详细内容（前10条）

1. ⭐ GSE311577 转录因子 NFE2 在调节急性髓系白血病中的氧化还原反应和化疗耐药性方面的新作用 [RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、RNA-seq
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusElevated activity of transcription factor NFE2 is sufficient to cause leukemic transformation in absence of a classical leukemic driver. However, the molecular mechanism promoting NFE2-driven leukemogenesis is not known. Here we report a previously unrecognized role for NFE2 as a key regulator of the oxidative stress response in leukemic cells. Through a comprehensive analysis of NFE2 genomic occupancy and its effect on chromatin accessibility and transcription, we demonstrate that NFE2 regulates glutathione homeostasis as well as the expression of central detoxifying enzymes. NFE2 constituted one of the highest scoring redox-dependencies in MLL-AF9-transformed primary leukemic cells, substantially more significant than the universally recognized redox regulator NRF2. Consequently, NFE2 knockdown sensitized leukemic cells to ferroptosis induction, GSH depletion as well as to cytarabine treatment. Deriving an NFE2 RedOx score, we demonstrate that increased NFE2 activity constitutes an independent predictor of inferior outcome in AML patients at diagnosis.
• 🔗 查看原文

2. ⭐ GSE311576 转录因子 NFE2 在调节急性髓系白血病中的氧化还原反应和化疗耐药性方面的新作用 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、ChIP-seq
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusElevated activity of transcription factor NFE2 is sufficient to cause leukemic transformation in absence of a classical leukemic driver. However, the molecular mechanism promoting NFE2-driven leukemogenesis is not known. Here we report a previously unrecognized role for NFE2 as a key regulator of the oxidative stress response in leukemic cells. Through a comprehensive analysis of NFE2 genomic occupancy and its effect on chromatin accessibility and transcription, we demonstrate that NFE2 regulates glutathione homeostasis as well as the expression of central detoxifying enzymes. NFE2 constituted one of the highest scoring redox-dependencies in MLL-AF9-transformed primary leukemic cells, substantially more significant than the universally recognized redox regulator NRF2. Consequently, NFE2 knockdown sensitized leukemic cells to ferroptosis induction, GSH depletion as well as to cytarabine treatment. Deriving an NFE2 RedOx score, we demonstrate that increased NFE2 activity constitutes an independent predictor of inferior outcome in AML patients at diagnosis.
• 🔗 查看原文

3. ⭐ GSE311575 转录因子 NFE2 在调节急性髓系白血病中的氧化还原反应和化疗耐药性方面的新作用 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、resistance、ATAC-seq
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusElevated activity of transcription factor NFE2 is sufficient to cause leukemic transformation in absence of a classical leukemic driver. However, the molecular mechanism promoting NFE2-driven leukemogenesis is not known. Here we report a previously unrecognized role for NFE2 as a key regulator of the oxidative stress response in leukemic cells. Through a comprehensive analysis of NFE2 genomic occupancy and its effect on chromatin accessibility and transcription, we demonstrate that NFE2 regulates glutathione homeostasis as well as the expression of central detoxifying enzymes. NFE2 constituted one of the highest scoring redox-dependencies in MLL-AF9-transformed primary leukemic cells, substantially more significant than the universally recognized redox regulator NRF2. Consequently, NFE2 knockdown sensitized leukemic cells to ferroptosis induction, GSH depletion as well as to cytarabine treatment. Deriving an NFE2 RedOx score, we demonstrate that increased NFE2 activity constitutes an independent predictor of inferior outcome in AML patients at diagnosis.
• 🔗 查看原文

