科研日报 2026-05-02
📅 Daily Report - 2026-05-02
今日筛选出 150 条内容,来自 3 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 空间转录组学揭示了肺部结节病(Sarcoidosis)中前萨泊辛(Prosaposin)作为新型治疗靶点(GSE263088, GSE262998)。
主要方向:
- 肿瘤免疫微环境与治疗:解析肝癌中TAMs与CD8+ T细胞的空间互作(GSE318324),探索NSCLC联合免疫治疗新策略(GSE317309),以及MEK抑制剂在T细胞激活中的作用(GSE311565, GSE311562)。
- 癌症进展机制与靶点:揭示ZNF25在胶质瘤进展中通过PI3K-AKT信号通路的作用(GSE272124),以及LRMDA对结直肠癌的抑制作用(GSE317858, GSE317857)。
- 细胞重编程与可塑性:研究工程化T细胞在默克尔细胞癌治疗中的应用(GSE326661),以及单细胞和空间图谱揭示前列腺癌的谱系可塑性与转移(GSE324131)。
技术亮点:
- 空间转录组学:广泛应用于肿瘤、神经退行性疾病和炎症性疾病研究,解析细胞微环境的空间异质性(GSE318324, GSE324131, GSE327284, GSE263088, GSE262998)。
- 单细胞RNA测序(scRNA-seq):用于研究免疫细胞功能(GSE322626, GSE296052)和肿瘤异质性(GSE326661, GSE324131)。
📊 学点生信
今日焦点: R语言新包
grouper为最优分组分配提供了自动化解决方案,旨在优化协作学习中的学生分组。
主要方向:
- 自动化生成考虑多种约束条件(如学生能力、偏好等)的最优学生分组。
- 提升协作学习的教学效果,促进学生对课程内容的深入理解和团队协作能力的培养。
技术亮点:
- 首次提出并实现基于优化算法的R语言包,用于解决协作学习中的复杂分组问题。
🧪 博客更新
今日焦点: 新型脂肪代谢机制被发现,改写了对脂肪组织平衡的传统认知。
主要方向:
- 肠道健康:研究揭示慢性压力与夜间进食对肠道健康双重负面影响。
- 单细胞数据整合:开发新型自监督学习方法,提升多组单细胞RNA测序数据的准确整合与分析。
- 脂肪代谢调控:发现关键蛋白在维持脂肪组织健康与平衡中的新功能。
技术亮点:
- scDecorr:一种用于多组单细胞实验自监督对齐的特征解相关表示学习方法,有效降低噪声并保留生物信号。
📚 分类浏览
🧬 数据前沿 (146条)
详细内容(前10条)
1. ⭐ GSE318324:对切除的肝细胞癌标本进行靶向RNA测序,以表征与PD-L1(+) TAM-CD8(+) T细胞空间相互作用相关的免疫基因表达。
- ✍️ 作者:未知作者
- 🏷️ 关键词:carcinoma、immune、T cell、sequencing、spatial
- 📝 描述:Contributors : Takuto Nosaka ; Masahiro Ohtani ; Junki Yamashita ; Yosuke Murata ; Yu Akazawa ; Tomoko Tanaka ; Kazuto Takahashi ; Tatsushi Naito ; Yoshiaki Imamura ; Kenji Koneri ; Takanori Goi ; Yasunari NakamotoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThis study investigates immune-related gene expression profiles associated with spatial interactions between PD-L1-positive tumor-associated macrophages (TAMs) and CD8-positive T cells in hepatocellular carcinoma (HCC). RNA was extracted from tumor regions of formalin-fixed paraffin-embedded (FFPE) specimens obtained from eight patients who underwent hepatectomy. Targeted RNA sequencing was performed using custom AmpliSeq panels covering cancer progression– and immunity-related genes. Raw sequencing data and processed gene expression matrices are provided to enable downstream reanalysis.
