详细内容（前10条）

1. ⭐ 最新10分生信，单细胞+空转多组学进行中性粒细胞亚型分析，识别 CTCF+TAN，靶向CTCF改善免疫治疗疗效！

• ✍️ 作者：东晓生物
• 🏷️ 关键词：免疫、单细胞、生信
• 🔗 查看原文

2. ⭐ 8.5生信，鉴定VSIG4+S100A10+巨噬细胞，影响免疫抑制及免疫治疗疗效。单细胞结合空转分析可增加结果可信度！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、单细胞、生信
• 📝 描述：点击查看详情
• 🔗 查看原文

3. ⭐ SMTdb：癌症空间元转录组资源

• ✍️ 作者：BMELab
• 🏷️ 关键词：癌症、空间转录组、转录组
• 📝 描述：SMTdb：癌症时空转录组资源
• 🔗 查看原文

4. ⭐ 文献分享–病灶修复过程中心脏免疫微环境的时空动态变化

• ✍️ 作者：单细胞空间交响乐
• 🏷️ 关键词：免疫、免疫微环境、心脏
• 📝 描述：文献分享–病灶修复过程中心脏免疫微环境的时空动态变化
• 🔗 查看原文

5. 最新14+干湿结合SCI，作者鉴定出干扰素诱导的衰老 CD8T 细胞并揭示其对免疫治疗的影响。衰老虽老，但是真的火！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：免疫、衰老
• 📝 描述：点击查看详情
• 🔗 查看原文

6. 44.5分顶刊发文，单细胞鉴定出乏氧巨噬细胞进行后续研究。前有衰老CD8T，现有乏氧巨噬。识别某种表型的XX细胞可发高分文章！

• ✍️ 作者：生信小课堂
• 🏷️ 关键词：衰老、单细胞
• 📝 描述：点击查看详情
• 🔗 查看原文

7. 衰老竟能抑制癌症！《自然》子刊：活到一定岁数，身体会开启抗癌模式

• ✍️ 作者：学术经纬
• 🏷️ 关键词：癌症、衰老
• 📝 描述：衰老的"意外益处"
• 🔗 查看原文

8. CR：识破肿瘤细胞的“装死”计谋！科学家发现，化疗激活WNT通路是乳腺癌细胞进入休眠状态的关键

• ✍️ 作者：奇点肿瘤探秘
• 🏷️ 关键词：肿瘤、通路
• 📝 描述：肿瘤细胞醒醒，这里不让睡
• 🔗 查看原文

9. 实验对象太珍贵？Nature Methods 验证：无需设备分析空间转录组

• ✍️ 作者：丁香学术
• 🏷️ 关键词：空间转录组、转录组
• 📝 描述：报名直播，赢惊喜好礼！
• 🔗 查看原文

10. 乳腺癌肺转移新机制！重庆医科大学发文：临床肿瘤免疫治疗的有效策略

• ✍️ 作者：转化医学网
• 🏷️ 关键词：肿瘤、免疫
• 📝 描述：本研究工作或许能为治疗乳腺癌肺转移提供一种颇具吸引力的策略。
• 🔗 查看原文

💡 该来源还有 13 条内容，详见 文末

详细内容（全部10条）

1. GSE305816 胆固醇外排蛋白 ABCA1 支持髓系免疫细胞的抗癌功能。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Contributors : Shruti V Bendre ; Rajendra K C ; Kevin VanBortle ; Erik R NelsonSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusBreast and other solid tumors respond poorly to immune therapy. Myeloid cells (MCs) such as macrophages contribute to resistance. Established clinical evidence links cholesterol to cancer outcomes, with MC function being regulated by cholesterol metabolism. We screened MC-expressed regulators of cholesterol homeostasis linked to survival and identified the cholesterol efflux protein ABCA1. ABCA1 activity increases anti-cancer functions of macrophages: enhancing tumor infiltration, decreasing angiogenic potential, reducing efferocytosis, and improving support of CD8+ T cell activity. Mechanistically, different AKT isoforms are involved, through both PI3K-dependent and independent mechanisms. Highlighting the clinical relevance of our findings are correlations between ABCA1 in macrophages and angiogenic potential, VEGFA, and CD8 T cell abundance and activity. The culmination of these activities was demonstrated through increased tumor growth and metastasis in mice lacking MC-expressed ABCA1. Tumors grown in these mice were also more resistant to immune therapy. Therefore, modulating ABCA1 activity within MCs may represent a novel approach to immune therapy.
• 🔗 查看原文

