详细内容（前10条）

1. ⭐ GSE338249 睡莲花器官发生的时空转录组图谱揭示了被子植物新性状的进化起源 [空间转录组学]

• ✍️ 作者：未知作者
• 🏷️ 关键词：spatial、spatial transcriptomics、transcriptome、transcriptomics
• 📝 描述：Contributors : Chang Liu ; Ge Wang ; Binbin Cao ; Yonglong Li ; Yamao Chen ; Chunce Guo ; Ji QiSeries Type : OtherOrganism : Nymphaea colorataPetals are a key evolutionary innovation of flowers that reshaped plant-pollinator interactions and underlie the dominance of angiosperms in terrestrial ecosystems, yet their evolutionary origin remains debated as the morphological inferences rarely connect directly to the regulatory programs inferred from extant flowering plants. We employed spatial transcriptome sequencing on serial floral buds of the basal angiosperm Nymphaea colorata, producing a spatiotemporal atlas of cell states during primordium initiation and the subsequent formation of tepals (sepals and petals), stamens and carpels. Our analyses identified multiple meristematic cell populations organized hierarchically at the floral base, with one population give rise to both initiating petals (or inner tepals) and stamens whereas a second population forms carpel primordia. Developmental trajectory reconstruction based on thousands of tissue-preferentially expressed genes uncovers a continuous fate transition from stamen primordia via developing stamens to inner tepals undergoing morphogenesis. Quantitative modeling of MADS-box tetramer composition reveals dosage-sensitive shifts that support the hypothesis that petaloid organs evolved from sterile stamens at the outer whorls. Trajectory modules further show stepwise incorporation of vegetative programs, particularly genes for polarity establishment and photosynthetic essential for leaf development into petal organogenesis. These findings support a model in which petal merger occurred through quantitative retuning and redeployment of ancestral regulatory networks that predate the origin of angiosperms, providing clues for understanding the evolutionary innovation and diversification of petaloid organs across flowering plants.
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2. ⭐ GSE302435 溴结构域抑制剂可预防神经鞘瘤对靶向激酶抑制剂产生耐药性 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：kinase、resistance、ChIP-seq
• 📝 描述：Contributors : Christina Fernandez-Valle ; Haley HardinSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensNeurofibromatosis type 2 (NF2) is an inherited disorder that promotes tumor growth on nerves throughout the nervous system. NF2 affects around 1 in 33,000 individuals worldwide and is caused by loss of function of the merlin tumor suppressor encoded by the NF2 gene. Tumor control early in life is critical for maintaining quality of life. Currently, treatments available for NF2-associated tumors are surgery and radiation therapy. Off-label use of cancer drugs are being tried, as there are no Food and Drug Administration (FDA)-approved drug therapies for NF2. As a member of the SYNODOS for NF2 consortium, we performed unbiased drug combination screening using schwannoma model cell lines. We identified a BRD4 and a PAK inhibitor that acted in concert to selectively slow growth of a human schwannoma line compared to its merlin-expressing parental line. BRD4 is a member of the BET family of bromodomain containing proteins that bind acetylated lysine in transcription regulatory proteins to alter gene expression. BRD proteins contribute to development of resistance to cancer drugs. Follow-up studies confirmed the drugs’ interaction in multiple mouse and human schwannoma lines. We will extend this research by assessing the ability of BRD4 inhibitors in combination with multiple PAK, PI3K, MEK, and FAK