4. ⭐ GSE320240 SUMO化缺失导致PRC1异常聚集和3D基因组重连，与H3K27me3无关 [Hi-C]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Hi-C、genome、clustering
• 📝 描述：Contributors : Nazli Akilli ; Paul-Swann Puel ; Marco Di Stefano ; Fernando Muzzopappa ; Lauriane Fritsch ; Fabian Erdel ; Daniel Jost ; Thierry Cheutin ; Giacomo CavalliSeries Type : OtherOrganism : Drosophila melanogasterPolycomb Repressive Complex 1 (PRC1) forms nuclear condensates that organize target chromatin domains. SUMOylation modulates PRC1 clustering, but its impact on condensate properties and 3D genome architecture remains unclear. Here, we show that depletion of SUMO in Drosophila wing imaginal discs transforms PRC1 condensates into large structures with reduced molecular dynamics. Strikingly, this biophysical reorganization occurs without global loss of the H3K27me3 mark. Instead, Hi-C reveals widespread rewiring of topologically associating domain (TAD) interactions. PRC1-bound TADs lose specific long-range contacts with each other while gaining ectopic interactions with active chromatin. These topological shifts correlate with gene misregulation independently of changes in canonical Polycomb histone modifications. Our results establish SUMOylation as a critical regulator of PRC1 condensates, demonstrating that post-translational control of biomolecular condensation dictates 3D genome architecture and transcriptional output through mechanisms separable from histone mark deposition.
• 🔗 查看原文

5. ⭐ GSE320239 SUMO化缺失导致PRC1异常聚集和3D基因组重连，与H3K27me3无关 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq、genome、clustering
• 📝 描述：Contributors : Nazli Akilli ; Paul-Swann Puel ; Marco Di Stefano ; Fernando Muzzopappa ; Lauriane Fritsch ; Fabian Erdel ; Daniel Jost ; Thierry Cheutin ; Giacomo CavalliSeries Type : Expression profiling by high throughput sequencingOrganism : Drosophila melanogasterPolycomb Repressive Complex 1 (PRC1) forms nuclear condensates that organize target chromatin domains. SUMOylation modulates PRC1 clustering, but its impact on condensate properties and 3D genome architecture remains unclear. Here, we show that depletion of SUMO in Drosophila wing imaginal discs transforms PRC1 condensates into large structures with reduced molecular dynamics. Strikingly, this biophysical reorganization occurs without global loss of the H3K27me3 mark. Instead, Hi-C reveals widespread rewiring of topologically associating domain (TAD) interactions. PRC1-bound TADs lose specific long-range contacts with each other while gaining ectopic interactions with active chromatin. These topological shifts correlate with gene misregulation independently of changes in canonical Polycomb histone modifications. Our results establish SUMOylation as a critical regulator of PRC1 condensates, demonstrating that post-translational control of biomolecular condensation dictates 3D genome architecture and transcriptional output through mechanisms separable from histone mark deposition.
• 🔗 查看原文

6. GSE343576 利用 ChIP-seq 对集胞藻 PCC 7942 中 NsrC 相关 DNA 区域进行全基因组定位

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、genome
• 📝 描述：Contributors : Li Wenzhe ; Liu Qian ; Fan Shoujin ; Chen Zhuo ; Zhang Jian ; Zhao GuoyanSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Synechococcus elongatus PCC 7942 = FACHB-805This study investigates the genome-wide DNA-binding profile of the small regulatory protein NsrC in Synechococcus elongatus PCC 7942. Chromatin immunoprecipitation sequencing was performed using a strain expressing NsrC fused to mNeonGreen and FLAG (D1339). Two biological ChIP replicates and their matched input controls were analyzed to identify NsrC-associated genomic regions and support evaluation of its role in regulating phycobilisome biosynthesis genes.
• 🔗 查看原文

7. GSE341214 多模态空间分析揭示了髓系定义的 ENKTL 亚群的不同特征以及肿瘤与髓系细胞在预后炎症微环境中的协同作用

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、spatial
• 📝 描述：Series Type : Other ; Expression profiling by arrayOrganism : Homo sapiensThis SuperSeries is composed of the SubSeries listed below.
• 🔗 查看原文