2. GSE248066 秋葵总黄酮通过上调 LncRNAAL137782 抑制 STAT3/EMT 信号通路，从而抑制结直肠癌细胞转移

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、pathway
• 📝 描述：Contributors : Qian Li ; Hui Zhang ; Yongshan He ; Conghui HanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTotal flavone of Abelmoschus manihot Lmedic (TFA) is a natural compound known for its anti-inflammatory, analgesic, and antioxidant properties. Despite extensive investigations into the therapeutic potential of TFA, there remains a paucity of reports regarding its impact on cancer treatment. This study aimed to elucidate the effects and mechanisms of TFA in CRC therapy. Subsequently, we employed RNA-seq technology to scrutinize differences in the gene expression profiles between TFA-treated and untreated CRC cells. Our findings underscore that TFA suppresses the growth, migration, and apoptosis of CRC cells. In animal models, TFA inhibits CRC cell growth and reduces hepatic metastasis. Mechanistically, we observed that TFA accomplishes this by upregulating long non-coding RNA AL137782, which, in turn, inhibits the EMT/STAT3 signaling pathway.
• 🔗 查看原文

3. GSE287801 卫星细胞分化中的 RNA 调控（RNA-seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusRNA regulation in satellite cell differentiation
• 🔗 查看原文

4. GSE244343 激活的 ATF6α 是一种内质网应激诱导癌蛋白，可代谢限制免疫监视 [Atf6 KO DEN/HFD 的批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Xin Li ; Cynthia Lebeaupin ; Randal J Kaufman ; Mathias HeikenwälderSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality with limited therapies. While endoplasmic reticulum (ER)-stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR-transducer activating transcription factor 6 alpha (ATF6α) remains unclear. In contrast to the well-characterized role of ATF6α-activation as an adaptive response to ER-stress, we here demonstrate its hitherto unknown function as an ER stress-inducing oncoprotein and metabolic master-regulator restricting cancer-immunosurveillance. In human HCC, ATF6α-activation significantly correlated with reduced patient-survival, tumor-progression, local immunosuppression, and higher recurrence rates of liver-cancer upon hepatectomy. Hepatocyte-specific ATF6α-activation in mice induced progressive hepatitis with ER-stress, immunosuppression, and hepatocyte-proliferation. Concomitantly, activated-ATF6α increased glycolysis and repressed gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP1). Restoring FBP1 expression prevented ATF6α-activation-related pathologies. Prolonged ATF6α-activation in hepatocytes triggered hepatocarcinogenesis, intratumoral T-cell infiltration, and nutrient-deprived immune-exhaustion. Immune-checkpoint blockade (ICB) efficiently restored immunosurveillance and dramatically reduced HCC. In line, HCC patients with a significantly higher ATF6α-activation signature presented complete response to ICB monotherapy. Targeting Atf6 via germline, hepatocyte-specific ablation, or therapeutic delivery of antisense-oligonucleotides dampened HCC in preclinical liver-cancer models. Thus, prolonged ATF6α-activation drives ER-stress, leading to aberrant glucose metabolism-dependent immunosuppression in liver cancer. Our findings propose persistently activated ATF6α as an oncoprotein, stratification-marker for liver-cancer ICB, and targetable therapeutic strategy against HCC.
• 🔗 查看原文

