详细内容（前10条）

1. ⭐ GSE312782 单细胞转录组学揭示牛传入淋巴中的树突状细胞亚群以及对卡介苗疫苗的免疫细胞反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、lymph、dendritic cell、regex:lymph(o|atic)?、transcriptomics
• 📝 描述：Contributors : Rachrapee Sukmak ; Heather A Mathie ; Richard S Taylor ; Jianxuan Sun ; Barbara Shih ; Charlotte R Bell ; Mark Gray ; Daniel J Macqueen ; Jayne C HopeSeries Type : Expression profiling by high throughput sequencingOrganism : Bos taurusBovine tuberculosis (bTB), caused by Mycobacterium bovis (M. bovis), remains an ongoing global issue for human and animal health. The Bacille Calmette Guerin (BCG) vaccine offers immunity against bTB, however, the mechanisms underlying the heterogenous protective response, including variations across species and age groups requires further investigation. In this study, we focused on dendritic cells (DCs), which are crucial for adaptive immune stimulation following BCG vaccination. By capturing afferent lymph DCs (ALDCs) migrating from the skin, we investigated shifts in DC profiles and potential subset-specific functions in response to BCG vaccination. Single-cell RNA sequencing (scRNA-seq) was performed on samples from n=3 Bos taurus calves before and after BCG vaccination, capturing the transcriptome of 20,761 individual cells expressing on average 3,036 unique genes, which were clustered into ALDCs, monocytes, T-cells, B-cells and NK cells. The ALDC subsets were further identified as cDC1 and cDC2. In homeostasis, ALDCs expressing potential subset-specific genes for cDC1, including ENSBTAG00000056208 (LINE-1), STX4, NEBL, ADAM23, ART3, and cDC2; FN1, PSPH, FGL2, SHOX2, and WWTR1 were identified. Following BCG vaccination, while both subsets exhibited gene expression signatures indicative of antigen-presenting function, migration, and DC maturation, cDC1 showed upregulation of genes consistent with metabolic alterations and lymphocyte recruitment, whereas cDC2 upregulated genes consistent with inflammatory responses. Overall, this study comprehensively describes the transcriptomic landscape of bovine ALDC subsets, providing evidence for the importance of subset-specific genes to BCG vaccination responses, while advancing knowledge on how ALDCs contribute to protective immunity against bTB.
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2. ⭐ GSE314480 SIRT7 将 H3K36ac 表观遗传调控与衰老小鼠睾丸中的基因组维持联系起来 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、ATAC-seq、genome、epigenetic
• 📝 描述：Contributors : A Guitart-Solanes ; M Romero ; I Fernandez-Duran ; A Gamez-Garcia ; B A Niedenberger ; C Madrid-Sandín ; N Spears ; I Roig ; C B Geyer ; A Vaquero ; K Schindler ; B N VazquezSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusReproductive aging is an increasing health concern affecting family planning and overall well-being. While extensively studied in females, the mechanisms driving male reproductive aging remain largely unexamined. Here we found that mammalian Sirtuin 7 (SIRT7) sustains spermatogenesis in an age-dependent manner through the control of histone 3 lysine 36 acetylation (H3K36ac). SIRT7 deficiency in mice resulted in increased levels of H3K36ac in spermatogonia and spermatocytes, a pattern also observed during natural testicular aging. SIRT7 deficiency altered chromatin accessibility, which was directly linked to H3K36ac activity in a germ cell line, and increased vulnerability to genotoxic stress. Importantly, undifferentiated spermatogonia, which are required for continuous sperm production, decreased prematurely in Sirt7-/- mice and showed enhanced genome damage accumulation during aging or under acute environmental stress. These changes were concurrent with age-dependent defects in double strand break (DBS) repair and partial meiotic arrest. Taken together, our results indicate that SIRT7 connects H3K36ac epigenetic regulation to long-term genome stability in male germ cells, ensuring steady-state spermatogenesis during the lengthy male reproductive lifespan.
