详细内容（前10条）

1. ⭐ GSE305116 空间转录组学揭示肠型胃癌与配对的正常胃黏膜之间独特的免疫微环境特征。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、spatial、spatial transcriptomics、transcriptomics、regex:intestin(e|al)
• 📝 描述：Contributors : Qingyuan Wang ; Jiajia Shen ; Sheng Yang ; Xiaochun Ping ; Lizong ShenSeries Type : OtherOrganism : Homo sapiensGastric adenocarcinoma, particularly the Lauren intestinal-type GAC (IGAC), leads to significant mortality in China due to the limited effectiveness of current treatments. We performed spatial transcriptomics to profile heterogeneous immune cell clusters in IGAC and validated our findings using scRNA-seq. Our study aims to investigate the mechanisms of immune suppression in IGAC to identify potential targets for enhancing immunotherapy outcomes.
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2. ⭐ GSE298286 利用GIS增强的空间转录组学对原发性和转移性肿瘤结构进行计算机模拟重建

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Jin Young Yoo ; Sabrina Akter ; Qianying Zuo ; Amir Kazemi ; Wenjun Wu ; Mahima Goel ; Audrey Lam ; Debapriya Dutta ; Betsy Barnick ; Melike Pekmezci ; Maria Grosse Perdekamp ; Aiman Soliman ; Zeynep Madak-Erdogan ; Matthew RillorazaSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensTumor microenvironment (TME) consists of different cell populations, whose interactions contribute to tumor heterogeneity and therapy response. Spatial transcriptomics (ST) offers valuable insights into spatial complexity and heterogeneity of TME. We established a Python package, Geographic Information System (GIS)-augmented In-Silico Reconstruction of Tumor Architecture (GIS-ROTA), based on application of GIS methods to ST data to examine/explore spatial heterogeneity of co-regulated gene sets, such as pathways and cell types within the TME. In our Visium dataset of primary and metastatic estrogen receptor positive breast tumor samples, GIS-ROTA revealed extensive co-localization of estrogen response with metabolic pathway gene sets and mutual exclusivity with metastasis-related and specific immune-related pathway gene sets. Our findings demonstrate the robustness of GIS-ROTA in quantitating tumor heterogeneity and identifying spatially significant regions while minimizing the subjectivity involved in interpreting the clusters from conventional statistical methods. Thus, GIS-ROTA enables the development of therapeutic strategies that target multiple cell populations.
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3. ⭐ GSE319069 利用抗体标记和流式细胞术富集神经嵴细胞，用于蜥蜴单细胞转录组学研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：antibody、single-cell、transcriptomics、enrichment
• 📝 描述：Contributors : Robin Pranter ; Cedric Patthey ; Nathalie FeinerSeries Type : Expression profiling by high throughput sequencingOrganism : Podarcis muralisSingle-cell transcriptomic data were generated from embryos of the common wall lizard (Podarcis muralis). Neural crest cells (NCCs) were enriched by fluorescence-activated cell sorting based on HNK-1 antibody staining. The dataset includes two unsorted samples representing all embryonic cells, one leniently sorted sample containing the top 15% of HNK-1–positive cells, and two strictly sorted samples containing the top 5% of HNK-1–positive cells. Unsorted and leniently sorted samples were generated from pools of three embryos each and sequenced using the 10x Genomics Chromium platform. Strictly sorted samples were generated from a single embryo, split across two plates, and sequenced using the Smart-seq3 protocol. These data enable characterization of NCC transcriptional profiles in a non-model vertebrate species and provide a resource for studying neural crest biology in systems lacking transgenic tools.
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4. ⭐ GSE318783 通过 LHRH-NanoTi 靶向递送 TGF-β 抑制剂可逆转卵巢癌中 NAT10/ac4C 介导的顺铂诱导的免疫抑制性肿瘤微环境 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、RNA-seq
• 📝 描述：Contributor : Fei LvSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Platinum-based chemotherapy for ovarian cancer is frequently compromised by the development of resistance, a process often accompanied by an immunosuppressive tumor microenvironment. The molecular mechanisms linking cisplatin resistance to immune evasion remain poorly understood, hindering the development of effective combination therapies. Results: This study reveals that cisplatin-induced immunosuppression and resistance are driven by a reduction in N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, which produces two parts of unfavorable effects: 1) activating the DNA damage repair pathway, thereby confers resistance to cisplatin; 2) enhancing the expression of TGF-β via NAT10’s interaction with ribosomal proteins RPS3 and RPS6. The elevated TGF-β increases the infiltration of myeloid-derived suppressor cells (MDSCs), M2 macrophages, exhausted CD8+ T cells, and regulatory T cells (Tregs) within the tumor microenvironment. To target this pathway, we developed a LHRH receptor-targeted nanodelivery system for a TGF-β inhibitor, which synergized with cisplatin to achieve superior antitumor efficacy by effectively reversing the immunosuppressive microenvironment. Conclusions: Our study defines the NAT10/ac4C–TGF-β axis as a pivotal mechanism coordinating cisplatin resistance and immunosuppression in ovarian cancer. These findings propose targeted inhibition of TGF-β signaling as a promising therapeutic strategy to overcome platinum resistance by revitalizing the antitumor immune response.
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5. ⭐ GSE319533 全基因组亚硫酸氢盐测序揭示甲醛诱导的鸡胚肝脏和骨骼肌DNA甲基化改变

