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1. ⭐ GSE290033 体外方法论证明小鼠训练免疫的五个步骤：对生物标志物发现、适应性免疫反应、小鼠品系、样本冷冻保存和基因消融的影响 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、RNA-seq
• 📝 描述：Contributors : Maria Gonzalez-Perez ; Jana Baranda ; Leticia Perez-Rodriguez ; Patricia Conde ; Carlos de la Calle-Fabregat ; Marcos J Berges Buxeda ; Alexander Dimitrov ; Javier Arranz ; Sergio Rius-Rocabert ; Alessia Zotta ; Ana Dopazo ; Nikita Poddar ; Xuedi Wang ; Estanislao Nistal-Villán ; Raphaël Duivenvoorden ; Joren Madsen ; David L Williams ; Dan Hasson ; Daniel Ojalvo-Lozano ; Florent Ginhoux ; Luke A.J. O’Neill ; Jordi OchandoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTrained immunity is defined by increased inflammatory cytokine production by macrophages that are sequentially activated by two stimuli, separated by a resting period. The models used to study trained immunity should reflect the definition of this process, which includes five different steps. Here, we developed an in vitro methodology to study trained immunity using murine bone marrow-derived macrophages (BMDM), following sequential stimulation with β-glucan and lipopolysaccharide (LPS). Kinetic analysis of cytokine production demonstrated, for the first time, that trained BMDM secrete high levels of tumor necrosis factor (TNF) and interleukin 6 (IL6) following stimulation with β-glucan (stimulus 1), compared to unstimulated BMDM (step 1). After a resting period, trained BMDM do not secrete significant levels of these cytokines (step 2), but rapidly produce enhanced levels of TNF and IL6 after secondary stimulation with LPS (stimulus 2), compared to BMDM stimulated with either β-glucan (step 3) or LPS (step 4) alone. In addition, the sum of cytokine levels produced by both BMDM stimulated with either β-glucan (stimulus 1) or LPS (stimulus 2) individually, was significantly lower than the cytokine levels produced by trained BMDM stimulated with both β-glucan and LPS (stimulus 1+2) (step 5). Our findings also demonstrate that trained BMDM produce higher levels of serum amyloid A3 (SAA3) protein due to metabolic and epigenetic reprogramming. Functionally, trained BMDM upregulate the expression of stimulatory molecules such as MHC-II, CD80, CD86, OX40L and PDL1; downregulate the inhibitory molecules ICOSL and CD206; and induce CD4+ and CD8+ T cell proliferation in vitro through a cell contact-dependent mechanism. Our results also revealed strain-specific differences in the training response among mice, the negative impact of cell cryopreservation on trained immunity, and the potential use of genetically modified mice in elucidating mechanisti…
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2. ⭐ GSE290032 体外方法论证明小鼠训练免疫的五个步骤：对生物标志物发现、适应性免疫反应、小鼠品系、样本冷冻保存和基因消融的影响 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、ATAC-seq
• 📝 描述：Contributors : Maria Gonzalez-Perez ; Jana Baranda ; Leticia Perez-Rodriguez ; Patricia Conde ; Carlos de la Calle-Fabregat ; Marcos J Berges Buxeda ; Alexander Dimitrov ; Javier Arranz ; Sergio Rius-Rocabert ; Alessia Zotta ; Ana Dopazo ; Nikita Poddar ; Xuedi Wang ; Estanislao Nistal-Villán ; Raphaël Duivenvoorden ; Joren Madsen ; David L. Williams ; Dan Hasson ; Daniel Ojalvo-Lozano ; Florent Ginhoux ; Luke A.J. O’Neill ; Jordi OchandoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTrained immunity is defined by increased inflammatory cytokine production by macrophages that are sequentially activated by two stimuli, separated by a resting period. The models used to study trained immunity should reflect the definition of this process, which includes five different steps. Here, we developed an in vitro methodology to study trained immunity using murine bone marrow-derived macrophages (BMDM), following sequential stimulation with β-glucan and lipopolysaccharide (LPS). Kinetic analysis of cytokine production demonstrated, for the first time, that trained BMDM secrete high levels of tumor necrosis factor (TNF) and interleukin 6 (IL6) following stimulation with β-glucan (stimulus 1), compared to unstimulated BMDM (step 1). After a resting period, trained BMDM do not secrete significant levels of these cytokines (step 2), but rapidly produce enhanced levels of TNF and IL6 after secondary stimulation with LPS (stimulus 2), compared to BMDM stimulated with either β-glucan (step 3) or LPS (step 4) alone. In addition, the sum