详细内容（前10条）

1. ⭐ GSE250385 空间转录组学揭示OP患者肺组织的功能区室化

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Ying Tang ; Cuilin Chu ; Siyuan Bu ; Qin Sun ; Airan Liu ; Lingyan Huang ; Hongmei WangSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensTo characterize the spatial characteristics of the lung tissue of OP patient, we collected lung samples for Visium CytAssist from one patient with OP
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2. GSE288402 NELF 可阻止癌细胞 DNA 复制区发生广泛的转录延伸 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ChIP-seq
• 📝 描述：Contributors : Nakayama Chihiro ; Daigaku Yasukazu ; Aoi Yuki ; Fang Qi ; Kimura Hiroshi ; Shilatifard Ali ; Tellier Michael ; Nojima TakayukiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRegulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is rewired in cancer to promote uncontrolled growth. Here, we find that gene expression of NELFCD, a known negative elongation factor, is up-regulated in colorectal tumours. To dissect the direct role of NELF-C on Pol II transcription in such cancer, we employed an auxin-dependent protein degradation system for NELF-C in combination with nascent transcript sequencing technologies. Strikingly, we demonstrate that the acute loss of NELF-C protein globally redistributes termination factors and perturbs Pol II transcription termination. These changes drive pervasive Pol II transcription into DNA replication zones leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. Our findings reveal a previously unrecognised role of NELF in transcription termination and highlight NELF as a potential therapeutic target in colorectal cancer.
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3. GSE253012 NELF 可阻止癌细胞 DNA 复制区发生广泛的转录延伸 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Chihiro Nakayama ; Yasukazu Daigaku ; Yuki Aoi ; Qi Fang ; Hiroshi Kimura ; Ali Shilatifard ; Michael Tellier ; Takayuki NojimaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRegulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is rewired in cancer to promote uncontrolled growth. Here, we find that gene expression of NELFCD, a known negative elongation factor, is up-regulated in colorectal tumours. To dissect the direct role of NELF-C on Pol II transcription in such cancer, we employed an auxin-dependent protein degradation system for NELF-C in combination with nascent transcript sequencing technologies. Strikingly, we demonstrate that the acute loss of NELF-C protein globally redistributes termination factors and perturbs Pol II transcription termination. These changes drive pervasive Pol II transcription into DNA replication zones leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. Our findings reveal a previously unrecognised role of NELF in transcription termination and highlight NELF as a potential therapeutic target in colorectal cancer.
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4. GSE253011 NELF 可阻止癌细胞 DNA 复制区发生广泛的转录延伸 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq
• 📝 描述：Contributors : Chihiro Nakayama ; Yasukazu Daigaku ; Yuki Aoi ; Qi Fang ; Hiroshi Kimura ; Ali Shilatifard ; Michael Tellier ; Takayuki NojimaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensRegulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is rewired in cancer to promote uncontrolled growth. Here, we find that gene expression of NELFCD, a known negative elongation factor, is up-regulated in colorectal tumours. To dissect the direct role of NELF-C on Pol II transcription in such cancer, we employed an auxin-dependent protein degradation system for NELF-C in combination with nascent transcript sequencing technologies. Strikingly, we demonstrate that the acute loss of NELF-C protein globally redistributes termination factors and perturbs Pol II transcription termination. These changes drive pervasive Pol II transcription into DNA replication zones leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. Our findings reveal a previously unrecognised role of NELF in transcription termination and highlight NELF as a potential therapeutic target in colorectal cancer.
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5. GSE313240 是来自 Alb-WT Bicd2fl/fl 和 Alb-Cre Bicd2fl/fl 小鼠（经 S-100 诱导的自身免疫性肝炎模型）肝脏免疫细胞的单细胞 RNA 测序数据。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、scRNA
• 📝 描述：Contributors : Wenyu Tian ; Weixuan Wang ; Dan LvSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo determine the changes in liver immune cells upon hepatic Bicd2 deficiency, we performed scRNA-seq to analyze the hepatic immune microenvironment in Alb-WT Bicd2fl/fl and Alb-Cre Bicd2fl/fl mice subjected to S-100 induced AIH model.
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6. GSE313194 柠檬酸肠衣菌及其相关肠道微生物群物种通过产生生物活性小分子来调节霍乱弧菌生物膜的形成

