科研日报 2026-05-12

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📅 Daily Report - 2026-05-12

今日筛选出 21 条内容,来自 1 个来源

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🤖 今日AI智能总结

🧬 数据前沿

今日焦点: 新型内源性脂质9-PAHSA显著增强T细胞抗肿瘤免疫功能和干性;m5C甲基转移酶NSUN3通过tRNA修饰驱动穿梭纳米管介导的线粒体转移,重塑胶质母细胞瘤免疫微环境。

主要方向

  • 肿瘤免疫逃逸与治疗抵抗机制(如胶质母细胞瘤、甲状腺癌、淋巴瘤、肺腺癌)
  • 肠道微生物组与宿主互作(如植物化学物对果蝇的影响)
  • 细胞通讯与信号通路(如线粒体转移、DNA感知、RNA修饰)

技术亮点

  • 创新的单细胞多组学分析技术(如Perturb-seq、Smart-seq3)用于解析细胞发育和疾病机制。
  • 新型网络分析方法(如D-SPIN)用于构建转录组调控网络模型。

📚 分类浏览

🧬 数据前沿 (21条)

详细内容(前10条)

1.GSE330057 9-PAHSA 调控 TCR-T 细胞命运以增强抗肿瘤免疫力 [RNA-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、immunity、T cell、RNA-seq
  • 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe identify the endogenous lipid 9-PAHSA as a potent enhancer of T cell anti-tumor function and stemness, validated in murine models and a clinical trial. Mechanistically, we identify ICAM2 as a direct surface sensor for 9-PAHSA and delineate a downstream signaling axis whereby the ICAM2-Ezrin-mTORC2 cascade drives FOXO1 O-GlcNAcylation at S318, facilitating its nuclear translocation to enact a stem-like transcriptional program. Translating this discovery, we engineered armored human TCR-T cells with potentiated ICAM2 expression, which achieve superior tumor control through their enhanced intrinsic efficacy and a remarkable ability to ignite a coordinated and durable host anti-tumor immune response. Our work establishes a new paradigm of metabolite-sensing in T cell biology and provides a compelling therapeutic strategy to potentiate cellular immunotherapy for intractable cancers.
  • 🔗 查看原文

2.GSE330166 植物化学物质干预引发果蝇肠道微生物组和转录组的性别特异性反应

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:transcriptome、gut、regex:gut(-?microbiome)?
  • 📝 描述:Contributors : Litzy Y Alvarado-Mata ; Nagamani Balagurusamy ; Umesh K ReddySeries Type : Expression profiling by high throughput sequencingOrganism : Drosophila melanogasterDietary phytochemicals are plant-derived bioactive compounds that can influence host physiology and gut microbial communities. However, the structural distinctiveness of phytochemicals and their modulation of host intestinal gene expression in a sex-dependent manner remain poorly understood. In this study, we used Drosophila melanogaster to investigate gut transcriptomic responses to four phytochemical-enriched diets, capsaicin, curcumin, resveratrol, and thymoquinone. Two-day-old mated female and male flies were exposed to control or phytochemical-supplemented diets for 10 days, after which gut tissues were dissected for bulk RNA sequencing. Transcriptomic analysis revealed that biological sex was a major source of variation in the gut, with female and male flies showing distinct expression profiles across dietary treatments. Phytochemical supplementation induced compound and sex-specific transcriptional responses. Curcumin produced the strongest transcriptional response, with females showing reduced expression of genes involved in carbohydrate digestion and trehalose metabolism, whereas males showed enrichment of xenobiotic detoxification pathways dominated by cytochrome P450 genes. Capsaicin also induced sex-dependent responses, including detoxification-associated transcriptional changes in females and increased expression of immune-related genes in males. These results indicate that dietary phytochemicals elicit sex-specific gut transcriptomic responses in Drosophila melanogaster and highlight biological sex as an important variable in studies of diet-host interactions.
  • 🔗 查看原文