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2. ⭐ GSE317309 CCL21基因修饰的树突状细胞疫苗与帕博利珠单抗联合应用可诱导非小细胞肺癌的免疫反应
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、immune、vaccine、dendritic cell
- 📝 描述:Contributors : Michael S Oh ; Aaron Lisberg ; Camelia Dumitras ; Ramin Salehi-Rad ; Linh M Tran ; Kostyantyn Krysan ; Edward B Garon ; Bin Liu ; Steven M DubinettSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusImmune checkpoint inhibitors (ICIs) have transformed treatment for non-small cell lung cancer (NSCLC), but resistance to these therapies is common. We report results from a phase I trial combining intratumoral administration of a CCL21-gene modified dendritic cell (CCL21-DC) vaccine with pembrolizumab in patients with advanced NSCLC. Among 23 patients that received trial therapy, there were no dose-limiting toxicities and a low incidence of treatment-related adverse events. Although no objective responses were observed, 36.8% of patients had a best response of stable disease (SD). Correlative analyses of longitudinal tumor biopsies revealed that disease stability was associated with reduced tumor mutational heterogeneity and increased intratumoral T cell receptor diversity following therapy. Post-treatment tumor biopsies exhibited increased CD4+ T cell infiltration and the presence of novel T cell clones that predominantly possessed CD4+ memory T cell phenotypes. These novel clones experienced greater clonal expansion and a transition towards exhausted phenotypes in SD samples. However, many novel clones failed to persist over time, and immunosuppressive myeloid signaling signatures were identified especially in progressive disease samples. Our findings demonstrated that CCL21-DC vaccination combined with pembrolizumab is safe and can promote antitumor immune responses in a subset of patients. However, efficacy may have been constrained due to limited tumor specificity of the T cell response and an inability to fully reprogram the immunosuppressive tumor microenvironment.
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3. ⭐ GSE272124泛癌分析结合RNA测序发现,ZNF25主要通过调节PI3K-AKT信号通路促进胶质瘤进展。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、glioma、RNA-seq、pathway
- 📝 描述:Contributors : Xiaohong Yi ; Xianwen Zhang ; Lijun Huang ; Yumei WangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBackground: ZNF25, a member of zinc finger proteins with KRAB domains family genes, is a transcription factor. Previous reports showed it is a biomarker of ovarian cancer. However, there are rarely reports about ZNF25 in other types of cancer, and its underlying mechanisms are not yet clear. Methods: Based on The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression Project (GTEx), cBioPortal, Human Protein Atlas (HPA), IntOGen, TIMER, TIMER2, TISIDB, MethSurv, TISIDB, and Cistrome Data Browser (CDB) databases, we adopted bioinformatics methods to excavate the potential tumor genomic features of ZNF25, including dissecting the correlation with prognosis, gene mutation, immune cell infiltration, and DNA methylation in different tumors, and evaluated the association with tumor heterogeneity and stemness, and co-expression with Tex cells, chemokines chemokine receptors, and immunomodulators in pan-cancer. Additionally, we knocked down ZNF25 in U87-MG cells and performed RNA-seq analysis, then differential expression genes (DEGs) were further analyzed and visualized, like GO, and KEGG to interpret the biological significance. Results: The results show that ZNF25 has early diagnostic potential and was associated with the immune infiltration of different tumors. ZNF25 is associated with most tumor immune-infiltrating cells in pan-cancer, especially in glioma. Additionally, ZNF25 correlates with DNA methylation, tumor heterogeneity, Tex, and stemness in many types of cancers, like glioma. Besides, our findings demonstrate a close relationship between ZNF25 and mutated IDH1 in gliomas. Furthermore, our experiments showed that ZNF25 is involved in cancer pathways, mainly in PI3K-AKT and MAPK pathways.Conclusion: Through pan-cancer analysis combined with RNA-seq data, we discovered that ZNF25 might influence the progression of glioma mainly via the PI3K-AKT signaling pathway, and suggested that ZNF25 could serve as an indicator for tumor diagnosis, treatment, and prognosis across various types of tumors, including glioma.
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4. ⭐ GSE309857 小胶质细胞 TDP-43 介导髓鞘精细化并抑制小鼠 Tyrobp 隐蔽外显子插入 [空间转录组学]
- ✍️ 作者:未知作者
- 🏷️ 关键词:spatial、spatial transcriptomics、transcriptomics
- 📝 描述:Contributors : Anne-Claire Compagnion ; Andranik Ivanov ; Anil Rana ; Felipe Espinoza ; Thomas Sandmann ; Fanny S Martineau ; Katia Monsorno ; Robera Facchineti ; Alessandro Matera ; Lionel Rougé ; Fernando G Ibáñez ; Clarissa Catale ; Mateo Bizzotto ; Sonia Garel ; Michela Matteoli ; Yutaro Kashiwagi ; Ryuta Koyama ; Christian Haass ; Marie-Eve Tremblay ; Dieter Beule ; Ileana Jelescu ; Valerio Zerbi ; Gilbert Di Paolo ; Rosa C PaoliceliSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTDP-43 proteinopathy is a hallmark of neurodegenerative disorders such as amyotrophic lateral sclerosis and frontotemporal dementia where mislocalization of TDP-43 has been observed in neurons and glial cells. However, the role of TDP-43 in microglia and the consequences of its loss-of-function remain unexplored. Combining magnetic resonance imaging, confocal, and electron microscopy we uncovered structural changes and myelin abnormalities in the early postnatal brain of mice lacking microglial TDP-43. Spatial transcriptomics further revealed an enriched interferon-response signature associated with oligodendrocyte dysfunction. Early microglial TDP-43 depletion resulted in motor deficits in adult mice. Mechanistically, knocking out TDP-43 impaired microglial ability to engulf and degrade myelin. It also led to cryptic exon inclusion in the Tyrobp mRNA, resulting in truncated DAP12 protein, thus causing defective TREM2 signaling. Our findings reveal a novel role for TDP-43 in regulating the TREM2-DAP12 axis in mice, highlighting a previously unrecognized mechanism by which TDP-43 controls microglial function.
