详细内容（全部6条）

1. ⭐ GSE316765 植物和悬浮细胞中关键免疫调节因子的亚家族水平比较转录组学揭示了新的水稻稻瘟病抗性基因

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、resistance、transcriptomics
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Oryza sativa Japonica GroupPlants activate pattern-triggered immunity (PTI) through key immune components, including pattern recognition receptors (PRRs), receptor-like cytoplasmic kinases (RLCKs), and transcription factors (TFs), to combat pathogens. However, a comprehensive transcriptional overview of these immune regulators at the subfamily level during biotic stress in rice is currently lacking. The aims of this study were to characterize the expression profiles of OsPRRs, OsRLCKs, and OsTFs and establish a robust pipeline for selecting novel candidate genes involved in plant immunity. We identified differentially expressed genes (DEGs) within these families using transcriptomic data from both rice plants infected with Magnaporthe oryzae infection and rice suspension cell treated with chitin treatment. Our analysis revealed the transcriptional regulation of well-known immune-related subfamilies of OsPRRs, OsRLCKs, and OsTFs, such as RLK-LRR-XII and RLCK-VII, and identified several novel subfamilies with high proportions of DEGs that may contribute to pathogen perception and plant defense. We demonstrated that selecting candidates from overlapping DEGs between plant and suspension cell systems is an effective strategy for screening genes involved in rice immunity. Using this pipeline, novel immune regulators were identified, and their functions were confirmed. Two RLCKs, i.e., OsRLCK298 and OsBSR1, act as positive regulators of immunity against rice blast fungus, whereas two transcription factors, i.e., OsERF65 and OsERF96.2, act as negative regulators. This study provides a valuable transcriptomic resource and establishes a validated pipeline for gene discovery that could be applied to other stress responses and in other plant species.
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2. GSE317491 糖尿病肾病小鼠肾脏转录组测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、transcriptome
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAging is a major risk factor for diabetic kidney disease (DKD), with both conditions exhibiting similar renal pathology. We identify the energy-sensing molecule Retinoic acid-related orphan receptor γ (RORγ) as significantly downregulated in diabetic and aged kidneys. Tubule-specific RORγ deficiency exacerbates kidney injury, whereas its overexpression protects. Mechanistically, RORγ stabilizes insulin-induced gene 1 (INSIG1) by upregulating the deubiquitinase YOD1 and enhancing AMPK activity via CAB39, which together promote INSIG1 phosphorylation and subsequent stabilization. Stabilized INSIG1 potently blocks the ER-to-Golgi transport and activation of SREBP2 (cholesterol synthesis) and STING (inflammatory signaling). In diabetes, RORγ itself is suppressed transcriptionally by CTCF and functionally by impaired AMPK/SIRT1 signaling, which hinders its activation. Importantly, administration of a RORγ agonist or RORγ-enriched exosomes effectively alleviates diabetic kidney injury. Thus, RORγ emerges as a key regulatory node that mitigates DKD and renal aging by co-regulating AMPK-mediated metabolic and STING-driven innate immune pathways through INSIG1 stabilization.
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3. GSE316251 NR3C1、LAX1 和 RCAN3 作为循环表观遗传生物标志物在转移性胰腺癌预后和化疗反应预测中的应用

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、epigenetic
• 📝 描述：Contributors : Pablo Cano-Ramírez ; Marta Toledano-Fonseca ; María T Cano-Osuna ; Nerea Herrera-Casanova ; Emilio Carrillo-Pecero ; Antonio Rodríguez-Ariza ; Enrique Aranda ; María V García-OrtizSeries Type : Methylation profiling by genome tiling arrayOrganism : Homo sapiensPancreatic cancer remains highly lethal, largely due to late diagnosis and limited efficacy of treatments. Improving first-line treatment selection and patient monitoring requires novel, non-invasive biomarkers beyond CA19-9 and imaging. This study investigates epigenetic biomarkers from liquid biopsy with prognostic and predictive potential in metastatic PDAC (mPDAC). Genome-wide methylation profiling of cell-free DNA (cfDNA) from healthy individuals and stage IV mPDAC patients identified thirteen gene-associated CpG sites with significantly altered methylation patterns. ddPCR validation confirmed consistent methylation differences in LAX1, NR3C1 and RCAN3 between healthy and patient groups. Elevated LAX1 and RCAN3 methylation and reduced NR3C1 methylation at diagnosis were associated with poor prognosis and correlated with high-risk circulating biomarker profiles, including CA19-9 levels, RAS MAF, cfDNA concentration, and cfDNA fragmentation. Notably, baseline NR3C1 methylation levels predicted response to first-line FOLFIRINOX-based treatment with an acceptable 75% sensitivity and a high specificity of 92.86%. These findings highlight the clinical significance of cfDNA methylation as a minimally invasive biomarker source, emphasizing LAX1, NR3C1 and RCAN3 as prognostic biomarkers in mPDAC. Specifically, baseline NR3C1 methylation emerges as a promising predictor of treatment response, supporting personalized therapeutic strategies in mPDAC.
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4. GSE310935 基于治疗性腺病毒治疗复发性胶质母细胞瘤效应试验 (TARGET) 的 Delta-24-RGD 治疗后长期生存的系统免疫相关性

