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1. ⭐ GSE336999 NT2.5、NT2.5LM 和 NT2.5LV 的全转录组测序：一种具有肺和肝转移倾向的 HER2 阳性小鼠乳腺癌细胞系系列

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、sequencing、transcriptome
• 📝 描述：Contributors : Batul Al-Zubeidy ; Edgar Gonzalez ; Aaron Baugh ; Marqus Dela Cruz ; Cheol Park ; Matthew Jacobo ; Isaac S Chan ; Michael Press ; Evanthia T Roussos TorresSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe NT2.5 cell line and its lung-preferential (NT2.5LM) and liver-preferential (NT2.5LV) metastatic derivatives constitute an isogenic HER2-positive murine breast cancer model derived from neu-N transgenic FVB/N mice. To define the transcriptional programs associated with organ-preferential metastatic colonization, we performed bulk poly(A) RNA-sequencing on the three cell lines grown in vitro. Differential expression analysis identified divergent, organ-correlated transcriptional programs distinguishing the lung- and liver-preferential derivatives on a conserved genomic background. These data accompany the whole-genome sequencing of the same cell line series deposited under the same BioProject.
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2. GSE335355 宿主来源的胆汁酸通过选择耐胆汁的差向异构化细菌来驱动炎症性肠病中的菌群失调

• ✍️ 作者：未知作者
• 🏷️ 关键词：bacteria、regex:bacter(ia|ial|ium)
• 📝 描述：Contributors : Maximilian Baumgartner ; Clarissa Campbell ; Georg BusslingerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe gut microbiome is a key regulator of intestinal homeostasis. Although dysbiosis is pervasively reported in inflammatory bowel diseases (IBD), its drivers and impact in disease pathophysiology are not yet fully understood. By integrating public metagenomic and metabolomic datasets from >5000 individuals across 12 ethnically diverse cohorts with independent validation cohorts and using neural-network based feature attribution, we identified epimerized bile acids (BAs) produced by microbial hydroxysteroid dehydrogenases (HSDHs) as a novel hallmark of IBD-associated dysbiosis. This shift occurs alongside previously reported changes including a depletion of microbe-derived C7-dehydroxylated BAs and an accumulation of host-derived C7-hydroxylated BAs. We show that increased levels of host-derived BA lead to epithelial remodelling during disease and are sufficient to recapitulate key features of IBD-related dysbiosis, including reduced microbial diversity and expansion of bile-resistant bacteria such as Mediterraneibacter gnavus and Escherichia coli. HSDHs found in IBD-enriched bacteria facilitate growth under high host-derived BA conditions by converting these molecules into urso- and iso-forms. While epimerized 7α-dehydroxylated BA have established immunoregulatory properties, the function of host-derived BA epimers remain poorly understood. We demonstrate that epimerized host-derived BAs exhibit reduced FXR agonist activity and that increased levels of these metabolites, or the bacteria that produce them, are associated with diminished ileal FXR signaling and altered circulating FGF19 and C4 levels in IBD patients. Our findings identify enhanced BA epimerization as a defining metabolic feature of IBD-associated dysbiosis and reveal a mechanism by which bile-resistant bacteria reshape BA signaling, linking microbial adaptation, impaired host-microbiome feedback regulation, and intestinal inflammation.
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3. GSE274929 骨髓来源巨噬细胞 (BMDM) 与 mEC25 癌细胞系共培养的 RNA 测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、RNA-seq
• 📝 描述：Contributors : Kun Chen ; Peng wang ; Zhengfei ZhuSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusOur findings revealed that when BMDMs cocultured with cancer cell lines in contact, auch as mEC25,their SIRPαexpression would upregulated compared with their coculture in a non-contact manner.To investigate the underlying mechanism and the altered signaling pathway involved in the SIRPα upregulation in BMDMs when their co-culture with cancer cell lines.We conduct RNA-seq based on sorting BMDMs after their co-culture with cancer cell lines in a direct or indirect way.
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4. GSE339459 5β-二氢睾酮和突变雄激素受体在前列腺癌中的脆弱性