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5. ⭐ GSE326661 重编程工程化自体 T 细胞以克服默克尔细胞癌的耐药性 [scRNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:carcinoma、resistance、scRNA
- 📝 描述:Contributors : Yuta Asano ; Cheng-Jung Sung ; Francesco Mazziotta ; Bo Lee ; Lauren Martin ; Philip D Greenberg ; Aude G ChapuisSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensImmune checkpoint inhibitors (CPIs) have transformed Merkel cell carcinoma (MCC) outcomes, but most patients with MCC develop resistance. We identified TCRMCC1, a highly-avid, HLA-A*02:01-restricted T cell receptor (TCR) targeting the Merkel Cell Polyoma Virus (MCPyV) oncoprotein LTAg15–23. Seven patients with CPI-refractory metastatic MCPyV+ MCC received TCRMCC1-transduced cells (TTCR-MCC1) following lymphodepleting chemotherapy or HLA-enhancing interventions (radiation or IFNg-1b [Actimmune®]), with concurrent CPIs (NCT03747484). TTCR-MCC1 trafficked to tumor sites and expressed a gene expression profile compatible with T cell activation, with tumor regression observed in two patients. However, therapeutic activity was limited by HLA class I silencing, a common mechanism of immune escape in MCC. In one patient, delayed tumor regression coincided with endogenous effector immune activation and restoration of MCC HLA expression, implying robust local responses could reverse HLA silencing. To overcome this barrier, we engineered CD4 and CD8 TTCR-MCC1 to co-express CD8ab and a CD200R-CD28 switch receptor, enabling CD4 T cell engagement and T cell co-stimulation. These modifications enhanced tumor infiltration, increased HLA expression, and improved control of HLAlow MCC in vivo in mice. These findings support the feasibility of TCR-engineered cell therapy for MCPyV+ MCC and provide a blueprint for overcoming immune evasion via targeted localized enhancement of antigen presentation.
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6. ⭐ GSE324131 前列腺癌的单细胞和空间图谱揭示了谱系可塑性和转移的基因模块的组合特性
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、single-cell、spatial
- 📝 描述:Contributors : Hanbing Song ; Sarah C Hsu ; Julia H Pham ; Yih-An Chen ; Hannah Weinstein ; Matthew R Cooperberg ; Nancy Greenland ; Franklin W HuangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensProstate cancer encompasses a spectrum of disease states driven by complex cellular heterogeneity. To delineate the transcriptional programs underlying lineage plasticity and metastasis, we constructed a comprehensive single-cell atlas of 128 patients, spanning localized, castration-resistant, and metastatic disease. Lineage plasticity was prevalent in localized disease, with subsets of tumor cells adopting distinct basal-like and club-like states. Luminal-like cancer cells also displayed extensive lineage infidelity, defined not by a binary loss of identity but by the combinatorial erosion of luminal gene modules associated with higher grade and stage. In the metastatic setting, gene program association analysis (GPAS) identified a broad induction of cell-cycle gene modules across organ sites as well as an induction of organ-specific gene modules, including osteomimetic signaling in bone, neuro-migratory genes in brain, and erythroid-like transitions in liver. Neuroendocrine prostate cancers (NEPCs) were not monolithic but defined by combinations of NE-associated gene modules including a novel HES6 program. Notably, these modules were detected at intermediate levels in localized samples, suggesting molecular plasticity precedes histological transformation. We also developed a refined NE signature that could distinguish NEPC tumors more accurately than previously published signatures. Within the tumor microenvironment (TME), we observed an elevation of pro-inflammatory Th17 T-cells in African American patients and identified a rare Schwann cell population. Finally, we present PCformer, a transformer-based foundation model trained on >500,000 cells to automate cell-state classification. Together, this comprehensive atlas demonstrates the complex nature of gene modules underlying lineage infidelity and plasticity in cancer cells and highlights distinct immune and stromal populations within the tumor ecosystem.
