科研日报 2026-01-24
📅 Daily Report - 2026-01-24
今日筛选出 41 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: 新型单细胞测序方法RoCK and ROI 增强转录组信息获取;空间组学技术Seq-Scope-X突破光学分辨率限制。
主要方向:
- 疾病机制探索:聚焦糖尿病肾病、阿尔茨海默病、COVID-19、皮肤癌、小细胞肺癌、葡萄膜黑色瘤肝转移、癫痫等疾病的关键调控因子与微环境重塑。
- 免疫细胞功能调控:深入研究CAR-T细胞功能、淋巴细胞适应性编程、单核细胞表型与免疫记忆形成。
- 代谢与表观遗传:阐明胆固醇代谢、β细胞功能、能量感知分子在疾病中的作用,以及代谢对表观遗传的重塑。
技术亮点:
- 单细胞多组学:结合scRNA-seq与scATAC-seq等技术,解析细胞异质性与基因调控。
- 空间组学:开发Seq-Scope-X等技术,实现高分辨率的空间转录组分析。
🧪 博客更新
今日焦点: 新型抗体有望攻克三阴性乳腺癌,长读长RNA测序技术在林奇综合征诊断方面取得突破。
主要方向:
- 针对三阴性乳腺癌的靶向治疗研究
- 利用长读长RNA测序技术改进林奇综合征的基因诊断
技术亮点:
- 发现并验证可靶向肿瘤生长相关蛋白的新型实验性抗体
- 应用靶向长读长RNA测序技术,有效识别致病性剪接缺陷,并解决林奇综合征中的不确定变异。
📚 分类浏览
🧬 数据前沿 (39条)
详细内容(前10条)
1. ⭐ GSE287840 RoCK 和 ROI:一种通过靶向富集转录本和预选区域特异性测序增强转录组信息的单细胞 RNA 测序方法 IV
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing、single-cell、transcriptome、enrichment
- 📝 描述:Contributors : Giulia Moro ; Izaskun Mallona ; Malwine J Barz ; Lorenz Bastian ; Claudia D Baldus ; Mark D Robinson ; Erich Brunner ; Konrad BaslerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMany scRNAseq-based methods suffer from a high number of non-detects and a bias towards the 3’ or 5’ end of transcripts. We developed a method termed RoCK and ROI to address these two biases. RoCK and ROI leads to the enrichment of the transcriptome profile of cells with information on transcripts of interest
- 🔗 查看原文
2. ⭐ GSE317266 能量感知分子RORγ在糖尿病肾病和衰老过程中调节胆固醇代谢和免疫信号传导
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、aging、metabolism
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAging is a major risk factor for diabetic kidney disease (DKD), with both conditions exhibiting similar renal pathology. We identify the energy-sensing molecule Retinoic acid-related orphan receptor γ (RORγ) as significantly downregulated in diabetic and aged kidneys. Tubule-specific RORγ deficiency exacerbates kidney injury, whereas its overexpression protects. Mechanistically, RORγ stabilizes insulin-induced gene 1 (INSIG1) by upregulating the deubiquitinase YOD1 and enhancing AMPK activity via CAB39, which together promote INSIG1 phosphorylation and subsequent stabilization. Stabilized INSIG1 potently blocks the ER-to-Golgi transport and activation of SREBP2 (cholesterol synthesis) and STING (inflammatory signaling). In diabetes, RORγ itself is suppressed transcriptionally by CTCF and functionally by impaired AMPK/SIRT1 signaling, which hinders its activation. Importantly, administration of a RORγ agonist or RORγ-enriched exosomes effectively alleviates diabetic kidney injury. Thus, RORγ emerges as a key regulatory node that mitigates DKD and renal aging by co-regulating AMPK-mediated metabolic and STING-driven innate immune pathways through INSIG1 stabilization.
