科研日报 2026-05-11

Page content

📅 Daily Report - 2026-05-11

今日筛选出 17 条内容,来自 2 个来源

Powered by 科研普拉斯 & Claude

🤖 今日AI智能总结

🧬 数据前沿

今日焦点

  • CRISPR Prime Editing赋能组蛋白修饰研究:利用高通量CRISPR Prime Editing技术,首次精确解析了哺乳动物组蛋白H3的关键赖氨酸在基因组上的功能(GSE319059, GSE319506, GSE319420)。
  • 单细胞多组学揭示TNBC药物作用机制:整合单细胞RNA测序与非靶向代谢组学,阐明了β-榄香烯在三阴性乳腺癌(TNBC)中的免疫和代谢调控作用(GSE329623)。

主要方向

  • 肿瘤分子机制与治疗:解析三阴性乳腺癌、神经母细胞瘤、喉部白斑以及T细胞淋巴瘤的转录组特征,探索药物(如β-榄香烯、HDAC抑制剂)的抗癌机制及耐药性(GSE329623, GSE292598, GSE292597, GSE292595, GSE296418, GSE330007, GSE302088)。
  • 神经系统疾病与细胞异质性:深入研究帕金森病患者腹侧黑质的细胞图谱,以及牙髓干细胞和牙周膜干细胞的单细胞转录组学,揭示细胞异质性(GSE329625, GSE329279)。
  • 表观遗传调控机制:探索组蛋白修饰(H3K36me3)在酵母中的基因组富集(GSE330204),以及哺乳动物组蛋白H3的关键赖氨酸作用(GSE319059, GSE319506, GSE319420),并研究了人类神经元表观基因组的后天重构(GSE330111)。

技术亮点

  • 高通量CRISPR Prime Editing:实现对哺乳动物组蛋白H3关键赖氨酸进行高精度、高通量的功能解析。
  • 单细胞RNA测序与代谢组学整合:为深入理解复杂疾病(如TNBC)的药物作用机制提供了多维度视角。

🧪 博客更新

今日焦点: 首次在小鼠模型中,利用年轻小鼠的肠道细菌成功逆转了衰老相关肝脏损伤,并有望预防肝癌。

主要方向

  • 肠道菌群重塑用于逆转衰老相关肝脏疾病。
  • 利用肠道菌群预防肝癌。

技术亮点

  • 通过移植年轻小鼠的肠道细菌,重塑衰老小鼠的肠道微生态。

📚 分类浏览

🧬 数据前沿 (16条)

详细内容(前10条)

1.GSE329623 整合单细胞 RNA 测序和非靶向代谢组学揭示 β-榄香烯在三阴性乳腺癌中的免疫和代谢调节作用

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer、immune、metabolic、metabolomics、sequencing、single-cell
  • 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTriple-negative breast cancer (TNBC) presents a significant challenge in women’s health due to its aggressive phenotype and the absence of targeted therapeutic options. β-Elemene, a sesquiterpene isolated from Curcuma wenyujin, has demonstrated clinical benefits against TNBC; however, its mechanisms of action, particularly with respect to the immune and metabolic tumor microenvironment, remain poorly characterized. In this study, we employed single-cell RNA sequencing and untargeted metabolomics to investigate how β-elemene reshapes the cellular and metabolic landscape of TNBC using a 4T1 orthotopic mouse model. Our findings are expected to provide the first comprehensive elucidation of β-elemene’s dual immunomodulatory and metabolic effects in TNBC, highlighting the potential of natural compounds to enhance antitumor immunity.
  • 🔗 查看原文

