详细内容（前10条）

1. ⭐ GSE313389 单细胞转录组分析揭示甲状腺癌淋巴结定植和进展的肿瘤免疫决定因素

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、immune、lymph、regex:lymph(o|atic)?、single-cell
• 📝 描述：Contributors : Anthony T Nguyen ; Stephen L Shiao ; Allen S HoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensLymph node (LN) metastases are a major driver of mortality across solid cancers, including thyroid carcinomas, which are known for high rates of nodal colonization. To elucidate the determinants of nodal spread, we isolated tumor-infiltrating leukocytes from primary thyroid tumors and matched metastatic LNs for single-cell RNA sequencing with validation by multiplex immunohistochemistry. Comparing the microenvironmental alterations between primary tumors and their LNs, we found that thyrocytes and tumor-associated macrophages downregulate the expression of multiple inflammatory cytokine receptors, including TNFRSF12A and CX3CR1, upon LN colonization. LNs were associated with the induction of regulatory T cells to suppress T cell-mediated cytotoxicity compared to matched primary tumors. Notably, tumor-infiltrating lymphocytes within LNs demonstrated increased expression of activation markers, including interleukin-7 receptor (IL7R). High LN expression of IL7R was significantly correlated with improved outcomes and can serve as a biomarker in this heterogeneous disease. Our findings on the dynamic equilibrium within LN metastases may offer conserved mechanisms for nodal colonization across solid tumors.
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2. ⭐ GSE307934 单细胞 RNA 测序揭示了 KPC 细胞移植小鼠模型中抗 VSIG4 抗体治疗对原位胰腺癌肿瘤微环境的影响

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment、sequencing、single-cell
• 📝 描述：Contributors : Guoling Huang ; Chenhui WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusImmune checkpoint blockade (ICB) therapies, such as PD-1/PD-L1 inhibitors, have revolutionized cancer treatment by reactivating exhausted T cells. However, their efficacy varies substantially among tumor types and is particularly limited in immunologically “cold” malignancies such as pancreatic ductal adenocarcinoma. These tumors exhibit minimal T-cell infiltration and a profoundly immunosuppressive tumor microenvironment (TME), leading to poor responses to ICB. VSIG4 is a B7-related transmembrane protein highly expressed by tissue-resident macrophages. Previous studies have shown that VSIG4 suppresses proinflammatory macrophage polarization by modulating pyruvate metabolism and enhances M2-like states via lactate-STAT3 signaling and fatty acid oxidation. VSIG4 also inhibits T-cell activation and proliferation, making it a candidate immune checkpoint molecule. Recent work has linked VSIG4⁺ tumor-associated macrophages to T-cell suppression and therapeutic resistance in multiple cancers, although the identity of the T-cell receptor for VSIG4 remains unknown. So we demonstrate that VSIG4 binds SLC3A2 to suppress Gln uptake and disrupt ion homeostasis, thereby impairing T-cell activation. Antibody-mediated VSIG4 blockade restores T-cell function and induces robust antitumor responses, especially in pancreatic cancer models. These findings define a novel VSIG4–SLC3A2 axis that integrates metabolic and ionic control to suppress immunity, offering a promising strategy to overcome resistance in “cold” tumors.
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3. ⭐ GSE314628 时间转录组分析鉴定分化 Caco-2 细胞中细胞因子诱导的肠道屏障破坏的核心调控因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：cytokine、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Cheng-Yuan Kao ; Hyo Shin Yoon ; Matt Kanke ; Chi-Ming Li ; Shining Ma ; Xin LouSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe intestinal epithelial barrier is a primary governor for gut homeostasis, and its disruption is a critical factor in the pathogenesis of many inflammatory diseases including Inflammatory Bowel Diseases (IBD). Although strategies to restore and enhance barrier function have been proposed as promising therapeutic approaches for treating inflammation-associated intestinal disorders, most therapies in development act on immune-cell response dampening rather than directly reinforcing epithelial function.