of cytokine levels produced by both BMDM stimulated with either β-glucan (stimulus 1) or LPS (stimulus 2) individually, was significantly lower than the cytokine levels produced by trained BMDM stimulated with both β-glucan and LPS (stimulus 1+2) (step 5). Our findings also demonstrate that trained BMDM produce higher levels of serum amyloid A3 (SAA3) protein due to metabolic and epigenetic reprogramming. Functionally, trained BMDM upregulate the expression of stimulatory molecules such as MHC-II, CD80, CD86, OX40L and PDL1; downregulate the inhibitory molecules ICOSL and CD206; and induce CD4+ and CD8+ T cell proliferation in vitro through a cell contact-dependent mechanism. Our results also revealed strain-specific differences in the training response among mice, the negative impact of cell cryopreservation on trained immunity, and the potential use of genetically modified mice in elucida…
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3. ⭐ GSE315077 KDM5蛋白介导卵巢癌的顺铂耐药性。[ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、resistance、ChIP-seq
• 📝 描述：Contributors : Jung Yoo ; So Hee KwonSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensHigh recurrence and relapse rates of ovarian cancer (OVC) make it one of the deadliest gynecological cancers and the 5th most common cause of death in women. It is well recognized that acquired resistance is accompanied by abnormal alteration of epigenetic regulation, yet there is a lack of in-depth mechanistic study on cisplatin-resistant OVC in epigenetic context. Herein, we investigate the role of lysine lysine demethylase 5 (KDM5) and how its abnormal overexpression correlates with cisplatin resistance and OVC tumor progression.
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4. GSE303973：利用 snATAC 测序技术对衰老小鼠心脏进行测序，以研究单细胞水平的染色质重塑。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、sequencing
• 📝 描述：Contributors : Michail Yekelchyk ; Julian Wagner ; Kathrin StilzSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTo study chromatin remodelig of the aging mouse heart, hearts from young and gaed mice were taken and nuclei were isolated via FACS. SnATAC Seq was performed using the 10X Genomics kit. Michail Yekelchyk (AG Braun) analysed the data)
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5. GSE242274 单细胞测序揭示颅外动静脉畸形中转录细胞谱系异质性

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Yi Sun ; Ren CaiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensExtracranial arteriovenous malformations (eAVMs) are rare congenital vascular anomalies consisting of abnormal artery-vein bypass with no intervening capillary network and can lead to disability and death. In this study, an integration of two cutting-edge technologies, single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST), was applied to uncover the underlying pathophysiology of eAVMs. Patient-matched eAVM tissue samples and normal tissue control data were analyzed. We identified different cell states of endothelial cells (ECs), perivascular cells and immune cells in eAVMs and characterized their spatial distributions with multiple immunofluorescence staining (mIF), immunostaining and spatial transcriptomics. Dysregulated cell-to-cell interactions among ECs, perivascular cells and immune cells that are associated with disease progression were cataloged. By performing scRNA-seq on 117,360 individual cells, we identified 14 transcriptomically defined cell lineages from eAVMs. We uncovered the presence of MAFB+ nidus ECs. Moreover, mesenchymal activation was observed in ECs, characterized by high expression of POSTN or FN1 and the upregulation of the NOTCH and TGF-β pathways. mIF and ST verified the location of MAFB+ nidus ECs and mesenchymal activation of eAVM ECs. We identified transcriptional variation within perivascular cells and the presence of smooth muscle–like pericytes in eAVMs. Ligand‒receptor-based cell‒cell interaction analysis indicated that Nd ECs might specifically communicate with perivascular cells through the MDK, VEGF, SEMA3 and ANGPT pathways, and this cellular crosstalk was supported by colocalization analysis of spatial transcriptomics. In addition, we found that hypoxia plays an important role in the development of eAVMs, and hyperbaric oxygen therapy (HBOT) was used to treat one large pelvic eAVM. Thus, correcting the hypoxic microenvironment could be a promising therapeutic strategy.