2. GSE319059 利用高通量 CRISPR 启动编辑技术揭示哺乳动物组蛋白 H3 中的关键赖氨酸 [RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:RNA-seq、histone
  • 📝 描述:Contributor : Aliaksandra RadzisheuskayaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHistone proteins are central to regulating eukaryotic genomes, and their post-translational modifications play key roles in controlling gene expression, DNA repair and chromatin structure. Understanding the functions of individual histone modifications is a significant challenge in mammalian chromatin biology, primarily due to the multiple copies of histone genes found in mammalian genomes. In this study, we present a high-throughput CRISPR prime editing platform that allows for base-precise, combinatorial, and reversible mutagenesis of all canonical and non-canonical histone H3 genes within their native genomic context. Using this system, we systematically substituted each lysine residue in histone H3 with arginine and compared each mutation against synonymous lysine-to-lysine controls. This unbiased functional screen revealed a core set of lysines, including H3K4, H3K9, H3K14, H3K18, and H3K79, whose mutations impair cellular fitness in mouse embryonic stem cells, highlighting the critical roles of their post-translational modifications in chromatin function. In addition, our approach demonstrated that H3K56 acetylation, previously linked to genome stability in yeast and Drosophila, plays a conserved role in safeguarding the genome in mammalian cells. Extending this approach, we generated double histone H3 mutants to probe functional redundancy between several lysine residues. While individual substitutions caused minimal defects, specific combinations, most notably H3K27R+H3K36R, revealed impairments in stem cell self-renewal and distinct transcriptional consequences, uncovering regulatory crosstalk not evident from single-site perturbations. This study presents the first comprehensive functional map of histone H3 lysines in a mammalian system, establishing a broadly applicable platform for dissecting histone modifications with advanced precision.
  • 🔗 查看原文

3. GSE330111 出生后甲基胞嘧啶向羟甲基胞嘧啶的转化重塑了人类神经元表观基因组

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:Neuronal、epigenome
  • 📝 描述:Contributors : Xu Heng ; Chien Jo-Fan ; Kozlenkov Alexey ; Vadukapuram Ramu ; Li Junhao ; Wei Yu ; Dwork Andrew J. ; Liu Chunyu ; Dracheva Stella ; Mukamek Eran A.Series Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensHealthy brain development requires a coordinated process of postnatal cellular maturation throughout the first two decades of life that transforms neuronal morphology, connectivity, physiology, and gene expression. The maturation and stable maintenance of neuron identity is driven, in part, by large-scale reconfiguration of the neuronal DNA methylome. Neurons have uniquely high levels of 5-hydroxy-methyl-cytosine (hmC) compared to other cell types, yet the relative contributions of 5hmC and 5-methyl-cytosine (mC) remain unknown because most experimental assays do not distinguish these marks. We measured mC and hmC using bisulfite- and oxidative-bisulfite sequencing in excitatory and inhibitory neurons, along with mRNA and histone modifications, from the prefrontal cortex of 103 human donors, ranging from 38 days to 77 years of age. Up to half of all CG dinucleotides convert from mC to hmC in a gradual process extending throughout the first decade of life, dramatically reshaping the neuronal methylome. Asymmetric enrichment of hmC on the sense strand of actively transcribed genes increases in a linear, clock-like fashion throughout the lifespan, indicating a mechanistic link between transcription and hmC. We found that sex differences in X-linked DNA methylation in the human brain are primarily driven by hmCG rather than mCG, suggesting an important role for hmC in X-chromosome inactivation (XCI) and escape gene expression. We found key changes in 5hmC at dynamic cis-regulatory elements marked by changing cell type-specific levels of active and repressive histone modifications. Collectively, our findings reveal the dynamic trajectory of hmC in human neurons across the lifespan and highlight the association of DNA hydroxymethylation with transcription, chromatin state, and sex-specific gene regulation.
  • 🔗 查看原文

4. GSE330007 转录组分析揭示了区分声带白斑和良性病变的分子特征:慢性炎症、免疫功能障碍和上皮屏障破坏的协同失调

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、inflammation
  • 📝 描述:Contributors : Zhixian Xiao ; Li Zhou ; Xiaocui Long ; Li Tian ; Xing LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensObjective: Vocal cord leukoplakia (VCL) represents a precancerous laryngeal lesion with a risk of malignant transformation. By employing transcriptomic analysis, this research sought to ascertain the key signatures and regulatory networks capable of distinguishing VCL from benign lesions. Methods: Surgically resected tissues from 8 individuals with VCL and 11 individuals with vocal cord polyps (VCP) were included for RNA sequencing and bioinformatics analysis. Core genes were identified through differential expression analysis, and functional enrichment analyses were utilized to characterize the associated biological processes. Results: The transcriptomic profile of VCL was characterized by abnormalities in three primary aspects: activation of inflammation-related pathways (e.g., NF-κB), downregulation of immune function-related genes (e.g., CD8A, CD19), and downregulation of epithelial barrier-related molecules (e.g., CLDN4). Conclusion: The transcriptomic signatures of VCL are linked to the coordinated dysregulation of pathways related to inflammation, immunity, and the epithelial barrier.
  • 🔗 查看原文

