详细内容（前10条）

1. ⭐ 文献分享|Gut Microbes：单细胞尺度解析克罗恩病：肠道微生物组的“疾病指纹”与“疗效密码”

• ✍️ 作者：王永成Lab
• 🏷️ 关键词：微生物、T细胞、B细胞、单细胞、肠道、gut、regex:gut(-?microbiome)?
• 🔗 查看原文

2. ⭐ 腾讯发表最新Nature子刊论文：推出AI大模型，从单细胞转录组翻译单细胞蛋白质组

• ✍️ 作者：生物世界
• 🏷️ 关键词：T细胞、单细胞、转录组、蛋白质组、组蛋白
• 📝 描述：scTranslator（单细胞翻译器）
• 🔗 查看原文

3. ⭐ IF:7.6！华科大团队发现LXR-β通过STAT6激活小胶，属于神经炎症+免疫细胞选题

• ✍️ 作者：神经岛
• 🏷️ 关键词：免疫、T细胞、炎症、神经
• 🔗 查看原文

4. ⭐ Nature重磅！解析癌症免疫中的树突状细胞

• ✍️ 作者：生信人
• 🏷️ 关键词：癌症、免疫、T细胞、树突状细胞
• 📝 描述：树突状细胞是连接innate 免疫（先天免疫）和adaptive 免疫（适应性免疫）的关键枢纽，在肿瘤免疫中既
• 🔗 查看原文

5. ⭐ Nature子刊：杨勇/王文广团队等开发通用型癌症疫苗，利用乙肝病毒表面抗原，清除实体瘤

• ✍️ 作者：生物世界
• 🏷️ 关键词：癌症、疫苗、抗原、抗体
• 📝 描述：HBsAg标记的肿瘤疫苗系统，通过病毒特异性记忆 T 细胞消除实体瘤
• 🔗 查看原文

6. ⭐ CellWhisperer让聊天式分析成为现实；肿瘤亚克隆进化分析新工具；人类皮肤淋巴管“新地图”；新策略解析B细胞多样性 等

• ✍️ 作者：单细胞天地
• 🏷️ 关键词：肿瘤、淋巴、B细胞
• 🔗 查看原文

7. ⭐ 最新8+生信，多组学识别三级淋巴结构（TLS）结构并进行针对性分析。预测预后及免疫治疗疗效，值得借鉴！

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

8. ⭐ 10月最新26+生信，多组学空间免疫谱分析确定了三级淋巴结构（TLS）的亚群并进行深入分析，建议收藏！

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

9. ⭐ Nat Med | APOE ε4 介导的免疫异常：神经退行性疾病的共同分子轨迹

• ✍️ 作者：人体蛋白质组导航计划
• 🏷️ 关键词：免疫、神经、轨迹
• 🔗 查看原文

10. ⭐ Nat Commun丨国家蛋白质科学中心（北京）唐丽团队合作发现巨噬细胞处理脂蛋白失调促进脂质代谢紊乱相关疾病的发展

• ✍️ 作者：人体蛋白质组导航计划
• 🏷️ 关键词：T细胞、巨噬细胞、代谢
• 🔗 查看原文

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详细内容（前10条）

1. ⭐ GSE300217 利用两种新型液滴式单细胞RNA测序平台：与10x Genomics的比较研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell、10x、genomics
• 📝 描述：Contributors : Alesia Maluchenko ; Ekaterina Avsievich ; Iaroslava Zvorygina ; Zoia Antysheva ; Denis Maksimov ; Margarita Boytsova ; Dmitry Tabakov ; Natalia Bodunova ; Olga Glazova ; Dmitry Tychinin ; Alexander Bolbat ; Ekaterina Petriaikina ; Dmitry Svetlichnyy ; Sergey Yudin ; Anton Keskinov ; Vladimir Yudin ; Mary Woroncow ; Veronika Skvortsova ; Julia Krupinova ; Pavel VolchkovSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusHere we performed a comparison of two droplet-based high-throughput single-cell platforms, namely, SeekOne and MobiDrop with a widely-used commercial platform from 10x Genomics. The use of different types of samples allowed us to evaluate the performance of the platforms on cell suspensions of varying complexity and quality. 10x showed generally superior performance, although all platforms compared in this study showed acceptable gene yield and allowed identification of all expected cell types. Taking into account the cost and availability of devices and reagents required for each platform and the flexibility in the number of samples loaded onto the chip, SeekOne and MobiDrop might serve as a good alternative. The results of the current comparison will support the community’s efforts to compare different aspects, including sample amount requirements, throughput, cell quality, gene capture efficiency and cell type representativeness.
• 🔗 查看原文