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6. GSE313975 表观遗传可塑性是大西洋鳉鱼可遗传污染耐受性的驱动因素 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、epigenetic
• 📝 描述：Contributors : Mathia Colwell ; Melissa K. Drown ; Nicole Flack ; Carrie Walls ; Christopher Faulk ; Samantha Carrothers ; Emma Weeks ; Caren WeinhouseSeries Type : Expression profiling by high throughput sequencingOrganism : Fundulus heteroclitusHeritable epigenetic adaptation to environmental stressors is a compelling but highly contested possibility. Previously, we showed evidence of a generationally heritable epigenetic memory at the cytochrome P450 1A (CYP1A) gene in wild Atlantic killifish (Fundulus heteroclitus) with evolved tolerance to PAH. This memory leads to blunted induction of CYP1A by PAH; this blunting that protects against polycyclic aromatic hydrocarbon (PAH)-induced cancer. Here, using Oxford Nanopore long-read sequencing in PAH-tolerant and sensitive wild-type embryos, we show that genome-wide, PAH-tolerant embryos showed reduced plasticity in DNA methylation response to PAH vs. PAH sensitive embryos that was not due to mutational loss of CpG sites. Notably, we observed population differences in gene methylation in pathways linked to the PAH tolerance phenotype, including AHR and voltage-gated potassium channel signaling, as well as developmental processes and energy metabolism. Specifically, we observed PAH-induced loss of CYP1A gene body methylation in PAH-sensitive (86% CpG methylation in control, decreased to 63% in exposed), but not -tolerant (84% control, 86% exposed), embryos. We observed similar patterns at CYP1B, CYP1C, and the aryl hydrocarbon receptor repressor, AHRR, which show similarly blunted expression. This genic methylation loss was correlated with decreased levels of natural anti-sense RNA transcripts in cis (cis-NATs), which may regulate transcription of these genes. Our data support the existence of stable epigenetic responses to chronic environmental stressors in a natural experimental setting, with broad implications for natural or directed adaptation strategies for other populations.
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7. GSE313974 表观遗传可塑性是大西洋鳉鱼可遗传污染耐受性的驱动因素 [ONT 长读测序；DNA]

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、epigenetic
• 📝 描述：Contributors : Mathia Colwell ; Melissa K. Drown ; Nicole Flack ; Carrie Walls ; Christopher Faulk ; Samantha Carrothers ; Emma Weeks ; Caren WeinhouseSeries Type : OtherOrganism : Fundulus heteroclitusHeritable epigenetic adaptation to environmental stressors is a compelling but highly contested possibility. Previously, we showed evidence of a generationally heritable epigenetic memory at the cytochrome P450 1A (CYP1A) gene in wild Atlantic killifish (Fundulus heteroclitus) with evolved tolerance to PAH. This memory leads to blunted induction of CYP1A by PAH; this blunting that protects against polycyclic aromatic hydrocarbon (PAH)-induced cancer. Here, using Oxford Nanopore long-read sequencing in PAH-tolerant and sensitive wild-type embryos, we show that genome-wide, PAH-tolerant embryos showed reduced plasticity in DNA methylation response to PAH vs. PAH sensitive embryos that was not due to mutational loss of CpG sites. Notably, we observed population differences in gene methylation in pathways linked to the PAH tolerance phenotype, including AHR and voltage-gated potassium channel signaling, as well as developmental processes and energy metabolism. Specifically, we observed PAH-induced loss of CYP1A gene body methylation in PAH-sensitive (86% CpG methylation in control, decreased to 63% in exposed), but not -tolerant (84% control, 86% exposed), embryos. We observed similar patterns at CYP1B, CYP1C, and the aryl hydrocarbon receptor repressor, AHRR, which show similarly blunted expression. This genic methylation loss was correlated with decreased levels of natural anti-sense RNA transcripts in cis (cis-NATs), which may regulate transcription of these genes. Our data support the existence of stable epigenetic responses to chronic environmental stressors in a natural experimental setting, with broad implications for natural or directed adaptation strategies for other populations.