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、genome、methylation
• 📝 描述：Contributors : Mustafa Özdemir ; Saffet Teber ; Ghulam Asghar Sajid ; Selma Büyükkılıç Beyzi ; Yunus Arzık ; Mehmet Kızılaslan ; Servet Yalçın ; Mehmet Ulas CinarSeries Type : Methylation profiling by high throughput sequencingOrganism : Gallus gallusPre-incubation formaldehyde (FA) fumigation of hatching eggs is widely implemented for microbial control, yet its epigenetic consequences in embryonic tissues remain unclear. Here, we profiled the methylome of chicken embryo liver and skeletal muscle following commercial-dose FA fumigation using whole-genome bisulfite sequencing (WGBS). We generated 16 WGBS libraries (per tissue: control n=4; FA n=4), producing ~1.80 billion clean reads with mapping rates of 88.1–89.9% and bisulfite conversion efficiencies of ~99.4–99.7%. Although global methylation patterns were largely maintained, FA exposure induced widespread locus-specific remodeling dominated by CpG hypomethylation in both tissues. We identified 10,496 DMRs in liver and 10,487 DMRs in muscle, with hypomethylated DMRs comprising 83.4% and 91.2%, respectively. Functional enrichment analyses revealed a tissue-specific adaptive logic. In liver, CG-DMR–associated genes were significantly enriched in Focal adhesion, Tight junction, and core signaling pathways (MAPK, Wnt, Insulin signaling). Notably, hypermethylated genes were enriched for Glycine, serine and threonine metabolism, whereas hypomethylated genes were enriched for Protein processing in endoplasmic reticulum and Autophagy. In the CHG context, hypomethylation preferentially involved ether lipid metabolism, glycerolipid metabolism, and cell–cell adhesion pathways (Adherens junction, Focal adhesion), while CHH-context hypermethylation enriched MAPK and tight junctions. In muscle, CG-DMRs were enriched for “housekeeping” stress-response pathways (Autophagy, Ubiquitin-mediated proteolysis), while a distinct metabolic signature emerged: hypermethylated genes were enriched for PPAR signaling and Biosynthesis of amino acids, whereas hypomethylated genes enriched for Fatty acid metabolism. A decisive metabolic switch was evident in the CHH context, where promoters of Biosynthesis of amino acids were hypermethylated, while catabolic energy pathways (Fatty acid degradation, Valine, leucine and isoleucine degradation, TCA cycle) were hypomethylated. Collectively, these data demonstrate that commercial-dose FA fumigation leaves tissue- and context-specific epigenetic imprints in embryonic liver and skeletal musc…
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6. ⭐ GSE319318 CDKN2A-ARF 失活促进 PDAC 肿瘤微环境的 p53 非依赖性重塑 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、tumor microenvironment、RNA-seq
• 📝 描述：Contributors : Brittany M Flowers ; Sofia Ferreira ; Laura D AttardiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe CDKN2A locus, which is frequently deleted in pancreatic ductal adenocarcinoma (PDAC), encodes two tumor suppressors, ARF and INK4A, that may influence tumorigenesis through distinct mechanisms. Distinguishing their individual contributions to cancer could help improve the understanding of PDAC pathogenesis and potentially uncover targetable vulnerabilities. Moreover, while ARF is known to enhance p53 function, defining its p53-independent activities could elucidate new processes that drive PDAC development. Here, we sought to understand ARF function in PDAC suppression. Analysis of gene expression and mutational patterns in human PDAC TCGA data indicated that CDKN2AARF and CDKN2AINK4A are commonly both affected by point mutations and/or deletions, suggesting that their combined inactivation contributes to PDAC development. In genetically engineered mouse models (GEMMs), Arf inactivation accelerated KRASG12D-driven PDAC development, both in the presence and absence of Trp53, demonstrating that ARF is a PDAC suppressor and can act in a p53-independent manner. Transcriptomic analyses of PDACs supported a p53-independent role for ARF, with ARF deficiency promoting extracellular matrix, collagen synthesis/assembly, and epithelial-mesenchymal transition gene expression programs. Accordingly, ARF-deficient PDACs displayed extensive remodeling of the tumor microenvironment (TME), associated with collagen deposition, increased tissue stiffness, and higher fibroblast content – hallmarks of aggressive and treatment-resistant PDAC stroma. Together, this study shows how ARF deficiency associated with CDKN2A inactivation sculpts the PDAC TME in a p53-independent fashion. Given the central role of the TME in PDAC progression and therapeutic resistance, these findings may provide insight critical for improving therapeutic interventions for PDAC.
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7. ⭐ GSE318784 通过 LHRH-NanoTi 靶向递送 TGF-β 抑制剂可逆转卵巢癌中 NAT10/ac4C 介导的顺铂诱导的免疫抑制性肿瘤微环境 [Ribo-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment
• 📝 描述：Contributor : Fei LvSeries Type : OtherOrganism : Mus musculusBackground: Platinum-based chemotherapy for ovarian cancer is frequently compromised by the development of resistance, a process often accompanied by an immunosuppressive tumor microenvironment. The molecular mechanisms linking cisplatin resistance to immune evasion remain poorly understood, hindering the development of effective combination therapies. Results: This study reveals that cisplatin-induced immunosuppression and resistance are driven by a reduction in N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, which produces two parts of unfavorable effects: 1) activating the DNA damage repair pathway, thereby confers resistance to cisplatin; 2) enhancing the expression of TGF-β via NAT10’s interaction with ribosomal proteins RPS3 and RPS6. The elevated TGF-β increases the infiltration of myeloid-derived suppressor cells (MDSCs), M2 macrophages, exhausted CD8+ T cells, and regulatory T cells (Tregs) within the tumor microenvironment. To target this pathway, we developed a LHRH receptor-targeted nanodelivery system for a TGF-β inhibitor, which synergized with cisplatin to achieve superior antitumor efficacy by effectively reversing the immunosuppressive microenvironment. Conclusions: Our study defines the NAT10/ac4C–TGF-β axis as a pivotal mechanism coordinating cisplatin resistance and immunosuppression in ovarian cancer. These findings propose targeted inhibition of TGF-β signaling as a promising therapeutic strategy to overcome platinum resistance by revitalizing the antitumor immune response.
• 🔗 查看原文