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7. ⭐ GSE322626 单细胞 RNA 测序数据表明,CD40 促进心肌梗死后巨噬细胞的吞噬作用。
- ✍️ 作者:未知作者
- 🏷️ 关键词:macrophage、sequencing、single-cell
- 📝 描述:Contributors : Linlin Zhang ; Canbiao Wang ; Longjiang ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCD40 expressed on the macrophage membrane is recognized as one of the characteristic biomarkers for their inflammatory phenotype. We demonstrated that macrophage CD40 functionally promotes post-myocardial infarction (MI) repair. To elucidate the role of CD40 in the post-MI repair process, we dissected infarct and border zones from the hearts of wild-type (WT) and CD40 knockout (KO) mice at 3 days post-MI. Mononuclear macrophages (CD45⁺CD11b⁺CD64⁺) were isolated via flow cytometry and subjected to single-cell RNA sequencing analysis. This study establishes that CD40 plays a critical role in macrophage efferocytosis. Furthermore, analysis of scRNA-seq data led to the identification of developmental precursor cells of repair-phenotype macrophages.
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8. ⭐ GSE317858 LRMDA抑制结肠炎症、结直肠癌和细菌感染[CRC_RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、inflammation、regex:bacter(ia|ial|ium)
- 📝 描述:Contributors : Liping Yang ; Yuyao Guo ; Bikun XiaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe leucine-rich melanocyte differentiation-associated protein (LRMDA), a recently characterized intracellular trafficking regulator, plays a critical yet unexplored role in intestinal homeostasis 1. Here, we show that LRMDA expression is downregulated in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and in colorectal tumor tissues. Similarly, we demonstrate that LRMDA deficiency exacerbates dextran sulfate sodium (DSS)-induced colitis, promotes tumorigenesis in azoxymethane (AOM)/DSS and AOM/Vil-Cre;Trp53fl/fl (VP) models and aggravates enteric pathogen infection. Mechanistically, LRMDA may positively regulate the normal exocytosis of mucins from intestinal goblet cells into the intestinal lumen via the dynein-dynactin-microtubule pathway by interacting with the ICD domain of DCTN1. These findings identify LRMDA as a novel regulator of intestinal mucosal barrier function.
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9. ⭐ GSE317857 LRMDA抑制结肠炎症、结直肠癌和细菌感染[Colitis_RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、inflammation、regex:bacter(ia|ial|ium)
- 📝 描述:Contributors : Liping Yang ; Yuyao Guo ; Bikun XiaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe leucine-rich melanocyte differentiation-associated protein (LRMDA), a recently characterized intracellular trafficking regulator, plays a critical yet unexplored role in intestinal homeostasis 1. Here, we show that LRMDA expression is downregulated in the inflamed mucosa of patients with inflammatory bowel disease (IBD) and in colorectal tumor tissues. Similarly, we demonstrate that LRMDA deficiency exacerbates dextran sulfate sodium (DSS)-induced colitis, promotes tumorigenesis in azoxymethane (AOM)/DSS and AOM/Vil-Cre;Trp53fl/fl (VP) models and aggravates enteric pathogen infection. Mechanistically, LRMDA may positively regulate the normal exocytosis of mucins from intestinal goblet cells into the intestinal lumen via the dynein-dynactin-microtubule pathway by interacting with the ICD domain of DCTN1. These findings identify LRMDA as a novel regulator of intestinal mucosal barrier function.
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10. ⭐ GSE280461 成纤维网状细胞驱动交感神经再生以适应肿瘤细胞引起的淋巴结扩张
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、lymph、regex:lymph(o|atic)?
- 📝 描述:Contributors : Jun Li ; Hui LiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusLymph nodes (LNs) are peripheral immune organs innervated by sympathetic and sensory nerves. Upon diverse stimuli, LNs undergo substantial structural reorganization and volume expansion. However, the adaptation of innervation to these changes remains poorly understood. In this study, whole-mount 3D imaging revealed that sympathetic nerve fibers, rather than sensory nerves, exhibited significant elongation and increased branching over time during tumor-induced lymph node enlargement (TLNE). Single-nucleus RNA Sequencing (snRNA-seq) analysis demonstrated that throughout TLNE, fibroblastic reticular cells (FRCs) are activatedand engage in neuro-related signaling pathways while secreting substantial amounts of hepatocyte growth factor (HGF). Moreover, the stiffness of the extracellular matrix (ECM) in LNs increased in the context of TLNE, further supporting FRC activation and HGF secretion. The role of HGF in promoting sympathetic nerve fiber outgrowth was confirmed by administering specific HGF inhibitors or using adeno-associated virus (AAV)-mediated HGF silencing. Collectively, HGF secreted by FRCs plays a pivotal role in TLNE, triggering adaptive sympathetic nerve outgrowth and reinnervation within LNs, providing novel insights into neuro-stromal-immune system crosstalk.