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3. ⭐ GSE253962 人类肝细胞癌的空间转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Joanne O’Rourke ; Daniel A Patten ; Dean Kavanagh ; Catherine Willoughby ; Josep Llovet ; Helen Reeves ; Peter Hewett ; Neena Kalia ; Tahir Shah ; Yuk T Ma ; Kelly Hunter ; Jack L McMurray ; Joe Flint ; Owen Cain ; Derek Mann ; Amy Naylor ; Victoria Heath ; Roy Bicknell ; Shishir ShettySeries Type : OtherOrganism : Homo sapiensBackground: Immune checkpoint inhibition is now standard of care for patients with advanced hepatocellular cancer (HCC) and yet many patients remain resistant to this therapy. The presence of innate immune populations in the tumour microenvironment (TME) have been implicated in regulating the efficacy of these agents. CLEC14A has previously been shown to be upregulated on tumour endothelial cells and we found endothelial upregulation of CLEC14A in a subset of HCC tumours as well as acute liver injuries. This led us to explore the role of CLEC14A in neutrophil recruitment, critical populations in both liver pathologies.Methods:Immunohistochemical analysis was undertaken of CLEC14A in human liver tissue across a range of liver diseases and HCC. CLEC14A regulation and function was then explored in primary human liver endothelial cells including responses to shear stress and flow based adhesion assays. Liver injury models were undertaken CLEC14A knockout mice followed by intravital microscopy. Finally, CLEC14A expression was studied in both publically available HCC data sets and through spatial transcriptomics of HCC tissue.Findings:We found that CLEC14A mediates neutrophil recruitment across liver endothelium in both in vitro and in vivo settings. This process appears to be independent of its interaction with its known ligand Multimerin-2. Additionally, we demonstrated a correlation of CLEC14A expression in human HCC with a neutrophil transcriptional signature.Interpretation:This study unveils a new link between a tumour angiogenic receptor and neutrophil infiltration to the liver and highlights the potential of combining current immunotherapy in HCC with agents targeting the CLEC14A pathway.
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4. ⭐ GSE316624 抗SLC7A11单克隆抗体通过对结直肠癌中CD4+和CD8+T细胞的双重作用抑制肿瘤进展[RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、antibody、RNA-seq
• 📝 描述：Contributors : Jichang Li ; Yuhang Yin ; Haopeng Hong ; Xiaoxue Pan ; Chang A Meng ; Jing Zhu ; Xin Wang ; Yucun Liu ; Pengyuan Wang ; Shanwen ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSLC7A11 is aberrantly overexpressed in numerous solid tumors, including colorectal cancer (CRC), where it serves as a key regulator of cystine import and ferroptosis. However, its therapeutic potential and feasible targeting strategies remain less well understood. Our findings reveal that elevated SLC7A11 expression is critical for the activation of regulatory T cells and is associated with advanced tumor grade, lymphatic metastasis, and poor prognosis in CRC patients. A monoclonal antibody that blocks the transporter function of SLC7A11 induces apoptosis across multiple cancer cell types and demonstrates significant therapeutic efficacy in preclinical mouse models of colon cancer. Additionally, inhibition of SLC7A11 reprograms the tumor immune microenvironment, transforming it from a ‘cold’ to a more immunogenic state by suppressing regulatory T cell activation. These results highlight the dual role of SLC7A11 in modulating CD4+ and CD8+ T cell responses, positioning SLC7A11 as a crucial orchestrator of tumor immune evasion and a promising therapeutic target.
