详细内容（前10条）

1. GSE343500 细胞外基质通过 YAP/TEAD 调控前列腺癌的谱系可塑性 [ATAC-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、ATAC-seq
• 📝 描述：Contributors : Han Teng ; Lange Matthew ; Cho Y Zoe ; Mcgillivray Patrick ; Buttner Maren ; Koche Richard ; Sawyers CharlesSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTreatment-related neuroendocrine prostate cancer (NEPC) is an increasingly frequent mechanism of resistance to androgen receptor pathway inhibitor (ARPI) therapy in prostate adenocarcinoma (PRAD). This lineage transition is dependent on upregulation of the NE-specifying transcription factor ASCL1, typically in a genetic background of RB1 and TP53 loss. Here we identify extracellular matrix-integrin-YAP1/TEAD signaling as a critical brake on NEPC lineage transition. Deletion of Itgb1, the shared B1 subunit required for collagen and laminin-mediated integrin activation, is sufficient to induce ASCL1 and NE lineage gene expression, by activating LATS1/2 kinases with subsequent inactivation of YAP1/TEAD signaling. Conversely, restoration of YAP1/TEAD signaling by pharmacological LATS1/2 inhibition, or by expression of constitutively active YAP1/TAZ mutants, prevents or reverts NEPC lineage transition. NOTCH and AR cooperate with YAP/TEAD to repress ASCL1, such that combined inhibition leads to complete reprograming of PRAD into NEPC in vitro, providing a dynamic platform to dissect the molecular events responsible for lineage transition over time. We find that lineage transition is accompanied by a redistribution of FOXA1 and TEAD cistromes from PRAD to NEPC-specific enhancers and requires the pioneering activity of FOXA1. Thus, extracellular matrix/integrin signaling in the PRAD tumor microenvironment restrains NE lineage plasticity, highlighting a potential path for pharmacological inhibitors in modulating treatment-induced lineage change.
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2. GSE275249：他克莫司和雷帕霉素治疗下小鼠角膜移植模型的单细胞RNA测序分析

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Yan He ; Tuo Deng ; Limin Xie ; Yating Liu ; Yingyi Liu ; Xixuan Huang ; Huanmin KangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIn this study, we utilized single-cell RNA sequencing (scRNA-seq) to investigate the effects of tacrolimus and rapamycin on corneal graft survival following penetrating keratoplasty in mice. Post-transplantation, the recipient mice were administered daily intraperitoneal injections of tacrolimus, rapamycin, or PBS. Fifteen days after treatment, scRNA-seq was employed to detect molecular and cellular changes within the corneal tissues.
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3. GSE331133 单细胞和空间多组学揭示雌激素介导的阴道壁微环境重塑和绝经后盆腔器官脱垂中的血管周围修复微环境

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial
• 📝 描述：Contributor : Xiaochun LiuSeries Type : Other ; Expression profiling by high throughput sequencingOrganism : Homo sapiensLocal estrogen is widely used to improve vaginal mucosal status and menopausal urogenital symptoms in pelvic organ prolapse despite variable clinical outcomes, highlighting a critical gap in our understanding of its actions within the native tissue architecture. To resolve this, we employed high-definition spatial transcriptomics, achieving a near-cellular resolution map of the postmenopausal vaginal wall. This spatial atlas reveals spatial patterns underlying estrogen’s action, the spatial organization of a structured HAS1+ fibroblast-pericyte cellular unit around vasculature. Estrogen is associated with the recruitment of TWIST1-related HAS1+ fibroblasts into this precise micro-anatomical location, enabling their functional coupling with pericytes. This co-localization facilitates a rewired fibroblast-pericyte signaling axis, enhancing intercellular communication. Computational pharmacology further suggests this unit as a potential druggable functional module. Our findings support a model in which estrogen’s effects involve spatially organized formation of a multicellular regulatory unit rather than general tissue stimulation. TWIST1, HAS1, and ECM remodeling are linked within this regulatory program, which may inform future tissue-modulating and symptom-directed strategies.
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4. GSE276743 肝移植患者外周血单核细胞转录组