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💡 该来源还有 136 条内容,详见 文末
📊 学点生信 (1条)
详细内容(全部1条)
1. grouper:用于最优分组分配的 R 包
- ✍️ 作者:未知作者
- 🏷️ 关键词:R package
- 📝 描述:Introduction Universities are increasingly using collaborative learning pedagogies, which can benefit learners through deeper understanding of course content and teamwork skills. However, the realisation of these sought-after benefits depend on how educators assign learners to groups. Educators have formulated various mathematical models to perform this assignment. Some have developed developed … Continue reading: grouper: An R package for Optimal Group Assignment
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🧪 博客更新 (3条)
详细内容(全部3条)
1. 压力和深夜进食会对你的肠胃造成“双重打击”。
- ✍️ 作者:未知作者
- 🏷️ 关键词:gut、regex:gut(-?microbiome)?
- 📝 描述:Chronic stress is already tough on your gut—but new research suggests late-night eating could make things even worse. Scientists analyzing thousands of people found that those under high stress who also ate a large portion of their calories after 9 p.m. were far more likely to suffer from constipation and diarrhea. The combination appears to hit the gut twice, not only disrupting digestion but also reducing the diversity of beneficial gut bacteria.
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2. scDecorr——基于特征去相关的表征学习方法,能够实现多个单细胞实验的自监督对齐。
- ✍️ 作者:未知作者
- 🏷️ 关键词:single-cell
- 📝 描述:RNA sequencing analysis with scDecorr improves integration of single-cell datasets by reducing noise and preserving biological signals, enabling more accurate clustering and…
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3. 一项惊人的肥胖症发现改写了数十年来关于脂肪代谢科学的认知
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolism
- 📝 描述:A key protein involved in fat metabolism has been found to do more than scientists once thought. Instead of just releasing fat, it helps maintain healthy fat tissue and balance in the body. When it’s missing or disrupted, the results can be surprisingly harmful. This finding reshapes how researchers think about obesity and metabolic disease.
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📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| cancer | 21 |
| RNA-seq | 18 |
| metabolic | 17 |
| sequencing | 16 |
| epigenetic | 15 |
| carcinoma | 10 |
| single-cell | 8 |
| spatial | 8 |
| immune | 8 |
| scRNA | 8 |
| transcriptome | 8 |
| resistance | 6 |
| genome | 5 |
| ATAC-seq | 5 |