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5. ⭐ GSE316623 抗SLC7A11单克隆抗体通过对结直肠癌中CD4+和CD8+T细胞的双重作用抑制肿瘤进展[scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、antibody、scRNA
• 📝 描述：Contributors : Jichang Li ; Yuhang Yin ; Haopeng Hong ; Xiaoxue Pan ; Chang A Meng ; Jing Zhu ; Xin Wang ; Yucun Liu ; Pengyuan Wang ; Shanwen ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSLC7A11 is aberrantly overexpressed in numerous solid tumors, including colorectal cancer (CRC), where it serves as a key regulator of cystine import and ferroptosis. However, its therapeutic potential and feasible targeting strategies remain less well understood. Our findings reveal that elevated SLC7A11 expression is critical for the activation of regulatory T cells and is associated with advanced tumor grade, lymphatic metastasis, and poor prognosis in CRC patients. A monoclonal antibody that blocks the transporter function of SLC7A11 induces apoptosis across multiple cancer cell types and demonstrates significant therapeutic efficacy in preclinical mouse models of colon cancer. Additionally, inhibition of SLC7A11 reprograms the tumor immune microenvironment, transforming it from a ‘cold’ to a more immunogenic state by suppressing regulatory T cell activation. These results highlight the dual role of SLC7A11 in modulating CD4+ and CD8+ T cell responses, positioning SLC7A11 as a crucial orchestrator of tumor immune evasion and a promising therapeutic target.
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6. ⭐ GSE295691 口腔鳞状细胞癌的多模态分析揭示了与嚼槟榔相关的基因组改变和表达程序[空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Shih-Chi Su ; Lung-Ching Chang ; Shun-Fa YangSeries Type : OtherOrganism : Homo sapiensBetel quid (BQ) chewing is a profound risk for oral squamous cell carcinoma (OSCC) in Southeast Asia. To decipher contributory genomic abnormalities and transcriptional reprogramming in these malignancies, we conducted a multi-omics survey, including exome sequencing of tumor-normal pairs, alone with integrated single-cell and spatial transcriptomics of a set of tumors. In addition to enrichment of significantly altered genes (e.g mutations of TP53 and CHUK, copy gains of MAP3K13 and FADD, copy losses of CDKN2A) and mutational signatures associated with BQ chewing, we demonstrated frequently altered oncogenic pathways (Hippo and p53 signaling) and potential combination therapy opportunities linked to BQ use. Moreover, a shift of tumor microenvironment in BQ-related OSCC, characterized by extensive cell-cell crosstalk and induced tissue hypoxia, dendritic immunosuppression, and endothelial sprouting, was observed. Collectively, these differences in genomic landscape and tumor niche suggest that BQ-positive OSCC could be an etiological subtype different from their BQ-negative counterparts.
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7. ⭐ GSE314213 SIRT7 将 H3K36ac 表观遗传调控与衰老小鼠睾丸中的基因组维持联系起来

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、genome、epigenetic
• 📝 描述：Contributors : A Guitart-Solanes ; M Romero ; I Fernandez-Duran ; A Gamez-Garcia ; B A Niedenberger ; C Madrid-Sandín ; N Spears ; I Roig ; C B Geyer ; A Vaquero ; K Schindler ; B N VazquezSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusReproductive aging is an increasing health concern affecting family planning and overall well-being. While extensively studied in females, the mechanisms driving male reproductive aging remain largely unexamined. Here we found that mammalian Sirtuin 7 (SIRT7) sustains spermatogenesis in an age-dependent manner through the control of histone 3 lysine 36 acetylation (H3K36ac). SIRT7 deficiency in mice resulted in increased levels of H3K36ac in spermatogonia and spermatocytes, a pattern also observed during natural testicular aging. SIRT7 deficiency altered chromatin accessibility, which was directly linked to H3K36ac activity in a germ cell line, and increased vulnerability to genotoxic stress. Importantly, undifferentiated spermatogonia, which are required for continuous sperm production, decreased prematurely in Sirt7-/- mice and showed enhanced genome damage accumulation during aging or under acute environmental stress. These changes were concurrent with age-dependent defects in double strand break (DBS) repair and partial meiotic arrest. Taken together, our results indicate that SIRT7 connects H3K36ac epigenetic regulation to long-term genome stability in male germ cells, ensuring steady-state spermatogenesis during the lengthy male reproductive lifespan.
