科研日报 2026-08-05
📅 Daily Report - 2026-08-05
今日筛选出 50 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 研究发现肠道微生物网络调控神经视网膜自身免疫(GSE327793),以及声波空化技术显著增强淋巴结微环境重塑,促进肿瘤疫苗接种(GSE341961)。
主要方向:
- 免疫与疾病:探索免疫检查点阻断在非小细胞肺癌中的生物标志物(GSE305086),解析免疫细胞(如树突状细胞、T/B细胞)在肿瘤免疫和自身免疫中的作用(GSE307145, GSE341912),以及疾病(如败血症)中的免疫失调机制(GSE342074)。
- 肿瘤转录组学:研究乳腺癌(GSE304137)、食管癌(GSE341901)和横纹肌肉瘤(GSE292876, GSE292872)的分子机制。
- 肠道与代谢:绘制小鼠肠道空间和单细胞转录组图谱(GSE341914, GSE341913),并揭示特定物质(如槲皮素)对炎症的调节作用(GSE304676)。
技术亮点:
- 单细胞与空间转录组学:广泛应用于解析复杂组织(如肠道、肿瘤)的细胞异质性和微环境(GSE341912, GSE341914, GSE341913, GSE342074)。
- 高通量测序技术:包括RNA-seq、ChIP-Seq和基因表达谱分析,是揭示疾病机制和寻找生物标志物的核心手段。
🧪 博客更新
今日焦点: 新型化合物靶向阿尔茨海默病关键蛋白TAOK-1,并发现激活剂;同时,RNA测序与空间转录组学揭示了休眠癌细胞的藏匿点,为治疗耐药性提供新思路。
主要方向:
- 靶向阿尔茨海默病早期病因,开发新型抑制剂和激活剂。
- 绘制休眠癌细胞微环境,探索联合疗法。
- 揭示衰老与脑部疾病(如ALS、亨廷顿病)的分子机制。
- 优化单细胞RNA测序数据分析,提高细胞周期预测精度。
- 探索免疫系统增强策略,对抗癌症和病毒。
技术亮点:
- 首创选择性抑制TAOK-1的化合物。
- RNA测序结合空间转录组学,精确定位休眠癌细胞。
📚 分类浏览
🧬 数据前沿 (45条)
详细内容(前10条)
1. ⭐ GSE327793 肠道微生物相互作用网络控制神经视网膜自身免疫
- ✍️ 作者:未知作者
- 🏷️ 关键词:regex:micro(b|be|bial|organism)、gut、regex:gut(-?microbiome)?
- 📝 描述:Contributors : Amy Zhang ; Reiko Horai ; Yingyos Jittayasothorn ; Jonathan Badger ; Zhichao Wu ; Guangpu Shi ; Akriti Gupta ; Vijayaraj Nagarajan ; John McCulloch ; Shilpa Kodati ; H Nida Sen ; Jung Wha Lee ; Jonathan Jacobs ; Xiaoyan Xu ; Mary Mattapallil ; Zixuan Peng ; Biying Xu ; Robert Palmer ; Nadim Majdalani ; Kenya Honda ; Colm O’hUigin ; Rachel CaspiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe gut microbiome influences the development of immune-mediated inflammatory diseases. One such condition is autoimmune uveitis, a sight-threatening ocular inflammation driven by retina-specific T cells. Using a model of spontaneous experimental autoimmune uveitis (sEAU) we showed that gut commensals provide immune stimuli that trigger the disease. Here we report that uveitis-promoting microbes are present in human gut flora and that colonization of germ-free (GF) mice with commensal flora from healthy human donors was sufficient to provoke disease. Severity of sEAU correlated with expansion of Akkermansia and contraction of short-chain fatty acid (SCFA)–producing Firmicutes, followed by decreased SCFA levels and a dominant gut Th1 effector response. Mechanistic gain-of-function experiments, enriching GF sEAU mice with Akkermansia, reproduced these microbiome, metabolite and immune phenotype shifts, and exacerbated disease. We propose that Akkermansia promotes autoimmunity by outcompeting SCFA-producers and enhancing Th1-type responses. Notably, an inverse correlation between Akkermansia (Verrucomicrobia) and Firmicutes was also present in fecal microbiome of patients with uveitis, multiple sclerosis and Crohn’s disease. These findings reveal a stereotypic gut microbial interaction network that regulates systemic immune balance, and may represent an ecologically conserved mechanism through which the gut microbiome modulates autoimmune and inflammatory diseases.
