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1. ⭐ 空间组学 | Nat.Genet. | 单细胞多组学与空间图谱揭示食管鳞状细胞癌中GPR116+周细胞在癌症转移中的免疫抑制作用

• ✍️ 作者：BioJournal Link
• 🏷️ 关键词：癌症、免疫、T细胞、单细胞、空间组学
• 🔗 查看原文

2. ⭐ 5月最新6+生信，单细胞+空转分析MMP1+ 肿瘤细胞对肿瘤-免疫相互作用的影响，识别某基因阳性的细胞亚群是目前流行的发文思路！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：肿瘤、免疫、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

3. ⭐ Cell |单细胞联合空间发现新型巨噬细胞靶向免疫细胞因子，看看咋实验验证的

• ✍️ 作者：生信钱同学
• 🏷️ 关键词：免疫、巨噬细胞、细胞因子、单细胞
• 📝 描述：清晰的组学和实验思路
• 🔗 查看原文

4. ⭐ 《细胞》：免疫治疗重磅炸弹诞生！科学家发明新型免疫治疗药物，能同时增强巨噬细胞、NK细胞和T细胞抗癌能力

• ✍️ 作者：奇点肿瘤探秘
• 🏷️ 关键词：免疫、T细胞、巨噬细胞、NK细胞
• 📝 描述：可以说是免疫治疗领域的重磅突破了！
• 🔗 查看原文

5. ⭐ 单细胞分辨率下肿瘤微环境的代谢图谱

• ✍️ 作者：生信菜鸟团
• 🏷️ 关键词：肿瘤、代谢、单细胞
• 🔗 查看原文

6. ⭐ 生信绘图不再愁！karyoploteR包，三分钟轻松绘制基因组数据，快速掌握染色体可视化与注释技巧！

• ✍️ 作者：云生信
• 🏷️ 关键词：基因组、生信、R包
• 🔗 查看原文

7. ⭐ 最新8+生信，结合单细胞+空转+ 18 种程序性细胞死，着重于对预后和免疫治疗疗效的预测及基因功能验证！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

8. ⭐ 7+生信，基于单细胞和空转识别生态位特异性转录和细胞组成特征，识别关键基因并进行验证。思路新颖！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：单细胞、转录组、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

9. scRNA与scBCR-seq识别不同年龄段健康供体腹膜腔和外周血中BCR双抗体B细胞

• ✍️ 作者：单细胞天地
• 🏷️ 关键词：B细胞、抗体
• 📝 描述：通过单细胞与免疫组库，系统比较不同年龄段人类与小鼠B细胞受体组成，发现双BCR B细胞随年龄增长而显著增加，且主要来源于B1细胞。该群体呈现独特基因表达谱，提示免疫衰老伴随B细胞受体多样性"质变"，为理解年龄相关免疫失调提供了新视角
• 🔗 查看原文

10. 选题想顺利搭上国自然？山大团队这篇“表型差异+免疫细胞+炎症基因”的框架就是现成模板！

• ✍️ 作者：神经岛
• 🏷️ 关键词：免疫、炎症
• 🔗 查看原文

💡 该来源还有 22 条内容，详见 文末

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1. ⭐ GSE310605 UHRF1 缺陷通过表观遗传调控 NPY1R 基因甲基化加剧肠道炎症

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、epigenetic、methylation、regex:intestin(e|al)
• 📝 描述：Contributor : Han YananSeries Type : Methylation profiling by arrayOrganism : Homo sapiensEpigenetic modifications play a crucial role in the pathogenesis of inflammatory bowel disease (IBD) by mediating gene–environment interactions. We previously showed that UHRF1, a central regulator of DNA methylation, contributes to cancer progression; however, its function in IBD remains poorly understood. Here, we revealed that UHRF1 is frequently reduced in inflamed tissues of IBD patients and that its deficiency exacerbates intestinal epithelial cell (IEC) damage. Through a multi-level approach incorporating human cell models and an intestinal epithelial-specific Uhrf1 knockout mouse model, we established UHRF1 as a key mitigator of IBD progression. Mechanistically, UHRF1 bound to the NPY1R promoter, promoting its methylation and leading to transcriptional suppression. The NPY1R upregulation resulting from UHRF1 deficiency attenuated cAMP–PKA–CREB signaling in IECs, thereby enhancing NF-κB activation and subsequent pro-inflammatory responses, which compromised intestinal epithelial barrier integrity. Furthermore, we identified miR-141 as a negative regulator of NPY1R, highlighting its potential as a therapeutic agent. Collectively, our results identified the UHRF1–NPY1R regulatory axis as a critical epigenetic mechanism in intestinal inflammation and underscored its dual promise for IBD diagnostics and therapy.
• 🔗 查看原文