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8. GSE291162 人源化小鼠模型中癌睾丸抗原BORIS发育沉默不完全会促进癌症易感性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、antigen
• 📝 描述：Contributors : Emma Price ; Victor LobanenkovSeries Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Mus musculusCancer-testis antigens are genes normally restricted to the germline but aberrantly activated in many cancers, where their role in tumorigenesis remains unclear. BORIS (CTCFL), a testis-specific paralog of the chromatin organizer CTCF, is one such antigen that shows limited conservation between humans and mice, complicating in vivo functional studies. Here, we generated humanized mice in which both alleles of the endogenous Boris locus are replaced with the full-length human BORIS gene, including its highly diverged cis-regulatory elements. These fully humanized mice maintain normal fertility, indicating accurate germline expression and preserved BORIS function despite evolutionary divergence. However, unlike the strictly testis-specific expression of mouse Boris, human BORIS escapes complete somatic silencing, producing mosaic expression in a minority of mouse somatic cells. This ectopic expression is associated with reduced survival, increased tumor incidence and a shift of tumor spectrum toward aggressive lymphomas. Transcriptomic and chromatin profiling revealed that ectopic human BORIS reactivates testes-specific genes in the soma, including regulators of meiosis and DNA repair, through direct chromatin binding. This transcriptional reprogramming was consistent across tissues and clonal cell lines, revealing a dominant tissue-independent gene activation program. These findings demonstrate that when human BORIS escapes epigenetic silencing in somatic cells, it connects aberrant germline gene activation with increased cancer susceptibility in vivo.
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9. GSE303738 在血管免疫母细胞性 T 细胞淋巴瘤 (AITL) 小鼠模型中鉴定出肿瘤性 Tfh 样细胞亚群

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymphoma、T cell
• 📝 描述：Contributors : Saba Mohammaei ; Antoine Bouchard ; Woong-Kyung SuhSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusNodal T-follicular helper cell lymphoma, angioimmunoblastic type (nTFHL-AI, or AITL), is an aggressive peripheral T cell lymphoma without effective treatments. It has been shown that genetic and epigenetic changes lead to the expansion of neoplastic CD4+ T cells originating from T follicular helper (Tfh) cells, which subsequently cause B cell expansion and tumor. However, it remains unclear if the Tfh-like cell populations contain a subset that drive tumor progression and, if so, whether such a subset may have druggable targets. Using a mouse model of AITL driven by heterozygous sanroque mutation (Roquinsan/+), we identified a tumor-enriched Tfh cell subset highly expressing CXCR6 and IL-18 receptor, termed “Double-Expressor (DE) Tfh” cells. DE Tfh cells also expressed higher levels of enhancer of zeste homolog 2 (EZH2). In vitro data indicated that IL-18 and EZH2 are required for the proliferation of DE Tfh cells. Furthermore, DE Tfh cells have a potent capacity to expand B cells when adoptively transferred to lymphopenic recipients. On the other hand, depletion of DE Tfh cells via Ezh2 gene deletion, inhibition of EZH2 (using FDA-approved drug, tazemetostat), or anti-CXCR6 mAb led to tumor regression. These findings may be relevant to a subset of AITL cases since we found that ~20-30% of AITL patient samples have concomittantly elevated expression of CXCR6, IL-18R1, and IFNG. Thus, our study identified a pathogenic Tfh-like subset essential for AITL tumor progression in a mouse model and suggests that identifying and targeting DE Tfh-like subset in AITL patients might be an effective strategy.
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10. GSE315815 KLHDC4 是一种新型预后生物标志物，可通过 PI3K/AKT 信号通路驱动透明细胞肾细胞癌的肿瘤进展。

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、carcinoma
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : HomoThe clinical significance and molecular mechanisms of KLHDC4 in malignancies, particularly in clear cell renal cell carcinoma (ccRCC), remain poorly understood. In this study, we integrated multi-omics data—including tran-scriptomic, proteomic, and single-cell RNA sequencing—to systematically evaluate the clinical relevance and func-tional role of KLHDC4, followed by experimental validation. Our results demonstrated that KLHDC4 is significantly upregulated in multiple cancer types and serves as an independent prognostic biomarker for poor survival in ccRCC. KLHDC4 expression was correlated with immune cell infiltration, tumor mutational profiles, and immune check-point expression. Furthermore, KLHDC4 levels predicted response to drug therapies, including immunotherapy and tyrosine kinase inhibitors. Functional experiments showed that KLHDC4 knockdown suppressed proliferation, mi-gration, and invasion in vitro, as well as tumor growth in vivo, whereas its overexpression promoted malignant phenotypes. Mechanistic investigations through RNA sequencing and Western blot analysis indicated that KLHDC4 activates the PI3K/AKT signaling pathway. Rescue assays confirmed that KLHDC4-driven oncogenic effects are partially mediated through this axis. Additionally, molecular docking identified ledipasvir as a potential KLHDC4 inhibitor. Collectively, our findings establish KLHDC4 as a novel prognostic biomarker and therapeutic predictor, highlighting the KLHDC4/PI3K/AKT axis as a potential target for ccRCC treatment.