• 🔗 查看原文

8. ⭐ GSE324039 药理学抑制 HIF-2α 可保护透明细胞肾细胞癌中的 T 细胞转录组

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、T cell、transcriptome
• 📝 描述：Contributor : Katrine N MadsenSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBelzutifan is a selective HIF-2α inhibitor currently in clinical trials for clear cell renal cell carcinoma (ccRCC). As belzutifan is being evaluated in combination with immune checkpoint inhibitors, we investigated whether pharmacologic HIF-2α inhibition affects T cell transcriptional programs. Primary human pan T cells isolated from blood from healthy donors and ccRCC patients and tumor-infiltrating T cells were isolated from ccRCC patients. These cells were treated with belzutifan (2 μM, 5 days) vs. control DMSO under hypoxic conditions. RNA sequencing revealed that belzutifan treatment preserved T cell transcriptional programs, supporting the rationale for combining belzutifan with immunotherapy in ccRCC.
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9. ⭐ GSE320258 Pan-Cancer Analysis Reveals Mutation-Driven TE Dysregulation as a Contributor to Immune Suppression [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、ATAC-seq
• 📝 描述：Contributors : Hongjian Qi ; Kai Tian ; Chicheng Ma ; Min Huang ; Yanxiao ZhangSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensSomatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data. Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
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10. ⭐ GSE320255 泛癌分析揭示突变驱动的转座元件失调是免疫抑制的促成因素 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、RNA-seq
• 📝 描述：Contributors : Hongjian Qi ; Kai Tian ; Chicheng Ma ; Min Huang ; Yanxiao ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSomatic mutations and transposable element (TE) dysregulation are hallmarks of cancer, yet how specific genetic alterations influence TE activity across tumor types remains unclear. Here, we mapped mutation–TE regulatory networks across 9,622 tumors representing 33 TCGA cancer types by integrating RNA-seq, whole-exome, and DNA methylation data. Comparative analysis of tumors with and without mutations identified 275 significant cancer–gene pairs associated with altered TE expression, many of which are transcription factors such as TP53, NSD1 and ARID1A. The changes in TE expression were also inversely correlated with DNA methylation changes in many cases. Unexpectedly, we observed that immune pathway activity is down-regulated when TE expression is induced, and up-regulated when TE is repressed. Functional validation in isogenic ARID1A- and CTNNB1-perturbed models recapitulated the changes in TE activity and immune responses observed in TCGA datasets. Together, these findings reveal mutation-driven TE activity reprogramming as a widespread feature and a potential source for immune modulation in human cancers.
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1. 非侵入性胶带条RNA测序追踪斑秃的疾病活动

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing from non-invasive tape strips reveals immune activity and treatment response patterns in alopecia areata, supporting improved disease monitoring and patient stratification…
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2. 你的DNA一直在移动——这或许可以解释癌症的成因。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have uncovered a surprising secret about our DNA: it’s not a static blueprint, but a constantly shifting, folding structure that helps control how genes turn on and off. Researchers at the Salk Institute found that different parts of the genome loop and unloop at different speeds, with more active regions constantly reshaping themselves to support gene activity.