2. ⭐ GSE310603 UHRF1 缺陷通过表观遗传调控 NPY1R 基因甲基化加剧肠道炎症 [基因表达]

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、epigenetic、methylation、regex:intestin(e|al)
• 📝 描述：Contributors : Han Yanan ; Bai XueSeries Type : Expression profiling by arrayOrganism : Homo sapiensEpigenetic modifications play a crucial role in the pathogenesis of inflammatory bowel disease (IBD) by mediating gene–environment interactions. We previously showed that UHRF1, a central regulator of DNA methylation, contributes to cancer progression; however, its function in IBD remains poorly understood. Here, we revealed that UHRF1 is frequently reduced in inflamed tissues of IBD patients and that its deficiency exacerbates intestinal epithelial cell (IEC) damage. Through a multi-level approach incorporating human cell models and an intestinal epithelial-specific Uhrf1 knockout mouse model, we established UHRF1 as a key mitigator of IBD progression. Mechanistically, UHRF1 bound to the NPY1R promoter, promoting its methylation and leading to transcriptional suppression. The NPY1R upregulation resulting from UHRF1 deficiency attenuated cAMP–PKA–CREB signaling in IECs, thereby enhancing NF-κB activation and subsequent pro-inflammatory responses, which compromised intestinal epithelial barrier integrity. Furthermore, we identified miR-141 as a negative regulator of NPY1R, highlighting its potential as a therapeutic agent. Collectively, our results identified the UHRF1–NPY1R regulatory axis as a critical epigenetic mechanism in intestinal inflammation and underscored its dual promise for IBD diagnostics and therapy.
• 🔗 查看原文

3. GSE310548 Etv2+ 和 Flk1+ 祖细胞对内皮、造血和心脏谱系的不同贡献 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac、RNA-seq
• 📝 描述：Contributors : Alleyne Dereck ; Kim Minseo ; Wu Jun ; Kwon Yoojung ; Kim Ye-Ram ; Ul Kabir Ashraf ; Ishahak Matthew ; Millman Jeffrey R. ; Fan Changxu ; Lee Hyung Joo ; Krchma Karen ; Xing Xiaoyun ; Lavine Kory ; Wang Ting ; Choi KyungheeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe ETS family transcription factor ETV2, VEGFA and its receptor FLK1 are essential for hematopoietic, vascular and cardiac development. Here, we combine dual Etv2 and Flk1 lineage tracing with molecular profiling to define how mesoderm progenitors are allocated to hematopoietic, endothelial, cardiomyocyte and smooth muscle lineages. We demonstrate that hematopoietic, endothelial, and cardiac valves arise from dual Etv2+ and Flk1+ lineages and that Etv2+ and Flk1+ mesoderm contributing to the hemangiogenic fate is molecularly distinct from those generating muscle. Mechanistically, we show that ETV2 cooperates with the BAF chromatin remodeling complex to establish accessibility at ETV2 target loci. Loss of Baf155 expression reduces chromatin accessibility at ETV2 target loci and impairs hemangiogenic lineage specification. This work defines lineage relationships and the molecular circuitry underlying hemangiogenic specification during cardiovascular development.
• 🔗 查看原文