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1. ⭐ SPLISOSM——利用空间转录组学数据绘制异构体及其调控机制图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Using RNA sequencing with spatial resolution, SPLISOSM maps isoform-specific patterns in brain and tumor tissues, revealing conserved splicing regulation and links to neurological disease…
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2. CONCORD——揭示单细胞数据集中一致的细胞状态图谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：CONCORD unifies batch correction and denoising to reveal coherent cell-state landscapes from RNA sequencing data, enabling high-resolution comparison of single-cell datasets across experiments and species…
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3. 仅仅10分钟的运动就能引发强大的抗癌效果

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A brief, intense workout may do more than boost fitness—it could help fight cancer. Researchers found that just 10 minutes of hard exercise releases molecules into the bloodstream that switch on DNA repair and shut down cancer growth signals. When these molecules were applied to bowel cancer cells, hundreds of cancer-related genes changed activity. The discovery helps explain how exercise lowers cancer risk and hints at future therapies inspired by movement.
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• GSE315687 抗CD4耗竭抗体通过激活CD8+ T细胞和抑制调节性T细胞在小鼠肺纤维化中发挥抗肿瘤作用
• GSE308920 AKPS转移性结肠癌模型的单细胞RNA测序
• GSE303889 KDM5 蛋白介导卵巢癌的顺铂耐药性。
• GSE222430：七氟烷暴露后老年小鼠转录组的10倍单细胞测序
• GSE315770：在固体琼脂平板上，于PD（100 mM NaCl）条件下对野生型秀丽隐杆线虫进行RNA-seq分析
• GSE315766 RNA-seq 分析秀丽隐杆线虫中低钾和 pmk-1 调控基因
• GSE315765 RNA-Seq 分析 Mapk14 敲除和 C2C12 细胞成肌分化
• GSE310159 蜕皮激素介导的肠道生长促进营养不良条件下微生物群驱动的发育可塑性
• GSE303574 ZBTB16抑制后HUVEC细胞的批量ATAC测序
• GSE287976 人类嗜碱性粒细胞单细胞组学分析揭示了两个转录组不同的细胞群
• GSE315788 β3-肾上腺素能受体下调导致肥胖症中脂肪细胞儿茶酚胺抵抗
• GSE315411 双线捕鱼：一种空间转录组发现的混合方法
• GSE312325 Grin2b 突变小鼠的异常 mRNA 剪接和海马神经发生受损 [RNAseq]
• GSE295012 糖蛋白非转移性黑色素瘤蛋白B (GPNMB) 的缺失会加剧感染挑战期间内皮细胞的通透性、代谢和存活率
• GSE268636 雄激素受体剪接变体表达与挽救治疗后前列腺癌复发
• GSE315860 DAXX 控制小鼠精子发生过程中 LINE1 的沉默 [ChIP-seq]
• GSE315521 乳酸介导的 KRT15 和 GPR68 之间的相互作用驱动 ECRSwNP 中的 2 型免疫。
• GSE315518 达芙妮汀通过调节DDIT3相关的应激反应，增强肝细胞癌细胞对化疗药物的敏感性并抑制恶性表型
• GSE312105 评估表观遗传抑制剂对转移性类器官向非转移性类器官染色质结构逆转的影响
• GSE285789 前列腺癌中 TGF-β 诱导的 M2 极化 TAM 来源的外泌体 miRNA 的作用和机制。
• GSE283937 高 MAPK、低 WNT 细胞状态驱动结直肠癌转移扩散
• GSE283935 转移性结直肠癌肿瘤中 MAPK 和 Wnt 信号通路的差异富集
• GSE252763 人类鼻腔气道上皮细胞培养物的 RNA 测序（对照组和结节病组）