8. GSE343197 Alox15 抑制糖酵解以支持蠕虫免疫期间 M2 巨噬细胞的效应功能。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、macrophage
• 📝 描述：Contributors : Dovran Ovezgeldiyev ; Vanessa Trefzer ; Rory Doolan ; Mati Moyat ; Gillian Coakley ; Lakshanie Wickramasinghe ; Carmel Daunt ; Beatrice Volpe ; Fiona Henkel ; Alexander Serra ; Maike Hartmann ; Shirin Rezaei ; Niki Ubags ; Alana Butler ; Roxanne Chatzis ; Benjamin Marsland ; Adam A Smith ; Deanna D Lucas ; Erin McGowan ; Katrina Binger ; Malcolm McConville ; Julia Esser-von Bieren ; Nicola Harris ; Tiffany BoucherySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMacrophage polarization by type-2 cytokines is central to anti-helminth immunity and tissue repair. While some hallmark changes in macrophages are well-characterized and associated with protection against helminths, it is still unclear how macrophages exert their anti-helminth effects. In this context, we investigated Arachidonate 15-lipoxygenase (Alox15), a lipoxygenase well known for its role in macrophage polarization in the context of metabolic diseases, and a hallmark of type-2 macrophage (M2) human polarization. We show that in the absence of Alox15, M2 cannot trap and kill helminths. Surprisingly, expression of M2 markers was normal despite a loss of function. Instead, we found a concomitant increase in pro-inflammatory responses due to an uncontrolled activation of glycolysis. We further show that activation of Peroxisome proliferator-activated receptor-delta (PPAR-δ) by lipids downstream of Docosapentaenoic acid (DPA) can restore normal glycolysis control, highlighting a novel role of lipids in the fine-tuning of the metabolic support required for optimal macrophage polarization.
• 🔗 查看原文

9. GSE336330 组蛋白阅读器 MLLT1 和 MLLT3 的浓度赋予 AID 活性位点特异性 [ChIP-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq、histone
• 📝 描述：Contributors : Noé Seija ; Sophia Gannon ; Kíra A Häfner ; Tim M Gemeinhardt ; Jana Ridani ; Mélanie Provencher ; Poorani G Subramani ; Diego Alvarez ; Christian Poitras ; Eva-Maria Piskor ; Tarik Möröy ; Nicholas Vonniessen ; Bruce Mazer ; Marcelo A Navarrette ; Nicole Francis ; François Robert ; Javier M Di NoiaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusActivation-induced deaminase (AID) drives antibody diversification through class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin (Ig) genes, but its mutagenic activity at several hundred other genes and enhancers contributes to B cell lymphoma. Despite its physiological and pathological relevance, how AID selectively mutates the Ig and a restricted set of off-target genes is unknown. Transcription is required for AID activity, but most transcribed genes are not mutated, and AID occupies more loci than it mutates. Here, we identify the Super Elongation Complex (SEC) histone readers MLLT1 and MLLT3 as determinants of selective AID activity. Combined loss of MLLT1 and MLLT3 abolishes all AID-dependent processes, phenocopying AID deficiency. AID-mutated genomic regions are precisely marked by high MLLT1 and MLLT3 occupancy (MLLT1/3high) in mouse and human B cells, while nascent transcription remains largely unchanged in MLLT1- or MLLT3-deficient cells, indicating a direct role in licensing AID activity. Mechanistically, MLLT1 and MLLT3 are dispensable for global AID chromatin tethering but link AID to transcription elongation. In mice, both readers bind AID and are partially redundant, but MLLT1 plays a dominant role through its intrinsically disordered region, which promotes condensate formation and selectively concentrates AID. Fusing AID to MLLT1 or MLLT3 is sufficient to restore CSR and mutagenesis in SEC-deficient cells. These findings reveal how MLLT1/3high licenses AID at a restricted subset of genomic regions by spatially confining and concentrating its activity, likely through condensate-based mechanisms.
• 🔗 查看原文