5. GSE318699 RNA测序,分析在正常培养基中培养或用TNFα+CD68+巨噬细胞上清液处理的mAECs

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:RNAseq
  • 📝 描述:Contributors : Li Wang ; Fangzhou Li ; Fang YaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe isolated TNFα+CD68+ macrophages from atherosclerotic mice, and transferred the conditioned medium to normal murine aortic endothelial cells (mAECs). mAECs cultured in normal medium was used as the negative control. Following a 48-h incubation in conditioned media, mAECs were subjected to bulk RNA-sequencing analysis.
  • 🔗 查看原文

6. GSE319506 利用高通量 CRISPR Prime Editing 揭示哺乳动物组蛋白 H3 中的关键赖氨酸 [CUT&Run]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:histone
  • 📝 描述:Contributor : Aliaksandra RadzisheuskayaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHistone proteins are central to regulating eukaryotic genomes, and their post-translational modifications play key roles in controlling gene expression, DNA repair and chromatin structure. Understanding the functions of individual histone modifications is a significant challenge in mammalian chromatin biology, primarily due to the multiple copies of histone genes found in mammalian genomes. In this study, we present a high-throughput CRISPR prime editing platform that allows for base-precise, combinatorial, and reversible mutagenesis of all canonical and non-canonical histone H3 genes within their native genomic context. Using this system, we systematically substituted each lysine residue in histone H3 with arginine and compared each mutation against synonymous lysine-to-lysine controls. This unbiased functional screen revealed a core set of lysines, including H3K4, H3K9, H3K14, H3K18, and H3K79, whose mutations impair cellular fitness in mouse embryonic stem cells, highlighting the critical roles of their post-translational modifications in chromatin function. In addition, our approach demonstrated that H3K56 acetylation, previously linked to genome stability in yeast and Drosophila, plays a conserved role in safeguarding the genome in mammalian cells. Extending this approach, we generated double histone H3 mutants to probe functional redundancy between several lysine residues. While individual substitutions caused minimal defects, specific combinations, most notably H3K27R+H3K36R, revealed impairments in stem cell self-renewal and distinct transcriptional consequences, uncovering regulatory crosstalk not evident from single-site perturbations. This study presents the first comprehensive functional map of histone H3 lysines in a mammalian system, establishing a broadly applicable platform for dissecting histone modifications with advanced precision.
  • 🔗 查看原文

7. GSE319420 利用高通量 CRISPR Prime Editing 揭示哺乳动物组蛋白 H3 中的关键赖氨酸 [CUT&Tag]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:histone
  • 📝 描述:Contributor : Aliaksandra RadzisheuskayaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHistone proteins are central to regulating eukaryotic genomes, and their post-translational modifications play key roles in controlling gene expression, DNA repair and chromatin structure. Understanding the functions of individual histone modifications is a significant challenge in mammalian chromatin biology, primarily due to the multiple copies of histone genes found in mammalian genomes. In this study, we present a high-throughput CRISPR prime editing platform that allows for base-precise, combinatorial, and reversible mutagenesis of all canonical and non-canonical histone H3 genes within their native genomic context. Using this system, we systematically substituted each lysine residue in histone H3 with arginine and compared each mutation against synonymous lysine-to-lysine controls. This unbiased functional screen revealed a core set of lysines, including H3K4, H3K9, H3K14, H3K18, and H3K79, whose mutations impair cellular fitness in mouse embryonic stem cells, highlighting the critical roles of their post-translational modifications in chromatin function. In addition, our approach demonstrated that H3K56 acetylation, previously linked to genome stability in yeast and Drosophila, plays a conserved role in safeguarding the genome in mammalian cells. Extending this approach, we generated double histone H3 mutants to probe functional redundancy between several lysine residues. While individual substitutions caused minimal defects, specific combinations, most notably H3K27R+H3K36R, revealed impairments in stem cell self-renewal and distinct transcriptional consequences, uncovering regulatory crosstalk not evident from single-site perturbations. This study presents the first comprehensive functional map of histone H3 lysines in a mammalian system, establishing a broadly applicable platform for dissecting histone modifications with advanced precision.
  • 🔗 查看原文

8. GSE330204 毕赤酵母 GS115 基因组上的 H3K36me3 富集

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:genome
  • 📝 描述:Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Komagataella phaffii GS115The goal of the study was to examine the the histone modification mark H3K36me3 occupancy in the ORF regions of K. phaffii.
  • 🔗 查看原文