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2. ⭐ GSE305086 免疫疗法下血液基因表达作为非小细胞肺癌免疫检查点阻断的潜在生物标志物
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、immune、regex:immuno(logy|therapy|suppression)
- 📝 描述:Contributors : Fabienne Lusky ; Petros ChristopoulosSeries Type : Expression profiling by arrayOrganism : Homo sapiensAbstractIntroduction: PD-(L)1 immunotherapy (IO) is a mainstay first-line (1L) treatment for advanced non-small-cell lung cancer without actionable alterations (aNSCLC), but reliable biomarkers are lacking. This study explored the potential utility of longitudinal blood gene expression profiling in this setting.Methods: 165 patients with aNSCLC and 1LIO as monotherapy (n=60), or combined with chemotherapy (CHTIO, n=71) were prospectively analyzed along with patients receiving 2LIO (n=34) and age-matched controls (n=21). PAXgene blood RNA was analyzed by quantitative PCR (qPCR) and Affymetrix U133 Plus 2.0 microarrays, including median fold changes [FC] and odds ratio (OR) between groups, with control of the false discovery rate (FDR). Progression-free survival (PFS) was verified through review of radiological images based on RECIST v1.1. Routine blood cell counts and PD L1 tumor proportion score (TPS) were available from the patients’ records.Results: Significantly higher neutrophil (FC 1.66, p1year (OR 12-19x, pConclusions: Transcriptomic perturbations are pronounced and readily detectable by qPCR in the blood of NSCLC patients. While the prognostic utility of immunologic gene expression alterations at baseline in the blood was limited by the patients’ initial leucocytosis, an upregulation of PD1, GATA3, FOXP3 and other T-cell related genes specifically under IO monotherapy was strongly associated with clinical benefit and could serve as a novel IO biomarker independent of blood cell counts and tumor PD L1 expression.
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3. ⭐ GSE341961 声空化增强淋巴结微环境重塑实现强效癌症疫苗的深层浸润
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、lymph、regex:lymph(o|atic)?
- 📝 描述:Contributors : Bihan Wu ; Xiaodan Xu ; Peile Jin ; Yijie Chen ; Xia Fang ; Yue Song ; Guowei Wang ; Jiajia Zhou ; Huaimin Wang ; Pintong HuangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe efficacy of peptide-based tumor vaccines is often constrained by the size-exclusion barrier of the subcapsular sinus (SCS), which restricts infiltration of macromolecules into the lymph node (LN) parenchyma essential for T-cell priming. Here, inspired by the clinical contrast agent Sonazoid, we developed an ultrasound-assisted vaccine platform with tunable phase-transition behavior for active modulation of the LN microenvironment. The system integrates phosphoserine-decorated lipid chemistry to promote cell-mediated LN trafficking, a covalently conjugated adjuvant–antigen construct for synchronized immunostimulation, and liquid-state perfluorocarbon nanodomains programmed for ultrasound-triggered liquid–gas transition. Upon localized ultrasound irradiation, the chemically programmed phase transition triggers cargo release, while the resultant acoustic cavitation generates transient openings in the SCS endothelium. This process enables deep parenchymal infiltration of vaccine components that would otherwise be excluded. Beyond the physical barrier disruption, RNA sequencing reveals that acoustic stimulation drives both structural and immunological reprogramming of LN into an immune-permissive niche. By synergizing mechanical stimulation with biological modulation, this strategy induces benign and persistent LN expansion, amplifies anti-tumor T-cell responses, and establishes durable immunological memory, resulting in both prophylactic and therapeutic outcomes. This approach is versatile across both model antigens and neoantigens, offering a bio-inspired, two-stage LN-targeted delivery strategy that serves as a framework for designing more effective therapeutic vaccines.