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4. ⭐ GSE313902 马衰老相关骨关节炎的多组学分析突显了肠道微生物组和代谢组的变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Lyndah Chow ; Lynn Pezzanite ; Steven DowSeries Type : Expression profiling by high throughput sequencingOrganism : Equus caballusAging-related osteoarthritis (OA) is a leading cause of lameness and reduced performance in horses. Mounting evidence in humans and laboratory species indicates both systemic and local inflammation play a role in OA pathogenesis, with increasing recognition that the gut microbiome contributes to a pro-inflammatory state. However, the role of the gut-joint-axis has not been fully explored in etiopathogenesis of equine OA. Therefore, the aim was to investigate fecal and leukocyte microbiome profiles and host gene expression patterns in horses with naturally occurring aging-related OA compared to controls.
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5. ⭐ GSE308704 P4HA3 通过促进 ACLY 介导的铁死亡抵抗来驱动宫颈癌淋巴转移 [HeLa, SiHa]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:lymph(o|atic)?、resistance
• 📝 描述：Contributors : Li Yuan ; Hongye Jiang ; Meng Xia ; Junxiu Liu ; Shuzhong Yao ; Chunyu ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe lymph node is the most common site of distant metastasis of cervical cancer (CCa), which elicits dismal prognosis and limited efficiency for treatment. Identification of the factors contributing to CCa lymphatic metastasis is needed to develop effective prevention and treatment strategies. Here, we found upregulation of prolyl 4-hydroxylase subunit alpha 3 (P4HA3), an α-subunit of prolyl hydroxylase, in lymphatic metastatic lesions of cervical cancer, which is strongly associated with poor prognosis. In vitro and in vivo experiments showed that P4HA3 promoted CCa lymphatic metastasis by conferring ATP-citrate lyase (ACLY)-mediated ferroptosis resistance. Mechanistically, P4HA3 stabilizes ACLY protein by competitively inhibiting its interaction with the E3 ubiquitin ligase UBR4, which prevents UBR4-mediated proteasomal degradation of ACLY. ACLY-derived acetyl-CoA enhances H3K27 acetylation (H3K27Ac) modification level in the promoter of SLC7A11 gene, ultimately enhancing SLC7A11 transcription and ferroptosis resistance. Collectively, our study provides a mechanistic understanding of the interplay between ferroptosis resistance and lymph node metastasis, providing a possibility to combat lymph node metastasis in cervical cancer.
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6. ⭐ GSE304077 P4HA3 通过促进 ACLY 介导的铁死亡抵抗来驱动宫颈癌淋巴转移。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:lymph(o|atic)?、resistance
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe lymph node is the most common site of distant metastasis of cervical cancer (CCa), which elicits dismal prognosis and limited efficiency for treatment. Identification of the factors contributing to CCa lymphatic metastasis is needed to develop effective prevention and treatment strategies. Here, we found upregulation of prolyl 4-hydroxylase subunit alpha 3 (P4HA3), an α-subunit of prolyl hydroxylase, in lymphatic metastatic lesions of cervical cancer, which is strongly associated with poor prognosis. In vitro and in vivo experiments showed that P4HA3 promoted CCa lymphatic metastasis by conferring ATP-citrate lyase (ACLY)-mediated ferroptosis resistance. Mechanistically, P4HA3 stabilizes ACLY protein by competitively inhibiting its interaction with the E3 ubiquitin ligase UBR4, which prevents UBR4-mediated proteasomal degradation of ACLY. ACLY-derived acetyl-CoA enhances H3K27 acetylation (H3K27Ac) modification level in the promoter of SLC7A11 gene, ultimately enhancing SLC7A11 transcription and ferroptosis resistance. Collectively, our study provides a mechanistic understanding of the interplay between ferroptosis resistance and lymph node metastasis, providing a possibility to combat lymph node metastasis in cervical cancer.
