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1. ⭐ GSE307853 利用测序 (ATAC-Seq) 对大麦 CI 16151 和感染白粉病真菌 (Blumeria hordei (Bh)；分离株 5874) 的快中子衍生免疫缺陷突变体进行转座酶可及染色质分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、sequencing、ATAC-seq
• 📝 描述：Contributors : Valeria Velasquez-Zapata ; Gregory Fuerst ; Roger P WiseSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Hordeum vulgareTranscriptional reprogramming is a key component of disease resistance. MLA (mildew locus a), is an immune receptor that interacts with several transcription factors (TFs), and thus, represents a model to explore regulatory architecture during defense. To characterize chromatin accessibility of barley during powdery mildew infection, a series of isogenic mutant genotypes and timepoints were subjected to ATAC sequencing. We designed our study around two diverse genes in host immunity, mildew locus a (Mla6), a nucleotide binding leucine-rich repeat (NLR) immune receptor, and the Blufensin1 (Bln1) basal defense regulator, which influence immunity in a resistance (R)-gene dependent and R-gene independent manner, respectively. In addition to the CI 16151 resistant progenitor (Mla6, Bln1), three mutants were utilized: the susceptible mla6-m18982, the resistant bln1-m19089, and the susceptible double mutant (mla6+bln1)-m19028 (Chapman et al., 2021; Velásquez-Zapata et al., 2024). Four infection timepoints (0, 16, 20, 32 HAI) were taken to sample across key pathogen life cycle events such as appressorial penetration and haustorial development. Validation of the ATAC-Seq dataset was performed using the correlation with gene expression profiles from RNA-Seq data; by checking the presence of epistatic events at the chromatin level, phenomenon that was recently described using RNA-Seq (Velásquez-Zapata et al., 2024).
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2. ⭐ GSE326101 微卫星稳定型转移性结直肠癌化疗免疫治疗反应的空间预测因子

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)、spatial
• 📝 描述：Contributors : Joan Choo ; Joseph J Zhao ; Mai Chan Lau ; Raghav Sundar ; Filippo PietrantonioSeries Type : OtherOrganism : Homo sapiensMicrosatellite-stable (MSS) colorectal cancers (CRC) are largely unresponsive to immune checkpoint inhibition (ICI). The MAYA trial used temozolomide (TMZ) in MGMT-silenced MSS mCRC, hypothesizing that TMZ-induced hypermutation could sensitize tumors to ICI; the primary endpoint was met, showing durable responses with TMZ plus ipilimumab and nivolumab. We perform integrated spatial, transcriptomic, and immune profiling of longitudinal tumor and blood samples from patients treated on the MAYA trial. Post-TMZ increases in tumor mutational burden associate with improved progression-free survival. Spatial profiling demonstrates that clinical benefit is greatest in permissive tumor microenvironments. Responders exhibit enrichment of cytotoxic T cells across tumor and stromal compartments, whereas non-responders display heterogeneous cellular neighborhoods, with fibroblasts in close spatial proximity to T cells, consistent with barriers to immune mediated clearance. Longitudinal peripheral immune profiling shows that early upregulation of TIGIT and PD-1 following TMZ exposure predicts resistance. Together, these findings indicate that both mutational evolution and spatial immune architecture contribute to immune sensitization in MGMT-silenced MSS CRC.