3.GSE330074 m5C甲基转移酶NSUN3通过tRNA修饰驱动隧道纳米管介导的线粒体转移重塑胶质瘤免疫微环境的机制研究[RNA-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、glioma、RNA-seq
  • 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGlioma is the most common and aggressive malignant tumor in the central nervous system, and its immunosuppressive microenvironment is closely associated with therapeutic resistance and poor prognosis. NSUN3, an m5C methyltransferase, catalyzes m5C modification on tRNA and regulates RNA translation and cellular metabolism. However, the role and transcriptomic mechanism of NSUN3 in remodeling the glioma immune microenvironment remain unclear. In this study, mRNA sequencing was performed on NSUN3-knockdown glioma cells and control cells to identify differentially expressed mRNAs and related signaling pathways. Total RNA was extracted, and mRNA was enriched for library construction and high-throughput sequencing. Bioinformatics analyses including quality control, read mapping, gene quantification, differential expression screening, and functional enrichment (GO, KEGG, GSEA) were conducted. We identified a series of differentially expressed mRNAs associated with tRNA modification, mitochondrial transfer, tunneling nanotube formation, and immune regulation. These mRNAs were significantly enriched in immune response, cellular metabolism, and tumor progression pathways. Our transcriptomic data provide a comprehensive resource for understanding the mechanism by which NSUN3 drives tunneling nanotube-mediated mitochondrial transfer and remodels the glioma immune microenvironment, and offer potential targets for glioma immunotherapy.
  • 🔗 查看原文

4. GSE330276 抑制的 cGAS-STING DNA 感知驱动间变性甲状腺癌的免疫逃逸

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、immune
  • 📝 描述:Contributors : Xuguang Zhu ; Manju Acharya ; Nathan Wong ; Sheue-yann ChengSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe used single-cell RNA sequencing to study the tumor immune microenvironment of thyroid tumors in a genetically engineered mouse model harboring triple mutations in Thrb1, Trp53, and Pten.
  • 🔗 查看原文

5. GSE330028 m5C甲基转移酶NSUN3通过tRNA修饰驱动隧道纳米管介导的线粒体转移重塑胶质瘤免疫微环境的机制研究

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、glioma
  • 📝 描述:Series Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensGlioma is characterized by an immunosuppressive tumor microenvironment (TME) that promotes immune escape and therapeutic resistance. Mitochondrial transfer mediated by tunneling nanotubes (TNTs) is critical for tumor-stroma crosstalk, yet the underlying epigenetic regulatory mechanism remains unclear. Here, we report that the RNA m5C methyltransferase NSUN3 drives TNT formation and intercellular mitochondrial transfer in glioma by catalyzing m5C modification on tRNAs. Using tRNA-specific bisulfite sequencing (tRNA-BSseq) on human glioma cells, we systematically profiled tRNA m5C methylation landscapes in NSUN3-overexpressing and control groups. We identified NSUN3-dependent m5C sites on tRNAs that modulate translation efficiency of key factors involved in TNT assembly and mitochondrial transport. Functional assays demonstrated that NSUN3-mediated tRNA m5C modification enhances TNT formation, facilitates mitochondrial transfer from stromal cells to glioma cells, and remodels the immune microenvironment by suppressing anti-tumor immunity and promoting immunosuppressive cell infiltration. Our study reveals a novel epitranscriptomic mechanism linking tRNA m5C methylation to intercellular organelle transfer and immune regulation in glioma, providing potential targets for glioma immunotherapy.
  • 🔗 查看原文