5. GSE244342 激活的 ATF6α 是一种内质网应激诱导癌蛋白，可代谢限制免疫监视 [TG-AAV-GFP/CRE、DEN/HFD 的批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Xin Li ; Cynthia Lebeaupin ; Randal J Kaufman ; Mathias HeikenwälderSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality with limited therapies. While endoplasmic reticulum (ER)-stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR-transducer activating transcription factor 6 alpha (ATF6α) remains unclear. In contrast to the well-characterized role of ATF6α-activation as an adaptive response to ER-stress, we here demonstrate its hitherto unknown function as an ER stress-inducing oncoprotein and metabolic master-regulator restricting cancer-immunosurveillance. In human HCC, ATF6α-activation significantly correlated with reduced patient-survival, tumor-progression, local immunosuppression, and higher recurrence rates of liver-cancer upon hepatectomy. Hepatocyte-specific ATF6α-activation in mice induced progressive hepatitis with ER-stress, immunosuppression, and hepatocyte-proliferation. Concomitantly, activated-ATF6α increased glycolysis and repressed gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP1). Restoring FBP1 expression prevented ATF6α-activation-related pathologies. Prolonged ATF6α-activation in hepatocytes triggered hepatocarcinogenesis, intratumoral T-cell infiltration, and nutrient-deprived immune-exhaustion. Immune-checkpoint blockade (ICB) efficiently restored immunosurveillance and dramatically reduced HCC. In line, HCC patients with a significantly higher ATF6α-activation signature presented complete response to ICB monotherapy. Targeting Atf6 via germline, hepatocyte-specific ablation, or therapeutic delivery of antisense-oligonucleotides dampened HCC in preclinical liver-cancer models. Thus, prolonged ATF6α-activation drives ER-stress, leading to aberrant glucose metabolism-dependent immunosuppression in liver cancer. Our findings propose persistently activated ATF6α as an oncoprotein, stratification-marker for liver-cancer ICB, and targetable therapeutic strategy against HCC.
• 🔗 查看原文

6. GSE244341 激活的 ATF6α 是一种内质网应激诱导癌蛋白，可代谢限制免疫监视 [TG-AAV-GFP/CRE/FBP1 的批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNAseq
• 📝 描述：Contributors : Xin Li ; Cynthia Lebeaupin ; Randal J Kaufman ; Mathias HeikenwälderSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusHepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality with limited therapies. While endoplasmic reticulum (ER)-stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR-transducer activating transcription factor 6 alpha (ATF6α) remains unclear. In contrast to the well-characterized role of ATF6α-activation as an adaptive response to ER-stress, we here demonstrate its hitherto unknown function as an ER stress-inducing oncoprotein and metabolic master-regulator restricting cancer-immunosurveillance. In human HCC, ATF6α-activation significantly correlated with reduced patient-survival, tumor-progression, local immunosuppression, and higher recurrence rates of liver-cancer upon hepatectomy. Hepatocyte-specific ATF6α-activation in mice induced progressive hepatitis with ER-stress, immunosuppression, and hepatocyte-proliferation. Concomitantly, activated-ATF6α increased glycolysis and repressed gluconeogenic enzyme fructose-1,6-bisphosphatase 1 (FBP1). Restoring FBP1 expression prevented ATF6α-activation-related pathologies. Prolonged ATF6α-activation in hepatocytes triggered hepatocarcinogenesis, intratumoral T-cell infiltration, and nutrient-deprived immune-exhaustion. Immune-checkpoint blockade (ICB) efficiently restored immunosurveillance and dramatically reduced HCC. In line, HCC patients with a significantly higher ATF6α-activation signature presented complete response to ICB monotherapy. Targeting Atf6 via germline, hepatocyte-specific ablation, or therapeutic delivery of antisense-oligonucleotides dampened HCC in preclinical liver-cancer models. Thus, prolonged ATF6α-activation drives ER-stress, leading to aberrant glucose metabolism-dependent immunosuppression in liver cancer. Our findings propose persistently activated ATF6α as an oncoprotein, stratification-marker for liver-cancer ICB, and targetable therapeutic strategy against HCC.
• 🔗 查看原文