• ✍️ 作者：未知作者
• 🏷️ 关键词：transcriptome
• 📝 描述：Contributors : Dong Jin Joo ; Byungjin Hwang ; Deok Gie Kim ; Su-Hyeon Lee ; Yuri ChoSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo explore immune cell dynamics in allograft rejection in LT patients, PBMC samples from recipients who experienced acute rejection and those without rejection were sequenced.
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5. GSE328227 KLF4/MLL3复合物轴驱动NRBP2转录以消除急性髓系白血病细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia
• 📝 描述：Contributors : Meng Yang ; Shangda Yang ; Ting Lu ; Hui Cheng ; Tao ChengSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAcute myeloid leukemia (AML) is a heterogeneous malignancy rooted in hematopoietic stem cell dysregulation. Despite therapeutic advances, clinical outcomes remain unsatisfactory. Here, we identify KLF4, a zinc-finger (ZnF) transcription factor with previously reported context-dependent roles in hematologic malignancies, as a negative regulator of AML proliferation. Mechanistically, KLF4 interacts with the MLL3 histone methyltransferase complex, comprising MLL3, WDR5, RBBP5 and ASH2L. KLF4 engages the catalytic subunit MLL3 and the allosteric regulator ASH2L through its ZnF and transrepression (TRD) domains, thereby activating transcription of the tumor suppressor gene NRBP2. Furthermore, integrated transcriptional analysis revealed TNIK as a convergent effector of the KLF4–NRBP2 tumor-suppressive circuit in acute myeloid leukemia. Pharmacological blockade of TNIK with the selective small-molecule inhibitor TNIK-IN-1 selectively impaired leukemic cell proliferation while sparing normal hematopoiesis. Consequently, our findings reveal a previously unrecognized KLF4–MLL3 complex–NRBP2 transcriptional axis that suppresses AML survival through TNIK, highlighting a potential therapeutic strategy for AML.
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6. GSE328080 KLF4/MLL3 复合物轴驱动 NRBP2 转录以消除急性髓系白血病细胞 [Cut & Tag]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia
• 📝 描述：Contributors : Meng Yang ; Shangda Yang ; Ting Lu ; Hui Cheng ; Tao ChengSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensAcute myeloid leukemia (AML) is a heterogeneous malignancy rooted in hematopoietic stem cell dysregulation. Despite therapeutic advances, clinical outcomes remain unsatisfactory. Here, we identify KLF4, a zinc-finger (ZnF) transcription factor with previously reported context-dependent roles in hematologic malignancies, as a negative regulator of AML proliferation. Mechanistically, KLF4 interacts with the MLL3 histone methyltransferase complex, comprising MLL3, WDR5, RBBP5 and ASH2L. KLF4 engages the catalytic subunit MLL3 and the allosteric regulator ASH2L through its ZnF and transrepression (TRD) domains, thereby activating transcription of the tumor suppressor gene NRBP2. Furthermore, integrated transcriptional analysis revealed TNIK as a convergent effector of the KLF4–NRBP2 tumor-suppressive circuit in acute myeloid leukemia. Pharmacological blockade of TNIK with the selective small-molecule inhibitor TNIK-IN-1 selectively impaired leukemic cell proliferation while sparing normal hematopoiesis. Consequently, our findings reveal a previously unrecognized KLF4–MLL3 complex–NRBP2 transcriptional axis that suppresses AML survival through TNIK, highlighting a potential therapeutic strategy for AML.
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7. GSE313017 CHTOP通过调节ROS稳态来调控结直肠癌的化疗耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Mingchao Mu ; Jing LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensChemotherapy resistance remains a significant challenge in colorectal cancer (CRC) treatment, with disrupted reactive oxygen species (ROS) homeostasis playing a central role. We identify CHTOP as a key regulator of ROS levels and chemoresistance in CRC. Mechanistically, CHTOP regulates ROS homeostasis by interacting with Nrf2 and modulating its SUMOylation via the SENP3-containing 5FMC complex. Notably, CHTOP expression is tightly controlled by a ROS-dependent feedback loop. The PSIP1/p52 isoform inhibits CHTOP expression by disrupting HNRNPH1-dependent splicing, leading to CHTOP degradation via nonsense-mediated decay (NMD). Meanwhile, ROS accumulation stabilizes SENP3, promoting the deSUMOylation and degradation of p52, thereby forming a ROS-SENP3-p52-CHTOP feedback loop. Thus, ROS levels both regulate and are regulated by CHTOP, maintaining redox balance. CHTOP downregulation in 5-FU-resistant CRC shifts cells into a higher-ROS steady state, which correlates with reduced 5-FU sensitivity. Both restoring CHTOP expression and inducing further depletion of CHTOP disrupt redox balance in 5-FU-resistant cells, reversing resistance and re-establishing sensitivity. These findings suggest that modulating CHTOP expression may offer a promising therapeutic strategy to overcome chemoresistance in CRC through redox regulation.
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8. GSE306746 KLF4/MLL3轴驱动NRBP2转录以消除急性髓系白血病细胞

