详细内容（前10条）

1. ⭐ GSE291210 MMTV-PyMT 乳腺癌小鼠模型中乳腺肿瘤的空间转录组学特征 [MERFISH]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Nitin Narwade ; Raúl Jiménez-Castaño ; Khalil K Youssef ; Angela NietoSeries Type : OtherOrganism : Mus musculus ; synthetic constructDisseminated cancer cells rarely succeed in forming macrometastases, yet they continue to be the most life-threatening cause of patient mortality. The determinants driving metastatic competence, however, are still poorly understood. Using data from human breast cancer patients and genetic mouse models, we uncover a non-linear relationship between the expression of the EMT transcription factor Prrx1 in the primary tumor and metastatic outcome. Multi-omics analyses in mouse tumors reveal that Prrx1 functions as a dual regulator, promoting invasive behavior while simultaneously inducing dormancy. Cells with intermediate Prrx1 levels exhibit the highest metastatic fitness, whereas extreme levels (negative or too high) lead to less metastasis, typical of a hormetic behavior, and respectively due to insufficient invasiveness or to dormancy. These findings provide mechanistic insight into the regulation of dormancy and its link to metastatic potential. Additionally, we propose that combined signatures of invasion and proliferation allow robust prognosis prediction in breast cancer patients. Our study further highlights Prrx1-driven heterogeneity, established in the primary tumor, as a key determinant of metastatic competence.
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2. ⭐ 对皮内（i.d.）感染结核分枝杆菌（Mtb）的 C57BL/6 小鼠的颈部淋巴结（cLNs）进行 GSE314979 空间全转录组分析（GeoMx；Nanostring），揭示了病变边缘的转录变化。

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、regex:lymph(o|atic)?、spatial、transcriptome
• 📝 描述：Contributors : Matt A Field ; Manoharan KumarSeries Type : OtherOrganism : Mus musculusHere, we used a mouse model of latent lymphatic M. tuberculosis (Mtb) infection (LTBI) to dissect the immunological mechanisms underlying LTBI containment versus reactivation. We show that immunosuppression-mediated reactivation of lymphatic LTBI and the subsequent induction of progressive disease can be prevented by vaccination with BCG or recombinant BCG (BCG::ESAT-6-PE25SS (abbreviated to PE25) even in the absence of CD4+ T cells. Spatial transcriptomics, network analysis and bioinformatic reveal that anti-CD4-mediated immunosuppression is associated with and enhanced immune response at the edge of TB lesions within the infection-draining cervical lymph nodes.
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3. ⭐ GSE314556 层粘蛋白A/C维持基因组拓扑结构并调控病毒驱动的B细胞活化所必需的转录程序。[Hi-C]

• ✍️ 作者：未知作者
• 🏷️ 关键词：B cell、Hi-C、genome
• 📝 描述：Contributors : Lisa B Caruso ; Italo TemperaSeries Type : OtherOrganism : Homo sapiensLamin A/C is a crucial structural component of the nuclear lamina that influences chromatin organization and gene regulation. In this study, we demonstrate that lamin A/C is vital for maintaining higher-order genome organization and transcriptional programs that support EBV-driven B-cell activation. Loss of lamin A/C in a B-lymphoblastoid cell line caused significant three-dimensional reorganization of the genome, evidenced by the loss of long-range chromatin loops, an increase in short-range contacts, and redistribution of H3K9me2- marked heterochromatin. These structural disruptions were linked to widespread changes in gene expression affecting metabolic, signaling, and differentiation pathways. Mechanistically, lamin A/C influences the nuclear positioning and transcription of CTCF-bound loci by preventing their relocation to the periphery and their association with lamin B1. Blocking H3K9me2 deposition mimicked the transcriptional effects of lamin A/C depletion and revealed increased sensitivity to PI3K inhibitors. Overall, our results identify lamin A/C as a key organizer of genome structure and epigenetic regulation in EBV-infected B cells, uncovering a lamin-dependent pathway that connects nuclear architecture, metabolism, and viral disease processes.