inhibitors, some of which are in NF2 clinical trials (selumetinib, crizotinib, brigatinib, trametinib) to reduce the viability of schwannoma lines. We will measure whether the combinations provide long-lasting inhibition of cell proliferation, induce cell death, and block compensatory escape pathways that often arise when cells are treated with a single kinase inhibitor. We will use an established mouse xenograft model to test the effectiveness of the best performing in vitro drug combination. Mechanisms of action studies will complete the preclinical evaluation of the advanced drug combination in a representative cell line. Our proposed study is timely because the results will indicate whether drug resistance could develop for several of the kinase inhibitors in ongoing NF2 clinical trials. Moreover, the results could indicate whether BRD4 inhibitors could serve as an adjuvant therapy to prevent drug resistance. By assessing the RNAome and methylome of single and dual treated human schwannoma cells, we will uncov…
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3. ⭐ GSE302434 溴结构域抑制剂可预防神经鞘瘤对靶向激酶抑制剂产生耐药性 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：kinase、resistance、RNA-seq
• 📝 描述：Contributors : Christina Fernandez-Valle ; Haley Hardin ; Anna NagelSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensNeurofibromatosis type 2 (NF2) is an inherited disorder that promotes tumor growth on nerves throughout the nervous system. NF2 affects around 1 in 33,000 individuals worldwide and is caused by loss of function of the merlin tumor suppressor encoded by the NF2 gene. Tumor control early in life is critical for maintaining quality of life. Currently, treatments available for NF2-associated tumors are surgery and radiation therapy. Off-label use of cancer drugs are being tried, as there are no Food and Drug Administration (FDA)-approved drug therapies for NF2. As a member of the SYNODOS for NF2 consortium, we performed unbiased drug combination screening using schwannoma model cell lines. We identified a BRD4 and a PAK inhibitor that acted in concert to selectively slow growth of a human schwannoma line compared to its merlin-expressing parental line. BRD4 is a member of the BET family of bromodomain containing proteins that bind acetylated lysine in transcription regulatory proteins to alter gene expression. BRD proteins contribute to development of resistance to cancer drugs. Follow-up studies confirmed the drugs’ interaction in multiple mouse and human schwannoma lines. We will extend this research by assessing the ability of BRD4 inhibitors in combination with multiple PAK, PI3K, MEK, and FAK inhibitors, some of which are in NF2 clinical trials (selumetinib, crizotinib, brigatinib, trametinib) to reduce the viability of schwannoma lines. We will measure whether the combinations provide long-lasting inhibition of cell proliferation, induce cell death, and block compensatory escape pathways that often arise when cells are treated with a single kinase inhibitor. We will use an established mouse xenograft model to test the effectiveness of the best performing in vitro drug combination. Mechanisms of action studies will complete the preclinical evaluation of the advanced drug combination in a representative cell line. Our proposed study is timely because the results will indicate whether drug resistance could develop for several of the kinase inhibitors in ongoing NF2 clinical trials. Moreover, the results could indicate whether BRD4 inhibitors could serve as an adjuvant therapy to prevent drug resistance. By assessing the RNAome and methylome of single and dual treated human schwannoma cells, we will uncove…
• 🔗 查看原文