2. ⭐ GSE310026 内在 RB 激活诱导肿瘤和基质抗肿瘤反应，从而限制三阴性乳腺癌 [scRNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、scRNA
• 📝 描述：Contributors : Yin Wan ; Jianxin Wang ; Thomas N O’Connor ; Vishnu Kumarasamy ; Ioannis Sanidas ; Scott I Abrams ; Agnieszka K Witkiewicz ; Erik S KnudsenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe RB tumor suppressor is a key regulator of cell cycle progression that is often inactivated in triple-negative breast cancer (TNBC). Recent studies indicate that drugs activating RB have multiple tumor-suppressing effects on the tumor and the tumor microenvironment (TME). Here, we utilize a constitutively active RB protein incapable of being phosphorylated and inactivated by CDKs (RBΔCDK) to assess the intrinsic sufficiency of RB activation on tumor suppression. Expression of RBΔCDK in TNBC cell lines uniformly inhibited proliferation. Transcriptomic analysis revealed suppression of cell cycle genes and the induction of genes associated with interferon response. Similarly, tumor growth and metastasis were suppressed in RBΔCDK expressing human xenograft and mouse syngeneic tumor models. RB activation was sufficient to dramatically alter the TME, wherein tumor growth suppression was mediated by CD8+ T cells. Together, these data indicate that active RB suppresses TNBC progression in cancer cell-autonomous and non-autonomous mechanisms.
• 🔗 查看原文

3. ⭐ GSE310025 内在 RB 激活诱导肿瘤和基质抗肿瘤反应，从而限制三阴性乳腺癌 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、RNA-seq
• 📝 描述：Contributors : Yin Wan ; Jianxin Wang ; Thomas N O’Connor ; Vishnu Kumarasamy ; Ioannis Sanidas ; Scott I Abrams ; Agnieszka K Witkiewicz ; Erik S KnudsenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusThe RB tumor suppressor is a key regulator of cell cycle progression that is often inactivated in triple-negative breast cancer (TNBC). Recent studies indicate that drugs activating RB have multiple tumor-suppressing effects on the tumor and the tumor microenvironment (TME). Here, we utilize a constitutively active RB protein incapable of being phosphorylated and inactivated by CDKs (RBΔCDK) to assess the intrinsic sufficiency of RB activation on tumor suppression. Expression of RBΔCDK in TNBC cell lines uniformly inhibited proliferation. Transcriptomic analysis revealed suppression of cell cycle genes and the induction of genes associated with interferon response. Similarly, tumor growth and metastasis were suppressed in RBΔCDK expressing human xenograft and mouse syngeneic tumor models. RB activation was sufficient to dramatically alter the TME, wherein tumor growth suppression was mediated by CD8+ T cells. Together, these data indicate that active RB suppresses TNBC progression in cancer cell-autonomous and non-autonomous mechanisms.
• 🔗 查看原文

4. ⭐ GSE309813 Deoxyguanosine Kinase Deficiency Couples Purine Metabolism to Innate Immune Activation and Lipid Accumulation in Hepatocytes