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3. ⭐ GSE297529 利用单细胞多组学测序发现与 COVID-19 严重程度相关的经典单核细胞表型中的关键调控因子
- ✍️ 作者:未知作者
- 🏷️ 关键词:monocyte、sequencing、single-cell
- 📝 描述:Contributors : Donggun Kim ; Sin Young Choi ; Eui Tae Kim ; Jihwan ParkSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensDysregulated immune responses often accompany severe COVID-19, but the underlying epigenetic mechanisms driving monocyte heterogeneity and disease progression remain poorly understood. Here, we applied single-cell multi-omics profiling to peripheral blood mononuclear cells from individuals across five COVID-19 severity stages. We identified two severity-associated classical monocyte subtypes-IL7R+ and CD163+-characterized by distinct transcriptional and epigenetic landscapes. Using constructing of gene regulatory network and in silico TF perturbations, we revealed ETS1 as a key driver of IL7R+ monocytes with T cell-like signaling features, and JDP2 as a repressor maintaining the pro-fibrotic, anti-inflammatory identity of CD163+ monocytes via suppression of AP-1 activity. These subtypes were enriched in moderate-to-critical stages and exhibited signaling pathways associated with tissue remodeling and immune suppression. Our findings define monocyte heterogeneity linked to COVID-19 severity and identify ETS1 and JDP2 as central regulators, offering insight into immune dysregulation and potential therapeutic targets for fibrosis and long-term sequelae.
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4. ⭐ GSE275131 抑制硬脂酰辅酶A去饱和酶(SCD)对阿尔茨海默病(AD)小鼠模型空间转录组的影响
- ✍️ 作者:未知作者
- 🏷️ 关键词:Alzheimer、spatial、transcriptome
- 📝 描述:Contributors : Audrey Hector ; Benoît Delignat-Lavaud ; Valerie MongrainSeries Type : OtherOrganism : Mus musculusHere, the effects of a stearoyl-CoA desaturase inhibitor (SCDi) on the mouse brain spatial transcriptome was investigated. More precisely, wild-type and 3xTg-AD female mice were infused in the brain left lateral ventricle with control (DMSO) or SCDi during 28 days (after the implantation of electrodes for electrocorticography and electromyography). Brains were sampled on the morning of Day 31 after the beginning of treatment, and immediately frozen. Brains were treated and libraries were prepared according to 10x Genomics protocols for Visium Spatial Gene Expression. Sequencing was conducted by Genome Quebec (Montreal, QC, Canada).
- 🔗 查看原文
5. ⭐ GSE287857 LDHA 通过代谢表观遗传重编程诱导糖尿病中的 β 细胞去分化 [RNA-Seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic、RNA-seq、epigenetic
- 📝 描述:Contributors : Xirui Li ; Haoqiang Gong ; Can Xiong ; Xinyue Huang ; Mei He ; Liangjun Sun ; Wenyue Yin ; Suyun Zou ; Min Sha ; Wanhua Guo ; Tijun Wu ; Qingguo Li ; Yaqin Zhang ; Fang ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAims/hypothesis Pancreatic β cell dedifferentiation underlies the reversible reduction in β cell mass and function in diabetes. Interventional targets and adjuvant therapies to prevent/reverse β cell dedifferentiation and transdifferentiation may provide evidence to support the effective treatment of diabetes, while the underlying molecular mechanism remains elusive. Methods LDHA expression and activity were analysed in islets obtained from humans with type 2 diabetes, hyperglycaemic db/db mice, and a high-fat diet (HFD)-induced mouse model of diabetes. The impact of LDHA inhibition on β cell function and identity was investigated in high-fat diet (HFD) feeding mice and db/db mice. ChIP-seq and RNA-seq were used to investigate the specific molecular mechanism underlying the effect of LDHA on the H3K9la enhancement and beta cell function under glucotoxic conditions. Results We demonstrated that inhibition of LDHA effectively preserved β cell identity, which not only delay disease progression in prediabetic stage, but also improve insulin output and glucose homeostasis in diabetic models. Mechanistically, the activation of LDHA led to a marked increase in histone H3 lysine 9 lactylation (H3K9la) in the promoter region of the β cells dedifferentiation markers Sox9, Hes1 and Aldh1a3, and facilitated their transcription, thereby triggering β cell dedifferentiation as well as impaired glucose homeostasis and β cell function in mice. Conclusions/interpretation We unraveled the role of lactate dehydrogenase A (LDHA)-mediated metabolic and epigenetic reprogramming in β cell dedifferentiation during diabetes development. This study suggests that LDHA inhibition could be a novel therapeutic strategy for diabetes treatment.