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3. GSE325221 SLC38A5依赖性谷氨酰胺代谢导致的氧化还原适应受损，促进了褪黑素介导的骨癌细胞凋亡敏感性和转移抑制

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、metabolism
• 📝 描述：Contributors : Bao-Tran Nguyen ; Chih-Hsin TangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMalignant bone cancer, including osteosarcoma and chondrosarcoma as popular subtypes, are aggressive neoplasms which arise from bone tissue and have lung metastasis. Tumor cells evade anoikis through reactive oxygen species (ROS)-mediated redox homeostasis, which modulates signaling cascades that promote proliferation, survival, and metastatic invasion into distant sites. Melatonin, synthesized primarily by the pineal gland, has been implicated in cancer prevention and therapy due to its inhibitory effects on bone cancer growth and progression. Little is known about the mechanisms underlying anoikis resistance in bone cancer cells or whether melatonin can therapeutically modulate this process. We demonstrated that glutamine metabolism is essential for bone cancer cells to maintain anoikis resistance. Melatonin treatment disrupted glutamine metabolism and altered redox homeostasis, as evidenced by increased ROS accumulation and reduced NADPH/NADP⁺ ratios under anchorage-independent conditions. Notably, solute carrier family 38 member 5 (SLC38A5), a glutamine transporter, was identified as a critical regulator of bone cancer progression, with higher SLC38A5 expression correlating with poorer clinical outcomes. Melatonin suppressed SLC38A5 expression and attenuated anoikis resistance through inhibition of the PI3K-Akt signaling pathway. Consistently, reduced SLC38A5 expression was associated with decreased lung metastasis in melatonin-treated groups in an orthotopic mouse model. Collectively, our findings reveal a previously unrecognized role of melatonin in modulating glutamine-dependent redox balance and anoikis resistance in bone cancer. This study highlights SLC38A5-mediated glutamine metabolism as a critical determinant of metastatic potential and supports melatonin and SLC38A5 as promising therapeutic targets for osteosarcoma and chondrosarcoma.
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4. GSE297781 DNMT1 缺失导致 DNMT3A 对一部分晚期复制结构域进行过度甲基化（组蛋白 ChIP-seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、histone
• 📝 描述：Contributor : Duncan SproulSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensLoss of DNA methylation is a hallmark of cancer that is proposed to promote carcinogenesis through gene expression alterations, retrotransposon activation and induction of genomic instability. Cancer-associated hypomethylation does not occur across the whole genome but leads to the formation of partially methylated domains (PMDs). However, the mechanisms underpinning PMD formation remain unclear. PMDs replicate late in S-phase leading to the proposal that they become hypomethylated due to incomplete re-methylation by the maintenance methyltransferase DNMT1 during cell division. Here we investigate the role of DNMT1 in the formation of PMDs in cancer by conducting whole genome bisulfite sequencing (WGBS), repli-seq and ChIP-seq on DNMT1 knockout HCT116 colorectal cancer cells (DNMT1 KO cells). We find that DNMT1 loss leads to preferential hypomethylation in late replicating, heterochromatic PMDs marked by the constitutive heterochromatic mark H3K9me3 or the facultative heterochromatic mark H3K27me3. However, we also observe that a subset of H3K9me3-marked PMDs gain methylation in DNMT1 KO cells. We find that, in DNMT1 KO cells, these hypermethylated PMDs remain late replicating but gain DNMT3A localisation. This is accompanied by loss of heterochromatic H3K9me3 and specific gain of euchromatic H3K36me2. Our observations suggest that hypermethylated PMDs lose their heterochromatic state, enabling their methylation by DNMT3A and the establishment of a hypermethylated, non-PMD state, despite their late replication timing. More generally, our findings suggest that the de novo DNMTs play a key role in establishing domain level DNA methylation patterns in cancer cells.