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7. ⭐ GSE294751 阿尔茨海默病小鼠模型的多组学单核分析表明 ACSS2 赋予神经元抵抗 tau 蛋白病变的能力 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、Neuronal、ChIP-seq
• 📝 描述：Contributors : Gabor Egervari ; Desi Alexander ; Hua Huang ; Greg Donahue ; Connor Hogan ; Mariel Mendoza ; Hong Xu ; Virginia Lee ; Ben A Garcia ; Nancy M Bonini ; Shelley L BergerSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusLoss of cell identity and global epigenomic dysregulation are emerging as key contributors to Alzheimer’s disease (AD). The mechanisms by which protective or risk-conferring epigenetic marks are established and maintained are under intense investigation. ACSS2 (Acetyl-CoA Synthetase 2) is a key metabolic enzyme that is nuclear-localized in neurons. In healthy brains, ACSS2 fuels histone acetylation and drives expression of neuronal genes that regulate learning and memory. Here, we examine how loss of ACSS2 contributes to AD-associated cellular, genomic and behavioral outcomes, focusing on long-term steady state changes. Using a mouse model of human pathological AD-Tau injection, we show that loss of ACSS2 exacerbates Tau-related memory impairments, while dietary supplementation of acetate rescues learning in an ACSS2-dependent manner. Combining state-of-the-art proteomic and genomic approaches, we demonstrate that this effect is accompanied by ACSS2-dependent incorporation of acetate into hippocampal histone acetylation, which facilitates gene expression programs related to learning. We identify the most severely affected hippocampal neuronal populations, including pyramidal cells of the perforant pathway and Cajal-Retzius cells. Overall, these results reveal ACSS2 as a neuroprotective metabolic enzyme in key hippocampal neuronal populations, and dysregulation of which may play an important role in the etiology of AD. These findings may guide development of future therapies for AD, other tauopathies and related dementia.
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8. ⭐ GSE294331 阿尔茨海默病小鼠模型的多组学单核分析揭示 ACSS2 赋予神经元抵抗 tau 蛋白病变的能力 [RNA-seq Acetate]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer、Neuronal、RNA-seq
• 📝 描述：Contributors : Gabor Egervari ; Desi Alexander ; Hua Huang ; Greg Donahue ; Connor Hogan ; Mariel Mendoza ; Hong Xu ; Virginia Lee ; Ben A Garcia ; Nancy M Bonini ; Shelley L BergerSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusLoss of cell identity and global epigenomic dysregulation are emerging as key contributors to Alzheimer’s disease (AD). The mechanisms by which protective or risk-conferring epigenetic marks are established and maintained are under intense investigation. ACSS2 (Acetyl-CoA Synthetase 2) is a key metabolic enzyme that is nuclear-localized in neurons. In healthy brains, ACSS2 fuels histone acetylation and drives expression of neuronal genes that regulate learning and memory. Here, we examine how loss of ACSS2 contributes to AD-associated cellular, genomic and behavioral outcomes, focusing on long-term steady state changes. Using a mouse model of human pathological AD-Tau injection, we show that loss of ACSS2 exacerbates Tau-related memory impairments, while dietary supplementation of acetate rescues learning in an ACSS2-dependent manner. Combining state-of-the-art proteomic and genomic approaches, we demonstrate that this effect is accompanied by ACSS2-dependent incorporation of acetate into hippocampal histone acetylation, which facilitates gene expression programs related to learning. We identify the most severely affected hippocampal neuronal populations, including pyramidal cells of the perforant pathway and Cajal-Retzius cells. Overall, these results reveal ACSS2 as a neuroprotective metabolic enzyme in key hippocampal neuronal populations, and dysregulation of which may play an important role in the etiology of AD. These findings may guide development of future therapies for AD, other tauopathies and related dementia.
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9. ⭐ GSE313089 转录组分析鉴定出细胞周期蛋白 D–CDK4/6 轴是膀胱癌顺铂耐药性的可药物靶向介质 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、RNA-seq
• 📝 描述：Contributors : Chun-Han Chen ; Tsung-Han HsiehSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPurpose Cisplatin resistance remains a critical challenge in bladder cancer (BC). This study aimed to define molecular drivers of cisplatin resistance and to assess potential therapeutic targets that may help restore treatment responsiveness. Methods Integrative transcriptomic analyses were performed using The Cancer Genome Atlas (TCGA) cohort to compare cisplatin non-responders with responders, alongside a cisplatin-resistant BC cell model to identify dysregulated pathways. Functional studies, including siRNA-mediated knockdown, SRB viability assays, flow cytometry, western blotting, and microarray-based transcriptomics, were used to characterize the dysregulated pathways. Results Both TCGA data and resistant BC cells exhibited upregulation of CCND1 and enrichment of E2F target genes. Silencing of Cyclin D1 restored cisplatin sensitivity in resistant cells. Abemaciclib selectively inhibited proliferation of cisplatin-resistant BC cells, reduced RB phosphorylation, induced sub-G1 accumulation, and suppressed expression of key regulators of cell-cycle progression and homologous recombination repair. Combined treatment with abemaciclib and cisplatin synergistically suppressed the proliferation of cisplatin-resistant BC cells in vitro and resulted in significantly greater tumor growth inhibition in an RT112 xenograft model in vivo. Conclusion Activation of the Cyclin D1/CDK4/6–E2F axis is a key driver of cisplatin resistance and demonstrate that CDK4/6 inhibition reduces proliferative capacity and DNA repair competency while enhancing cisplatin responsiveness. Targeting this pathway represents a rational therapeutic strategy for advanced or refractory BC.