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6. ⭐ GSE284026 NR2F6 缺失可恢复 CAR-T 细胞功能并诱导实体瘤中抗原非特异性免疫记忆
- ✍️ 作者:未知作者
- 🏷️ 关键词:immune、T cell、antigen
- 📝 描述:Contributors : Dominik Humer ; Victoria Klepsch ; Dietmar Rieder ; Gottfried BaierSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusCAR‑T cell therapy is effective in hematologic malignancies but remains challenging in solid tumors owing to antigen heterogeneity and tumor microenvironment‑induced exhaustion. Here, gene editing of the nuclear receptor NR2F6 restores CAR‑T cell functionality, sustaining a TCF1⁺ progenitor‑exhausted T cell phenotype, enhancing metabolic fitness, and preserving cytotoxic potency under chronic antigen exposure. In immunocompetent models, Nr2f6‑deficient CAR‑T cells suppress solid tumor growth and induce robust, polyclonal host antitumor responses, as shown by protection in tumor re‑challenge experiments. Although infused CAR‑T cells disappear within 2 weeks, durable tumor control coincides with epitope spreading and secondary immune responses, likely via dendritic and other antigen‑presenting cell reactivation. Protection against antigen‑negative tumors and transferable immunity reveal a dual mode of direct cytotoxicity followed by durable immune reprogramming. This broadened host immunity may offset immune escape driven by antigen loss and tumor heterogeneity, establishing NR2F6 inhibition as a promising CAR‑T engineering strategy for durable, antigen‑agnostic solid‑tumor immunotherapy.
- 🔗 查看原文
7. GSE308414 逐步表观遗传信号整合控制细胞毒性淋巴细胞的适应性编程 [ATAC-seq AP1抑制剂]
- ✍️ 作者:未知作者
- 🏷️ 关键词:ATAC-seq、epigenetic
- 📝 描述:Contributors : Simon Grassmann ; Hyunu Kim ; Joseph SunSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusLymphocyte differentiation depends on activation via antigen and cytokines during the immune response to infection. How the timing and integration of these signals program the epigenetic and functional fate of these cells is not completely understood. In this study, we find that inflammatory cytokine signals received by innate and adaptive lymphocytes have a context-dependent role for immune memory formation. Without preceding and sufficient antigen receptor signaling, inflammatory cytokines drive terminal differentiation into short-lived effector cells. In contrast, sufficient antigen-receptor signaling redirects inflammatory cytokine signals to promote memory differentiation via cooperation of STAT and AP-1 transcription factors. By this crucial epigenetic mechanism, optimally equipped lymphocytes are selected for memory formation rather than a terminal effector cell fate. Whereas T cells are hardwired to be shielded from premature inflammatory signals, NK cells rely on coincidental early antigen receptor signaling for adaptive responses. Together, step-wise integration of antigen and cytokine signaling optimizes both effector and memory differentiation, allowing for promiscuous recruitment into the acute immune response while promoting avidity maturation in memory populations of both innate and adaptive lymphocytes.
- 🔗 查看原文
8. GSE304036 非侵入性表皮取样用于基于DNA甲基化的皮肤癌表型预测
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、methylation
- 📝 描述:Contributors : Manuel Rodríguez-Paredes ; Yan Feng ; Oliver Gilliam ; Katrin Wegner ; Günter Raddatz ; Elke Grönniger ; Frank LykoSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensThe epidermis is uniquely exposed to the effects of environmental factors such as ultraviolet radiation, which induce progressive genetic and epigenetic modifications contributing to aging and the onset of keratinocyte carcinomas. DNA methylation is the best-characterized epigenetic modification and a valuable biomarker for assessing epidermal health. However, broad screening approaches have been hindered by the limited quantity and quality of the genomic DNA obtained from the epidermis and the resulting need for invasive sampling methods. Here we describe an integrated method that enables the non-invasive sampling of epidermal DNA for subsequent analysis by DNA methylation microarrays. This procedure combines a gel-based adhesive tape for keratinocyte collection, a robust gDNA extraction protocol and a curated selection of microarray probes optimized for low-input DNA conditions. Analysis of >100 corresponding methylomes demonstrates that our approach can be used for both the training of epigenetic clocks capable of predicting epidermal age with high accuracy, as well as the investigation of various DNA methylation-based biomarkers relevant to keratinocyte cancer development. These findings underscore the potential of our method for broad and non-invasive skin health assessment and cancer prevention strategies.