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、metabolism、kinase
• 📝 描述：Contributors : Maija Corey ; Sonia Sharma ; Jeamin JungSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMitochondrial DNA depletion syndromes (MDS) encompass a heterogeneous set of metabolic disorders caused by defects in enzymes responsible for maintaining mitochondrial nucleotide pools and genome integrity. Among these, deoxyguanosine kinase (DGUOK) acts within the mitochondrial purine-salvage pathway and loss-of-function mutations give rise to DGUOK deficiency, a severe hepatocerebral form of MDS marked by liver failure, neurodevelopmental impairment, and systemic metabolic inflammation. Although the clinical manifestations of DGUOK deficiency have been primarily ascribed to defective mitochondrial DNA (mtDNA) replication, some patients exhibit hepatic steatosis and inflammation despite preserved mtDNA content, suggesting that DGUOK deficiency may deregulate additional metabolic and immune pathways. Here we show that DGUOK depletion reprograms hepatocellular metabolism and innate immune signaling through a purine-dependent mechanism operating independently of mtDNA depletion. In Human hepatocellular carcinoma (HEPG2) hepatocytes subjected to siRNA-mediated DGUOK silencing, mitochondrial architecture and respiration remained intact but cells exhibited pronounced lipid droplet accumulation and a robust cell-intrinsic innate immune type I interferon response. Bulk RNA sequencing revealed widespread transcriptional reprogramming, including upregulation of human endogenous retroviruses (HERVs) and interferon-stimulated genes (ISGs), suppression of lipid metabolic pathways, and changes in purine, methionine, and methylation-associated gene networks. Perturbing purine homeostasis through deoxyadenosine (dAdo) supplementation in wild-type cells phenocopied DGUOK disruption, causing cellular DNA hypomethylation and activation of viral mimicry pathways. Together, these findings identify DGUOK as a central regulator of the purine-regulated lipid-immune axis in hepatocytes, demonstrating that mitochondrial nucleotide salvage preserves hepatic immune and metabolic homeostasis beyond its canonical role in mtDNA synthesis. By linking purine imbalances to steatosis and type I interferon activation, this study establishes a mechanistic framework for immunometabolic pathology in DGUOK deficiency.
• 🔗 查看原文

5. ⭐ GSE238130 Single-cell genomics highlight MYC-upregulation, metabolic activation, and altered cell interactions in T-PLL progression

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolic、single-cell、genomics
• 📝 描述：Contributors : Linus Wahnschaffe ; Marco Herling ; Tea Pemovska ; Philipp B Staber ; Marek Franitza ; Theodore Georgomanolis ; Kerstin BeckerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensT-prolymphocytic leukemia (T-PLL) is a rare T-cell malignancy usually associated with rapid tumor progression already at first diagnosis. A small subset of 15-25% of T-PLL patients, however, presents at a primarily indolent disease stage. These patients feature asymptomatic lymphocytosis with stable tumor load over several months to years, before inevitably progressing into active-stage T-PLL. In this study, we employed single-cell RNA sequencing of longitudinally acquired samples to investigate the pathobiologic mechanism underlying this transition from indolent to active T-PLL. We detected consistent deregulations of relevant cancer-associated pathways, centered around a strong upregulation of MYC target gene signatures that highly correlated with an enhanced energy metabolism in active-stage T-PLL cells. Both in silico and ex vivo analyses identified a marked restriction of cell energy metabolism during the indolent disease stage that strongly confined the outgrowth of T-PLL cells. Active T-PLL cells were capable to surpass this metabolic restriction. Analyses of immune-signaling pathways of T-PLL cells as well as the tumor microenvironment further revealed a progressive detachment from immune-related survival signals and escape from the homeostatic control. In summary, we identified both global alterations of gene expression patterns as well as patient-specific lesions that enabled the transformation into active-stage T-PLL. This study provides the first single-cell-resolved genomic analysis of T-PLL, providing valuable and novel insights into the intra-tumor heterogeneity of T-PLL, mechanisms of tumor evolution, as well as its interaction with the tumor microenvironment.
• 🔗 查看原文