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• GSE318688 单细胞 RNA 测序揭示了小鼠脓毒症模型中间充质干细胞治疗相关的 M2 样巨噬细胞特征
• GSE315928 差异性 T 细胞克隆动力学是晚期胃癌一线化疗免疫疗法疗效的基础 [配对 scRNA/TCR-seq]
• GSE314069 饮食和毛状假毛细线虫（Pt）感染对斑马鱼肠道转录组的影响
• GSE300697 丝氨酸代谢确保正常的次要合子基因组激活（ZGA），特别是调节小鼠合子雄原核的组蛋白甲基化和DNA完整性
• GSE294814 哺乳动物组织中宿主和细菌RNA的空间分辨分析
• GSE294211 巨噬细胞介导的IL1β/IL23信号通路调节γδT细胞对非结核分枝杆菌的免疫反应
• GSE291185 新生儿肌腱细胞的再生潜能受其内在抗炎能力和T细胞分泌的支持性因子调控
• GSE289926 用于评估 T 细胞积累和细胞毒性的免疫肿瘤基质屏障体外 3D 模型
• GSE326495 整合单细胞 RNA 和空间分析揭示新生儿脑出血病理生理和修复机制 [scRNA-seq]
• GSE326000 启动子差异甲基化作为上皮性卵巢癌组织学分型的工具
• GSE325479 单细胞多组学比较分析揭示了介导自然视网膜衰老的进化保守且物种特异性的细胞机制
• GSE316497 基因型-表观基因组-表型整合揭示外周免疫细胞对双相情感障碍发病机制、表型异质性和治疗的贡献
• GSE298311 RNA测序：16D前列腺癌细胞系中OGDHL基因敲低
• GSE326238 大鼠体细胞基因组编辑实现ER+乳腺癌建模
• GSE324062 RAS通路激活驱动FLT3和BCL2抑制剂耐药中的克隆选择和单核细胞分化。
• GSE320398 泛癌分析揭示突变驱动的转座元件失调是免疫抑制的促成因素
• GSE320262 泛癌分析揭示突变驱动的转座元件失调是免疫抑制的促成因素 [WGBS]
• GSE320261 泛癌分析揭示突变驱动的转座元件失调是免疫抑制的促成因素 [CUT&Tag]
• GSE315929 差异性 T 细胞克隆动力学是晚期胃癌一线化疗免疫疗法疗效的基础 [TCR-seq]
• GSE315149 核 FGF2、雄激素受体和 Wnt 通路激活定义了抗孕激素耐药性管腔型乳腺癌的一个可靶向亚群
• GSE311053 SIRT1 是治疗先天性钴胺素代谢异常中蛋氨酸合成酶缺乏引起的脑代谢和发育后果的靶点
• GSE307677 真菌根内生菌在功能上增强了宿主的免疫力并减轻了拟南芥的自然免疫变异
• GSE303625 MYST 乙酰转移酶是 SETBP1 突变白血病中可靶向治疗的脆弱点 [RNA-Seq]
• GSE296012 NeuID 是一种新型的神经元特异性长链非编码RNA，它在阿尔茨海默病中调控神经元功能。
• GSE294970 Pin1 通过抑制转座元件介导纤维化乳腺癌的免疫逃逸 [ChIP-seq]
• GSE294478 冬眠哺乳动物基因组趋同性揭示下丘脑代谢调控的遗传学 [bulk RNA-seq]
• GSE294456 左心房单细胞TCR谱分析揭示补体通路参与心房颤动
• GSE293568 Arglabin及其衍生物对NLRP3/CCR2的阻断可抑制髓系驱动的免疫抑制并增强抗PD-L1免疫疗法在肝细胞癌中的疗效
• GSE293538 镉诱导的肠道菌群失调先于小鼠海马依赖性学习和记忆缺陷的发生
• GSE283439 用源自葡萄糖缺乏的肝细胞癌细胞的微囊泡处理的中性粒细胞的 RNA 测序。
• GSE279089 胰腺肿瘤发生过程中 KRAS 突变体表型分化的分子动力学驱动因素 [RNA-Seq]
• GSE279088 分子动力学驱动胰腺肿瘤发生中 KRAS 突变体表型分化 [ATAC-Seq]