7. GSE292906 LUMINIDEPENDENS 蛋白是拟南芥中转录的一般抑制因子 [RNA-Seq 2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Clara Bergis-Ser ; Qingyi Wang ; Xiaoning He ; Maherun Nisa ; Vickie Kaiser ; Christelle Mazubert ; Jeannine Drouin-Wahbi ; Rim Brik-Chaouche ; Layla Chmaiss ; Jeele Van Leene ; Geert de Jaeger ; Jose Gutierrez-Marcos ; Catherine Bergounioux ; Clara Richet-Bourbousse ; David Latrasse ; Moussa Benhamed ; Cécile RaynaudSeries Type : Expression profiling by high throughput sequencingOrganism : Arabidopsis thalianaGenomic integrity is constantly challenged by transcription/replication conflicts, a major source of replication stress and instability across all life forms. While extensive studies have uncovered transcription/replication conflicts resolution mechanisms in animals, yeast, and prokaryotes, their counterparts in plants remain largely unexplored. Through a forward genetic screen, we identified the LUMINIDEPENDENS (LD) protein, previously known for regulating the flowering repressor FLC, as a key player in mitigating replication stress in plants. Strikingly, transcriptomic analyses reveal that loss of LD results in the upregulation of over 13,000 genes, establishing LD as a global transcriptional repressor. Consistent with this role, LD binds a substantial portion of the Arabidopsis genome and interacts with the MED18 subunit of the Mediator complex to modulate RNA polymerase II phosphorylation. These findings uncover a fundamental function of LD in fine-tuning transcription genome-wide, with an additional role in suppressing transcription/replication conflicts by locally dampening transcription and promoting replication fork progression. Our work highlights a previously unrecognized genome-protective strategy in plants, opening new avenues for understanding transcription/replication conflict management in eukaryotic systems.
• 🔗 查看原文

8. GSE292381 LUMINIDEPENDENS 蛋白是拟南芥中转录的一般抑制因子 [LD ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：ChIP-seq
• 📝 描述：Contributors : Clara Bergis-Ser ; Qingyi Wang ; Xiaoning He ; Maherun Nisa ; Vickie Kaiser ; Christelle Mazubert ; Jeannine Drouin-Wahbi ; Rim Brik-Chaouche ; Layla Chmaiss ; Jeele Van Leene ; Geert de Jaeger ; Jose Gutierrez-Marcos ; Catherine Bergounioux ; Clara Richet-Bourbousse ; David Latrasse ; Moussa Benhamed ; Cécile RaynaudSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Arabidopsis thalianaGenomic integrity is constantly challenged by transcription/replication conflicts, a major source of replication stress and instability across all life forms. While extensive studies have uncovered transcription/replication conflicts resolution mechanisms in animals, yeast, and prokaryotes, their counterparts in plants remain largely unexplored. Through a forward genetic screen, we identified the LUMINIDEPENDENS (LD) protein, previously known for regulating the flowering repressor FLC, as a key player in mitigating replication stress in plants. Strikingly, transcriptomic analyses reveal that loss of LD results in the upregulation of over 13,000 genes, establishing LD as a global transcriptional repressor. Consistent with this role, LD binds a substantial portion of the Arabidopsis genome and interacts with the MED18 subunit of the Mediator complex to modulate RNA polymerase II phosphorylation. These findings uncover a fundamental function of LD in fine-tuning transcription genome-wide, with an additional role in suppressing transcription/replication conflicts by locally dampening transcription and promoting replication fork progression. Our work highlights a previously unrecognized genome-protective strategy in plants, opening new avenues for understanding transcription/replication conflict management in eukaryotic systems.
• 🔗 查看原文