6. GSE298237 幼稚样记忆T细胞的代谢静止状态先于并维持抗原特异性T细胞记忆

• ✍️ 作者：未知作者
• 🏷️ 关键词：antigen、metabolic
• 📝 描述：Contributors : Sina Frischholz ; Ev-Marie Schuster ; Myriam Grotz ; Christine Schülein ; Julia Benz ; Katharina Kocher ; Lucia Klotz ; Szilard Varga ; Theresa Hiltner ; Rayya Alsalameh ; Jan Esse ; Johannes Träger ; Jürgen Held ; Frederik Graw ; Jürgen Pahle ; Bernd Spriewald ; Luca Gattinoni ; Veit R Buchholz ; Felix Drost ; Benjamin Schubert ; Simon Rothenfußer ; Dirk H Busch ; Christian Bogdan ; Kilian SchoberSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMetabolic activity shapes cell fate but remains challenging to capture in vivo with high resolution. We performed longitudinal metabolic and phenotypic profiling of human antigen-specific CD8+ T cells after yellow-fever vaccination on the single-cell level. During the acute phase, T cells upregulated glycolysis to fuel anabolic needs of proliferation, but predominantly used oxidative phosphorylation for energy production, as assessed via protein translation rates. Central memory T cells were the most active subset, while effector cells underwent metabolic shut-down. In contrast, weakly differentiated naïve-like memory T cells showed minimal activity, relying solely on oxidative phosphorylation already during the acute phase. Reinforcing the link between cellular quiescence and longevity, naïve-like memory cells were preferentially maintained even 26 years post vaccination. This association between differentiation degree and metabolic activity was conserved after SARS-CoV-2 vaccination and in two murine infection models. Our study dissects the metabolic profile of antigen-specific T-cell responses ex vivo, highlighting quiescence as a key feature for long-term immunological memory formation in humans.
• 🔗 查看原文

7. GSE310176 果蝇 OSC 基因组：转座子和 piRNA 生物学研究资源 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、genome
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Drosophila melanogasterAccurate genome assemblies are critical for understanding small RNA-mediated genome defense. In animals, the PIWI-interacting RNA (piRNA) pathway protects genome integrity by silencing transposable elements. Studying how piRNAs are generated and how they guide heterochromatin formation requires complete reconstruction of genomic piRNA source loci and detailed transposon maps. Here, we present a high-quality de novo genome assembly of Drosophila melanogaster ovarian somatic cells (OSCs), a widely used cell line that recapitulates nuclear piRNA biology. The OSC genome differs substantially from the reference genome, with major differences in transposon content and piRNA cluster composition. Our assembly resolves the 700 kb flamenco locus, the primary piRNA cluster in OSCs, and provides a genome-wide transposon map. Using this resource, we characterize piRNA source loci, reveal how piRNA cluster composition determines transposon-derived piRNA profiles, and clarify the widespread impact of the nuclear piRNA pathway on heterochromatin. Finally, we provide an open platform for integrating user-generated datasets with the OSC genome, creating a community resource for studying transposon control and piRNA biology.
• 🔗 查看原文

8. GSE250428 NAT10 通过染色质相关 tRNA 调节 p300/CBP 活性来促进癌症转移 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq
• 📝 描述：Contributors : Ruhul Amin ; Ngoc-Han Ha ; Tinghu Qiu ; Ronald Holewinski ; Huaitian Liu ; Andy D Tran ; Maxwell P Lee ; Supuni T Gamage ; Thorkell Andresson ; Jordon L Meier ; Kent W HunterSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusAcetylation of proteins and RNA is crucial for development and cancer progression. NAT10 is the sole RNA acetylase responsible for N4-acetylcytidine (ac4C) modification of various RNAs. Our study reveals that NAT10 loss significantly reduces lung metastasis in breast cancer mouse models. NAT10 interacts with a mechanosensitive, metastasis-susceptibility protein complex at the nuclear pore. Mechanistically, NAT10-mediated acetylation of chromatin-associated tRNAs enhances p300/CBP activity. Without NAT10, acetylation of these tRNAs decreases, leading to p300/CBP inactivation and mislocalization. As a result, NAT10 depletion disrupts enhancer organization, altering gene transcription critical for metastasis, including reduced chemokines that recruit myeloid cells and create a less metastasis-prone tumor microenvironment. Our findings highlight the distinct role of NAT10 in acetylated tRNA-dependent regulation of enhancer function in metastatic tumor cells and its impact on tumor-immune interactions influencing metastasis.
• 🔗 查看原文