9. GSE329959 真核生物染色质调控状态的多样性和演化 [ChIP-Seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:ChIP-seq
  • 📝 描述:Contributors : Arnau Sebe-Pedros ; Cristina Navarrete ; Sean A MontgomerySeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Acanthamoeba castellanii ; Arabidopsis thaliana ; Bigelowiella natans ; Creolimax fragrantissima ; Dictyostelium discoideum ; Guillardia theta ; Naegleria gruberi ; Nematostella vectensis ; Physcomitrium patens ; Saccharomyces cerevisiae ; Spizellomyces punctatus ; Tetrahymena thermophilaHistone post-translational modifications (hPTMs) are key regulators of chromatin states, influencing gene expression, epigenetic memory, and transposable element repression across eukaryotic genomes. While many hPTMs are evolutionarily conserved, the extent to which the chromatin states they define are similarly preserved remains unclear. Here, we developed a combinatorial indexing ChIP-seq method to simultaneously profile specific hPTMs across diverse eukaryotic lineages, including amoebozoans, rhizarians, discobans, and cryptomonads. Our analyses revealed highly conserved euchromatin states at active gene promoters and gene bodies. In contrast, we observed diverse configurations of repressive heterochromatin states associated with silenced genes and transposable elements, characterized by various combinations of hPTMs such as H3K9me3, H3K27me3 and/or different H3K79 methylations. These findings suggest that while core hPTMs are ancient and broadly conserved, their functional readout has diversified throughout eukaryotic evolution, shaping lineage-specific chromatin landscapes.
  • 🔗 查看原文

10. GSE329625 帕金森病患者腹侧黑质的深度细胞图谱揭示了其与胰岛素抵抗的遗传和分子重叠

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:resistance
  • 📝 描述:Contributors : Viola Volpato ; David Menassa ; Preethi Sheshadri ; Stefania Giussani ; Michal Rokicki ; Lucia Cardo ; Marirena Bafaloukou ; Ann-Kathryn Schalkamp ; Agata Zaremba ; Jimena Monzón-Sandoval ; Ngoc-Nga Vinh ; Joanne Morgan ; Michele Hu ; Scott Miners ; Richard Wade-Martins ; Cynthia Sandor ; Laura Parkkinen ; Caleb WebberSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensParkinson’s disease (PD) is a complex neurodegenerative disorder characterised by selective neuronal loss. We integrate deep full-length single-nuclei sequencing of the human substantia nigra with novel genome-wide association studies (GWAS) identifying genetic and cellular drivers of PD. Genetic risk converges on AGTR1+ dopaminergic neurons and perineuronal oligodendrocytes (pODCs), both reduced in PD, as well as oligodendrocyte precursor cells, enriched among disease-disrupted intercellular interactions. AGTR1+ neurons represent a metabolically stressed state, characterised by renin-angiotensin system (RAS) and MAPK activation, oxidative stress, and mitochondrial dysfunction, rather than a distinct subtype. AGTR1+ neurons and pODCs link PD risk to metabolic traits; in pODCs, this association reflects insulin resistance with downregulated PI3K–AKT signalling.
  • 🔗 查看原文

💡 该来源还有 6 条内容,详见 文末

🧪 博客更新 (1条)

详细内容(全部1条)

1.在一项惊人的研究中,科学家利用年轻的肠道细菌逆转了肝脏衰老。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:aging、bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
  • 📝 描述:Rebooting the gut microbiome with bacteria from youth may help stop aging-related liver damage and even prevent liver cancer, according to new research in mice. Older mice that received their own preserved youthful microbiome showed less inflammation, reduced DNA damage, and no signs of liver cancer. Researchers also found that the treatment suppressed a cancer-linked gene called MDM2, making older mice biologically resemble younger ones.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
histone3
RNA-seq2
immune2
ChIP-seq2
cancer2
single-cell2
RNAseq1
genome1
Neuronal1
epigenome1
inflammation1
resistance1
metabolic1
metabolomics1
sequencing1
lymphoma1
scRNA1
aging1
bacteria1
regex:bacter(iaial

📎 更多内容

🧬 数据前沿 其他内容 (6条)

📅 报告生成时间:2026-05-10 22:07
🤖 由 GitHub Actions 自动生成