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10. ⭐ GSE297164 RNA-seq 分析放射性碘处理的分化型甲状腺癌细胞揭示碘耐受过程中 DDR 通路的调控

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq、pathway
• 📝 描述：Contributors : Xiaotong Qiu ; Yongji Jiang ; Simin Liu ; Li Zhao ; Chuanzi Zuo ; Yanlei Huo ; Chao MaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAim: To investigate the role of ataxia-telangiectasia mutated (ATM) in thyroid cancer (TC) progression and radioactive iodine (RAI) resistance, exploring its potential as a therapeutic target. Methods: Single-cell RNA sequencing of 28 TC tumors / normal tissues traced ATM dynamics during dedifferentiation. Clinical validation used tissue microarrays (TMAs) on 89 RAI resistance (RAIR) and RAI-avid differentiated thyroid cancer (DTC) specimens. Preclinical models evaluated the synergy between the ATM inhibitor AZD1390 and RAI. Mechanistic studies employed RNA-seq, comet assays, cell cycle analysis, and AP site quantification. Results: scRNA-seq revealed progressive ATM upregulation during malignant progression, correlating with cell cycle dysregulation. TMAs confirmed elevated ATM expression in anaplastic thyroid cancer (ATC) vs. papillary thyroid cancer, PTC and RAIR tumors. In vivo, AZD1390 + 131I synergistically suppressed tumor growth and enhanced apoptosis. RAI predominantly induced apurinic/apyrimidinic (AP) sites rather than double-strand breaks (DSBs). ATM inhibition disrupted base excision repair (BER) coordination and G2/M checkpoint control, forcing cells with unresolved AP sites into mitotic catastrophe. Conclusion: ATM mediates RAIR in thyroid cancer by promoting AP site repair and inducing cell cycle arrest. Inhibiting ATM converts repairable damage into lethal DNA lesions, restoring RAI sensitivity, suggesting ATM as a therapeutic target for RAI-refractory thyroid cancer.
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1. 科学家可能已经找到了阿尔茨海默病真正的诱因