9. GSE290980 靶向反义寡核苷酸治疗挽救脊髓性肌萎缩症类器官的发育异常 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：scRNA
• 📝 描述：Contributors : Irene Faravelli ; Paola Rinchetti ; Monica Tambalo ; Illia Simutin ; Lisa Mapelli ; Sara Mancinelli ; Matteo Miotto ; Mafalda Rizzuti ; Andrea D’Angelo ; Chiara Cordiglieri ; Giulia Forotti ; Clelia Peano ; Paolo Kunderfranco ; Luca Calandriello ; Giacomo P Comi ; Elvezia Paraboschi ; Eleonora Pali ; Francesca Beatrice ; Egidio D’Angelo ; Serge Przedborski ; Monica Nizzardo ; Simona Lodato ; Stefania CortiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSpinal muscular atrophy (SMA) is a severe neurological disease caused by mutations in the SMN1 gene, characterized by early onset and degeneration of lower motor neurons.Understanding early neurodevelopmental defects in SMA is crucial for optimizing therapeutic interventions. Using spinal cord and cerebral organoids generated from multiple SMA type I donors, we revealed widespread disease mechanisms beyond motor neuron degeneration. Single-cell transcriptomics uncovered pervasive alterations across neural populations, from progenitors to neurons, demonstrating SMN-dependent dysregulation of neuronal differentiation programs. Multi-electrode array analysis identified consistent hyperexcitability in both spinal and brain organoids, establishing altered electrical properties as a central nervous system-wide feature of pathogenesis. Early administration of an optimized antisense oligonucleotide (ASO) that restored SMN levels rescued morphological and functional deficits in spinal cord organoids across different genetic backgrounds. Importantly, this early intervention precisely corrected aberrant splicing in newly identified SMN1 targets enriched at critical nodes of neuronal differentiation. Our findings demonstrate that early developmental defects are core features of SMA pathogenesis that can be prevented by timely therapeutic intervention, providing new insights for optimizing treatment strategies.
• 🔗 查看原文

10. GSE290979 靶向反义寡核苷酸治疗挽救脊髓性肌萎缩症类器官的发育异常 [bulk RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Irene Faravelli ; Paola Rinchetti ; Monica Tambalo ; Illia Simutin ; Lisa Mapelli ; Sara Mancinelli ; Matteo Miotto ; Mafalda Rizzuti ; Andrea D’Angelo ; Chiara Cordiglieri ; Giulia Forotti ; Clelia Peano ; Paolo Kunderfranco ; Luca Calandriello ; Giacomo P Comi ; Elvezia Paraboschi ; Eleonora Pali ; Francesca Beatrice ; Egidio D’Angelo ; Serge Przedborski ; Monica Nizzardo ; Simona Lodato ; Stefania CortiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSpinal muscular atrophy (SMA) is a severe neurological disease caused by mutations in the SMN1 gene, characterized by early onset and degeneration of lower motor neurons.Understanding early neurodevelopmental defects in SMA is crucial for optimizing therapeutic interventions. Using spinal cord and cerebral organoids generated from multiple SMA type I donors, we revealed widespread disease mechanisms beyond motor neuron degeneration. Single-cell transcriptomics uncovered pervasive alterations across neural populations, from progenitors to neurons, demonstrating SMN-dependent dysregulation of neuronal differentiation programs. Multi-electrode array analysis identified consistent hyperexcitability in both spinal and brain organoids, establishing altered electrical properties as a central nervous system-wide feature of pathogenesis. Early administration of an optimized antisense oligonucleotide (ASO) that restored SMN levels rescued morphological and functional deficits in spinal cord organoids across different genetic backgrounds. Importantly, this early intervention precisely corrected aberrant splicing in newly identified SMN1 targets enriched at critical nodes of neuronal differentiation. Our findings demonstrate that early developmental defects are core features of SMA pathogenesis that can be prevented by timely therapeutic intervention, providing new insights for optimizing treatment strategies.
• 🔗 查看原文

详细内容（全部1条）

1. 勘误表：接受全身性癌症治疗的老年患者脆弱性的实际评估和管理：ASCO 指南更新

• ✍️ 作者：未知作者
• 🏷️ 关键词：癌症
• 📝 描述：Secret hovertext: 临床肿瘤学杂志，印刷前。
• 🔗 查看原文

详细内容（全部1条）

1. 神经科学家发现可能延缓衰老的免疫细胞。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、aging
• 📝 描述：A newly recognized set of T helper cells seems to guard against aging by eliminating harmful senescent cells. Their presence in supercentenarians suggests they may be a key to maintaining a healthier, age-balanced immune system.
• 🔗 查看原文

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