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4. ⭐ GSE341912 C57BL/6小鼠结肠中B细胞、T细胞和髓系细胞亚群的单细胞转录组验证
- ✍️ 作者:未知作者
- 🏷️ 关键词:T cell、B cell、single-cell
- 📝 描述:Contributors : Tailiang Chai ; Yang Chen ; Weiming Liang ; Ruizhen Zhao ; Yifei Sheng ; Fuhua Lu ; Fangxiao DongSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis dataset serves as a validation cohort for single-cell transcriptomic changes observed in germ-free (GF) and specific pathogen-free (SPF) mice. Single-cell RNA sequencing was performed on B cell, T cell, and myeloid subsets isolated from the colon of C57BL/6 mice. The dataset captures immune heterogeneity in the absence of microbiota and enables direct comparison with the KM mouse cohort.
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5. ⭐ GSE307145 CCR7+活化树突状细胞对于自发性和免疫疗法驱动的抗肿瘤免疫至关重要
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、immunity、regex:immuno(logy|therapy|suppression)
- 📝 描述:Contributors : Eduardo Bonavita ; Victoria S Pelly ; Maria Koufaki ; Richard Reeves ; Sudhakar Sahoo ; Santiago ZelenaySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSingle-cell transcriptomics identifies a convergent activation state of conventional dendritic cells (cDCs) shared by type 1 and type 2 cDCs (cDC1s and cDC2s). These activated DCs (actDCs) are characterized by co-expression of T cell-stimulating and inhibitory molecules. Here, we examined the functional contribution of actDCs to anti-tumor immunity by developing mouse models that leverage CCR7 expression to conditionally label or ablate actDCs. The capacity of cDCs to stimulate tumor-specific cytotoxic T lymphocytes (CTLs) was restricted to the actDC state. cDC1- and cDC2-derived actDCs supported CTL priming through cross-presentation and cross-dressing, respectively, with the latter occurring in a cancer type-dependent manner. actDCs were required for the activation of naive CTLs in tumor-draining lymph nodes and for sustaining effector CTL function within tumors. Consequently, ablation of actDCs impaired spontaneous tumor control and responses to immune checkpoint blockade or adoptive T cell therapy. Thus, the actDC state emerges as a critical determinant of cDC-mediated anti-tumor immunity.
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6. ⭐ GSE342074 CYP1B1介导的代谢重编程驱动脓毒症中的免疫失调:单细胞转录组学和治疗探索
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、metabolic、single-cell
- 📝 描述:Contributors : Jinyan Xie ; Yinshan Wu ; Feng GuoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSepsis, a life-threatening condition characterized by dysregulated immune responses, poses significant clinical challenges due to high mortality and limited therapeutic strategies. Emerging evidence highlights immune-metabolic dysregulation, particularly in monocytes and macrophages, as a critical driver of sepsis pathogenesis. Here, we performed single-cell RNA sequencing (scRNA-seq) on peripheral blood mononuclear cells (PBMCs) from patients with sepsis and healthy controls, revealing significant alterations in immune cell composition. Sepsis patients exhibited increased myeloid cells and decreased T, NK, and B/plasma cells. CD8+ T cells displayed enhanced activation, while macrophages showed disrupted amino acid metabolism, with upregulated tryptophan pathways (e.g., CYP1B1, HADHA) and downregulated arginine and proline metabolism. In vitro, lipopolysaccharide (LPS)-stimulated macrophages exhibited elevated CYP1B1 expression, and its inhibition by (E)-2,3’,4,5’-tetramethoxystilbene (TMS) suppressed pro-inflammatory cytokine production (IL1B, TNFA). In a murine sepsis model, TMS administration reduced systemic inflammation, attenuated organ damage, and decreased myeloid cell infiltration. These findings identify CYP1B1 as a novel metabolic checkpoint in sepsis-associated hyperinflammation and demonstrate the therapeutic potential of TMS in rebalancing immune dysregulation. Our study provides insights into precision immunometabolic interventions for sepsis management.
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7. GSE322572 植入后第 21 天引流淋巴结中 Kaede red+ CD45+ 细胞的 scRNA 测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:lymph、regex:lymph(o|atic)?