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：Contributor : Antunes L CaetanoSeries Type : Expression profiling by high throughput sequencingOrganism : Vibrio cholerae C6706Cholera is a deadly diarrheal disease that affects millions of people globally. Although V. cholerae, the causative agent of the disease, has been extensively studied in isolation, it was relatively recently that scientists started investigating its interactions with the gut microbiota. Our group and others previously showed that microbiota-derived metabolites significantly influence V. cholerae behavior. By investigating how an organic extract of human feces affects V. cholerae gene expression, we recently showed that gut metabolites strongly suppress swimming motility, a virulence factor important for host colonization. Interestingly, extracts of pure cultures of a single gut commensal, Enterocloster citroniae, recapitulated this inhibitory effect. Here, we present a comprehensive examination of the effect of small molecules produced by E. citroniae and related species on V. cholerae behavior. We show that E. citroniae small molecules inhibit motility by various V. cholerae strains. We also show that several phylogenetically related species produce this activity, although the magnitude of the effect varies between strains. Using biofilm formation assays in static and shear flow conditions, we show that V. cholerae strongly induces biofilm formation in response to E. citroniae metabolites. Transcriptome and reporter analyses show that several genes involved in the synthesis of an extracellular polysaccharide are induced by growth in the presence of E. citroniae metabolites. Lastly, we show that V. cholerae interactions with host epithelial cells are also modulated by compounds produced by this commensal. These findings advance our understanding of microbiome-pathogen interactions and how commensal bacteria influence V. cholerae virulence through the production of small molecules. In the future, this knowledge may be used to design novel microbiome-based therapeutic approaches to combat cholera and other infections.
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7. GSE313132 炎症诱导的lncRNA SNHG1通过IL-17A信号通路调控非梗阻性无精子症中的精原细胞发育

• ✍️ 作者：未知作者
• 🏷️ 关键词：inflammation、pathway
• 📝 描述：Contributors : Yongtong Zhu ; Maocai Li ; Xiaomin Zhan ; Li Liu ; Cairong Chen ; Yao Zhou ; Pei He ; Rui HuaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusNon-obstructive azoospermia (NOA) is a critical subtype of male infertility associated with inflammation. However, the molecular mechanisms underlying this phenomenon remain poorly understood. This study investigated the role of the inflammation-activated long non-coding RNA SNHG1 in NOA pathogenesis. Using lipopolysaccharide (LPS)-induced orchitis mouse models and spermatogonium cell lines (GC-1 spg and TCAM-2), we observed that both SNHG1 and the transcription factor SP1 were significantly upregulated, correlating with spermatogonium proliferation and loss of stemness. Mechanistically, SP1 directly binds to and transcriptionally activates the SNHG1 promoter, whereas SNHG1 knockdown rescued LPS-induced spermatogonium dysfunction without affecting SP1 expression. RNA-seq revealed that SNHG1 overexpression activated the IL-17A signaling pathway. Notably, IL-17A receptor blockade (Brodalumab) reversed the SNHG1-mediated proliferation arrest and stemness. Our findings demonstrated that the SP1-SNHG1-IL-17A axis drives inflammatory spermatogenic failure, suggesting that IL-17A inhibition is a potential therapeutic strategy for NOA.
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8. GSE255449 PAPOLA介导的poly(A)延长在白血病中的功能和机制[RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、RNA-seq
• 📝 描述：Contributors : Siyao Guo ; Shuibin LinSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe polyadenylation of mRNA is pivotal for mRNA stability and efficient mRNA translation. The length of poly(A) tail is dynamically changed under various physiological conditions; however, the functions and mechanisms of aberrant poly(A) length control in cancers remain poorly understood. Here we uncovered the aberrant lengthening of poly(A) tail and particularly upregulated expression of poly(A) polymerase alpha (PAPOLA) in acute myeloid leukemia (AML), and the elevated PAPOLA expression significantly correlated with unfavorable AML outcomes. We further demonstrated the critical oncogenic functions of PAPOLA-mediated poly(A) lengthening in promoting AML leukemogenesis and leukemia stem cell self-renewal using human primary AML samples, AML cells and various mouse leukemogenesis models. Mechanistically, we identified GSTM2 as a key downstream target of PAPOLA that regulated metabolic reprogramming through the HNE-DLD axis to promote AML initiation and progression. Moreover, PAPOLA inhibitor cordycepin effectively blocked metabolic reprogramming and AML leukemogenesis in vivo. Overall, our study uncovers the novel functional link between aberrant poly(A) lengthening and cellular metabolic reprogramming in AML, and provides a molecular basis for development of an effective therapeutic strategy for AML patients.
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9. GSE294329 单细胞 RNA 测序揭示增生性玻璃体视网膜病变膜中成纤维细胞的异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Contributors : Fengjuan Gao ; Yuqiao Ju ; Lili Zhang ; Ting Zhang ; Qing Chang ; Shunxiang Gao ; Xin Huang ; Yuan Zong ; Gezhi XuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensProliferative vitreoretinopathy (PVR) is a vision-threatening fibrotic disorder characterized by pathological membrane formation, yet its cellular and molecular mechanisms remain incompletely understood. Here, we employed single-cell RNA sequencing (scRNA-seq) to profile 18,213 cells from 5 human PVR membranes (PVRMs), uncovering cellular heterogeneity and novel pathogenic pathways.
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10. GSE287936 DNA甲基化和lncRNA表达控制印记基因区域的异步DNA复制