4. GSE298248 选择性消除供体细菌可实现接合早期阶段质粒基因表达的全局分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Contributors : Meng Wen ; Nathan Fraikin ; Emma Mettouchi ; Christian Lesterlin ; Elena Espinosa ; Yoshiharu YamaichiSeries Type : Expression profiling by high throughput sequencingOrganism : Escherichia coli ; Sinorhizobium melilotiConjugative plasmids are a major driving force for the dissemination of antimicrobial resistance. During conjugation, plasmid DNA is transferred from the donor cell as a single-stranded (ss) linear molecule. Recent researches highlighted intriguing DNA reactions at the early stage of conjugation that are important for plasmid establishment in the recipient cell, including prompt expression of anti-defense genes. However, genomics-based approaches to investigate plasmid establishment have been challenging, because identical, fully established plasmids in donor cells mask transconjugant-specific signals. To overcome this limitation, we developed a new EDTA method which exploits a donor mutant hypersensitive to hypoosmotic shock. It allows unprecedently quick and efficient Elimination of Donor population for Transconjugant Accumulation. RNAseq analysis revealed highly selective and robust induction of plasmid genes during early stage of conjugation. We experimentally identified +1 sites of 6 possible operons that are matched with ssDNA promoter predictions. We also showed gene expression program is altered in different recipient cells in which plasmid establishment is perturbed. As the EDTA method is straightforward and broadly applicable, it will further understanding of the plasmid establishment processes in new host cell, not only gene expression but also ss to double-stranded DNA conversion and plasmid circularization.
• 🔗 查看原文

5. GSE280954 分泌BiTE的T细胞与PD-1阻断剂合理联合，促进局部免疫微环境重塑，从而增强卵巢癌的治疗反应持久性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Contributors : Long Mark ; McGray AJ Robert ; Chiello Jessie LSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusscRNA-seq (5’ GEX) was used to examine the peritoneal TME in IE9-mp1-hFRa cells bearing animals treated with FRB-T cell + anti-PD1 therapies. We observed unique TME composition associated with acute and durable responses to combination therapy that was disrupted in progressive disease. Further we found that providing an AD-OVA immunization boost along the course of therapy enhanced favorable TME composition and overall tumor control.
• 🔗 查看原文

6. GSE280910 人类-小鼠嵌合脑模型用于研究人类神经胶质细胞-神经元和巨胶质细胞-小胶质细胞相互作用 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、scRNA
• 📝 描述：Contributors : Jin Mengmeng ; Ma Ziyuan ; Jiang PengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHuman-mouse chimeric brain models, generated by transplanting human induced pluripotent stem cell (hiPSC)-derived neural cells, are valuable for studying the development and function of human neural cells in vivo. Understanding glial-glial and glial-neuronal interactions is essential for unraveling the complexities of brain function and developing treatments for neurological disorders. To explore these interactions between human neural cells in vivo, we co-engrafted hiPSC-derived neural progenitor cells together with primitive macrophage progenitors into the neonatal mouse brain. This approach creates human-mouse chimeric brains containing human microglia, macroglia (astroglia and oligodendroglia), and neurons. Using super-resolution imaging and 3D reconstruction techniques, we examine the dynamics between human neurons and glia, and observe human microglia pruning synapses of human neurons, and often engulfing neurons themselves, as well as the interactions between human oligodendrocytes and neurons. Single-cell RNA sequencing analysis of the chimeric brain uncovers a close recapitulation of the human glial progenitor cell population, along with a dynamic stage in astroglial development that mirrors the processes found in the human brain. Furthermore, cell-cell communication analysis highlights significant neuronal-glial and macroglial-microglial interactions, especially the interaction between adhesion molecules neurexins and neuroligins. This innovative co-transplantation model opens up new avenues for exploring the complex pathophysiological mechanisms underlying human neurological diseases. It holds particular promise for studying disorders where glial-neuronal interactions and non-cell-autonomous effects play crucial roles.
• 🔗 查看原文

