录组学揭示腺样体肥大和过敏性鼻炎的不同致病机制
• GSE329269 利用单核和批量RNA测序对人iPSC衍生的瘙痒感受器进行转录组分析
• GSE329092 骨骼肌发育和功能成熟调控增强子和转录因子的鉴定 [RNA-Seq]
• GSE329091 骨骼肌发育和功能成熟调控增强子和转录因子的鉴定 [ChIP-Seq]
• GSE328820 对接受司库奇尤单抗治疗前后 4 周采集的斑块状银屑病患者的外周血单核细胞进行批量 RNA 测序，这些患者的 52 周临床反应轨迹各不相同
• GSE328393 健康人和 IPF 原代人肺成纤维细胞中 DNA 损伤诱导衰老的多组学分析 [ATAC-seq]
• GSE328392 健康人和 IPF 原代人肺成纤维细胞中 DNA 损伤诱导衰老的多组学分析 [RNA-seq]
• GSE322936 CVID 合并 GLILD 患者的支气管肺泡灌洗液来源免疫细胞与结节病患者不同
• GSE311094 出芽酵母中 RNA 聚合酶 III 的 ChIP-seq 分析。
• GSE310124 衰老标志物及相关转录组变化在阿尔茨海默病早期神经病理学改变中表达，但与痴呆状态无独立相关性
• GSE305873 野生型和PGRN基因敲除小鼠的单细胞RNA测序数据比较基因表达谱分析。[scRNA-Seq]
• GSE305180 WT 和 PGRN-KO 小鼠 RNA-seq 数据的比较基因表达谱分析。
• GSE304660 基因组折叠和核斑点共同调控成纤维细胞活化
• GSE301515 人类类器官揭示 PTEN 驱动的中内胚层分化通过抑制视黄酸信号通路实现 [单细胞 RNA 测序]
• GSE301161 人类类器官揭示了 PTEN 驱动的中内胚层分化通过抑制视黄酸信号通路实现 [ATAC-Seq]
• GSE301159 人类类器官揭示了 PTEN 驱动的中内胚层分化通过抑制视黄酸信号通路实现 [RNA-Seq]
• GSE283632 Linc01446 通过调控 APEX1 参与铁死亡防御和食管鳞状细胞癌的进展
• GSE281431 揭示T-PLL中大规模编码和非编码转录组失调
• GSE269527 拟南芥 Col-0 msh1 记忆基因第 1 代、第 7 代和非记忆基因的 sRNA 测序
• GSE269287 拟南芥 Col-0 msh1 记忆基因第 1 代、第 7 代和非记忆基因的亚硫酸氢盐测序
• GSE269286 拟南芥 Col-0 msh1 记忆蛋白的同源异构体测序
• GSE252998 细胞因子基因组合对iPS细胞衍生的T细胞具有协同作用，可改善实体瘤中的迁移、增殖和记忆形成
• GSE220292 利用siControl和siNsun2对E14细胞系中5-甲基胞嘧啶(m5C)甲基化进行分析
• GSE343669：T细胞急性淋巴细胞白血病中CD38的多模态分析揭示联合治疗策略
• GSE343668 新生儿D-β-羟基丁酸替代疗法和早期母体TUDCA干预后P7海马体批量RNA测序
• GSE334830 追踪心脏修复中新生冠状动脉侧支循环形成的起源 [CUT&RUN]
• GSE320081 肿瘤自主性IL-6信号传导在肝内胆管癌中的分子和细胞后果
• GSE314312 急性降解介导的 RUNX1 丢失重编程增强子活性，与上皮不稳定和癌症标志的启动有关 [PRO-seq]
• GSE306054 MEF2B突变型套细胞淋巴瘤（MCL）新生RNA谱分析，旨在明确其即时转录程序
• GSE287511 交感神经元介导的雄激素信号传导调节过敏性肺部炎症
• GSE275756 小鼠健康脾脏、肿瘤脾脏和肿瘤 Treg 细胞的转录特性。
• GSE335071 体外转录的经 5-甲氧基尿嘧啶修饰的 eGFP mRNA 的直接 RNA 测序
• GSE315701 唾液蛋白NlSP2与OsCBSX3–SNAC3模块相互作用，增强水稻免疫力
• GSE313502 5-甲氧基尿嘧啶修饰的体外转录mRNA的直接RNA测序
• GSE312827 RNA 测序：对转染 RNA 的细胞做出反应，包括未修饰的 RNA、5 甲氧基尿嘧啶修饰的 RNA 和 N1 甲基假尿苷修饰的 RNA。
• GSE304591 利福平作用下大肠杆菌转录组的调控机制
• GSE300261 Plakophilin 1 通过 DExD/H 解旋酶抑制角质形成细胞的固有免疫反应
• GSE275525 通过整合系统生物学重新定义恶臭假单胞菌中的 HexR 调控格局 [RNA-Seq]