4. GSE338068 全基因组 RRBS 甲基化谱分析发现 NLRP7 启动子高甲基化与单纯性大疱性表皮松解症的疾病严重程度相关

• ✍️ 作者：未知作者
• 🏷️ 关键词：genome、methylation
• 📝 描述：Contributors : Lubna Khair ; Ofer Sarig ; Rawaa Ishtewy ; Yoni Moskovitz ; Kiril Malovitski ; Angi Zenab ; Thomas Kocher ; Julia Hummel ; Josefina Hofbauer ; May Arad ; Eylon Sharoni ; Naama Adam ; Ben Avshalom ; Ulrich Koller ; Verena Wally ; Liat Samuelov ; Eli SprecherSeries Type : Methylation profiling by high throughput sequencingOrganism : Homo sapiensReduced representation bisulfite sequencing (RRBS) was performed to investigate DNA methylation profiles in patients with epidermolysis bullosa (EB) exhibiting variable disease severity. Differential methylation analysis identified a differentially methylated region within the NLRP7 promoter and first exon. The dataset provides genome-wide DNA methylation profiles generated from peripheral blood leukocyte DNA and is intended to facilitate studies of epigenetic mechanisms associated with EBS disease severity.
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5. GSE338036 睡莲花器官发生的时空转录组图谱揭示了被子植物新性状的进化起源 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、transcriptome
• 📝 描述：Contributors : Chang Liu ; Ge Wang ; Binbin Cao ; Yonglong Li ; Yamao Chen ; Chunce Guo ; Ji QiSeries Type : Expression profiling by high throughput sequencingOrganism : Nymphaea colorataPetals are a key evolutionary innovation of flowers that reshaped plant-pollinator interactions and underlie the dominance of angiosperms in terrestrial ecosystems, yet their evolutionary origin remains debated as the morphological inferences rarely connect directly to the regulatory programs inferred from extant flowering plants. We employed spatial transcriptome sequencing on serial floral buds of the basal angiosperm Nymphaea colorata, producing a spatiotemporal atlas of cell states during primordium initiation and the subsequent formation of tepals (sepals and petals), stamens and carpels. Our analyses identified multiple meristematic cell populations organized hierarchically at the floral base, with one population give rise to both initiating petals (or inner tepals) and stamens whereas a second population forms carpel primordia. Developmental trajectory reconstruction based on thousands of tissue-preferentially expressed genes uncovers a continuous fate transition from stamen primordia via developing stamens to inner tepals undergoing morphogenesis. Quantitative modeling of MADS-box tetramer composition reveals dosage-sensitive shifts that support the hypothesis that petaloid organs evolved from sterile stamens at the outer whorls. Trajectory modules further show stepwise incorporation of vegetative programs, particularly genes for polarity establishment and photosynthetic essential for leaf development into petal organogenesis. These findings support a model in which petal merger occurred through quantitative retuning and redeployment of ancestral regulatory networks that predate the origin of angiosperms, providing clues for understanding the evolutionary innovation and diversification of petaloid organs across flowering plants.
• 🔗 查看原文

6. GSE328364 miR-142 的 Canonical 和 isomiR 产物增强树突状细胞重编程 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：dendritic cell、ATAC-seq
• 📝 描述：Contributors : Nejc Arh ; Ilia Kurochkin ; Beatriz Lourenço Vaz ; Carlos-Filipe PereiraSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensMicroRNAs (miRNAs) regulate gene expression and generate isoforms (isomiRs) with distinct targeting properties, but their roles in cellular specification and reprogramming remain poorly understood. Here, we investigated miRNAs and isomiRs during direct reprogramming to conventional type 1 dendritic cells (cDC1s), identifying miR-124 and miR-142 as facilitators of the process. The canonical miR-124-3p strand induced a permissive chromatin landscape enriched for cooperative transcription factor motifs, thereby transiently increasing reprogramming efficiency. In contrast, miR-142 enhanced lineage fidelity by repressing fibroblast identity and activating cDC1-specific programs through cooperating isomiRs that drove XCR1 expression and increased type III interferon production. In addition, miR-142 mimics enhanced cancer cell reprogramming and anti-tumor immunity in vivo. Finally, we developed RNA-based cDC1 reprogramming using transcription factor mRNAs combined with miRNA mimics. Together, these findings uncover miRNA isoform diversity as a programmable regulatory layer in immune cell specification and establish RNA-driven reprogramming as a non-viral strategy for cancer immunotherapy.
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7. GSE324642 miR-142 的经典和异构体 miR 产物增强树突状细胞重编程 [bulk RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：dendritic cell、RNA-seq
• 📝 描述：Contributors : Nejc Arh ; Ilia Kurochkin ; Beatriz Lourenço Vaz ; Carlos-Filipe PereiraSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMicroRNAs (miRNAs) regulate gene expression and generate isoforms (isomiRs) with distinct targeting properties, but their roles in cellular specification and reprogramming remain poorly understood. Here, we investigated miRNAs and isomiRs during direct reprogramming to conventional type 1 dendritic cells (cDC1s), identifying miR-124 and miR-142 as facilitators of the process. The canonical miR-124-3p strand induced a permissive chromatin landscape enriched for cooperative transcription factor motifs, thereby transiently increasing reprogramming efficiency. In contrast, miR-142 enhanced lineage fidelity by repressing fibroblast identity and activating cDC1-specific programs through cooperating isomiRs that drove XCR1 expression and increased type III interferon production. In addition, miR-142 mimics enhanced cancer cell reprogramming and anti-tumor immunity in vivo. Finally, we developed RNA-based cDC1 reprogramming using transcription factor mRNAs combined with miRNA mimics. Together, these findings uncover miRNA isoform diversity as a programmable regulatory layer in immune cell specification and establish RNA-driven reprogramming as a non-viral strategy for cancer immunotherapy.
• 🔗 查看原文