9. GSE250284 NAT10 通过染色质相关 tRNA 调节 p300/CBP 活性来促进癌症转移 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Ruhul Amin ; Ngoc-Han Ha ; Tinghu Qiu ; Ronald Holewinski ; Huaitian Liu ; Andy D Tran ; Maxwell P Lee ; Supuni T Gamage ; Thorkell Andresson ; Jordon L Meier ; Kent W HunterSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcetylation of proteins and RNA is crucial for development and cancer progression. NAT10 is the sole RNA acetylase responsible for N4-acetylcytidine (ac4C) modification of various RNAs. Our study reveals that NAT10 loss significantly reduces lung metastasis in breast cancer mouse models. NAT10 interacts with a mechanosensitive, metastasis-susceptibility protein complex at the nuclear pore. Mechanistically, NAT10-mediated acetylation of chromatin-associated tRNAs enhances p300/CBP activity. Without NAT10, acetylation of these tRNAs decreases, leading to p300/CBP inactivation and mislocalization. As a result, NAT10 depletion disrupts enhancer organization, altering gene transcription critical for metastasis, including reduced chemokines that recruit myeloid cells and create a less metastasis-prone tumor microenvironment. Our findings highlight the distinct role of NAT10 in acetylated tRNA-dependent regulation of enhancer function in metastatic tumor cells and its impact on tumor-immune interactions influencing metastasis.
• 🔗 查看原文

10. GSE310215 FFPE 和冷冻结直肠癌组织的空间转录组分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、spatial
• 📝 描述：Contributors : Kullanist Thanormjit ; Thanawat Suwatthanarak ; Vitoon Chinswangwatanakul ; Pariyada TanjakSeries Type : OtherOrganism : Homo sapiensThis dataset contains spatial whole-transcriptome profiles from colorectal cancer (CRC) tissues preserved using formalin-fixed paraffin-embedded (FFPE), fresh frozen (FF), and snap frozen (SF) methods. Samples were obtained from a patient with stage IV CRC during surgical resection at Siriraj Hospital, Mahidol University, Thailand. Each tissue type was sectioned, stained for Pan-cytokeratin (PanCK), CD45, and SYTO13, and analyzed using the NanoString GeoMx Digital Spatial Profiler with the Human Whole Transcriptome Atlas panel. A total of 36 areas of illumination (AOIs) representing epithelial (PanCK⁺), immune (CD45⁺), and stromal (PanCK⁻/CD45⁻) compartments were collected. Sequencing was performed on an Illumina NovaSeq 6000 platform, and raw counts were processed using NanoString DSP Analysis Suite v3.1 and R for normalization and quality control. This dataset provides spatially resolved gene-expression information across different preservation conditions of CRC tissues to support comparative analysis and method evaluation in spatial transcriptomics.
• 🔗 查看原文

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1. 哨兵淋巴结活检改善宫颈癌的外科治疗

• ✍️ 作者：未知作者
• 🏷️ 关键词：淋巴
• 📝 描述：Secret hovertext:
• 🔗 查看原文

详细内容（全部2条）

1. ⭐ Foli-seq——粪便脱落组测序——可捕捉健康和炎症肠道的免疫动态

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、sequencing、gut、regex:gut(-?microbiome)?
• 📝 描述：Foli-seq uses fecal human cells to reveal gut and immune activity, expanding RNA sequencing to noninvasive monitoring of intestinal health and inflammation…
• 🔗 查看原文