- 📝 描述:Contributors : Ines Delclaux ; Katherine S Ventre ; Naomi R Besson ; Tara Muijlwijk ; Milad Ibrahim ; Guanning Wang ; Taylor A Heim ; Maria M Steele ; Alexander C Huang ; Markus Schober ; Iman Osman ; Amanda W LundSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusSuccessful neoadjuvant immune checkpoint blockade (ICB) therapy depends on the maintenance of a pool of stem-like CD8+ T cells that are enriched in tumor-draining lymph nodes (LN). Upon ICB, stem-like CD8+ T cells activate and proliferate to generate effector T cells that seed the intratumoral response. Yet, how the stem-like niche is maintained over time in cancer remains poorly understood. Here, we identify a continuous lymphatic circuit that sustains the stem-like CD8+ T cell pool. Using photoconvertible fate-mapping, we demonstrate that effector CD8+ T cells egress from the tumor microenvironment via tumor-associated lymphatic vessels, and migrate back to the draining LN. These tumor-specific, migratory effector T cells avoid chronic antigen stimulation in the tumor, re-express the transcription factor associated with self-renewal, TCF1, and subsequently enter a stem-like state in the LN. We find that chronic antigen presentation in LNs by dendritic cells drives the local proliferation and transient residence of tumor-egressing T cells thereby inflating the LN stem-like population. Consequently, maintenance of stem-like T cells and ICB response depends on constitutive lymphatic transport, which sustains both effector egress and antigen presentation in the LN. Finally, we find that metastasis disrupts the stem-like LN niche in patients and impairs response to ICB in mice. We, therefore, define a continuous, peripheral lymphatic circuit that recycles tumor-experienced effector T cells to fuel durable systemic anti-tumor immune responses, providing mechanistic insight into the enhanced efficacy of neoadjuvant immunotherapy and highlighting the importance of preserving lymphatic transport for optimal cancer immunotherapy outcomes.
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8. GSE304676:基于少样本学习的叶黄素通过葡萄糖代谢抑制Th1介导的炎症
- ✍️ 作者:未知作者
- 🏷️ 关键词:inflammation、metabolism
- 📝 描述:Contributor : Zonghui WeiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensArtificial intelligence (AI)-driven drug discovery is often hindered by the “few-shot” data bottleneck and the limited representational power of traditional two-dimensional models, challenging the accurate identification of functional molecules. In this study, we addressed these challenges by establishing a high-precision screening platform, which leverages transfer learning to recognize the key 3D molecular features of T cell inhibitors. Using this approach, we identified Lutein as a novel, specific immunomodulatory agent from a natural product library. Integrated multi-omics analyses revealed that Lutein activates peroxisome proliferator-activated receptor gamma (PPARγ), suppressing glucose uptake and glycolysis, thereby selectively inhibiting Th1 cell differentiation. In a dextran sulfate sodium (DSS)-induced mouse model of ulcerative colitis, Lutein treatment significantly restored Th1-mediated immune balance and alleviated pathological tissue damage. Our findings not only highlight the great potential of “few-shot” AI strategies that leverage transfer learning and 3D molecular features for the discovery of bioactive natural compounds, but also identify Lutein as a promising therapeutic candidate for ulcerative colitis.
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9. GSE304137 巨噬细胞和三阴性乳腺癌细胞在三维共培养模型中的表型变化
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、macrophage
- 📝 描述:Contributors : Chen Cheng ; Brett A McGregor ; Junguk Hur ; Colin K CombsSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTumor-associated macrophage (TAM) infiltration is a characteristic of triple-negative breast cancer (TNBC) related to drug resistance and poor prognosis. Unraveling intricate cell-cell interactions in the tumor microenvironment (TME) remains challenging, especially when using a standardized 3D culture system. This study used the TNBC cell line, MDA-MB-231, and polarized M1-like or M2-like macrophages derived from THP-1 monocytes to establish 3D co-culture spheroids for mimicking the TME environment. Drug efficacy, epithelial-mesenchymal transition (EMT) in cancer cells, macrophage phenotypes, and RNA sequencing of spheroids were performed. We observed that M2 macrophages increased the viability and proliferation rate of MDA-MB-231 cells in the 3D spheroids, while both M1 and M2 macrophages increased the chemosensitivity of MDA-MB-231 cells to doxorubicin and paclitaxel. Interestingly, instead of maintaining their phenotypes, M1 and M2 macrophages lost some polarization when 3D co-cultured with MDA-MB-231 cells. Compared with 2D cultures, an expected mesenchymal transition was observed in 3D spheroid MDA-MB-231 cells. However, both M1 and M2 macrophages induced a partial epithelial reversion in co-cultured spheroids. Deconvolution of our bulk RNA sequencing results verified the existence of phenotypic transitions between M1 and M2 macrophages when co-cultured with MDA-MB-231 cells in 3D spheroids. In conclusion, our findings suggest that a 3D co-culture system of polarized macrophages and breast cancer cells can serve as an effective platform for studying the dynamic cellular phenotype changes that occur in a heterogeneous environment contributing to chemoresistance. This 3D co-culture system may provide a valuable tool for drug screening to identify targeted therapies for cancer.