8. GSE311882 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [scRNA_MYOD1]

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、transcriptomics
• 📝 描述：Contributors : Rosa De Santis ; Lorenzo Vaccaro ; Davide CacchiarelliSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPredicting the pathogenic effect of rare genetic variants is hampered by the limited cohort of diagnosed patients and the difficulty in evaluating the effect of existing and novel variants. To address this issue, we leveraged a protein Multiplexed Assay of Variants Effect (MAVE) to functionally assess the effect of ~2,300 missense variants of the TP63 gene, some of which cause autosomal dominant developmental disorders. The activity of each variant was measured using an optimized fibroblast-to-keratinocyte conversion protocol, and a subset of mutants was validated using a wide range of functional tests. To expand MAVEs to any disease-driving gene without a specific predefined assay, we developed SCRAMseq (Single Cell RNAseq Associated with MAVEs by sequencing), which can retrieve each variant and characterize the functional consequences at the single-cell level through full-length scRNAseq. The dataset generated and validated here reclassified hundreds of variants present in the general population and definitively classified a Variant of Unknown Significance as pathogenic in a patient with ectodermal dysplasia. This work provides a robust and easy-to-use workflow to dissect the effect of gene variants for any possible disease-driving gene.
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9. GSE311881 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [scRNA_P63noconv]

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、transcriptomics
• 📝 描述：Contributors : Rosa De Santis ; Lorenzo Vaccaro ; Davide CacchiarelliSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPredicting the pathogenic effect of rare genetic variants is hampered by the limited cohort of diagnosed patients and the difficulty in evaluating the effect of existing and novel variants. To address this issue, we leveraged a protein Multiplexed Assay of Variants Effect (MAVE) to functionally assess the effect of ~2,300 missense variants of the TP63 gene, some of which cause autosomal dominant developmental disorders. The activity of each variant was measured using an optimized fibroblast-to-keratinocyte conversion protocol, and a subset of mutants was validated using a wide range of functional tests. To expand MAVEs to any disease-driving gene without a specific predefined assay, we developed SCRAMseq (Single Cell RNAseq Associated with MAVEs by sequencing), which can retrieve each variant and characterize the functional consequences at the single-cell level through full-length scRNAseq. The dataset generated and validated here reclassified hundreds of variants present in the general population and definitively classified a Variant of Unknown Significance as pathogenic in a patient with ectodermal dysplasia. This work provides a robust and easy-to-use workflow to dissect the effect of gene variants for any possible disease-driving gene.
• 🔗 查看原文

10. GSE311880 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [scRNA_P63conv]

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、transcriptomics
• 📝 描述：Contributors : Rosa De Santis ; Lorenzo Vaccaro ; Davide CacchiarelliSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPredicting the pathogenic effect of rare genetic variants is hampered by the limited cohort of diagnosed patients and the difficulty in evaluating the effect of existing and novel variants. To address this issue, we leveraged a protein Multiplexed Assay of Variants Effect (MAVE) to functionally assess the effect of ~2,300 missense variants of the TP63 gene, some of which cause autosomal dominant developmental disorders. The activity of each variant was measured using an optimized fibroblast-to-keratinocyte conversion protocol, and a subset of mutants was validated using a wide range of functional tests. To expand MAVEs to any disease-driving gene without a specific predefined assay, we developed SCRAMseq (Single Cell RNAseq Associated with MAVEs by sequencing), which can retrieve each variant and characterize the functional consequences at the single-cell level through full-length scRNAseq. The dataset generated and validated here reclassified hundreds of variants present in the general population and definitively classified a Variant of Unknown Significance as pathogenic in a patient with ectodermal dysplasia. This work provides a robust and easy-to-use workflow to dissect the effect of gene variants for any possible disease-driving gene.
• 🔗 查看原文