2. CRISPR技术为攻克耐药性肺癌开辟新途径

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists used CRISPR to disable the NRF2 gene, restoring chemotherapy sensitivity in lung cancer cells and slowing tumor growth. The technique worked even when only a fraction of tumor cells were edited, making it practical for real-world treatment. Since NRF2 fuels resistance in several cancers, the approach could have broad impact.
• 🔗 查看原文

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• Nature重磅：鲸鱼长寿且不患癌症，关键在于这个DNA修复蛋白，或可帮助人类延长寿命
• 中国学者一作兼通讯Nature论文：发现黄热病毒入侵人类细胞的受体
• Nature子刊：我国学者证实，运动对女性心脏健康的帮助更大
• Nature Aging：王宏林团队发现阿尔茨海默病治疗新靶点，并找到潜在药物
• STTT：郑州大学×复旦大学开发光遗传学疗法，治疗青光眼等视网膜神经退行性病变
• Cell Stem Cell：陈跃军/熊曼合作开发新型帕金森病细胞疗法
• CNS论文单细胞时空组学与机器学习课题思路设计
• 疾病恢复期不想吃肉？华人学者Cell论文证实，这是身体通过肠道-大脑信号在自救
• Cell子刊：浙江大学孔娜团队开发“以癌治癌”策略，防止癌症复发
• 铁死亡抗癌新突破！背靠背两篇Nature：靶向FSP1，促进癌症铁死亡
• 东南大学×南京大学合作Cell子刊：利用细胞外囊泡蛋白质组和脂质组，早期诊断帕金森病
• Cell重磅：AI大模型，设计生成人类单克隆抗体，对抗新型病毒
• 超越CRISPR：基于ADAR的RNA编辑技术，正在重塑癌症等疾病的治疗
• 复旦大学Cell子刊：全面揭示口腔微生物组与口腔健康在食管癌中的作用
• Nature子刊：无需手术和药物，超声可清除中风后大脑中有害碎片，减轻炎症、改善预后
• Nature Aging：学一门外语，让大脑更年轻
• Cell子刊：华人学者证实，母亲糖尿病，儿子易患心血管疾病，女儿则不受影响
• 国产CAR-NK细胞疗法登上《柳叶刀》：安全有效治疗系统性红斑狼疮
• 南京医科大学胡志斌团队发现，母亲孕期缺乏胆固醇，后代先天性心脏病风险升高
• 超越青蒿素，克服耐药性！首个非青蒿素抗疟疾药物即将上市
• Nature连发4篇论文，揭开这种RNA编辑酶在自身免疫疾病中的作用
• 代谢调控新靶点！《Phytomedicine》揭示HSYA改善心肌损伤的全新机制