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10. GSE341914 KM小鼠肠段的空间转录组图谱
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、regex:intestin(e|al)
- 📝 描述:Contributors : Tailiang Chai ; Yang Chen ; Weiming Liang ; Ruizhen Zhao ; Yifei Sheng ; Fuhua Lu ; Fangxiao DongSeries Type : OtherOrganism : Mus musculusThis study generated spatial transcriptomic profiles of ileum, cecum, and colon from specific pathogen-free (SPF) and germ-free (GF) Kunming (KM) mice using the BGI Stereo-seq platform. The dataset captures spatial organization and segment-specific immune niches in the absence of microbiota.
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💡 该来源还有 35 条内容,详见 文末
🧪 博客更新 (5条)
详细内容(全部5条)
1. 深度学习提高了基于单细胞RNA测序的细胞周期预测精度
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing、single-cell
- 📝 描述:RNA sequencing combined with deep learning improves cell cycle phase prediction, helping researchers better interpret single-cell data and reduce confounding effects in biological…
- 🔗 查看原文
2. 一种简单的补充剂或许就能帮助免疫系统对抗癌症和病毒。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、immune
- 📝 描述:Low arginine levels may allow cancer cells and viruses to slip past the immune system by reducing production of a crucial cellular warning protein. In mice, arginine-rich diets led to fewer colon tumors and milder viral infections, suggesting a simple supplement could have powerful therapeutic potential.
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3. 科学家绘制出休眠癌细胞的藏身之处,为治疗开辟了新的靶点。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer
- 📝 描述:RNA sequencing and spatial transcriptomics reveal dormant breast cancer cell niches that may help explain treatment resistance and support more effective combination therapies…
- 🔗 查看原文
4. 两种新化合物或将揭示阿尔茨海默病的潜在驱动因素
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer
- 📝 描述:Vanderbilt researchers created the first selective compound designed to inhibit TAOK-1, a poorly understood protein connected to Alzheimer’s disease. They also discovered a second compound that activates the entire TAOK protein family, offering scientists an unexpected new research tool. Together, the compounds could reveal hidden disease mechanisms and point toward new treatment strategies.
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5. 科学家可能已经发现了衰老引发脑部疾病的隐秘诱因。
- ✍️ 作者:未知作者
- 🏷️ 关键词:aging
- 📝 描述:Scientists have identified a molecular switch that may help explain why aging makes the brain more vulnerable to diseases such as ALS and Huntington’s. In worms, the protein EPS8 builds up with age and triggers signaling that encourages toxic proteins to clump together, damaging neurons and shortening lifespan. Reducing EPS8 activity prevented these harmful aggregates and preserved nerve function.