7. GSE280909 人类-小鼠嵌合脑模型研究人类神经胶质细胞-神经元和巨胶质细胞-小胶质细胞相互作用 [批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、RNA-seq
• 📝 描述：Contributors : Jin Mengmeng ; Ma Ziyuan ; Jiang PengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHuman-mouse chimeric brain models, generated by transplanting human induced pluripotent stem cell (hiPSC)-derived neural cells, are valuable for studying the development and function of human neural cells in vivo. Understanding glial-glial and glial-neuronal interactions is essential for unraveling the complexities of brain function and developing treatments for neurological disorders. To explore these interactions between human neural cells in vivo, we co-engrafted hiPSC-derived neural progenitor cells together with primitive macrophage progenitors into the neonatal mouse brain. This approach creates human-mouse chimeric brains containing human microglia, macroglia (astroglia and oligodendroglia), and neurons. Using super-resolution imaging and 3D reconstruction techniques, we examine the dynamics between human neurons and glia, and observe human microglia pruning synapses of human neurons, and often engulfing neurons themselves, as well as the interactions between human oligodendrocytes and neurons. Single-cell RNA sequencing analysis of the chimeric brain uncovers a close recapitulation of the human glial progenitor cell population, along with a dynamic stage in astroglial development that mirrors the processes found in the human brain. Furthermore, cell-cell communication analysis highlights significant neuronal-glial and macroglial-microglial interactions, especially the interaction between adhesion molecules neurexins and neuroligins. This innovative co-transplantation model opens up new avenues for exploring the complex pathophysiological mechanisms underlying human neurological diseases. It holds particular promise for studying disorders where glial-neuronal interactions and non-cell-autonomous effects play crucial roles.
• 🔗 查看原文

8. GSE280054 抑制 ADSS2 介导的从头 AMP 生物合成可使急性髓系白血病对 BH3 模拟物重新敏感 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、scRNA
• 📝 描述：Contributors : Xin He ; Wei Chen ; Ling LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensDe novo purine synthesis is required to promote tumor growth; however, its role in therapy resistance remains elusive. Here, through a dynamic BH3-priming based CRISPR-Cas9 screen, we found that deletion of ADSS2, which encodes for an enzyme functioning in de novo AMP synthesis, re-sensitizes drug resistant acute myeloid leukemia (AML) cells to BH3 mimetics. Single-cell sequencing and metabolomics analyses reveal that high ADSS2 activity in leukemia samples including those with TP53 aberrations inversely correlates with venetoclax responsiveness. Further, we developed anADSS2 antagonist, exhibiting synergism with BH3 mimetics in preclinical AML models. Mechanistically, sensitization to BH3 mimetics mediated by ADSS targeting was associated with downregulated AMPK activity, which governs mitochondrial homeostasis. AMPK activity in resistant cells promotes mitophagy to eliminate damaged mitochondria upon BH3 mimetics treatment. These data demonstrate that AMP synthesis governs venetoclax resistance, and that combining ADSS targeting with BH3 mimetic treatment could represent a promising approach against AML.
• 🔗 查看原文

9. GSE310067 人类输卵管上皮类器官携带TP53突变，重现浆液性输卵管上皮内癌（STIC）的特征 - RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、sequencing
• 📝 描述：Contributors : Judith Kraiczy ; Bo YuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHuman fallopian tube epithelial organoids with TP53 mutation recapitulate features of serous tubal intraepithelial carcinoma (STIC),Judith Kraiczy, Bo Yu,Gynecologic Oncology, Volume 203,2025, Pages 198-208, ISSN 0090-8258,https://doi.org/10.1016/j.ygyno.2025.10.038.SUMMARY Objective Serous tubal intraepithelial carcinoma (STIC) is the immediate precursor lesion for high-grade serous ovarian carcinoma (HGSOC) and harbors universal TP53 mutations. The lack of an appropriate in vitro model for STIC presents a major challenge in studying its pathogenesis. We aimed to develop a human in vitro model that mimics STIC lesions. Methods Using CRISPR-Cas9 gene editing, we generated human fallopian tube epithelial organoids with TP53 loss-of-function mutations (TP53-/- FTOs). We characterized TP53-/- FTOs on a cellular and molecular level using immunofluorescence confocal imaging, copy number variation (CNV) analysis, and RNA sequencing. TP53-/- FTOs recapitulated key features of STIC lesions. They exhibited increased proliferation and nuclear abnormalities, including nuclear enlargement and atypical mitotic figures. Copy number variation analysis revealed aneuploidy in some TP53-/- FTOs. Compared to unedited controls, TP53-/- FTOs demonstrated significant transcriptomic changes, including the downregulation of DNA repair genes and upregulation of epithelial-mesenchymal transition (EMT) pathways. Similar to STIC lesions, TP53-/- FTOs showed a marked reduction in ciliated cells and ciliogenesis-associated gene expression. Conclusions These findings suggest that p53 loss in FTOs promotes a proliferative and genomically unstable state that is conducive to carcinogenesis. The TP53-/- FTO model we have generated provides a valuable tool for studying early events in ovarian carcinogenesis and for developing new strategies for the early detection and prevention of ovarian cancer.
• 🔗 查看原文