6. GSE329793 ALK 融合肺腺癌的全面分析揭示了突变 p53 驱动的 DNA 复制和修复失调在靶向治疗耐药中的作用 [ChIP-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:resistance、ChIP-seq
  • 📝 描述:Contributors : Esther Redin ; Yingqian A Zhan ; Charles M RudinSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAcquired resistance to ALK tyrosine kinase inhibitors (TKIs) remains a major barrier in ALK-fusion lung adenocarcinoma (LUAD), with up to 50% of resistant tumors lacking known resistance drivers. Here, we performed integrated genomic, transcriptomic, and single-cell analyses of clinical specimens and patient-derived xenografts (PDXs) to define previously uncharacterized mechanisms of resistance. Transcriptomic profiling revealed marked intratumoral heterogeneity, with multiple distinct and independent pathways contributing to ALK inhibitor resistance. While secondary ALK mutations were detected in ~30% of resistant tumors, approximately half harbored no known actionable alterations. However, TP53 mutations, particularly DNA-binding domain missense variants, were significantly enriched in these TKI-resistant tumors and were associated with activation of DNA replication and repair programs. We find that missense mutant p53 acquired gain-of-function activity by directly binding promoters of replication and repair genes and engaging the chromatin remodeler EP400, thereby enhancing DNA damage repair and promoting survival under ALK inhibition. Therapeutically, combining lorlatinib with the proteasome inhibitor carfilzomib selectively depleted mutant p53, suppressed replication programs, and overcame resistance in TP53-mutant ALK-fusion PDX models. Together, these findings identify mutant p53–driven replication and repair as a previously unrecognized common mechanism of ALK TKI resistance and nominate a rational combination strategy for targeting a substantial fraction of TKI-refractory ALK-fusion LUAD.
  • 🔗 查看原文

7. GSE292335 定量 RNA 假尿苷图谱揭示细菌假尿苷化的功能信息

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:bacteria、regex:bacter(ia|ial|ium)
  • 📝 描述:Contributors : Xin Deng ; Letong XUSeries Type : OtherOrganism : Bacillus cereus ATCC 14579 ; Escherichia coli K-12 ; Klebsiella pneumoniae ; Pseudomonas aeruginosa PAO1 ; Pseudomonas savastanoi pv. phaseolicola 1448APseudouridine (Ψ) modifications play crucial roles in RNA regulation, yet their distribution and functional significance in bacteria remain largely unexplored compared to eukaryotic systems. Here, we present the first comprehensive transcriptome-wide mapping of Ψ modifications across five diverse bacterial species (Klebsiella pneumoniae, Escherichia coli, Bacillus cereus, Pseudomonas aeruginosa, Pseudomonas syringae) using bisulfte-induced deletion sequencing at single-base resolution. Ψ modifications exhibit enriched distribution in coding sequences and notable conservation across orthologous genes involved in central metabolism. Comparative analysis revealed evolutionarily conserved modification patterns in operons, such as the atp operon, and growth phase-dependent dynamics, particularly elevated modification levels in transfer RNA T-arms and transfer-messenger RNAs under stress conditions. We uncovered that Ψ modifications modulate mRNA translation in Pseudomonas syringae under nutrition-limited condition and enhance interactions with the RNA chaperone Hfq in Pseudomonas aeruginosa under stationary growth phase. We found local RNA architecture significantly influences modification levels, with highly modified sites sharing distinct structural features reminiscent of different type of RNA. To facilitate broader studies, we developed an integrated deep learning framework combining convolutional neural networks with transformer architecture to effectively capture both sequence patterns and RNA secondary structural features, enabling accurate prediction of Ψ modification sites across bacterial transcriptomes. Overall, our study provides fundamental insights into bacterial RNA Ψ modification landscapes and establishes a foundation for future mechanistic studies.
  • 🔗 查看原文

8. GSE256008 斑马鱼颅神经嵴单细胞多组学研究 [scRNA-seq (Direct Capture Perturb-seq)]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:single-cell、scRNA
  • 📝 描述:Contributors : Zhiyuan Hu ; Sarah Mayes ; Tatjana Sauka-SpenglerSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Danio rerioSingle-cell multiomic study of zebrafish cranial neural crest
  • 🔗 查看原文