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9. GSE316934 高脂饮食后野生型和Camk2d髓系条件性敲除小鼠eWAT基质血管组分细胞的单细胞RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:RNA-seq、single-cell
- 📝 描述:Contributors : Yifan Tu ; Ke Sui ; Zheng Wang ; Jiawei Zhang ; Ying GuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusEpididymal white adipose tissue (eWAT) stromal vascular fraction (SVF) cells were profiled by 10x Genomics Chromium Single Cell 3′ v1 scRNA-seq to characterize immune-cell states in diet-induced obesity. SVF cells were isolated by collagenase digestion, filtered, and processed when viability exceeded 85%. Libraries were sequenced on an Illumina NovaSeq 6000 (PE150). Reads were aligned to mm10 and gene–cell count matrices were generated with Cell Ranger count v5.0.0 and aggregated across samples with Cell Ranger aggr. Downstream analyses were performed in Seurat v4.1.1 with QC filtering, ambient RNA correction (SoupX v1.3.0), doublet detection (DoubletFinder v2.0.2), batch correction (fastMNN), clustering/UMAP, and differential expression testing (MAST). Cell types were annotated using SingleR v1.4.1 and canonical markers; non-immune cells were excluded for immune-focused analyses. Additional analyses included pseudotime inference (Monocle2 v2.14.0) and cell–cell communication analysis (CellChat v0.0.2).
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10. GSE287891 转录因子 Traffic jam 协调果蝇卵巢中的体细胞 piRNA 通路 [RNA-seq]
- ✍️ 作者:未知作者
- 🏷️ 关键词:RNA-seq、pathway
- 📝 描述:Contributors : Azad Alizada ; Aline Martins ; Nolwenn Mouniée ; Julia V Rodriguez Suarez ; Benjamin Bertin ; Nathalie Gueguen ; Vincent Mirouse ; Anna-Maria Papameletiou ; Austin J Rivera ; Nelson C Lau ; Abdou Akkouche ; Stéphanie Maupetit-Mehouas ; Gregory J Hannon ; Benjamin Czech Nicholson ; Emilie BrassetSeries Type : Expression profiling by high throughput sequencingOrganism : Drosophila melanogasterThe PIWI-interacting RNA (piRNA) pathway is essential for transposable element (TE) silencing in animal gonads. While the transcriptional regulation of piRNA pathway components in germ cells has been documented in mice and flies, their control in somatic cells of Drosophila ovaries remains unresolved. Here, we demonstrate that Traffic jam (Tj), the Drosophila orthologue of large Maf transcription factors in mammals, is a master regulator of the somatic piRNA pathway. Tj binds to regulatory regions of somatic piRNA factors and the major piRNA cluster flamenco, which carries a Tj-bound enhancer downstream of its promoter. Depletion of Tj in somatic follicle cells causes downregulation of piRNA factors, loss of flam expression and de-repression of gypsy-family TEs. We propose that the arms race between the host and TEs led to the co-evolution of promoters in piRNA pathway genes as well as TE regulatory regions that both rely on a shared transcription factor.
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💡 该来源还有 29 条内容,详见 文末
🧪 博客更新 (2条)
详细内容(全部2条)
1. 靶向长读长RNA测序提高了林奇综合征的诊断率。
- ✍️ 作者:未知作者
- 🏷️ 关键词:sequencing
- 📝 描述:Targeted long-read RNA sequencing reveals pathogenic splicing defects and resolves uncertain variants in Lynch syndrome, highlighting the clinical value of transcript-level analysis…
- 🔗 查看原文
2. 这种新型抗体或许能够阻止最致命的乳腺癌之一的发生。
- ✍️ 作者:未知作者
- 🏷️ 关键词:antibody
- 📝 描述:Researchers have identified a promising new weapon against triple-negative breast cancer, one of the most aggressive forms of the disease. An experimental antibody targets a protein that fuels tumor growth and shuts down immune defenses, effectively turning the immune system back on. In early tests, the treatment slowed tumor growth, reduced lung metastases, and destroyed chemotherapy-resistant cancer cells.