10. GSE305876 组蛋白精氨酸去甲基酶 JMJD7 通过调节 α-酮戊二酸代谢促进骨形成

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、histone
• 📝 描述：Contributors : Re-Wen Wu ; Wei-Shiung Lian ; Yu-Han Lin ; Tu-Shan Chen ; Shao-Yu Wang ; Shin-Long Wu ; Mei-Yao Lin ; Holger Jahr ; Feng-Sheng WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHistone methylation plays a critical role in chromatin accessibility and transcription regulation, with implications for various disorders, including osteoporosis. Jumonji C domain-containing protein 7 (JMJD7) demethylates arginine (R) residues on histones, influencing tissue metabolism and integrity. However, its role in bone tissue remains uncharacterized. We have discovered JMJD7 loss in human osteoporotic bone biopsies, and neonatal osteoblast-specific Jmjd7 knockout mice exhibit delayed cranial suture closure and premature mortality. Adult female Jmjd7 knockout mice, but not males, develop a smaller stature with hallmark features of osteoporosis and visceral adiposity. Forced Jmjd7 expression mitigates estrogen deficiency-induced bone loss. Jmjd7 deletion alters the transcriptomic landscape and promotes the H3R2me1-enriched epigenome, particularly affecting cellular energy metabolism and suppressing osteogenic differentiation of bone marrow mesenchymal cells. Runx2 was, among others, a functional epigenomic target of Jmjd7. Mechanistically, Jmjd7 loss disrupts energy production by shifting towards anaerobic glycolysis at the expense of mitochondrial oxidative phosphorylation. This metabolic shift is mediated through inhibition of complex I activity and reduced production of isocitrate dehydrogenase (Idh) and its intermediate α-ketoglutarate (α-KG). Notably, α-KG supplementation reverses H3R2me1-dependent transcriptional repression and mitigates post-translational arginine methylation and ubiquitination of Idh and Runx2, counteracting Jmjd7 deletion-induced loss of mineralized matrix synthesis. Furthermore, α-KG supplementation improves osteogenic differentiation and bone formation, attenuating both Jmjd7 loss- and estrogen deficiency-induced osteoporosis. Taken together, Jmjd7 is indispensable for bone integrity, and its loss accelerates osteoporosis through epigenetic repression of α-KG production, affecting mitochondrial energy metabolism and Runx2 signaling. This study reveals a novel anabolic function of Jmjd7 in maintaining bone mass homeostasis and emphasizes the essential role of its cofactor α-KG in promoting bone health.
• 🔗 查看原文

💡 该来源还有 14 条内容，详见 文末

详细内容（全部2条）

1. 导致老年人关节疼痛加剧的常见错误

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Aging gradually wears down the cartilage and fluid that protect our joints, but avoiding movement may actually make matters worse. Exercise helps nourish cartilage, strengthens the muscles that protect joints, and can reduce osteoarthritis pain. Low-impact activities such as swimming, cycling, tai chi, yoga, and walking on varied terrain may also improve balance and mobility. Even a few minutes of the right kind of movement can make a difference.
• 🔗 查看原文

2. 一种鲜为人知的蛋白质可能正在加剧阿尔茨海默病——科学家们找到了阻断它的方法。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：An experimental Alzheimer’s compound prevented damaging protein clumps from forming in the brains of mice, helping nerve cells survive longer and reducing amyloid buildup. The treatment also appeared to improve heart health and slow some signs of aging, raising hopes for an entirely new way to combat dementia.
• 🔗 查看原文

• GSE320399 SUMO化缺失导致PRC1异常聚集和3D基因组重连，且与H3K27me3无关
• GSE320241 SUMO化缺失导致PRC1异常聚集和3D基因组重连，与H3K27me3无关 [CUT&Run]
• GSE319380 散发性阿尔茨海默病患者来源星形胶质细胞的转录组和表型数据
• GSE343732 美洲原住民血统富集的eQTL调控HER2扩增子基因，并与哥伦比亚女性乳腺癌预后相关
• GSE343650 177Lu标记的DOTA-EB-RGD作为甲状腺癌治疗的候选药物
• GSE343610 MACF1通过ATF4介导的ASNS调控促进结直肠癌进展
• GSE343584 尿毒症血清改变基因表达谱和信号通路活性
• GSE338505 FFPE结肠组织完整细胞解离增强了scRNA-seq中的细胞回收率和基因检测
• GSE336466 组蛋白阅读器 MLLT1 和 MLLT3 的浓度赋予 AID 活性位点特异性
• GSE336464 组蛋白阅读器 MLLT1 和 MLLT3 的浓度赋予 AID 活性位点特异性 [TT-seq]
• GSE325317 构建整合心外膜的人类 iPSC 衍生心脏组织以模拟 Hutchinson-Gilford 早衰症 [Infinium Methylation EPIC]
• GSE305717 tRNA 修饰是应激颗粒形成和黑色素瘤转移所必需的 [RNA-seq]
• GSE303386 METTL1的药理学抑制作为一种新型抗癌策略
• GSE338847 一套全面的 HA 标记 PRC1 工具包可实现果蝇染色质分析和蛋白质组学分析的标准化 [ChIP-seq]