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia
• 📝 描述：Contributors : Meng Yang ; Cong Chen ; Shangda Yang ; Hui Cheng ; Tao ChengSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensAcute myeloid leukemia (AML) is a heterogeneous malignancy rooted in hematopoietic stem cell dysregulation. Despite therapeutic advances, clinical outcomes remain unsatisfactory. Here, we identify KLF4, a zinc-finger (ZnF) transcription factor with previously reported context-dependent roles in hematologic malignancies, as a negative regulator of AML proliferation. Mechanistically, KLF4 interacts with the MLL3 histone methyltransferase complex, comprising MLL3, WDR5, RBBP5 and ASH2L. KLF4 engages the catalytic subunit MLL3 and the allosteric regulator ASH2L through its ZnF and transrepression (TRD) domains, thereby activating transcription of the tumor suppressor gene NRBP2. Furthermore, integrated transcriptional analysis revealed TNIK as a convergent effector of the KLF4–NRBP2 tumor-suppressive circuit in acute myeloid leukemia. Pharmacological blockade of TNIK with the selective small-molecule inhibitor TNIK-IN-1 selectively impaired leukemic cell proliferation while sparing normal hematopoiesis. Consequently, our findings reveal a previously unrecognized KLF4–MLL3 complex–NRBP2 transcriptional axis that suppresses AML survival through TNIK, highlighting a potential therapeutic strategy for AML.
• 🔗 查看原文

9. GSE343585 父系心脏损伤引发炎症信号传递至性腺，并在脊椎动物中产生代际心脏效应 - Bulk_RNA-seq_F1_heart_ZF 数据集

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac
• 📝 描述：Contributors : Benedetta Coppe ; Prateek Arora ; Nadia MercaderSeries Type : Expression profiling by high throughput sequencingOrganism : Danio rerioThe blood-gonadal barrier protects the germline from parental exposures. A phenomenon known as intergenerational inheritance suggests that, exceptionally, this barrier can be surpassed with consequences for the subsequent generation. Specific diet regimes and early traumatic experiences have been among the chronic stressors shown to be able to lead to intergenerational inheritance in mammals. Less is known about how acute stress can affect the germline. Cardiac damage leads to several alterations in peripheral organs and overall affects alterations in blood flow, metabolism, and the immune response. Whether cardiac damage can also affect the reproductive system is not known and might offer new insights into the potential inheritance of CVD. Here, we used the zebrafish and mouse models to explore the intergenerational role of cardiac damage and repair. As early as one week after a cardiac cryolesion, male gonads and gametes activated responses associated with inflammation. In sperm, chromatin accessibility was altered in response to cardiac cryolesion and offspring of cryoinjured zebrafish males, revealing changes in cardiac function and cardiac gene expression. Induction of systemic sterile inflammation in the paternal generation mimicked a cardiac injury effect in the following generation, while anti-inflammatory treatments in the injured paternal generation partially recovered F1 cardiac features. Chromatin accessibility was also altered in mouse testis after a neonatal injury, and F1 hearts revealed alterations in gene expression associated with the immune response, suggesting a conserved role of sterile inflammation as a vector for intergenerational transmission of cardiac injury. This submission covers the Bulk_RNA-seq_F1_heart_ZF assay.
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10. GSE343579 父系心脏损伤引发炎症信号传递至性腺，并在脊椎动物中产生代际心脏效应 - Bulk_RNA-seq_testes_ZF 数据集