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📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| RNA-seq | 8 |
| cancer | 6 |
| ATAC-seq | 4 |
| epigenetic | 4 |
| transcriptome | 4 |
| sequencing | 3 |
| methylation | 3 |
| single-cell | 3 |
| scRNA | 3 |
| immune | 2 |
| aging | 2 |
| metabolism | 2 |
| spatial | 2 |
| genome | 2 |
| metabolic | 2 |
| monocyte | 1 |
| TME | 1 |
| Alzheimer | 1 |
| scATAC | 1 |
| regex:intestin(e | al) |
📎 更多内容
🧬 数据前沿 其他内容 (29条)
- GSE287858 LDHA通过代谢表观遗传重编程诱导糖尿病β细胞去分化
- GSE287823 两种获得性癫痫大鼠模型中基因表达和甲基化变化的共性 [RNA-seq]
- GSE317298 多组学分析揭示微环境重塑是屋尘螨诱发肺癌进展的关键驱动因素
- GSE309245 逐步信号整合控制淋巴细胞的适应性编程 [bulkRNA-seq 和 ATAC-seq 6 小时刺激]
- GSE308415 逐步表观遗传信号整合控制细胞毒性淋巴细胞的适应性编程 [CUT&RUN STAT1 STAT5 cJun]
- GSE294461 比较两种不同类型肿瘤(B16/F10-BrM 和 H2030-BrM)脑肿瘤微环境中的 CD74+ 与 CD74- 小胶质细胞/巨噬细胞
- GSE292377 逐步信号整合控制淋巴细胞的适应性编程 [bulkRNA-seq 和 ATAC-seq]
- GSE292296 逐步信号整合控制淋巴细胞的适应性编程 [scRNA-seq]
- GSE317349 GDF15 重编程微环境以驱动葡萄膜黑色素瘤肝转移的发展 [scRNA-seq]
- GSE317347 GDF15 重编程微环境以驱动葡萄膜黑色素瘤肝转移的发展 [bulk RNA-seq]
- GSE316978 米索霉素改变 EWS::FLI1 DNA 结合和 RNA 聚合酶 II 加工能力以抑制新生转录 [RNA-seq]
- GSE316811 Seq-Scope-eXpanded (Seq-Scope-X): 超越光学分辨率的空间组学
- GSE303770 ISL1:小细胞肺癌中一种新型神经内分泌亚型预测对鲁比替定的持久反应
- GSE298610 经典 BAF 复合物通过辅因子引导的染色质重塑来调控间充质干细胞微环境组成和命运 [RNA-Seq]
- GSE298609 经典 BAF 复合物通过辅因子引导的染色质重塑来调控间充质干细胞微环境组成和命运 [scATAC-seq]
- GSE298608 经典 BAF 复合物通过辅因子引导的染色质重塑来调控间充质干细胞微环境组成和命运 [scRNA-seq]
- GSE281433 贝特类药物苯扎贝特对腹水介导的上皮癌细胞转录变化的影响
- GSE281415 卵巢癌腹水暴露对上皮癌细胞系的影响
- GSE317332 用于探测人类 iPSC 衍生肠道类器官对基质信号的转录反应的完整定义方案和基于 PEG 的平台
- GSE315629 全基因组鉴定 786-O 细胞中 H4K12 乳酸化和 GR 的转录靶点(无论是否用地塞米松处理)。
- GSE315326 全基因组鉴定透明细胞肾细胞癌 (ccRCC) 细胞中 H4K12 乳酸化的转录靶点
- GSE314501 Mettl18缺陷胚胎的综合转录组分析
- GSE308156 CARM1介导的富含次黄嘌呤的外泌体生物合成重塑CD8+ T细胞的肌苷代谢并削弱其抗肿瘤能力
- GSE306334 靶向KEAP1失活肺癌中的泛素信号通路脆弱性
- GSE289768 衰老通过激活整合应激反应促进转移 [RNA-Seq OE]
- GSE288033 通过整合基因组分析和验证对卵巢衰老相关基因 NDUFS5 和 UBE2L3 进行功能解析
- GSE287822 两种获得性癫痫大鼠模型中基因表达和甲基化变化的共性 [RRBS]
- GSE281507 慢性轻度应激以性别依赖的方式改变终纹前背侧核床的转录组和信号传导特性
- GSE263687 衰老通过激活整合应激反应促进转移(ATAC-Seq)
📅 报告生成时间:2026-01-23 21:39
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