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5. GSE319934 CCL信号通路驱动小鼠结肠中慢性克氏锥虫感染期间的T细胞-巨噬细胞相互作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：T cell、macrophage
• 📝 描述：Contributors : Erica Silberstein ; Spyros Karaiskos ; Nikki Tirrell ; Charles C Chung ; Supriya Kumar ; Jung-Sun Cho ; Alain DebrabantSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChagas disease, caused by the protozoan Trypanosoma cruzi, is a chronic infection characterized by low levels of parasite persistence in tissues such as the heart, gastrointestinal tract, and skeletal muscle. The mechanisms underlying digestive Chagas disease (DCD), particularly within the colon, remain incompletely defined. To characterize the immune landscape during chronic infection, we used a murine model of DCD and performed single-cell RNA sequencing of colonic lamina propria cells. Immune profiling revealed infiltration of T cells, B cells, and macrophages, with T cells representing the predominant immune population in the chronically infected colon. Computational cell–cell communication analysis predicted activation of chemokine signaling pathways, including the CCL5–CCR5 axis, mediating interactions between CD8+ T cells and macrophages. Processed single-cell gene expression matrices and associated metadata are provided in this submission
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6. GSE293201 异位 MYC 表达重编程表观遗传景观和转录因子网络，从而驱动 AML 中的分化阻滞和恶性转化 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ATAC-seq、epigenetic
• 📝 描述：Contributors : David Dominguez-Sola ; Eirini Papapetrou ; Saul CarcamoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensOverexpression of MYC is a common convergent consequence of genetic driver mutations in acute myeloid leukemia (AML). However, despite extensive research, the mechanisms by which this proto-oncogene promotes leukemogenesis remain incompletely understood. Here, we developed models of deregulated MYC expression in human pluripotent stem cell (hPSC)-derived myelopoiesis. We show that MYC overexpression from the endogenous locus maintaining physiological regulation is insufficient for leukemogenesis. Rather, constitutive MYC overexpression from ectopic alleles is necessary for driving and sustaining leukemia-associated phenotypes. These phenotypes depend on the widespread disruption of epigenetic landscapes imposed by MYC overexpression, which in turn underlies a differentiation arrest and dysregulation of the BACH1 transcription factor network, identified here as a mediator of these changes. Our findings shed new light into the mechanisms underlying MYC-induced malignant transformation and leukemogenesis, suggesting novel therapeutic targets for AML.
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7. GSE293056 异位 MYC 表达重编程表观遗传景观和转录因子网络，从而驱动 AML 中的分化阻滞和恶性转化 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、epigenetic
• 📝 描述：Contributors : David Dominguez-Sola ; Eirini Papapetrou ; Saul CarcamoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensOverexpression of MYC is a common convergent consequence of genetic driver mutations in acute myeloid leukemia (AML). However, despite extensive research, the mechanisms by which this proto-oncogene promotes leukemogenesis remain incompletely understood. Here, we developed models of deregulated MYC expression in human pluripotent stem cell (hPSC)-derived myelopoiesis. We show that MYC overexpression from the endogenous locus maintaining physiological regulation is insufficient for leukemogenesis. Rather, constitutive MYC overexpression from ectopic alleles is necessary for driving and sustaining leukemia-associated phenotypes. These phenotypes depend on the widespread disruption of epigenetic landscapes imposed by MYC overexpression, which in turn underlies a differentiation arrest and dysregulation of the BACH1 transcription factor network, identified here as a mediator of these changes. Our findings shed new light into the mechanisms underlying MYC-induced malignant transformation and leukemogenesis, suggesting novel therapeutic targets for AML.
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8. GSE211070 多重增强简化代表性亚硫酸氢盐测序 (mERRBS) 分析成人骨髓增生异常综合征 (MDS)/急性髓系白血病 (AML) 伴孤立性 7 号染色体单体与对照组的比较

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、sequencing
• 📝 描述：Contributors : Cristina Mecucci ; Anair G Lema Fernandez ; Carlotta NardelliSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensMonosomy 7 is one of the most frequent aneuploidies in myeloid malignancies, associated to heterogeneous phenotypes. Its poor prognosis differentiates it from aberrations leading to partial/complete loss of 7q region. Underlying pathogenic mechanisms are still undetermined. We performed a comprehensive epi-genomic study of karyotypically isolated monosomy 7 in adult Myelodysplastic Syndromes/Acute Myeloid Leukemias.
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9. GSE211032 表达分析（RNA-Seq）成人骨髓增生异常综合征（MDS）/急性髓系白血病（AML）伴孤立性7号染色体单体与对照组的比较

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、RNA-seq
• 📝 描述：Contributors : Cristina Mecucci ; Anair G Lema Fernandez ; Carlotta NardelliSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMonosomy 7 is one of the most frequent aneuploidies in myeloid malignancies, associated to heterogeneous phenotypes. Its poor prognosis differentiates it from aberrations leading to partial/complete loss of 7q region. Underlying pathogenic mechanisms are still undetermined. We performed a comprehensive epi-genomic study of karyotypically isolated monosomy 7 in adult Myelodysplastic Syndromes/Acute Myeloid Leukemias.