• GSE309815 Single-cell RNA-seq of undirected human cerebral organoids (HuCOs) infected with MV1 or MV2 compared with uninfected controls at 120 and 180 days post-infection
• GSE282705 BLU-222, a Potent CDK2 Inhibitor, Synergizes with CDK4/6 Inhibitors to Overcome Drug Resistance in HR–Positive and Triple-Negative Breast Cancer by Inducing p21 and p27
• GSE267549 A functional genomics atlas enhanced by convolutional neural networks facilitates clinical interpretation of disease relevant variants in non-coding regulatory elements [wt RNA-seq]
• GSE263338 A functional genomics atlas enhanced by convolutional neural networks facilitates clinical interpretation of disease relevant variants in non-coding regulatory elements [ATAC-seq]
• GSE263337 A functional genomics atlas enhanced by convolutional neural networks facilitates clinical interpretation of disease relevant variants in non-coding regulatory elements [ChIP-seq]
• GSE263336 A functional genomics atlas enhanced by convolutional neural networks facilitates clinical interpretation of disease relevant variants in non-coding regulatory elements [plasmid DNA-seq]
• GSE263335 A functional genomics atlas enhanced by convolutional neural networks facilitates clinical interpretation of disease relevant variants in non-coding regulatory elements [STARR-RNA-seq]
• GSE310063 杆状病毒介导的冈比亚按蚊雌性细胞中雄性基因的表达 [RNA-seq]
• GSE307420 EVT0185 对乙酰辅酶A代谢酶的抑制作用可损害肝星状细胞活化，并逆转小鼠模型中的 MASH 和纤维化。
• GSE301764：一项无偏倚的全基因组开放阅读框过表达筛选鉴定出B3GALT2，一种新型的细胞ASO活性诱导因子
• GSE294955 ZFTA-RELA 室管膜瘤产生衣康酸作为癌代谢物以维持致病融合表达 [ChIP-Seq]
• GSE294954 ZFTA-RELA 室管膜瘤产生衣康酸作为致癌代谢物以维持致病融合表达 [ATAC-Seq]
• GSE287905 BPTF 通过增强染色质可及性和稳定 AR-FOXA1 相互作用来调节雄激素受体活性 [RNA-Seq]
• GSE287901 BPTF 通过增强染色质可及性和稳定 AR-FOXA1 相互作用来调节雄激素受体活性 [ATAC-Seq]
• GSE276076 巨型病毒创造亚细胞环境以克服密码子-tRNA 错配 [RNA-seq]
• GSE310178 果蝇 OSC 基因组：转座子和 piRNA 生物学研究资源 [smallRNA-Seq]
• GSE310177 果蝇 OSC 基因组：转座子和 piRNA 生物学研究资源 [PRO-Seq]
• GSE310174 果蝇 OSC 基因组：转座子和 piRNA 生物学研究资源 [HiC]
• GSE310097 LsrL 调节 Lsr2 诱导的染色质结构以调节委内瑞拉链霉菌中的生物合成基因簇调控 [RNA-seq]
• GSE304800 胆汁酸通过对脂肪酸吸收的选择性作用来调节脂质代谢
• GSE293705 19号染色体miRNA簇保护滋养层细胞免受过度活跃的先天免疫反应
• GSE280504 NAT10 通过染色质相关 tRNA 调节 p300/CBP 活性来促进癌症转移 [RNA-ChIP]
• GSE279482 Nrf2 协调表观遗传调控，并在砷诱导的细胞转化过程中作为 KLF4 表达和活性的主调控因子
• GSE268723 p53 介导磷脂头部基团清除 [RNA-seq]
• GSE268722 p53 介导磷脂头部基团清除 [ChIP-seq]
• GSE255610 定制基于 CRISPR/Cas 的表观基因组编辑器以实现可编程染色质酰化并降低细胞毒性
• GSE250430 NAT10 通过染色质相关 tRNA 调节 p300/CBP 活性，从而促进癌症转移
• GSE228745 HOXB13 通过与 SWI/SNF 复合物的相互作用改变前列腺癌中的染色质可及性
• GSE310021 酒精暴露早期适应期间肝脏巨噬细胞的变化
• GSE271715 利用隐形RNA载体生成倭黑猩猩诱导多能干细胞并进行转录组分析：一项与人类和黑猩猩的三方比较研究
• GSE254894 Netrin-1 通过 PPAR(γ) 依赖性 WNT-catenin(β) 信号通路调控高脂饮食诱导的脂肪生成
• GSE309838 Nascent strand sequencing of U2OS cells
• GSE305332 LincRNA-EPS regulates iron metabolism and osteoclastogenesis under inflammatory micro-environment
• GSE290662 MYC-FACT Interactions Drive Z-DNA Formation to Modulate Transcriptional Dynamics [ChIP-seq]
• GSE290661 MYC-FACT Interactions Drive Z-DNA Formation to Modulate Transcriptional Dynamics [RNA-seq]
• GSE290659 MYC-FACT Interactions Drive Z-DNA Formation to Modulate Transcriptional Dynamics [RNA-seq CC & CL]
• GSE282220 Mitochondrial translation drives activated CD8+ T cell dysfunction
• GSE278811 EZHIP-mediated PRC2 inhibition is required to maintain H3K27me3-dependent imprinting post fertilization [ChIP-Seq]
• GSE218454 RNA-seq of B16F10 tongue xenografts with or without inhibition of LN-innervating nociceptive nerves