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Samual Adams ; Lindsey Phelan ; Therese Lewis ; Josie Behm ; Aggie Law ; Xianglin Shi ; Guangyuan Li ; Jianneng LiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensBACKGROUND Bipolar androgen therapy (BAT) exploits the paradoxical vulnerability of castration-resistant prostate cancer (CRPC) to supraphysiologic androgen, but current BAT uses testosterone (T), which broadly activates wild-type androgen receptor (AR) in normal androgen-responsive tissues and can cause systemic androgenic effects. 5β-Dihydrotestosterone (5β-DHT), a naturally occurring T metabolite, has been considered androgenically inactive because of weak wild-type AR activity. Here, we examined whether 5β-DHT and related 5β-reduced metabolites activate mutant AR signaling and reproduce BAT-like growth suppression. METHODS Six 5β-reduced T metabolites were evaluated in C4-2 and LNCaP prostate cancer cells under androgen-depleted and BAT-like conditions. AR dependence and mutant-specific activity were assessed using enzalutamide, AR-null PC-3 cells, and PC-3 cells expressing AR-W742C or AR-H875Y. Cell proliferation, AR-responsive reporter activity, RT-qPCR, RNA sequencing with gene set enrichment analysis, immunoblotting, and senescence-associated β-galactosidase staining were used to characterize ligand responses. RESULTS At nanomolar concentrations, 5β-DHT and 3β-etiocholanediol (3β-ecdiol) induced AR target genes and promoted AR-dependent C4-2 and LNCaP growth, although less potently than T. RNA sequencing showed that both metabolites activated the T-regulated AR transcriptional program with smaller differentially expressed gene footprints. At high concentrations, 5β-DHT, but not the weaker agonist 3β-ecdiol or progesterone-class steroids, suppressed C4-2 and LNCaP proliferation. High-dose 5β-DHT also activated AR and suppressed growth in PC-3 cells expressing AR-W742C or AR-H875Y, whereas AR-null PC-3 cells were unaffected. High-dose 5β-DHT enriched androgen-response and senescence programs, suppressed G2M, E2F, and MYC-associated pathways, increased p21, p27, and p57, reduced RB phosphorylation and SKP2, and induced senescence-associated β-galactosidase activity.
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5. GSE273662 威尔姆斯肿瘤的分子特征：单核分析揭示威尔姆斯肿瘤的发生发展机制

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor
• 📝 描述：Contributors : Mike Adam ; James GellerSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWilms tumors are known to arise from and maintain features of the embryonic kidney associated with a surprisingly heterogenous genetic and molecular landscape. To further investigate both intra-tumor and inter-tumor variability, single nucleus RNA-sequencing (snRNA-seq) was performed on favorable histology Wilms tumors capturing blastema, epithelial, and stromal components, which were analyzed in comparison to a normal kidney reference atlas established from kidney samples (including patient-matched adjacent kidney) as well as publicly available single-cell RNA-seq from 18-week human fetal kidney. The transcriptomic profiles from Wilms tumor nuclei were shown to recapitulate its known triphasic histology, with similar gene expression signatures corresponding to nephron progenitor cells as well epithelial and stromal cells from human fetal kidneys. Tumors additionally show a high percentage of cycling cells in the G2/S phase, including tumor samples with blastemal cells both resembling “uninduced” nephron progenitors as well as tumor samples with blastema expressing more “differentiated” signatures of early proximal tubules, podocytes, as well as stromal/muscle genes. Furthermore, pathway enrichment analyses in the blastemal components show nephron/kidney epithelial development as expected, but interestingly also show neuronal/axon signatures across the majority of tumor samples. Additionally, enriched pathways in a subset of the tumors include WNT and TGF-beta signaling in the non-cycling blastema and polycomb repressive complex in cycling blastemal cells, suggesting that Wilms tumor blastema not only shows significant heterogeneity in its differentiation state/trajectory but also in its potential biological pathways/drivers.
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6. GSE342586 CD8 T 细胞中 LCK 缺乏导致小鼠增殖减少和效应 T 细胞形成增加 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：scRNA
• 📝 描述：Contributors : Valeria Uleri ; Veronika Niederlova ; Juraj Michalik ; Ondrej StepanekSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusLCK is an SRC-family kinase that mediates the initial steps in T-cell antigen receptor signaling and governs positive and negative selection during thymocyte development. While its developmental role is well established, its functions in peripheral T-cell responses remain poorly defined. Here, we investigated the responses of wild-type and LCK-deficient TCR-transgenic OT-I T cells across two infection models and an autoimmune diabetes model. LCK-deficient T cells exhibited reduced antigen-induced proliferation but, paradoxically, displayed enhanced effector differentiation in vivo. This phenotype likely reflects dysregulation of specific TCR signaling pathways, as LCK was more critical for ERK and NFAT activation than for NFκB, AP-1, or AKT/mTOR signaling. T cells deficient in a related kinase FYN also showed a slight increase in effector cell formation, suggesting that effector differentiation is regulated by their combined activity rather than distinct non-redundant roles. Our results reveal that LCK has two intrinsic roles in T-cell responses – promoting proliferation while restraining effector differentiation. These findings provide new insight into the molecular mechanisms of T-cell activation in vivo with implications for understanding the pathophysiology of LCK deficiency in humans and optimizing adoptive T-cell therapies.
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7. GSE342585 CD8 T 细胞中 LCK 缺陷导致小鼠增殖减少和效应 T 细胞形成增加 [批量 RNA 测序]