8. ⭐ GSE316760 原发性皮肤黑色素瘤的空间转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributor : Amaya VirósSeries Type : OtherOrganism : Homo sapiensWe performed spatial transcriptomics on primary cutaneous melanoma samples to characterise the tumour microenvironment
• 🔗 查看原文

9. ⭐ GSE313807 错配修复缺陷产生的胞质DNA结构协调结直肠癌的抗肿瘤免疫

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immunity
• 📝 描述：Contributors : Kristi Baker ; Shayla MosleySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPatients with the microsatellite instable (MSI) subtype of colorectal cancer (CRC) have better prognosis and immunotherapy response than patients with the chromosomally instable (CIN) subtype due to improved cytotoxic T cell responses. This is in part due to high production of the chemokines CXCL10 and CCL5 from constitutive activation of the cytosolic DNA (cyDNA) sensor cGAS/STING by specific features of MSI cyDNA that lead to more effective cGAS/STING pathway activation. Here, we investigate MSI and CIN cyDNA structure and show that MSI cyDNA is enriched in G-quadruplexes which improve cGAS/STING and CD8+ T cell activation. We also show that micronuclei are less effective at inducing anti-tumor immunity and instead increase Treg activation and IL10 production. Overall, these data highlight the role of specific cyDNA structures in anti-tumor immunity and provide knowledge for improved design of therapeutic DNA-based cGAS/STING agonists to improve the prognosis of poorly immunogenic tumors like CIN CRCs.
• 🔗 查看原文