10. GSE283535 METTL3 通过调控 CDC25A 和 AURKB mRNA 的稳定性，促进非小细胞肺癌细胞系对奥希替尼的耐药性。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance
• 📝 描述：Contributors : Ryusuke Suzuki ; Minoru Terashima ; Akihiko Ishimura ; Makiko Meguro-Horike ; Shin-ichi Horike ; Yuka Kubota ; Sasithorn Wanna-udom ; Seiji Yano ; Takahisa Takino ; Takeshi SuzukiSeries Type : Expression profiling by arrayOrganism : Homo sapiensOsimertinib, a third-generation EGFR tyrosine kinase inhibitor, is used as a first-line therapy for non-small cell lung cancer (NSCLC) harboring EGFR mutations. Nevertheless, the emergence of acquired drug resistance poses a significant challenge, leading to poor clinical outcomes. METTL3, a key methyltransferase responsible for N6-methyladenosine (m6A) modification of RNA, has been implicated in cancer development and progression across various cancer types. In this study, we explored the role of METTL3 in acquired resistance to osimertinib and assessed its potential as a therapeutic target. Using METTL3 knockdown EGFR-mutated NSCLC cell lines, we found that downregulation of METTL3 suppressed the acquisition of osimertinib resistance. Microarray analysis and qRT-PCR revealed that CDC25A and AURKB are downstream target genes of METTL3, with METTL3 facilitating the stabilization of their mRNAs. Downregulation of these METTL3 target genes also attenuated osimertinib resistance. Furthermore, we evaluated the effects of combining osimertinib with either a METTL3 inhibitor or a CDC25A inhibitor, both of which increased drug efficacy by promoting apoptosis. Collectively, this study highlights the involvement of METTL3 in the initial acquisition of osimertinib resistance and the therapeutic potential of targeting the METTL3-mediated regulatory pathway.
• 🔗 查看原文

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1. ⭐ 对FFPE组织中成像空间转录组学平台进行系统性基准测试

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：A comparison of imaging spatial transcriptomics platforms reveals strengths and tradeoffs across technologies using FFPE tissues and integrates insights with RNA sequencing…
• 🔗 查看原文

2. 这种小小的药丸可能会改变我们诊断肠道健康的方式。

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：Tiny ingestible spheres filled with engineered bacteria can detect intestinal bleeding by glowing when they encounter heme. Early tests in mice suggest they could become a quick, noninvasive way to monitor gut disease.
• 🔗 查看原文

3. 三联疗法可引发针对白血病的强效免疫攻击。

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、immune
• 📝 描述：A cutting-edge approach to immunotherapy shows that forcing cancer cells to die through necroptosis can dramatically boost the body’s anti-tumor defenses. By combining three existing drugs, scientists reprogrammed malignant B cells so they release danger signals that rally immune cells to fully eliminate leukemia in preclinical models.
• 🔗 查看原文

4. scSpecies——增强比较单细胞研究中的网络结构对齐

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：A new deep learning tool improves cross species single cell comparisons and integrates insights with RNA sequencing to enhance…
• 🔗 查看原文