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📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| cancer | 8 |
| RNA-seq | 6 |
| single-cell | 5 |
| transcriptome | 5 |
| immune | 4 |
| regex:onco(logy | logist |
| tumor | 3 |
| ChIP-seq | 3 |
| regex:intestin(e | al) |
| methylation | 3 |
| sequencing | 2 |
| inflammation | 2 |
| genome | 2 |
| cardiac | 2 |
| lymph | 2 |
| regex:lymph(o | atic)? |
| epigenetic | 2 |
| regex:immuno(logy | therapy |
| enrichment | 2 |
| Alzheimer | 1 |
📎 更多内容
🧬 数据前沿 其他内容 (35条)
- GSE341913 KM小鼠肠段单细胞转录组图谱
- GSE341901 RNA-seq 分析稳定敲低 HOXC11 的人类食管鳞状细胞癌细胞
- GSE341504 乳酸-Chac1轴调控铁死亡相关细胞死亡和肿瘤进展 [A549_LAC RNA-seq]
- GSE341473 RNA-seq 血液转录组学数据集揭示了枢纽基因在非结核分枝杆菌肺炎 (NTM-PD) 患者中的价值
- GSE292876 FANCM 是 PAX3::FOXO1 驱动的横纹肌肉瘤致癌程序所必需的 [ChIP-Seq]
- GSE292872 FANCM 是 PAX3::FOXO1 驱动的横纹肌肉瘤致癌程序所必需的 [RNA-Seq]
- GSE282948 H2A.Z 变体相对丰度的扰动改变了拟南芥中 H3K27me3 的富集 [RNA-Seq]
- GSE282947 H2A.Z 变体相对丰度的扰动改变了拟南芥中 H3K27me3 的富集 [ChIP-Seq]
- GSE210515 全转录组测序揭示了鼻窦后孔息肉的炎症内型和潜在生物标志物
- GSE334556 RNA-seq 分析了 LPS 诱导的急性炎症后 Fpr2 基因敲除小鼠和野生型小鼠的小胶质细胞在炎症反应中的变化
- GSE306319 基于激光捕获显微切割的肿瘤性肥大细胞转录组分析揭示了犬肥大细胞肿瘤各级别中的新型分子改变
- GSE305653 全基因组染色质记录解析动态细胞状态变化
- GSE341748 3D 人类 iPSC 衍生心脏类器官用于抗纤维化药物筛选
- GSE338502 阿托伐他汀调节六氯苯诱导的大鼠肝癌前病变中的致癌和保护性转录组特征
- GSE320003 机械隔离建立和维持心脏起搏细胞表型。
- GSE310884 林奇综合征携带者的运动相关表观遗传重塑和 TCR 库动态(MEDIP-seq)
- GSE309783 林奇综合征携带者 (RRBS) 的运动相关表观遗传重塑和 TCR 库动态
- GSE304560 拟南芥 Col-0、ces-D、35S:CES_YFP、ces-tM、ces-qM 突变体的转录组分析
- GSE341968 TSPAN8(一种可塑性标记物)在前列腺癌细胞中通过DUSP19和BRD4的相互作用进行转录调控
- GSE341964 SNAPC1 基因重复产生 snRNA 和性别特异性 piRNA 的转录因子 [ChIP-Seq]
- GSE341487 对受辐射皮肤的单细胞转录组分析揭示了成纤维细胞亚群的变化和caveolin表达的变异性
- GSE341465:小鼠造血细胞中H19 RNA编辑和miR-675-3p重定向的批量RNA测序、小RNA测序和miRNA下拉分析
- GSE339117 开放场爆炸损伤后小鼠角膜的长期免疫和细胞外基质重塑
- GSE336555 利用内源性环状 RNA 适体靶向剪接因子 hnRNP M 可抑制癌症转移 [shhnRNPM]
- GSE335525 利用内源性环状RNA适体靶向剪接因子hnRNP M可抑制癌症转移
- GSE306256 PD-L1的细胞内在功能激活自噬并阻止细胞因子诱导的细胞凋亡
- GSE304171 烟雾病颞肌转录组
- GSE292882 FANCM 是 PAX3::FOXO1 驱动的横纹肌肉瘤致癌程序所必需的 [CRISPR 筛选]
- GSE337745 Zfp57 和 Gzf1 的相互结合(依赖于甲基化)在发育重编程过程中保护 Dlk1-Dio3 印记
- GSE337304 Zfp57 和 Gzf1 的相互结合(依赖于甲基化)在发育重编程过程中保护 Dlk1-Dio3 印记
- GSE319402 锌缺乏诱导的肠杯状细胞基因表达变化
- GSE317740 混合牙列期快速上颌扩张后的DNA甲基化变化
- GSE306886 肺炎克雷伯菌泛基因组中全局转录调控网络的拓扑结构和演化
- GSE294384 热适应种鸡空肠黏膜组织在急性热应激下的转录组谱分析
- GSE294383:热适应和热敏感种鸡空肠黏膜组织在急性热应激下的转录组谱分析
📅 报告生成时间:2026-08-04 22:33
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