10. GSE319696 Setdb1 介导的 H3K9 甲基化在非活性 X 染色体上富集，并在其表观遗传沉默中发挥作用 [MEF_RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：epigenetic、methylation
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe presence of histone 3 lysine 9 (H3K9) methylation on the mouse inactive X chromosome has been controversial over the last 15 years, and the functional role of H3K9 methylation in X chromosome inactivation in any species has remained largely unexplored. Here we report the first genomic analysis of H3K9 di- and tri-methylation on the inactive X: we find they are enriched at the intergenic, gene poor regions of the inactive X, interspersed between H3K27 tri-methylation domains found in the gene dense regions. Although H3K9 methylation is predominantly non-genic, we find that depletion of H3K9 methylation via depletion of H3K9 methyltransferase Set domain bifurcated 1 (Setdb1) during the establishment of X inactivation, results in failure of silencing for around 150 genes on the inactive X. By contrast, we find a very minor role for Setdb1-mediated H3K9 methylation once X inactivation is fully established. In addition to failed gene silencing, we observed a specific failure to silence X-linked long-terminal repeat class repetitive element. Here we have shown that H3K9 methylation clearly marks the murine inactive X chromosome. The role of this mark is most apparent during the establishment phase of gene silencing, with a more muted effect on maintenance of the silent state. Based on our data, we hypothesise that Setdb1-mediated H3K9 methylation plays a role in epigenetic silencing of the inactive X via silencing of the repeats, which itself facilitates gene silencing through alterations to the conformation of the whole inactive X chromosome.
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1. ⭐ CubaseBio 结束隐秘运营，获得 590 万欧元融资，旨在实现真正的 3D 空间转录组学规模化应用。

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：CubaseBio secures €5.9 million to advance 3D spatial transcriptomics powered by DNA microscopy and RNA sequencing, enabling scalable volumetric gene expression mapping for drug discovery and disease research…
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2. 一项重大癌症突破：一个干细胞即可生成1400万个杀伤肿瘤的NK细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer
• 📝 描述：Scientists in China have unveiled a breakthrough way to mass-produce powerful cancer-fighting immune cells in the lab. By engineering early-stage stem cells from cord blood—rather than trying to modify mature natural killer (NK) cells—they created a streamlined process that generates enormous numbers of highly potent NK cells, including CAR-equipped versions designed to hunt specific cancers.
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3. 阿尔茨海默病首个细胞类型特异性基因调控图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Integrating RNA sequencing with whole-genome data, researchers built causal gene maps in Alzheimer’s brain cells, identifying hub genes and rewired networks that may drive neurodegeneration…
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4. 神秘的RNA引导科学家发现了癌症的隐藏层面。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A mysterious RNA found in breast cancer led scientists to uncover an entire hidden class of cancer-specific RNAs across dozens of tumor types. These molecules form unique molecular signatures that identify cancer type and subtype with remarkable accuracy. Some even drive tumor growth and metastasis. Because many are released into the bloodstream, a simple blood test can track how patients respond to treatment and predict survival.
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5. 科学家发现能够清除阿尔茨海默病斑块的大脑开关

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Researchers have identified two brain receptors that help the brain clear away amyloid beta, a hallmark of Alzheimer’s disease. By stimulating these receptors in mice, scientists increased levels of a natural amyloid-breaking enzyme, reduced buildup in the brain, and improved memory-related behavior. Because these receptors are common drug targets, the findings could open the door to affordable pill-based treatments with fewer side effects.
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6. 突破性的CRISPR系统有望逆转抗生素耐药性危机