• ✍️ 作者：未知作者
• 🏷️ 关键词：methylation
• 📝 描述：Contributors : Yui Imaizumi ; Robert Feil ; Jean-Charles CadoretSeries Type : Genome variation profiling by genome tiling arrayOrganism : Mus musculusEukaryotic genomes are structured in zones that replicate predominantly early or late. Besides these genome-wide patterns of replication timing (RT), some genes display asynchronous replication between the two alleles in certain stem cells, brought about by stochastic processes and genetic polymorphisms. To what extent epigenetic modifications control asynchronous replication remains unclear. As a paradigm to address this question we explored imprinted chromosomal domains, at which parental DNA methylation imprints mediate parental allele-specific gene expression. Our genome-wide and locus-specific RT assays in mono-parental and hybrid mouse embryonic stem cells (mESCs) reveal a pronounced replication asynchrony between the parental chromosomes at the Dlk1-Dio3 and Snrpn domains. This asynchrony is strictly parent-of-origin dependent. By generating a range of mutant mESC lines, we find that the replication asynchrony at Dlk1-Dio3 is mediated by parental allele-specific methylation at DMRs (Differentially Methylated Regions). Moreover, lncRNA polycistron expression controls early replication across parts of the domain on the maternal chromosome. As a result, at these imprinted domains, RT domains become unlinked from 3D chromatin architecture as assayed by Hi-C. Our combined data highlight how parental DNA methylation imprints and lncRNA expression can locally be used to override intrinsic RT domain organization.
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💡 该来源还有 11 条内容，详见 文末

• GSE254009 NELF 可阻止癌细胞 DNA 复制区发生广泛的转录延伸 [TT-seq]
• GSE253121 NELF 可阻止癌细胞 DNA 复制区发生广泛的转录延伸。
• GSE253120 NELF 可阻止癌细胞 DNA 复制区发生广泛的转录延伸 [POINT-seq]
• GSE298740 生物制剂治疗的 T2 高危重症哮喘患者的转录组学：抗 IgE、抗 IL-5 和抗 IL-5R 靶向治疗的比较。
• GSE294022 人类子宫浆液性癌细胞和肿瘤对 CTX-439 的反应
• GSE313231 RNA-seq 数据来自接受 S-100 诱导的自身免疫性肝炎 (AIH) 模型处理的 Alb-WT Bicd2fl/fl 和 Alb-Cre Bicd2fl/fl 小鼠的肝组织。
• GSE308896 癌细胞通过胶原蛋白丝中包含的microRNA转移侵袭性
• GSE294315 PAPOLA介导的poly(A)延长在白血病（小鼠）中的功能和机制
• GSE255668 PAPOLA介导的poly(A)延长在白血病中的功能和机制
• GSE255667 PAPOLA介导的poly(A)延长在白血病中的功能和机制[FLAM-Seq]
• GSE255603 PAPOLA介导的poly(A)延长在白血病中的功能和机制[RIP-Seq]