| regex:intestin(e | al) |
| tumor | 5 |
| T cell | 4 |
| inflammation | 4 |
| ChIP-seq | 4 |
| Alzheimer | 3 |
📎 更多内容
🧬 数据前沿 其他内容 (136条)
- GSE263088 空间转录组学鉴定出前蛋白酶原(PSAP)是肺结节病的新型治疗靶点 [小鼠_空间]
- GSE262998 空间转录组学鉴定出前蛋白酶原(PSAP)是肺结节病的新型治疗靶点
- GSE327284 阿尔茨海默病、CADASIL 和创伤性脑损伤小鼠模型中异质性小胶质细胞反应性与稳定的血管转录程序形成对比(空间数据)
- GSE311565 无序蛋白 LAT 编码 T 细胞活化中信号通路的相对水平 [Perturb-ATAC-seq]
- GSE311562 无序蛋白 LAT 编码 T 细胞活化中信号通路的相对水平 [ATAC-seq]
- GSE303210 分化的人类 iPSC 类器官衍生的肾小管(iPSCod 肾小管)的单细胞 RNA 测序
- GSE302836 研究发现,肝细胞 PI3Kα 的缺失可通过改变脂质代谢基因表达来保护小鼠免受肝细胞癌的侵害。
- GSE299925 子宫内膜样癌前病变的表观基因组分析
- GSE299307 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE299225 Metabolic-epigenetic reprogrammed splenic TRNP1hiCD8+ T cells exacerbate liver fibrosis
- GSE298191 Metabolic-epigenetic reprogrammed splenic TRNP1hiCD8+ T cells exacerbate liver fibrosis
- GSE298190 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE298189 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE296052 嗜酸性粒细胞协调肠道重塑并在生殖过程中促进先天防御 [scRNA-seq]
- GSE295403 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295188 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295187 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295185 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295182 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295172 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295170 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295167 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295165 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- GSE295162 代谢表观遗传重编程的脾脏 TRNP1hiCD8+ T 细胞加剧肝纤维化
- 利用RNA测序技术分析小鼠脑血管周围巨噬细胞(PVM)的转录组(GSE329151)。
- GSE326662 重编程工程化自体 T 细胞以克服默克尔细胞癌的耐药性 [TCR-Seq]
- GSE326660 重编程工程化自体 T 细胞以克服默克尔细胞癌的耐药性 [Xenium]
- GSE316970 CYD-4-61 通过靶向 SOX9-CDK4 驱动的致癌程序抑制胃肿瘤生长并增强抗 PD-1 疗法
- GSE316887 scRNA-seq 揭示了 Ad5-HA-VLP 驱动的肺部免疫微环境重塑
- GSE315448 单细胞 RNA 测序图谱揭示了山楂叶的发育图景。
- GSE314413 对接受免疫检查点抑制剂治疗的患者的 T 细胞进行高通量测序 [P365-5]
- GSE314283:接受免疫检查点抑制剂治疗的患者的T细胞高通量测序
- GSE313650 激活的干扰素信号抑制年龄依赖性肝癌 [RNA-Seq]
- GSE310671 RNA-seq 分析了经 HDAC 抑制剂 Largazole 处理的 PRDX6 敲低和对照 A223 鳞状细胞癌细胞。
- GSE309849 组蛋白乳酸化增强 m6A 介导的 PDK4 稳定性,从而驱动钙化性主动脉瓣疾病中的成骨分化 [RNAseq-PDK4]
- GSE301056 染色质分离RNA纯化(ChIRP)-随后对人白血病细胞系MOLMO13和OCI-AML4进行RNA测序,此前已进行过lncRNA CRISPR/Cas9编辑和胞嘧啶碱基编辑
- GSE299042 斑马鱼肝脏发育过程中肝细胞(含或不含GFP)的转录组测序
- GSE297875 用头孢菌素处理小鼠乳腺癌细胞系 4T1 进行 RNA 测序
- GSE297537 喉鳞状细胞癌从癌前病变到癌变的单细胞转录组图谱
- GSE296755 孕期摄入益生元可减轻长期抗生素对肠-乳轴的干扰并调节乳腺发育