• GSE228942 TL1A 在克罗恩病患者和小鼠中的过表达会改变潘氏细胞生物学和肠道菌群，从而促进回肠炎症
• GSE96752 人类心脏衰老基因表达谱
• GSE326496 整合单细胞 RNA 和空间分析揭示新生儿脑出血病理生理和修复机制 [Xenium]
• GSE324956 衰老过程中 Apex1 条件性敲除和热量限制小鼠海马体的表达谱分析
• GSE313468 野生型和Sirt7-/-小鼠精原细胞的RNA测序分析
• GSE291621 RNA-seq 分析 FOXF1/2 和 p300/CBP 缺失的衰老 IMR-90 细胞
• GSE291619 ATAC-seq 分析，用于研究 FOXF1/2 在衰老细胞中的作用。
• GSE262555 KDM5B组蛋白赖氨酸去甲基化酶缺陷小鼠表现出自闭症样表型和NMDAR2D表达增加
• GSE325239 RNA-seq 分析 P2 大鼠新生心房肌细胞，这些细胞转染了非靶向（对照）和 Pitx2c（KD）siRNA。
• GSE318825 靶向 eIF4E 帽结合域的治疗揭示前列腺癌谱系命运的控制 [CUT&Run]
• GSE305032 胶带条捕获主要罕见鱼鳞病中的免疫和表皮增生标志物
• GSE301507 靶向 eIF4E 帽结合域的治疗揭示了前列腺癌谱系命运的控制
• GSE288728 NIPBL 敲低诱导的粘连蛋白环挤出改变对 hESC 分化为胰腺谱系过程中 CTCF 环、增强子-启动子连接和 PRC 结构域接触的影响 [Hi-C]
• GSE326480 ACSS2 通过 E2F1-SLC7A11 信号通路抑制乳腺癌脑转移中的铁死亡
• GSE326430 内源性神经元RNA颗粒的独特动力学和组成
• GSE326265 核膜深内陷协调染色质的空间组织
• GSE326230 人类转录组中必需的长链非编码RNA
• GSE326178 Sprague-Dawley大鼠脑出血模型的RNA测序
• GSE326172 基质TNF-NFκB信号通过炎症驱动的上皮-基质串扰损害嵌合唾液腺类器官中的腺泡分化
• GSE325206 T细胞和NK细胞淋巴瘤细胞培养物的基因表达谱分析
• GSE324574 DNA甲基化影响转录因子结合，超越了经典的CpG序列——阵列6
• GSE324573 DNA甲基化影响转录因子结合，超越了经典的CpG序列——阵列5
• GSE324572 DNA甲基化影响转录因子结合，超越了经典的CpG序列——阵列4
• GSE324571 DNA甲基化影响转录因子结合，超越了经典的CpG序列 - 阵列2
• GSE324570 DNA甲基化影响转录因子结合，超越了经典的CpG序列 - 阵列1
• GSE324373 DNA甲基化影响转录因子结合，超越了经典的CpG序列——阵列3
• GSE324208 表观遗传重编程驱动脂肪肉瘤的细胞和表型可塑性
• GSE324206 平滑肌肉瘤空间分辨多组学图谱鉴定出两种具有临床意义的表观遗传驱动细胞状态 [scMultiomic]
• GSE324038 HIF-1α 和 HIF-2α 调控原代人类 T 细胞中重叠和不同的转录程序 [RNA-Seq]
• GSE322533 滑膜基因表达谱分析揭示了肱骨小头骨软骨炎患者自体骨软骨移植术后骨赘形成相关的心血管通路
• GSE320334 从大鼠和牛白色脂肪组织中分离细胞核用于单核RNA测序
• GSE320176 减肥的代价：索马鲁肽和 PYY3-36 会加重雌性大鼠已存在的代谢性骨质疏松症
• GSE318772 新型生物制剂治疗心力衰竭，通过调节免疫和基质网络促进内源性修复
• GSE317902 单核细胞亚群预测纤维化过敏性肺炎的临床结局
• GSE316178 LncRNAs协调强力霉素诱导的人类iPSCs基因表达反应（RNA-seq）