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4. ⭐ GSE314543 Lamin A/C 维持基因组拓扑结构并调节病毒驱动的 B 细胞活化所必需的转录程序 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：B cell、ChIP-seq、genome
• 📝 描述：Contributors : Lisa B Caruso ; Italo TemperaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensLamin A/C is a crucial structural component of the nuclear lamina that influences chromatin organization and gene regulation. In this study, we demonstrate that lamin A/C is vital for maintaining higher-order genome organization and transcriptional programs that support EBV-driven B-cell activation. Loss of lamin A/C in a B-lymphoblastoid cell line caused significant three-dimensional reorganization of the genome, evidenced by the loss of long-range chromatin loops, an increase in short-range contacts, and redistribution of H3K9me2- marked heterochromatin. These structural disruptions were linked to widespread changes in gene expression affecting metabolic, signaling, and differentiation pathways. Mechanistically, lamin A/C influences the nuclear positioning and transcription of CTCF-bound loci by preventing their relocation to the periphery and their association with lamin B1. Blocking H3K9me2 deposition mimicked the transcriptional effects of lamin A/C depletion and revealed increased sensitivity to PI3K inhibitors. Overall, our results identify lamin A/C as a key organizer of genome structure and epigenetic regulation in EBV-infected B cells, uncovering a lamin-dependent pathway that connects nuclear architecture, metabolism, and viral disease processes.
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5. ⭐ GSE314537 层粘蛋白A/C维持基因组拓扑结构并调控病毒驱动的B细胞活化所必需的转录程序。[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：B cell、RNA-seq、genome
• 📝 描述：Contributors : Lisa B Caruso ; Italo TemperaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensLamin A/C is a crucial structural component of the nuclear lamina that influences chromatin organization and gene regulation. In this study, we demonstrate that lamin A/C is vital for maintaining higher-order genome organization and transcriptional programs that support EBV-driven B-cell activation. Loss of lamin A/C in a B-lymphoblastoid cell line caused significant three-dimensional reorganization of the genome, evidenced by the loss of long-range chromatin loops, an increase in short-range contacts, and redistribution of H3K9me2- marked heterochromatin. These structural disruptions were linked to widespread changes in gene expression affecting metabolic, signaling, and differentiation pathways. Mechanistically, lamin A/C influences the nuclear positioning and transcription of CTCF-bound loci by preventing their relocation to the periphery and their association with lamin B1. Blocking H3K9me2 deposition mimicked the transcriptional effects of lamin A/C depletion and revealed increased sensitivity to PI3K inhibitors. Overall, our results identify lamin A/C as a key organizer of genome structure and epigenetic regulation in EBV-infected B cells, uncovering a lamin-dependent pathway that connects nuclear architecture, metabolism, and viral disease processes.
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6. ⭐ GSE307496 利用空间转录组学解析牛睾丸组织的发育

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Haoyan Jin ; Lingkai ZhangSeries Type : OtherOrganism : Bos taurusMammalian spermatogenesis is critical for the transmission of male genetic information, and single-cell sequencing technology can reveal its complex process. However, at present, there is no research on the dynamic transcription of bovine germ cell population. In this study, we used Stereo-seq to construct a spatial transcription map of bovine testicular tissue at two ages. Four germ cell groups and five somatic cell groups were determined, and functional enrichment characterized their different biological functions and the differences between calves and adult bovines. At the same time, we also defined the subpopulations of cells and marker genes, then, clarified the communications between germ cells. These data laid the foundation for the study of spermatogenesis in large mammals and elucidated the process of transcriptional changes for the mechanism of male germ cells.
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7. ⭐ GSE285389 将组蛋白 H2B 变体整合到染色质中可改变染色质可及性，从而诱导乳腺癌中上皮间质转化 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq、histone
• 📝 描述：Contributors : Hejer Dhahri ; Kin LauSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensHistones scaffold genomic DNA and regulate access to the transcriptional machinery. However, naturally occurring histone variants can alter histone-DNA interactions, DNA and histone modifications, and the chromatin interactome. Hence, alterations in histone variant deposition can disrupt chromatin, and are increasingly recognized as a way to trigger various disease (including cancer). While significant attention has been placed on the biochemical and functional roles of H2A and H3 variants, H2B variants remain largely understudied. Here, we show that H2B variants are dysregulated in breast cancer and that certain variants are associated with specific breast cancer subtypes. HIST1H2BO overexpression (in particular) is more common in Asian, African American/Black, and young female populations and is associated with a worse prognosis. In vitro, H2B1O compacts chromatin, and incorporating H2B1O into chromatin activates pro-inflammatory and oncogenic pathways and the epithelial-to-mesenchymal transition (EMT), and generates resistance to first-line chemotherapeutic agents. Thus, H2B1O acts much like an onco-histone, with H2B variant expression being a prognostic biomarker for breast cancer and a potential new target for drug therapies to enhance treatment efficacy.