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：Scientists may have uncovered a hidden trigger behind Alzheimer’s disease. Instead of plaques being the root cause, amyloid beta appears to interfere with tau, a protein that helps keep neurons functioning properly. This disruption could set off the damage that eventually leads to the disease’s most recognizable brain changes.
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• GSE296368 羟基脂肪酸脂肪酸酯（FAHFA）衍生物作为肥胖症中脂质代谢和肠道微生物群的双重调节剂
• GSE309019 结核分枝杆菌利用单核细胞微环境逃避淋巴结免疫
• GSE334984 IL-26驱动的表观遗传重塑促进结直肠癌的免疫逃逸
• GSE333935：单细胞RNA测序分析肠上皮细胞GSK3B缺失对AOM/DSS诱导的结肠癌模型的影响
• GSE331548 Rab44缺失通过调节免疫反应和嗜酸性粒细胞功能减弱卵清蛋白诱导的过敏性气道炎症
• GSE319700 鲍曼不动杆菌的 VgrG2 效应蛋白通过抑制 Csu 菌毛组装和触发吞噬细胞的甲氧化来介导免疫逃避 [scRNA-seq]
• GSE313099 对化疗敏感的小细胞肺癌细胞系 H82 和 DMS114 及其相应的化疗耐药对应细胞系进行高通量测序
• GSE309464 EO771肿瘤样本的批量RNA测序 Gq_DREADD vs. Ctr
• GSE309463 CRH神经元对照组与肿瘤组的批量RNA测序
• GSE304916 转移RNA修饰驱动人类共生细菌家族的全基因组同义重编码
• GSE302889 代谢重编程驱动胰腺 β 细胞从 α 细胞新生 [RNA-Seq 2]
• GSE302787 代谢重编程驱动胰腺β细胞从α细胞新生 [ATAC-seq 2]
• GSE302786 代谢重编程驱动胰腺β细胞由α细胞新生 [RNA-Seq]
• GSE302785 代谢重编程驱动胰腺β细胞由α细胞新生 [ATAC-seq]
• GSE300132 亲代和乐伐替尼耐药的TPC-1甲状腺癌细胞的转录组分析
• GSE299763：对乐伐替尼耐药的乳头状甲状腺癌细胞中KRT15敲低的转录组分析
• GSE328877 单细胞 RNA 测序揭示了鹅胚胎发生过程中卫星细胞的异质性和发育动态
• GSE318541 母体降温措施移除对后代生长、免疫、耐热性和肝脏转录组学的影响
• GSE313088 转录组分析鉴定出细胞周期蛋白 D–CDK4/6 轴是膀胱癌顺铂耐药性的可药物靶向介质 [array]
• GSE293501 从猪骨骼肌中分离的体外培养细胞的单细胞转录组数据。
• GSE287738 探索巨噬细胞标志物 CD68 在儿童急性髓系白血病中的作用
• GSE271179 唐氏综合征相关髓系白血病 (ML-DS) 细胞系/患者来源异种移植 (PDX) 样本的转录组分析
• GSE335269 烟酰胺核苷通过促进记忆分化和代谢适应性增强过继性T细胞疗法
• GSE335102 对假结核耶尔森菌感染回肠的空间转录组分析揭示了新的肠细胞转录状态和细菌定位
• GSE314772 NOD/ShiLtJ小鼠干燥综合征模型中的纤维化重塑：来自单细胞转录组学和人工智能驱动的定量分析的见解
• GSE270357：姜黄素或姜黄素-铜复合物干预下棕榈酸处理的HepG2细胞的转录组测序
• GSE333943 肠上皮细胞 GSK3B 缺失对 AOM/DSS 诱导的结肠癌模型中染色质可及性的影响
• GSE333942 GSK3B 对结肠癌 RKO 细胞中全基因组 H3K27ac 的影响
• GSE333940：结肠癌RKO细胞中GSK3B敲除(KO)引起的转录组变化
• GSE333936 肠上皮细胞 GSK3B 缺失对 AOM/DSS 诱导的结肠癌模型转录组谱的影响
• GSE307714 RNAi介导的突变NPM1沉默通过恢复KAT7和P300依赖的组蛋白乙酰化抑制AML进展[ATAC-seq]
• GSE307713 RNAi介导的突变NPM1沉默通过恢复KAT7和P300依赖的组蛋白乙酰化抑制AML进展[RNA-Seq]
• GSE335848 RNA-seq 和 TrAEL-seq 分析了奥希替尼处理的 PC9 细胞在特定细胞周期阶段的情况
• GSE335660 缺氧预处理的肌腱干细胞来源的细胞外囊泡通过调节巨噬细胞异质性促进肌腱再生
• GSE335600 微需氧铜胁迫改变金黄色葡萄球菌的丙酮酸代谢，并揭示了与 CopL 相关的氮反应。