• GSE315516 胶质母细胞瘤细胞模拟人类神经元兴奋性
• GSE315440 LncRNAs协调强力霉素诱导的人类iPSCs基因表达反应（ATAC-seq）
• GSE315379 p53的表观遗传调控是滑膜肉瘤中一个可靶向的依赖性因素
• GSE314768 奥沙利铂耐药性结直肠癌细胞的转录组分析
• GSE312987 膳食人乳低聚糖 (HMO) 和毛虫 (Tm) 感染对小鼠盲肠转录组的影响
• GSE312767 放线菌属 SE50/110 在阿卡波糖发酵全过程中的转录组时间序列数据
• GSE311966 甘蓝型油菜和模式植物拟南芥中精氨酸/N-降解途径的功能差异
• GSE311713 KANSL1 缺陷小鼠及其对照小鼠胸腺 DP 细胞的 RNA-seq。
• GSE309147 基质 Erbb3 塑造子宫腺体形态发生 [RNA-seq]
• GSE303627 MYST 乙酰转移酶是 SETBP1 突变白血病中可靶向治疗的脆弱点 [CUT&Run]
• GSE302884 棕榈酸处理和IL-6/sIL-6R复合物刺激下肝窦内皮细胞（LSEC）的转录组分析
• GSE295947 Tfh scRNA-Seq
• GSE295937 Tfh 和 Th1 RNA-seq 数据
• GSE295641 多模态分析揭示了与嚼槟榔相关的口腔鳞状细胞癌的基因组改变和表达程序
• GSE295590 ILC2 和 TH2 细胞在回忆性肺 2 型免疫中的非冗余作用
• GSE294974 Pin1 通过抑制转座元件介导纤维化乳腺癌的免疫逃逸 [RNAseq_MCF7]
• GSE294973 Pin1 通过抑制转座元件介导纤维化乳腺癌的免疫逃逸 [mouse_py]
• GSE294971 Pin1 通过抑制转座元件介导纤维化乳腺癌的免疫逃逸 [RNAseq_4T1]
• GSE293985 肺炎链球菌和大肠杆菌中 I 型限制修饰系统的表观遗传基因调控
• GSE293933 地西他滨对多柔比星和紫杉醇耐药乳腺癌细胞系治疗反应的影响
• GSE293468转录组分析揭示健脾化脂丸（JPHZW）在缓解DSS诱导的溃疡性结肠炎中的调控作用
• GSE293063 甲苯咪唑处理下THP-1细胞的全基因组CRISPR缺失筛选
• GSE291647 野生型和AaegGr34埃及伊蚊脂肪体和脑组织的RNA测序分析
• GSE287319 免疫疗法联合粒子疗法治疗伴有大血管侵犯的晚期肝细胞癌：Ib期DEPARTURE试验
• GSE285810 ATF3依赖的polyQ表达的人类iPSC衍生神经元中包涵体的形成赋予细胞保护作用[RNA测序]
• GSE282968 无葡萄糖微囊治疗后的肝细胞癌
• GSE281448 秀丽隐杆线虫成虫和胚胎中poly(U)突变体的测序实验
• GSE281237 广泛的基因-环境相互作用塑造了对SARS-CoV-2感染的免疫反应
• GSE270211 对 RIPK3 被 siRNA 敲低的 NCI-H441 细胞系中 TNFα 或坏死性凋亡诱导刺激的转录组分析。
• GSE263559 通过移植人类iPS细胞衍生的3D类器官治疗代谢性肝病的新疗法
• GSE229883 小鼠滋养层干细胞 (mTSC) 中 METTL3 敲低与否的 N6-甲基腺苷 (m6A) 测序
• 利用 GS​​E229859 对敲低和未敲低 METTL3 的小鼠滋养层干细胞 (mTSC) 进行 mRNA 测序
• GSE229371 骨细胞来源的 Semaphorin3A 表达降低导致 GSD 小鼠模型淋巴管扩张
• 来自亲代和SLX4IP耗竭的D2.OR细胞的GSE200622 RNA-seq表达数据
• GSE96750 人类左心室的衰老
• GSE96749 人类左心房老化
• GSE300270 研究发现，WWOX 缺失通过调控 EMT 驱动皮肤鳞状细胞癌 (cSCC) 的发生。