9. GSE312966 基于网络的分析揭示了 SOX10 缺失的葡萄膜黑色素瘤中 microRNA 对致癌通路潜在的调控作用

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:regex:onco(logy|logist|gene|genic)
  • 📝 描述:Contributors : Xin Lai ; Chunyan Luan ; Anja Wessely ; Markus Heppt ; Julio VeraSeries Type : Non-coding RNA profiling by high throughput sequencingOrganism : Homo sapiensSOX10 is essential for melanocyte development and maintenance and plays a critical role in uveal melanoma (UM) initiation and progression. While SOX10’s transcriptional regulation of protein-coding genes is well characterized, its role on microRNA (miRNA) regulatory landscape in UM remains unexplored. Here, we employed network-based modeling to systematically characterize miRNA regulatory functions following SOX10 depletion in UM. First, we profiled mRNA and miRNA expression levels in SOX10 wild-type and knockdown UM cells. Then, we integrated the transcriptomic data, a UM network, and a Bayesian model to quantify miRNAs’ regulatory activities and identify key miRNAs. Subsequently, we employed pathway enrichment analysis combined with literature mining to elucidate the functional roles of identified miRNAs through their target genes and associated signaling pathways in UM. We identified 17 miRNAs that show significant changes in regulatory activities following SOX10 knockdown in UM cells. These miRNAs regulate the expression of genes involved in cancer hallmark pathways, including cell cycle progression, mTORC1 signaling, and fatty acid metabolism. Notably, miR-34a, miR-25, miR-186, and miR-211 have tumor-suppressive potential by targeting genes involved in UM progression and metastasis. Our results suggested that SOX10 depletion in UM can activate tumor-suppressive mechanisms through regulating miRNAs.
  • 🔗 查看原文

10. GSE330067 PEDV不连续转录产生一种新型亚基因组RNA,以增强免疫逃逸和病毒适应性

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune
  • 📝 描述:Contributor : Dehua LuoSeries Type : Expression profiling by high throughput sequencingOrganism : Porcine epidemic diarrhea virusDuring viral evolution, RNA viruses accumulate advantageous mutations that enhance replicative, adaptability, and evasion of host immune responses. While most studies have focused on amino acid substitutions that alter protein function, functional RNA-level mutations remain largely underexplored. In this study, we employed RNA-seq and Ribo-seq for the first time to analyze viral gene expression during replication of the porcine epidemic diarrhea virus (PEDV). We identified a novel subgenomic RNA (sgRNA) that encodes a truncated nucleocapsid isoform, designated N1. Evolutionary analysis revealed that a double-point mutation within the GII-b subclade facilitated the emergence of a functional transcriptional regulatory sequence (TRS-B) and a translation initiation codon. N1 promotes viral replication but is unable to substitute for the full-length N protein in the assembly of infectious virions. Mechanistically, N1 binds double-stranded RNA (dsRNA) and suppresses dsRNA-induced phosphorylation of protein kinase R (PKR) and eukaryotic translation initiation factor 2α (eIF2α), thereby inhibiting the formation of host stress granules (SG). Mutations at residues R133 and R134 markedly impair the dsRNA-binding capacity of N1 and its ability to inhibit SG formation. Further transcriptomic analysis of infected cells revealed that the absence of N1 enhances activation of host innate immune response following viral infection, thereby suppressing viral replication. Our findings demonstrate that PEDV can promote the generation of novel innate immune antagonists through the evolution of TRS-B, thereby enhancing its immune evasion ability and adaptation to the host.
  • 🔗 查看原文

💡 该来源还有 11 条内容,详见 文末

📊 关键词统计

关键词出现次数
immune5
RNA-seq5
resistance3
glioma2
ChIP-seq2
scRNA2
single-cell2
regex:onco(logylogist
cancer1
transcriptome1
gut1
regex:gut(-?microbiome)?1
tumor1
immunity1
T cell1
ATAC-seq1
sequencing1
bacteria1
regex:bacter(iaial

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🧬 数据前沿 其他内容 (11条)

📅 报告生成时间:2026-05-11 22:31
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