- GSE295541 TCN2 通过 IL-1β-STAT3 通路促进银屑病皮肤炎症和角质形成细胞增殖
- GSE274618 胰腺癌前病变的空间结构揭示腺泡化生细胞的异质性 [scRNA-seq]
- GSE268320 转录周期的调控导致 BET 溴结构域抑制剂耐药性 [RNA-seq]
- GSE260626 通过RNA测序分析子宫腺肌症患者正常子宫内膜和原位子宫内膜间充质干细胞的转录组
- GSE232557 抗CD40激动剂和卡博替尼对小鼠肝细胞癌免疫微环境的影响
- GSE171081 研究揭示了胶质瘤相关小胶质细胞和巨噬细胞在脑免疫反应中的不同作用
- GSE137966 WT 和 IkB 缺陷型小鼠早期 B 细胞祖细胞和前体细胞群的单细胞转录组和免疫球蛋白谱分析
- GSE329296 MURV-seq 揭示了痘病毒转录本中 5’ 末端和前导序列的全基因组多样性
- GSE318960 阿尔茨海默病、CADASIL 和创伤性脑损伤小鼠模型中异质性小胶质细胞反应性与稳定的血管转录程序形成对比(ArcSwe 数据)
- GSE311572 无序蛋白 LAT 编码 T 细胞活化中信号通路的相对水平 [Perturb-CITE-seq]
- GSE309858 小胶质细胞 TDP-43 介导髓鞘精细化并抑制小鼠 Tyrobp 隐蔽外显子插入 [RNA-seq]
- GSE300113 阿尔茨海默病、CADASIL 和创伤性脑损伤小鼠模型中异质性小胶质细胞反应性与稳定的血管转录程序形成对比(主数据集)
- GSE296053 嗜酸性粒细胞在生殖过程中协调肠道重塑并促进先天防御
- GSE290843 SUMO蛋白酶Ulp1突变对出芽酵母染色质相关SUMO化全基因组的影响
- GSE290842 表达SUMO蛋白酶Ulp1突变体的出芽酵母转录组分析
- GSE253631 FAM60A 的缺失会破坏 Sin3/HDAC 对 Hippo 信号通路的调控,并促进致癌基因 YAP1 的激活。
- GSE329633 单核分析揭示,心肌细胞丢失和炎症驱动早期 PKP2 缺陷型 ARVC 的微环境重塑。
- GSE329577 鸡胚卵黄囊膜内胚层上皮细胞脂蛋白转运的单细胞转录组分析
- GSE329498 负载超稳定新白细胞介素-2/15的抗原支架可扩增具有适用于过继细胞治疗的有利表型的抗原特异性T细胞
- GSE329420 内皮细胞外泌体重塑癌细胞染色质可及性和超级增强子,促进肝转移定植
- GSE329198 PGC-1α通路失调破坏脊髓延髓肌萎缩症小鼠模型中的肌纤维分化。
- GSE329095 草原田鼠雌雄伏隔核的批量 RNA-seq 数据
- GSE328823 先天性和获得性转录程序塑造肿瘤细胞对 PARP、Akt 和 CDK4/6 抑制剂的异质性反应
- GSE328755 半乳糖凝集素-1的过表达促进肿瘤-脑机械界面模型中独特的迁移性胶质母细胞瘤亚群的细胞侵袭
- GSE327314 人类大脑发育过程中的 R 环景观与神经分化和细胞类型特异性转录有关 [scRNA-seq]
- GSE327247 早期B细胞耐受失败和可能的BCR信号失调是NF155介导的自身免疫性结节病的基础
- GSE326894 HSF2-HSP110轴通过支持RNA聚合酶II依赖性转录和DNA修复基因表达来促进基因组稳定性[CUT&Run]
- GSE326884 HSF2-HSP110轴通过支持RNA聚合酶II依赖性转录和DNA修复基因表达来促进基因组稳定性[PRO-Seq]
- GSE325089 研究发现,柠檬苦素 DDK 通过促进 SDHA 脱乙酰化和 SDH 复合物活性,恢复线粒体氧化还原稳态,从而缓解代谢功能障碍相关的脂肪性肝炎。
- GSE325047 炎症性乳腺癌肿瘤和外周血单核细胞中普遍增强的转录影响血浆中的RNA剪接和内含子RNA
- GSE324922 Atg14f/f 和 Atg14f/f-LysM-cre 小鼠肺细胞总 RNA 测序。
- GSE324645 靶向 Y593 磷酸化的 DDX5 可引发线粒体功能障碍,并与 BCL2 抑制剂在急性髓系白血病中产生协同作用
- GSE324347 人类大脑发育过程中的 R 环景观与神经分化和细胞类型特异性转录有关 [RNA-seq]
- GSE323164 RNA-seq 分析高渗应激模型下人角膜上皮细胞的干眼症
- GSE322548 线虫捕食真菌寡孢节丛孢菌中Aohog1的转录组分析
- GSE319841 出生体重和代乳粉蛋白含量对完全人工饲养仔猪生长及小肠、肝脏和肌肉转录组谱的影响
- GSE319130 多组学分析揭示 SLE 中具有不同免疫表型的分子亚型 [RNA-Seq]
- GSE318682 FGF4-整合素β1轴通过恢复定向集体运动来协调糖尿病伤口再生[ChIP-Seq]
- GSE315907 p53 维持健康老龄化
- GSE315421 金黄色葡萄球菌腹膜炎的体内抗菌治疗效果和免疫稳态分析
- GSE314411 p53 维持健康衰老 [P53KO_PTENKO_RNAseq]
- GSE314410 p53 维持健康衰老 [P53KO_HFD_RNAseq]
- GSE313885 激活的干扰素信号抑制年龄依赖性肝癌 [MYC_WL_MethylArray]
- GSE313862 激活的干扰素信号抑制年龄相关的肝癌 [methylation_all]
- GSE313704 激活的干扰素信号抑制年龄依赖性肝癌 [MERFISH]
- GSE313700 激活的干扰素信号抑制年龄依赖性肝癌 [CosMx_Stat1KO]
- GSE313696 激活的干扰素信号抑制年龄依赖性肝癌 [snRNAseq]