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详细内容（全部3条）

1. 这种蛙源细菌只需单次注射即可清除小鼠体内的癌性肿瘤。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:bacter(ia|ial|ium)
• 📝 描述：A naturally occurring bacterium from amphibian intestines completely eliminated colorectal tumors in mice with a single treatment by both attacking cancer cells and activating the immune system. The findings point to a promising new type of cancer therapy that could one day work against many solid tumors.
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2. 一种隐藏的免疫备份系统可能增强mRNA癌症疫苗的效力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Researchers found that mRNA cancer vaccines can recruit an unexpected immune cell to launch powerful tumor-fighting responses, overturning a long-held assumption about how the vaccines work. The discovery could lead to more effective cancer vaccines and help scientists tailor treatments for better patient outcomes.
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3. QutRNA2——基于纳米孔直接tRNA测序的稳健tRNA修饰发现方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing with QutRNA2 enables faster, more accurate detection of transfer RNA modifications from direct Nanopore sequencing, supporting large scale studies of RNA biology…
• 🔗 查看原文

• GSE311879 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [RNAseq_P63noconv]
• GSE311878 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [RNAseq_MYOD]
• GSE311877 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [RNAseq_mutants]
• GSE311876 基因型-表型单细胞转录组学用于大规模并行评估遗传变异 [MITE_SAM]
• GSE311874 基因型-表型单细胞转录组学用于大规模并行评估遗传变异
• GSE338167 甲基化时钟不能预测遗传混合个体的年龄或阿尔茨海默病风险
• GSE333876 人类 Tr1 细胞的表观遗传景观、关键转录调控因子和体内鉴定 [ATAC-seq]
• GSE333496 人类 Tr1 细胞的表观遗传景观、关键转录调控因子和体内鉴定 [RNA-Seq]
• GSE337810 衰老过程中鳉鱼视网膜-RPE的批量RNA测序
• GSE302409 脑脊液动态单细胞图谱揭示隐球菌性脑膜炎期间的免疫抑制状态
• GSE238011 ApoE-/- 小鼠和 MSC_ITGB3 处理的 ApoE-/- 小鼠主动脉细胞的单细胞 RNA 测序
• GSE330047 CRISPR/Cas9介导的IMR32神经母细胞瘤细胞中PHOX2B功能敲除通过离子通道基因失调损害神经元兴奋性
• GSE328357 miR-142 的经典和异构体 miR 产物增强树突状细胞重编程 [lenti_hairpins]
• GSE322812 miR-142 的经典和异构体 miR 产物增强树突状细胞重编程 [smRNA]
• GSE321699 miR-142 的 Canonical 和 isomiR 产物增强树突状细胞重编程 [Cut&Tag]
• GSE317727 异双功能蛋白结合剂通过细胞内富集实现细胞类型特异性杀伤
• GSE338229 研究发现，奈非那韦联合顺铂可通过 caspase-8/caspase-3/GSDME 通路诱导铂耐药卵巢癌细胞发生裂解性细胞死亡。
• GSE333877 人类Tr1细胞的表观遗传图谱、关键转录调控因子和体内鉴定
• GSE313296 SHIP1 是 T 细胞监视隐匿性恶性肿瘤所必需的
• GSE261033 人类 Tr1 细胞的表观遗传景观、关键转录调控因子和体内鉴定 [scMultiome]
• GSE337807 扩展 ASXL1 突变谱：遗传性 ASXL1 错义突变导致过度生长表型的转录组和代谢失调
• GSE337671 胸腺-卵巢轴失调促进虚拟记忆T细胞极化，从而加剧多囊卵巢综合征的病理
• GSE299993 神经软骨素 (NCDN) 缺失和对照 U251 胶质母细胞瘤细胞的转录组学分析
• GSE338314 跨平台转录组数据中细胞类型反卷积的基准测试 [Visium]
• GSE312785 脾脏 IgG1 或 IgM 浆细胞的 RNA-seq 分析
• GSE312596 生发中心来源脾脏IgG1或IgM浆细胞的RNA测序分析