• ✍️ 作者：未知作者
• 🏷️ 关键词：resistance
• 📝 描述：Antibiotic resistance is racing toward a global crisis, with “superbugs” projected to cause over 10 million deaths annually by 2050. Now, scientists at UC San Diego have unveiled a powerful new CRISPR-based tool that doesn’t just fight resistant bacteria—it can actively strip away their drug resistance. Inspired by gene drives used in insects, the technology spreads a genetic “fix” through bacterial populations, even inside stubborn biofilms that shield microbes from antibiotics.
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• GSE302204 人鼻咽癌细胞在 BALF2​​-LR 和 BALF2​​-HR 过表达组中的 RNA-seq
• GSE292264 缺氧条件下 Hif1a 和 Ahr 对 NK 细胞转录组的调控
• GSE318858 CDC14A-KMT5A信号通路对向心性与离心性心脏肥大平衡的调控
• GSE273669 皮肤细菌诱导的共生菌3D黑色素瘤皮肤模型中的基因表达变化
• GSE319783 整合多组学分析和 CRISPR 筛选鉴定小鼠免疫系统中的功能性非经典翻译位点 [RNA-Seq]
• GSE316050 高效小分子可控碱基编辑用于体内癌症功能基因组学
• GSE277536 高复杂度条形码狂犬病毒用于利用单细胞和单核测序进行可扩展的电路映射
• GSE319313 CDKN2A-ARF 失活促进 PDAC 肿瘤微环境的 p53 非依赖性重塑 [WES]
• GSE290140 SET1/COMPASS 亚基 RBBP5 协调全局蛋白质稳态和 12 小时振荡器的表观遗传控制，以保障代谢和细胞稳态
• GSE243523 在高分辨率单细胞 3D 基因组中观察到的突出转录延伸环 [RNA-seq 和 Smart-seq3、拓扑异构酶抑制和黏连蛋白耗竭、mESC]
• GSE224898 在高分辨率单细胞 3D 基因组中观察到的突出转录延伸环 [Micro-C、CUT&TAG、RNA-Seq、拓扑异构酶抑制（DMSO、ETO、TPT）、GM12878]
• GSE308091 SWI/SNF 的 SMARCA4 亚基可防止 G 四链体处的基因组不稳定性
• GSE300441 ERRα-KDM5C 抑制 STING 增强子活性以调节乳腺癌进展中的 I 型干扰素信号传导
• GSE298679 Transcriptomic Profiling of Ferroptosis in Enteric Neurons: Bulk RNA-Seq of IM-FEN Cells Treated with Palmitate
• GSE297210 亨廷顿病 DNA 甲基化谱分析揭示纹状体中与疾病相关的改变
• GSE287197 识别转移进展的代谢机制
• GSE286294 Polycomb复合物染色质结合失衡导致神经发育障碍[scRNA-Seq]
• GSE286289 Polycomb复合物染色质结合失衡导致神经发育障碍[ChIP-Seq]
• GSE286288 Polycomb复合物染色质结合失衡导致神经发育障碍[ATAC-Seq]
• GSE286287 Polycomb复合物染色质结合失衡导致神经发育障碍[RNA-Seq]
• GSE279064 LARP6 影响纤维化基因的 mRNA 翻译 [RNA-seq]
• GSE231768 维生素D结合蛋白诱导骨骼肌萎缩，并独立于维生素D水平参与癌症相关的肌肉萎缩。
• GSE319795 脱碘酶基因表达谱揭示了牛品种特异性甲状腺代谢和热应激耐受性的基础
• GSE313685 单次静脉注射临床相关剂量的铁剂可诱导心血管代谢性心力衰竭患者发生心肌铁死亡
• GSE302289 miR-146a-5p 和 miR-146b-5p 限制多发性创伤期间脂肪组织中 IL-1β 介导的炎症
• GSE301368 急性激素信号诱导的 3D 染色质环重组控制脂肪细胞产热 [ChIP-seq 人类]
• GSE301366 急性激素信号诱导的 3D 染色质环重组控制脂肪细胞产热 [ChIP-seq 小鼠，CTCF，SMC1，MED1]
• GSE301359 急性激素信号诱导的 3D 染色质环重组控制脂肪细胞产热 [RNA-seq 人类]
• GSE261413 急性激素信号诱导的 3D 染色质环重组控制脂肪细胞产热 [RNA-Seq 小鼠]
• GSE261412 急性激素信号诱导的 3D 染色质环重组控制脂肪细胞产热 [ChIP-Seq 小鼠，H3K27ac，H3K4me3，H2AZ]
• GSE261410 急性激素信号诱导的 3D 染色质环重组控制脂肪细胞产热 [ATAC-Seq 小鼠]
• GSE319794 对接受新辅助 BO-112 和低分割放射治疗（伴或不伴 nivolumab）的软组织肉瘤患者的软组织肉瘤进行批量 RNA 测序
• GSE319779 整合多组学分析和 CRISPR 筛选鉴定小鼠免疫系统中的功能性非经典翻译位点 [Guide-seq]
• GSE319768 两例集合管癌患者的肾脏
• GSE263517 小鼠皮层星形胶质细胞核转录组分析（Fmr1 KO 和 Smad4 条件性 KO）
• GSE319591 异质品系大鼠全脑组织转录组学
• GSE319577 Single-Cell Profiling of HDAC Inhibitor-Induced EBV Lytic Heterogeneity Defines Abortive and Refractory States in B Lymphoblasts
• GSE315069 Smad4-p65 相互作用驱动 BMP 介导的抗炎症细胞死亡保护作用 [RNA-Seq]
• GSE315063 Smad4-p65 相互作用驱动 BMP 介导的抗炎症细胞死亡保护作用 [ATAC-Seq]
• GSE315062 Smad4-p65 相互作用驱动 BMP 介导的抗炎症细胞死亡保护作用 [ChIP-Seq]
• GSE288123 解析多 RRM 内体 mRNA 转运蛋白 Rrm4 的结合行为 [RNA-seq]
• GSE243525 在高分辨率单细胞3D基因组中观察到的突出转录延伸环
• GSE243524 在高分辨率单细胞 3D 基因组中观察到的突出转录延伸环 [Micro-C 和 CUT&TAG、Rpb1 耗竭、mESC]
• GSE222243 在高分辨率单细胞 3D 基因组中观察到的突出转录延伸环 [Smart-seq2, GM12878]