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8. ⭐ GSE284679 靶向 PKMYT1 可增强去势抵抗性前列腺癌的抗肿瘤免疫反应 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune、scRNA
• 📝 描述：Contributors : Lin Gao ; Bo Han ; Jing HuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAlthough immunotherapy has been successful in various tumors, its efficacy in castration resistant prostate cancer (CRPC) is minimal, due to reduced presence of intratumoral immune effector cells in CRPC. How CRPC cells escape immune surveillance is not fully defined. Here we demonstrate that PKMYT1 expression is elevated in CRPC cases, which related to low immune infiltration in these patients. Patients with high PKMYT1 expression exhibit low CD8+ T cells signature and resistance to ICB therapy. Targeting PKMYT1 can suppress CRPC progression, accompanied with increased intratumoral CD8+ T cells. Selective PKMYT1 inhibitor, RP-6306, augmented ICB in a manner dependent on CD8+ T cells. PKMYT1 inhibitors alone or in combination with PD-L1 blockade causes CD8+ T cell infiltration and remarkable tumor suppression, which suggests a promising immunotherapeutic approach in CRPC. Mechanically, targeting PKMYT1 activated the cGAS-STING pathway, which increases expression of type I and II interferon response genes and led to upregulation of key immune regulators. These findings highlight a key role of PKMYT1 in CRPC progression and rationalize PKMYT1 as a potential therapeutic target.
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9. ⭐ GSE272303 α-突触核蛋白病转基因小鼠模型的空间转录组成像

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Liam Horan-Portelance ; Michiyo Iba ; Dominic J Acri ; J R Gibbs ; Mark R CooksonSeries Type : OtherOrganism : Mus musculusOne of the unifying pathological hallmarks of the age-related neurodegenerative disorders Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) is the presence of misfolded, aggregated, and often phosphorylated forms of the protein α-synuclein (α-syn) in neurons. α-syn pathology appears in select populations of neurons throughout various cortical and subcortical regions, and little is currently known about why some neurons develop pathology while others are spared. Here, we utilized subcellular-resolution imaging-based spatial transcriptomics (IST) in a transgenic mouse model which overexpresses wild-type human α-syn (α-syn-tg) to evaluate patterns of selective neuronal vulnerability to α-syn pathology. By performing post-run immunofluorescence for α-syn phosphorylated at Ser129 (pSyn), we identified cell types in the cortex and hippocampus of these mice which were vulnerable or resistant to developing pSyn pathology. Next, using a set of custom probes to detect genes involved in α-syn processing and toxicity, we investigated the transcriptional underpinnings of the observed selective vulnerability; this pointed to expression of the kinase-substrate pair Plk2, which phosphorylates α-syn at Ser129, and human SNCA (hSNCA), as a driving mechanistic force behind these neurons’ selective vulnerability to pSyn pathology in this model. Finally, we performed differential gene expression analysis, comparing non-transgenic cells to pSyn- and pSyn+ α-syn-tg cells; this revealed gene expression changes downstream of hSNCA overexpression and pSyn pathology which were conserved across cell types, including some genes which were differentially expressed in a pSyn-specific manner. This study provides one of the most comprehensive use cases of newly developed IST to date, yielding new biological insights into the formation of α-syn pathology and its downstream effects in a PD/DLB mouse model.