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac
• 📝 描述：Contributors : Benedetta Coppe ; Prateek Arora ; Nadia MercaderSeries Type : Expression profiling by high throughput sequencingOrganism : Danio rerioThe blood-gonadal barrier protects the germline from parental exposures. A phenomenon known as intergenerational inheritance suggests that, exceptionally, this barrier can be surpassed with consequences for the subsequent generation. Specific diet regimes and early traumatic experiences have been among the chronic stressors shown to be able to lead to intergenerational inheritance in mammals. Less is known about how acute stress can affect the germline. Cardiac damage leads to several alterations in peripheral organs and overall affects alterations in blood flow, metabolism, and the immune response. Whether cardiac damage can also affect the reproductive system is not known and might offer new insights into the potential inheritance of CVD. Here, we used the zebrafish and mouse models to explore the intergenerational role of cardiac damage and repair. As early as one week after a cardiac cryolesion, male gonads and gametes activated responses associated with inflammation. In sperm, chromatin accessibility was altered in response to cardiac cryolesion and offspring of cryoinjured zebrafish males, revealing changes in cardiac function and cardiac gene expression. Induction of systemic sterile inflammation in the paternal generation mimicked a cardiac injury effect in the following generation, while anti-inflammatory treatments in the injured paternal generation partially recovered F1 cardiac features. Chromatin accessibility was also altered in mouse testis after a neonatal injury, and F1 hearts revealed alterations in gene expression associated with the immune response, suggesting a conserved role of sterile inflammation as a vector for intergenerational transmission of cardiac injury. This submission covers the Bulk_RNA-seq_testes_ZF assay.
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1. 当肠道微生物缺乏纤维时，它们可能会开始吃掉你。

• ✍️ 作者：未知作者
• 🏷️ 关键词：gut、regex:gut(-?microbiome)?
• 📝 描述：Gut microbes need something to eat, and when fiber is limited, they may begin consuming proteins from the mucus lining that protects the gut. Researchers found that fiber can suppress this process, while indigestible plant proteins help microbes produce more beneficial compounds.
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• GSE343555 干旱和盐碱条件下葡萄品种和砧木的比较转录组分析
• GSE343538 父系心脏损伤引发炎症信号传递至性腺，并在脊椎动物中产生代际心脏效应 - snATAC-seq_testes_M 数据集
• GSE343529 父系心脏损伤引发炎症信号传递至性腺，并在脊椎动物中产生代际心脏效应 - Bulk-RNA-seq_F1_heart_M 数据集
• GSE343528 父系心脏损伤引发炎症信号传递至性腺，并在脊椎动物中产生代际心脏效应 - ATAC-seq_sperm_ZF 数据集
• GSE343523 父系心脏损伤引发炎症信号传递至性腺，并在脊椎动物中产生代际心脏效应 - DNA_Met_sperm_M 数据集
• GSE343504 细胞外基质通过 YAP/TEAD 调控前列腺癌的谱系可塑性 [scMultiome]
• GSE343502 细胞外基质通过YAP/TEAD调控前列腺癌细胞谱系可塑性
• GSE343498 细胞外基质通过 YAP/TEAD 调控前列腺癌的谱系可塑性 [Cut & Run]
• GSE343352 机械损伤诱导的大鼠食管狭窄模型揭示炎症相关的纤维化重塑
• GSE338648 肝细胞 MLKL 通过线粒体功能障碍驱动肥胖驱动的肝细胞癌进展，且该过程独立于坏死性凋亡（MASLD）。