• GSE334417 呼吸道合胞病毒抑制I型干扰素信号传导以维持CD1c+树突状细胞中HLA-DM的表达
• GSE332551 阿尔茨海默病iPSC衍生小胶质细胞模型中与疾病相关的RNA和蛋白质特征
• GSE330200 p.Ser143Pro lamin A/C 突变导致扩张型心肌病，并在敲入小鼠模型中激活未折叠蛋白反应通路
• GSE329418 单细胞RNA测序上游细胞保存方法的多中心评估
• GSE328018 双相情感障碍中的脉络丛炎症
• GSE324036 心血管运动通过挽救异常剪接驱动脊髓小脑性共济失调1型的神经保护作用
• GSE320526 出生后早期发育过程中巨噬细胞的耗竭导致牙根发育紊乱和 Gli1⁺ MSC 轨迹改变
• GSE320067 I型干扰素重编程肠道上皮细胞，使接受抗逆转录病毒治疗的HIV-1感染者CD4+ T细胞中的HIV-1病毒得以持续潜伏
• GSE314867 小鼠视网膜单链RNA在Atf4和Bach1敲低中的应用
• GSE313339 对晚期肺腺癌患者血浆 EV 中癌症相关血栓形成的转录组进行分析。
• GSE304964 通过核糖体谱分析 (Ribo-seq) 和 RNA-seq 整合量化 shNC 和 shGm26917 FGSC 之间的翻译效率 (TE) 变化 [Ribo-Seq]
• GSE304963 鉴定 shNC 和 shGm26917 女性生殖系干细胞 (FGSC) 之间的差异表达基因 (DEG) [RNA-Seq]
• GSE300744 小鼠 MASH 和纤维化模型的肝脏单细胞图谱
• GSE300008 解码胰腺癌对PP2A抑制剂的反应
• GSE298460 新冠肺炎住院患者的DNA甲基化谱
• GSE282572 miR-4800-3p 过表达对胰腺癌细胞系（MIA PaCa-2 和 PSN-1）转移相关基因表达的影响
• GSE245656 褪黑素在挽救炎症引起的细胞线粒体功能障碍和成牙骨质细胞分化中的双重作用
• GSE327586 癫痫持续状态改变脑源性细胞外囊泡的功能 [BV2-RNA-seq]
• GSE327585 癫痫持续状态改变脑源性细胞外囊泡的功能 [N2A-RNA-Seq]
• GSE327253 IL15 — 驱动肝窦内皮细胞与 CD8⁺ 组织驻留记忆 T 细胞之间的串扰促进酒精相关性肝炎的炎症
• GSE327118 纳米纤维上培养的人类iPSC衍生少突胶质细胞的RNA测序分析
• GSE318601 MeCP2 突变对 Rett 综合征患者来源的人类皮质类器官功能网络的早期差异性影响 [RNA-Seq]
• GSE316794 ELAV的多聚化对于指导神经元选择性剪接和多聚腺苷酸化程序至关重要
• 利用 GS​​E315356 RNA-seq 技术鉴定 HFD 处理的 Lyve1-Cre;Heg1fl/fl 小鼠肝细胞中的关键差异表达基因。
• GSE310768 内皮细胞 AGO1 缺陷可降低小鼠乳腺癌负荷
• GSE308927 对呼伦贝尔短尾羊和湖羊胚胎在 E16 和 E19 阶段的单细胞转录组分析揭示了 T 基因突变介导的尾长表型调控机制
• GSE308104 DLK1敲除CMK细胞的转录组分析
• GSE302312 通过空间图案化的稳定和肥大软骨类器官植入物同步再生骨软骨缺损
• GSE302106 Gak缺失导致足细胞溶酶体功能障碍和免疫调节
• GSE296084 RNA测序分析未分化和分化的CT27人滋养层干细胞
• GSE293835 猪骨骼肌分离体外培养细胞的转录组数据
• GSE291701 FMRP 调控含有停滞核糖体的神经元 RNA 颗粒，而非核糖体停滞的位置
• GSE196382 定义胶质母细胞瘤中受 RBBP4/p300 复合物调控的转录本 [RNA-seq]
• GSE196381 绘制胶质母细胞瘤中由 RBBP4/p300 复合物调控的染色质图谱 [ChIP-seq]
• GSE335693 PIK3CA突变型结直肠癌中DHODH抑制的转录组分析
• GSE335522 女性特异性肝脏m6A重塑与高脂饮食的转录后代谢适应相关
• GSE300354 KMT2A-MLLT3 AML 中 KRAS 突变的建模促进白血病进展和转录组重塑
• GSE333948 载体或富马酸二甲酯处理的小鼠骨髓来源中性粒细胞的基因组 H3K36me2 富集谱
• GSE333945 对 RKO 细胞进行 ATAC-seq 分析，并进行 H1FX 和 GSK3B 的组合遗传扰动。
• GSE333941 GSK3B 对结肠癌 RKO 细胞中可及染色质区域的影响
• GSE308929 健康人皮肤毛囊皮脂腺单元的整合转录组图谱
• GSE307716 RNAi介导的突变NPM1沉默通过恢复KAT7和P300依赖的组蛋白乙酰化抑制AML进展[CUT&Tag]