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10. ⭐ GSE254444 利用单细胞转录组学研究冯·希佩尔-林道综合征相关肾癌的肿瘤异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、transcriptomics
• 📝 描述：Contributors : Isaline Rowe ; Giulia Scotti ; Giovanni Pipitone ; Andrea SaloniaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensVon Hippel-Lindau (VHL) dìsease is a rare inherited disorder caused by the loss of the VHL gene and characterized by benign and malignant tumors in several organs. Patients with VHL disease have risk of developing multiple primary clear cell renal carcinomas (ccRCC). Patients are managed with multiple sessions of renal surgery causing renal failure and complication of dialysis or systemic progression and cancer-specific mortality. Our hypothesis states that multiple independent tumors from one VHL patient may display inter-tumoral heterogeneity characterized by differences in tumor grade, metabolic, stromal, and immune cell features that may cause different response to systemic therapy. We took advantage of a nephrectomy from one VHL patient to investigate molecular and microenvironmental factors in five independent primary tumors.
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详细内容（全部3条）

1. 是静止期还是衰老期？癌症中心的研究有助于识别更易复发的癌症。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Using single-cell RNA sequencing, researchers identified a continuum between quiescent and senescent cancer cells after chemotherapy, offering insights into tumor dormancy and the…
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2. 科学家发现生活经历如何重塑免疫系统

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Why does the same virus barely faze one person while sending another to the hospital? New research shows the answer lies in a molecular record etched into our immune cells by both our genes and our life experiences. Scientists at the Salk Institute have created a detailed epigenetic map of human immune cells, revealing how inherited traits and past exposures—like infections, vaccines, or even environmental chemicals—shape immune responses in different ways.
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3. 这种开菲尔和膳食纤维的组合在减轻炎症方面胜过omega-3。

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation
• 📝 描述：A six-week study from the University of Nottingham suggests that pairing fermented kefir with a diverse prebiotic fiber mix may deliver a powerful anti-inflammatory boost. This “synbiotic” combination outperformed omega-3 supplements and fiber alone, leading to the broadest drop in inflammation-related proteins in healthy adults. By feeding beneficial microbes and helping them produce compounds like butyrate, the combo appeared to improve overall immune balance and metabolic health.
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• GSE318726 苯丙氨酸重编程 MASH-HCC 中的 TLS 成熟和浆细胞分化 [空间转录组学]
• GSE318590 野生型和 App NL-G-F 小鼠后皮层的空间转录组学数据
• GSE309787 MGMT 与 cGAS/STING 通路交叉调控巨噬细胞的先天免疫反应
• GSE289441 白血病中肿瘤抑制程序的表观遗传再激活
• GSE317406 靶向 PKMYT1 可增强去势抵抗性前列腺癌的抗肿瘤免疫反应。
• GSE314658 早期胎儿生长受限妊娠胎盘的全基因组DNA甲基化分析
• GSE314558 Lamin A/C 维持基因组拓扑结构并调节病毒驱动的 B 细胞活化所必需的转录程序。
• GSE310687 表观遗传可塑性和代谢及细胞壁动力学的调控重塑驱动小麦基因型特异性胚胎发生
• GSE306502 激活时巨噬细胞中糖皮质激素转录组 [RNA-seq]
• GSE300736 免疫激活基因的转录水平在 circRNACRT-E7E6 治疗后肿瘤中发生改变
• GSE297421 改进的用于胞内细菌沃尔巴克氏体 wAlbB RNA 测序的 RNA 制备方法
• GSE290960 肠道菌群通过 Toll 样受体 2 对小鼠神经胶质瘤的生长产生负面影响
• GSE285392 将组蛋白 H2B 变体整合到染色质中可改变染色质可及性，从而诱导乳腺癌的上皮间质转化
• GSE285391 将组蛋白 H2B 变体整合到染色质中可改变染色质可及性，从而诱导乳腺癌中上皮间质转化 [RNA]
• GSE285390 将组蛋白 H2B 变体整合到染色质中可改变染色质可及性，从而诱导乳腺癌上皮间质转化 [CUT&RUN]
• GSE283458 靶向 PKMYT1 可增强去势抵抗性前列腺癌的抗肿瘤免疫反应
• GSE281596 偏头痛小鼠模型 Sp5C 中 miRNA 的差异表达和生物信息学分析
• GSE312483 靶向代谢脆弱性：REV-ERB激动剂SR9009增强索拉非尼在肝癌中的疗效
• GSE307476 ATGL 通过调节 CEBPα/SCD1 轴抑制急性髓系白血病细胞的铁死亡，并诱导吉瑞替尼耐药性。
• GSE294340 ETS1 内皮特异性敲除和对照胚胎 E14.5 小鼠心室组织的单细胞 RNA 测序
• GSE291211 Prrx1 敲除后 MMTV-PyMT 乳腺癌小鼠模型中乳腺肿瘤的单细胞 RNA 分析
• GSE291199 MMTV-PyMT乳腺癌小鼠模型中乳腺肿瘤的单细胞ATAC分析
• GSE275648 癌症相关成纤维细胞通过与内皮细胞和恶性上皮细胞相互作用在晚期胃癌预后分层中的作用 [AGC scRNA-seq]
• GSE269621 单细胞 RNA 测序分析 SW620 异种移植瘤在裸鼠体内的模型
• GSE263150 新一代测序技术有助于对接受 KAT8 抑制剂治疗的骨髓来源巨噬细胞进行定量分析
• GSE263149 新一代测序技术促进野生型和KAT8缺陷型骨髓来源巨噬细胞转录组的定量分析
• GSE319280 全基因组DNA甲基化调查揭示水杨酸诱导的独特低甲基化与针对生物营养型病原体的防御反应有关
• GSE319044：肺部免疫细胞单细胞多组学分析鉴定出新的哮喘风险基因和细胞类型特异性功能
• GSE318886 ALDH18A1促进胃癌进展并调节PI3K-Akt信号通路
• GSE317207 利用批量RNA测序对人肝细胞癌活检样本进行转录组分析
• GSE309346 PI3K 和 MAPK 信号节点作为结直肠癌相关成纤维细胞表型可塑性的不同驱动因素 [scRNA-Seq]
• GSE289419 评估大鼠足底电击模型在创伤后应激障碍研究中研究肠脑相互作用和肠易激综合征相关基因表达的适用性
• GSE315428 柯里拉京通过激活TXNIP-Caspase-3-GSDME通路诱导AML细胞发生焦亡
• GSE310104 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 [ChIP-seq]
• 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]
• GSE306053 INO80 调控启动子相关的 R 环，从而协调转录并维持胚胎干细胞的基因组稳定性
• GSE305730 精准医学方法解读先天性心脏病患儿的 GATA4 基因变异 [RNA-seq]
• GSE304121 人类基因组暴露于艰难梭菌 TcdB 后 CTCF（CCCTC 结合因子）结合模式。
• GSE299397基因表达谱分析鉴定出人结肠癌细胞系中与铁死亡相关的基因
• GSE293873 研究表明，双调蛋白和表皮调蛋白通过氧化磷酸化赋予食管鳞状细胞癌放射抗性。