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10. GSE325164 Kurarinone 通过调节小鼠肠道菌群-吲哚-3-乙醛-芳烃受体轴改善实验性自身免疫性脑脊髓炎

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：Contributors : Xinyan Han ; Jiaqi Ding ; Weitai He ; Xue Kang ; Cong Zhao ; Yi Li ; Di Wu ; Zonghao Pan ; Hongzeng Li ; Kaixi Ren ; Jiaji Lin ; Jun GuoSeries Type : OtherOrganism : metagenomeMultiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease primarily driven by Th17 and Th1 cells, and the gut microbiota is associated with MS onset and progression. Kurarinone (KU), a key component of the traditional Chinese medicine Radix Sophora Flavesvara, exhibits anti-inflammatory and immune-regulatory effects and can modulate the gut microbiota. However, it is unclear whether KU affects MS via a gut microbiota-mediated mechanism. Herein, we demonstrated that KU significantly alleviated experimental autoimmune encephalomyelitis (EAE), an animal model of MS, by modulating the gut microbiota, particularly by enriching Akkermansia muciniphila. The disease-alleviating effect of KU was achieved in a manner dependent on A. muciniphila. Meanwhile, KU significantly upregulated the tryptophan metabolite indole-3-acetaldehyde (IAAld). The IAAld content was positively correlated with the relative abundance of A. muciniphila and negatively with the severity of EAE in mice. In vitro, A. muciniphila alone could also facilitate the tryptophan metabolism to produce IAAld. Oral IAAld suppresses Th17 and Th1 differentiation to ameliorate EAE. In vitro, IAAld activates AhR and inhibits STAT3/STAT4 phosphorylation, thereby reducing Th17/Th1 differentiation. Collectively, this study identifies a novel mechanism by which KU ameliorates EAE via the gut microbiota-indole-3-acetaldehyde-AhR axis and unveils the potential therapeutic targets for MS.
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1. 前列腺癌细胞“图谱”为早期检测开辟了新途径

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：RNA sequencing combined with spatial analysis reveals early cellular changes and distinct cell states in prostate cancer, uncovering hidden disease progression and new targets for diagnosis…
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2. 科学家发现与新冠后遗症疲劳和症状相关的免疫细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Long COVID remains a frustrating medical mystery, affecting up to 1 in 10 people long after the initial infection fades. Now, scientists have uncovered a crucial clue hidden deep within the immune system. By analyzing individual immune cells, they identified a distinct molecular state in key white blood cells—especially common in patients who initially had mild or moderate COVID.