5. 简单的氨基酸补充剂能显著减轻阿尔茨海默病造成的损害。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers discovered that the common amino acid arginine can block harmful Aβ aggregation and reduce its toxic effects in Alzheimer’s disease models. In flies and mice, oral arginine lowered plaque levels, reduced inflammation, and improved behavior. Its strong safety record and low cost make it a promising repurposing candidate. The findings hint at a surprisingly simple path toward more accessible AD therapies.
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• 最新10分生信，单细胞+空转识别ECM 重塑相关成纤维细胞，并确定关键基因进行实验验证，干湿结合值得借鉴！
• 衰老不是磨损，而是泄漏！Nature揭示炎症新源头！
• 浅谈生物信息个性化分析
• 纯生信分析的天花板！哈医大利用多组学+泛癌分析，还能融合单细胞，拿下6分SCI实至名归！
• IF=16.6 Cancer Res 文献解读| 梗阻性肠癌的脂代谢陷阱被揭开，香草酮抑制方案可直接套用！
• Cell Rep：王璋/郑雪燕揭示环境污染驱动呼吸道抗生素耐药基因的富集与传播
• 不止是能量：代谢调控如何重塑免疫细胞的命运与功能
• 新机制见解！同济大学附属东方医院等单位发文：克服肿瘤耐药性和提高病理缓解率的潜在策略
• 最新10+纯生信，空转Visium+COSMx定义治疗反应相关的niche！生信分析新思路，值得收藏学习！
• M2巨噬细胞迁移体双重信号导引干细胞归巢
• 刚刚发表的7.5分生信，一种用于精准泛癌分类的多表征深度学习框架！只要有技术，还做什么实验！
• 对话 | 全球14亿人血压失控！斯坦福专家教你用八招守护心脏健康 | Bilingual
• kmodR：带异常检测的 K-Means 聚类
• 解码卵巢癌前病变：空间蛋白组学勾勒输卵管上皮内癌向高分级浆液性卵巢癌的演化进程
• scUnified：单细胞数据分析的AI标准化资源
• 67分巨作，带你用爆火的代谢重编程实现弯道超车
• Cell Genom最新力作！多组学+孟德尔随机化分析，破解血清代谢物与慢性疾病的遗传关联！
• 28 样本 IF40.4！解密王红阳院士团队的单细胞创新密码
• 最新27+生信，原来只做了这些操作！
• NM｜死亡风险飙升 22.4 倍！1250 例数据揭示，相比远处转移，这件事才是癌症致死的“头号杀手”！
• 地球健康的隐形守护者——微生物丨Cell Press Live
• Cell子刊：GLP-1类药物，发挥全身性抗衰老作用

• GSE282695 STAT3 通过重编程炎症诱导的微生物防御反应来调节巨噬细胞中的病原体控制和清除。
• GSE279638 利用转座子进行生物传感器引导的全基因组诱变测序结果
• GSE310716 不同细胞外基质硬度下神经母细胞瘤细胞的全转录组学数据
• GSE310396 Etv2+ 和 Flk1+ 祖细胞对内皮、造血和心脏谱系的不同贡献
• GSE304598 人类iPSc分化为胸腺上皮祖细胞的批量RNA测序时间进程
• GSE295457 多组学研究揭示 CCL3 驱动不明原因慢性瘙痒中的神经元敏化
• GSE291111 转移性三阴性乳腺癌的全身化疗可极化效应T细胞分化
• GSE290679 代谢适应以亚群特异性方式重塑人类危重疾病（伴或不伴脓毒症）中的 CD4 T 细胞
• GSE271812 病毒和免疫损伤与组织修复之间的平衡可预防致命性流感感染导致的死亡
• GSE300561 低氮和有益细菌对根和茎生长的拟南芥的影响。
• GSE280009 抑制 ADSS2 介导的从头 AMP 生物合成可使急性髓系白血病对 BH3 模拟物重新敏感
• GSE310557 多组学分析揭示了微生物群-胆汁酸-TLR信号通路驱动间质性膀胱炎膀胱损伤的作用
• GSE310429 人类输卵管上皮类器官携带TP53突变，重现了浆液性输卵管上皮内癌（STIC）的特征 - LP-WGS
• GSE303156 糖尿病患者（伴或不伴代谢功能障碍相关脂肪性肝炎）循环外泌体microRNA谱分析
• GSE291949 HMGN1 和 HMGN2 被募集到乙酰化和含有组蛋白变体 H2A.Z 的核小体上，从而调节染色质状态和转录
• GSE291947 HMGN1 和 HMGN2 被募集到乙酰化和含有组蛋白变体 H2A.Z 的核小体上，从而调节染色质状态和转录
• GSE310181 Vnut 缺失对 CD4+ T 细胞分化为 Th1 细胞过程中基因表达的影响
• GSE297896 人类异种移植排斥反应中的克隆性 T 细胞反应
• GSE289110 不同的免疫调节通路介导恶性周围神经鞘瘤的放射治疗反应 [scRNA-Seq]