- GSE313664 评估弱信号RNA-Seq数据分析流程性能的双重方法
- GSE313655 激活的干扰素信号抑制年龄依赖性肝癌 [WGBS]
- GSE313654 激活的干扰素信号抑制年龄依赖性肝癌 [RNAseq_MycRux]
- GSE313640 激活的干扰素信号抑制年龄依赖性肝癌 [RNAseq_IFNblockade]
- GSE313598 高通量测序研究
- GSE313597 对接受免疫检查点抑制剂治疗的患者进行B细胞和T细胞的高通量测序
- GSE313596 唐氏综合征供体T细胞的高通量测序
- GSE311717 脂质相关巨噬细胞极化通过 APOE-SDC2 信号通路驱动慢性异种移植纤维化
- GSE309862 水稻中DDM1调控的小RNA位点的全基因组鉴定
- GSE309520 组蛋白乳酸化增强 m6A 介导的 PDK4 稳定性,从而驱动钙化性主动脉瓣疾病中的成骨分化
- GSE302427 HMGB2 通过 MTA2 驱动的代谢重编程促进心肌细胞增殖和心脏再生
- GSE300262 头孢菌素通过抑制 PKCζ/NF-κB 驱动的 PARP1 表达触发实体瘤中的免疫原性细胞死亡,并与免疫疗法产生协同作用
- GSE298511 SUV39H1 调节平滑肌细胞表型可塑性中的 KLF4 和染色质重塑 [ATAC-Seq]
- GSE298510 SUV39H1 调控平滑肌细胞表型可塑性中的 KLF4 和染色质重塑 [RNA-Seq]
- GSE298102 单核 RNA 测序揭示了食蟹猴眼外肌和股四头肌功能和生理差异的分子决定因素
- GSE297704 PhoP介导的细胞膜维持对于结核分枝杆菌的甲基乙二醛耐药性至关重要
- GSE297323 Bcl11b-Cxxc1 轴调控胸腺细胞发育过程中的阶段特异性染色质可及性 [RNA-seq]
- GSE297322 Bcl11b-Cxxc1 轴调控胸腺细胞发育过程中的阶段特异性染色质可及性 [ChIP-seq]
- GSE296908 神经元间隙连接抑制诱导神经保护并部分恢复视觉功能 II
- GSE296907 神经元间隙连接抑制诱导神经保护并部分恢复视觉功能
- GSE296817 DRG RNA-seq 数据
- GSE296649 克隆进化允许耐药的 LMPP 样早期祖细胞在复发性 NPM1c AML 中过度生长 [scRNA-Seq]
- GSE296241 持续的 MYB 活性驱动新兴增强子激活和精确的增强子-启动子相互作用 [ChIP-seq]
- GSE296161 持续的 MYB 活性驱动新兴增强子激活和精确的增强子-启动子相互作用 [RNA-seq]
- GSE296152 持续的 MYB 活性驱动新兴的增强子激活和精确的增强子-启动子相互作用 [ATAC-seq]
- GSE296132 细胞周期蛋白 D3 的阶段特异性降解调控髓系造血并抑制 MPN 发展 [scRNA-seq]
- GSE296131 细胞周期蛋白 D3 的阶段特异性降解调控髓系造血并抑制 MPN 发展 [RNA-seq]
- GSE294338 黄芪多糖通过提高灭活疫苗的效力来抑制虹鳟(Oncorhynchus mykiss)感染性造血细胞坏死病毒引起的鳃和皮肤损伤
- GSE292838 Dlx1&2 直接促进 Cxcl14 的表达以控制突触发育和中间神经元存活 [scRNA-seq]
- GSE292837 Dlx1&2 直接促进 Cxcl14 的表达以控制突触发育和中间神经元存活 [ChIP-seq]
- GSE291942 拟南芥 PRMT5 转录组分析及其在高温胁迫响应调控中的作用
- GSE288818 暴露于急性与慢性木烟冷凝物的人原代支气管上皮细胞:采用批量RNA测序评估其反应
- GSE285906 奥沙利铂通过小鼠肌肉和脂肪组织中不同的转录途径诱导癌症样恶病质
- GSE283623 子宫内膜异位症恶性转化为透明细胞癌的分子机制研究
- GSE277415 炎症性肠病患者的同工型解析转录组
- GSE274621 胰腺癌前病变的单细胞转录组和空间结构揭示腺泡化生细胞的异质性
- GSE274617 胰腺癌前病变和癌症的单细胞转录组揭示腺泡化生细胞的异质性 [MERFISH]
- GSE268319 转录周期的调控导致 BET 溴结构域抑制剂耐药性 [CUT&RUN]
- GSE267779 Sfp1 缺失引起的组蛋白翻译后修饰变化
- GSE263006 mTORC1依赖的CCL24-CCR3轴调控控制结节病中的肉芽肿形成和维持[RNA测序]
- GSE253081 波形纳米纹理介导的干细胞成骨启动,通过机械转导机制和染色质重编程 [ATAC-seq]
- GSE252983 波状纳米纹理介导的干细胞成骨启动,通过机械转导机制和染色质重编程 [RNA-seq]
- GSE233778 双氢青蒿素可增强多发性骨髓瘤癌细胞对铁死亡的敏感性
- GSE230535 NLRP3抑制对肠道成纤维细胞基因表达的影响
- GSE228579 慢性应激通过ADRB2信号通路破坏肝脏稳态并加速肝癌进展
- GSE212128:从Gpr65缺陷型和野生型小鼠中分离的B16和MC38肿瘤浸润CD45+ TILs的单细胞水平基因表达谱
- GSE156767 神经干细胞单细胞3’UTR测序
- GSE151088 miR-375 调控肠隐窝细胞的形态、增殖和再生能力
- GSE322762 USP40沉默小鼠足细胞的转录组分析
📅 报告生成时间:2026-05-01 22:09
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