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• GSE310868 小鼠转移性乳腺癌细胞的批量 RNA 测序 TUBO
• GSE293125 DNA甲基化差异与女性生殖衰老相关
• GSE293085 淋巴细胞凋亡和17型免疫功能受损是DOCK8缺陷导致黏膜念珠菌病的基础，可通过IL-7免疫疗法挽救。
• GSE292970 空间组织数百万愈伤组织细胞，识别出能够促进番茄芽再生的核心网络 [RNA-Seq]
• GSE281581 转移性乳腺癌小鼠模型原发肿瘤和肺转移灶的单细胞RNA测序
• GSE281491 小鼠转移性乳腺癌细胞的批量 RNA 测序
• GSE281490 人类单细胞RNA测序：三个乳腺癌转移灶和三个正常乳腺组织
• GSE281489 MMTV-PyMT小鼠转移性乳腺癌模型肺转移灶的原位单细胞分析
• GSE281488 对 HER2+ 乳腺癌患者的脑转移瘤和 8 例 TNBC 患者的原发肿瘤进行原位单细胞分析。
• GSE281487 人类转移性乳腺癌细胞的批量 RNA 测序
• GSE276260 H2O2诱导的星形胶质细胞胶原蛋白触发缺血性中风中的神经元死亡[RNA-seq]
• GSE324927 合胞素-a 缺乏通过抑制 PRL/PGE2 和 PI3K/AKT/mTOR 通路损害小鼠精子功能
• GSE323311 人类巨噬细胞通过训练免疫编码先前暴露的刺激特异性信息
• GSE319745 DNMT1 缺失导致 DNMT3A 对一部分晚期复制结构域进行过度甲基化（RNA-seq）
• GSE311539 微生物组产生的烟酸控制结肠区域特性和损伤易感性（批量RNA测序）
• GSE310813 PWWP 突变体转录辅助因子 JASPer 改变启动子和增强子活性并抑制果蝇位置效应变异 [Hi-C]
• GSE310811 PWWP 突变体转录辅助因子 JASPer 改变启动子和增强子活性并抑制果蝇中的位置效应变异 [ChIP-Seq]
• GSE297779 DNMT1 缺失导致 DNMT3A 对一部分晚期复制结构域进行过度甲基化（H3K36me2 天然 ChIP-seq）
• GSE294435 转录延伸因子 SPT6 维持小鼠表皮稳态并抑制皮肤炎症
• GSE287897 SPT6 通过抑制 NF-κB 正反馈环路来维持表皮稳态，从而防止过度炎症反应。
• GSE254974 双重 RNA-seq 分析揭示了鱼类病原体鲑鱼立克次体 (Piscirickettsia salmonis) 的生物学特性
• GSE319667 Tet2 缺陷会改变 CD4+ T 细胞功能，并促进具有 TFH 细胞免疫表型的 T 细胞淋巴瘤。
• GSE281662 SARS-CoV-2 mRNA疫苗免疫小鼠骨髓单细胞水平基因表达谱
• GSE250125 横纹肌肉瘤转录组学研究：PAX3-FOXO1 与其他融合蛋白联合拯救后的转录组学分析
• GSE211048 Affymetrix SNP芯片数据，用于分析伴有孤立性7号染色体单体的成人骨髓增生异常综合征（MDS）/急性髓系白血病（AML）。
• GSE326056 CCR5 调控 DNA 损伤修复和乳腺癌干细胞扩增
• GSE325692 多组学分析揭示海湾战争综合征小鼠模型中，压力和毒物暴露导致脑血一致性和持续性神经免疫重编程 [RNA-Seq]
• GSE325684 多组学分析揭示海湾战争综合征小鼠模型中，压力和毒物暴露导致脑血一致性和持续性神经免疫重编程 [ATAC-seq]
• GSE325668 皮质酮处理后MCF-7细胞的转录组学
• GSE325667 皮质酮处理后4T1细胞的转录组学
• GSE325548 手术伤口的时间分辨转录组分析揭示了残余卵巢癌的阶段特异性治疗靶点
• GSE310201 小鼠 4T1 细胞 ETV4 KO 的批量 RNA 测序 [FGF]
• GSE310157 小鼠 4T1 细胞 ETV4 敲除的批量 RNA 测序
• GSE310156 人类MDA细胞ETV4敲除的批量RNA测序
• GSE310155 小鼠 4T1 细胞 FGFR2 敲除的批量 RNA 测序
• GSE300231 年龄相关基因表达改变对机械力和 TGFβ 信号的反应 [ATAC-seq]
• GSE293046 空间组织数百万愈伤组织细胞，识别出能够促进番茄芽再生的核心网络 [ncRNA-Seq]
• GSE281582 三个转移性患者来源类器官 (PDO) 的人类 ChIP-seq
• GSE281580 人类单细胞RNA测序，包括三例原发性乳腺癌和五例转移性乳腺癌
• GSE281492 乳腺癌转移细胞状态的分子特征
• GSE198803 雄性大鼠重复轻度创伤性脑损伤控制性皮质冲击模型后的小RNA测序
• GSE275852 耻垢分枝杆菌 mc2 155 中 napM 缺失菌株的转录组