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Contributors : Valeria Uleri ; Veronika Niederlova ; Juraj Michalik ; Ondrej StepanekSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusLCK is an SRC-family kinase that mediates the initial steps in T-cell antigen receptor signaling and governs positive and negative selection during thymocyte development. While its developmental role is well established, its functions in peripheral T-cell responses remain poorly defined. Here, we investigated the responses of wild-type and LCK-deficient TCR-transgenic OT-I T cells across two infection models and an autoimmune diabetes model. LCK-deficient T cells exhibited reduced antigen-induced proliferation but, paradoxically, displayed enhanced effector differentiation in vivo. This phenotype likely reflects dysregulation of specific TCR signaling pathways, as LCK was more critical for ERK and NFAT activation than for NFκB, AP-1, or AKT/mTOR signaling. T cells deficient in a related kinase FYN also showed a slight increase in effector cell formation, suggesting that effector differentiation is regulated by their combined activity rather than distinct non-redundant roles. Our results reveal that LCK has two intrinsic roles in T-cell responses – promoting proliferation while restraining effector differentiation. These findings provide new insight into the molecular mechanisms of T-cell activation in vivo with implications for understanding the pathophysiology of LCK deficiency in humans and optimizing adoptive T-cell therapies.
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8. GSE342353 一种纳摩尔级亲和力抗体，可实现 O-GlcNAc 的灵敏标记和高分辨率基因组定位

• ✍️ 作者：未知作者
• 🏷️ 关键词：antibody
• 📝 描述：Contributors : Weiyao Hong ; Che Zhang ; Xiaoyang GuoSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusHigh-affinity O-GlcNAc-specific antibodies are crucial for the sensitive detection and functional study of O‑GlcNAcylation. Here, we report the development of a pan-specific, nanomolar-affinity O-GlcNAc antibody named EPR19847 by using a degenerate O‑GlcNAcylated peptide as the immunogen. The EPR19847 antibody can be used for O‑GlcNAc detection, imaging, isolation, and chromatin immunoprecipitation. Using this novel antibody, O-GlcNAcylated proteins were enriched and identified in mouse embryonic stem cells (mESCs). Chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) demonstrates that O-GlcNAc is enriched around the promoters of highly expressed genes, and that its genomic distribution is positively correlated with transcription-activating marks including H3K4me3, H3K9ac, and RNA Pol II in mESCs. Further analysis suggests a high occupancy of O-GlcNAcylation within super-enhancers. We anticipate that EPR19847 will serve as a powerful tool for the highly-sensitive detection and systematic functional dissection of O-GlcNAc.
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9. GSE324312 先天免疫细胞纤溶活性的时间调节

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Contributors : Paula A Klavina ; Roger J Preston ; Annie M CurtisSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPeritoneal macrophages are important for pathogen clearance, forming cell-pathogen aggregates held together by fibrin. This can be beneficial in limiting the spread of pathogens, however, persistent fibrin deposits can lead to abdominal adhesions which give rise to multiple comorbidities. How this process is regulated is poorly understood. Under inflammatory conditions, macrophages secrete PAI-1, a potent inhibitor of fibrinolysis. We found that macrophage fibrinolytic activity is dependent on the time of day. PAI 1 secretion by peritoneal macrophages was increased at the onset of activity (ZT13) compared to at the onset of rest (ZT1), both basally and following in vivo LPS stimulation. Furthermore, the fibrinolytic response was reduced at ZT13 compared to ZT1. We also establish a novel role for the Rev-erbα agonist SR9009 in reversing macrophage anti-fibrinolytic activity. The chrono-dependency of macrophage fibrinolytic activity was confirmed using SR9009, which potently inhibited PAI-1 and PAI-2 secretion from LPS-stimulated macrophages, boosting plasmin generation and fibrin clot lysis in the presence of both macrophages and endothelial cells. Moreover, SR9009 promoted intraperitoneal fibrinolysis in LPS-administered mice. Collectively, these data highlight a novel role for circadian regulation of macrophage fibrinolytic activity.
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10. GSE275198 探索 CM-白血病的转录组变化

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia
• 📝 描述：Contributors : Lianjun Zhang ; Yu-Hsuan Fu ; Ya-Huei KuoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTo explore the transcriptome change in CM-leukemia, we performed RNA-seq for bone marrow mononuclear cells from CM mice at the leukemic stage and control littermate.
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1. 一种比血液循环更古老的蛋白质可能彻底改变癌症免疫疗法。

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：A protein that evolved long before the human circulatory system may help unlock stronger cancer treatments. When C3 is produced inside tumors, it blocks immune-suppressing cells and gives immunotherapy a better chance to work. Researchers were even able to recreate this effect in resistant tumors, significantly improving survival in mice.
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• GSE274441 RNA-seq 检测了 CMK 和 M07E 细胞系在有或无 GNE987 存在的情况下的情况。
• GSE304561 COPD/肺气肿发病机制中B细胞和上皮细胞衰老的异质性[scRNA-seq]