• GSE292899 Loss of H3K9me3 maintenance leads in human neural progenitor cells leads to transcriptional activation of L1 retrotransposons [Bulk RNA-seq]
• GSE290344 USH2A 外显子 13 中的无义突变激活 Müller 胶质细胞的先天免疫反应
• GSE290309 通过 BCL6-FXR 肠肝串扰预防胆汁淤积性肝病 [RNA-seq]
• GSE290307 通过 BCL6-FXR 肠肝串扰预防胆汁淤积性肝病 [ChIP-seq]
• GSE287825 METTL3-YTHDC1轴介导RNA结构m6A修饰，从而调节MLLr+ AML基因组中染色质TAD的完整性
• GSE287122 研究表明，Neuregulin-1β 治疗可增强代偿性重塑并改善压力负荷过重时的心脏功能。
• GSE277139 LOXL2 保护颞下颌关节免受线粒体功能障碍、细胞凋亡和骨关节炎样进展的影响 [RNA-Seq]
• GSE254446 患有冯·希佩尔-林道病患者的肾细胞癌和囊肿
• GSE254445：冯·希佩尔-林道病患者肾细胞癌和囊肿的转录组分析
• GSE223246 前列腺素D2合成酶调控雪旺细胞代谢
• GSE155631 DIS3突变在多发性骨髓瘤中的致癌机制
• GSE319253 二十碳五烯酸重编程脑血管代谢并损害脑损伤后的修复，与慢性创伤性脑病相关 [human_brain_OnurE_RNA-seq]
• GSE319252 二十碳五烯酸重编程脑血管代谢并损害脑损伤后的修复，与慢性创伤性脑病相关 [mouse_brain_OnurE_RNA-seq]
• GSE318724 苯丙氨酸重编程 MASH-HCC 中的 TLS 成熟和浆细胞分化 [scRNA-seq]
• GSE313644 激活的干扰素信号抑制年龄相关的肝癌 [RNAseq_WholeLiver]
• GSE313615 NSD2受高危型HPV E6/E7上调，并调节HPV相关头颈癌的上皮分化。
• GSE310024 CYP4F11 耗竭对肺癌细胞系 NCI-H460 细胞系增殖和迁移的影响。
• GSE303158 单细胞 CRISPR 筛选揭示了调控人类多能性的基因调控网络，该网络存在于已启​​动和未启动细胞中。
• GSE300652 MED8 敲低对膀胱癌细胞 T24 基因表达的影响。
• GSE299752 脓毒症引起的骨骼肌萎缩可通过药物抑制小鼠 STAT3 信号传导来缓解 [RNA-seq]
• GSE289162 表观基因组衰老的可塑性导致个体对早期环境暴露的脆弱性，从而重塑成年细胞和特定方向的发育轨迹
• GSE280617 H3K27me3 染色质异质性揭示了细胞对雌激素和内分泌治疗的不同反应 [RNA-seq]
• GSE275656 保护视网膜神经节细胞：抑制 PAX6-JNK3 轴可防止青光眼模型中 NMDA 诱导的兴奋性毒性 [RNA-seq]
• GSE275655 保护视网膜神经节细胞：抑制 PAX6-JNK3 轴可防止青光眼模型中 NMDA 诱导的兴奋性毒性 [ChIP-seq]
• GSE269391 高级别胶质瘤血浆细胞外囊泡取样显示了一种指示疾病的小 RNA 特征，并将 lncRNA RPPH1 鉴定为高级别胶质瘤生物标志物。
• GSE268613 铁过载通过WNT信号通路重编程Glul+肝细胞命运，诱导小鼠脂肪变性和纤维化
• GSE263148 RNA-seq 分析了 IMQ 诱导的银屑病模型中 KAT8 cKO 和 WT 小鼠的耳部皮肤
• GSE263147 R848刺激的骨髓来源巨噬细胞的H4K16ac Cut&Tag谱分析
• GSE263146 KAT8 Cut&Tag 分析 R848 刺激的骨髓来源巨噬细胞
• 利用 GS​​E263145 ATAC-seq 分析 R848 刺激的 BMDM 的染色质可及性
• GSE319264 RNA-seq cas9-核糖核蛋白复合物产生的植物甾烯脱氢酶敲除类胡萝卜素缺陷微藻突变体
• GSE318896 CUT&Tag 分析 AC16 心肌细胞中 Irx3 结合位点，为心脏调控机制的研究提供支持
• GSE318779 The VgrG2 effector of Acinetobacter baumannii mediates immune evasion by repressing Csu pilus assembly and triggering phagocyte methuosis
• GSE317960 来自肝细胞 Tet1 过表达 MASH 小鼠的肝脏 RNA 测序
• GSE316707 小鼠肝肿瘤单细胞RNA测序：早期治疗、晚期治疗和对照
• GSE311241 心肌梗死模型中经 AAV9-cTnT-Rbm22 治疗的成年小鼠心肌细胞的 ATAC-seq 分析
• GSE309233 PI3K 和 MAPK 信号通路节点作为结直肠癌相关成纤维细胞表型可塑性的不同驱动因素
• GSE295696 ATAC-seq 分析 RBM22 沉默和对照原代心肌细胞的染色质可及性
• GSE295695 新一代测序技术促进了RBM22沉默和对照原代新生小鼠心肌细胞转录组的定量分析
• GSE279430 增强T细胞中蛋白酶体活性可缓解T细胞耗竭并改善抗肿瘤免疫力
• GSE278200 尼达尼布在博来霉素诱导的大鼠肺纤维化模型中的作用：转录组分析
• GSE224344 鞣花酸处理的小鼠骨髓间充质干细胞的转录组分析
• GSE189768 Dnmt1 中的显性突变导致表观遗传改变（RNA-BS-seq）
• GSE189763 Dnmt1 中的显性突变导致表观遗传改变（RIPseq）