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune
• 📝 描述：Contributors : Chibawanye I Ene ; Sanjay Singh ; Thiagarajan Venkataraman ; Lynette M Phillips ; James P Long ; Deep Singh ; Nam D Tran ; Frank Tufaro ; P J Anand ; Nicholas Navin ; Sujit Prabhu ; Jeffrey S Weinberg ; Benjamin Larman ; Candelaria Gomez-Manzano ; Juan Fueyo ; Frederick F LangSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensPurpose: Treatment of high grade gliomas, particularly glioblastoma (GBM), with the oncolytic adenovirus Delta-24-RGD has previously produced anti-tumor effects in phase 1 clinical trials. These effects are mediated through direct oncolysis and activation of an anti-tumor immune response. In this study, we combined Delta-24-RGD with interferon gamma (IFN-𝛾), a potent activator of T-helper 1 CD8+ cell immune response. Patients and Methods: In the Phase 1b, multicenter, randomized, study (NCT02197169), we evaluated the combination of intratumoral injected Delta-24-RGD with subcutaneous administered IFN-𝛾 in 37 patients with recurrent high grade glioma and investigated potential systemic immune correlates of long-term survival. Twenty-seven patients were randomized 2:1 into two cohorts; Delta-24-RGD with IFN-𝛾 or Delta-24-RGD alone via a standard nashold biopsy needle. In an expansion cohort, 10 patients received intra-tumoral injected Delta-24-RGD via the MEMS Cannula (Neela Therapeutics). Results: Although the addition of IFN-𝛾 to Delta-24-RGD did not significantly increase the percentage of long term survivors compared to Delta-24RGF alone, the IFN-𝛾 cohort has the longest surviving patients after treatment (OS 44.2, 23.7, 20.6 and 20.1 months). Post-hoc analysis of plasma and peripheral blood mononuclear cells using viral phage immunoprecipitation sequencing antibody reactome profiling of viral epitopes (VirScan) and single cell RNA sequencing (scRNA seq) revealed that levels of circulating anti-adenovirus specific IgG and CD8+ NKT-like cells 2 months after treatment with Delta-24-RGD distinguished long term survivors from short term survivors. Conclusions: Immunological fitness assessed by an anti-adenoviral specific antibody response and higher levels of activated CD8+ NKT-like cells after Delta-24-RGD treatment could be used as early surrogates of a robust systemic immune response that correlates with rate of tumor growth and long-term survival.
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5. GSE309030 IFN-γ 通过 Meis1 诱导肿瘤细胞造血干细胞髓系造血

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor
• 📝 描述：Contributors : Xue Han ; Minyi Zhao ; Kexin Wang ; Weiwei Ma ; Songqi Zhu ; Ruiqing Zhou ; Uet Yu ; Bangxue Jiang ; Xiaoqing Bai ; Peng Lei ; Shunqing WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackgroundTumors associated overproduction of tissue-damaging myeloid cells and loss of lymphoid cell production were caused by chronic inflammation. Hematopoietic stem cells (HSCs) were the origin of all innate and adaptive immune cells and differentiate through a series of lineage-biased multipotent progenitors (MPPs) dependent on situations.MethodsMC38 tumor and Lewis lung cancer models were performed to evaluate HSCs differentiation biased. Through elisa assay and bioinformatic analysis, the key pro-inflammatory cytokine was selected, which promoted myeloid-biased differentiation of HSCs. Next, the main transcription factor was found in tumor induced myeloid-biased differentiation. Finally, HSC-derived myeloid-derived suppressor cells (MDSCs) and impaired T cell functions were measured to evaluate the reason of tumor progression. By targeting myeloid-biased HSCs, Emapalumab was used to suppress tumor progression.ResultsHere we found HSCs preserved myeloid-biased differentiation in MC38 tumor and Lewis lung cancer models, which reflected extensive properties in tumor models, and was induced by one of pro-inflammatory cytokines, IFN-γ. Transcriptional profiling indicated Meis homeobox 1 (Meis1) was enriched in tumor primed HSCs, and ablation of Meis1 in HSCs prevented HSCs-associated myeloid cell differentiation. HSC-derived MDSCs, which were primary factors, promoted tumor progression. Targeting myeloid differentiated HSCs, combination of anti-PD-1 and Emapalumab, an anti-IFN-γ antibody, inhibited HSC-derived MDSCs and enhanced T cells associated adoptive immune response to suppress tumor progression. Myelodysplastic syndrome (MDS), which was displayed abnormal myeloid cell differentiation induced by hematopoietic failure, was improved by treated with Emapalumab or Meis1 inhibitor.ConclusionsThese results suggested that targeting HSCs was a new approach to treat tumor, and combination of PD-1 and Emapalumab might serve as a novel therapeutic strategy to improve the response and efficacy of anticancer therapy.
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6. GSE287461 无线、无电池迷走神经电刺激：一种通过H3K18乳酸化介导的线粒体自噬抑制心脏肥大的新方法

• ✍️ 作者：未知作者
• 🏷️ 关键词：cardiac
• 📝 描述：Contributors : Pilong Shi ; Yang Liu ; Yuetong Sha ; Jiaxin Wang ; Jiajun Zhou ; Kai Liu ; Hongli SunSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Rattus norvegicusBackground: Electrical stimulation (ES) has been established as a reliable and beneficial approach in therapeutic rehabilitation, exhibiting negligible side effects. Nevertheless, research focusing on the application of ES for cardiac hypertrophy remains limited, as it fails to provide an enduring remedy for chronic diseases. Battery-free implants have been surgically placed on the surface of the vagus nerve in rats, and wireless ES has been applied for four weeks to observe potential alterations in cardiac hypertrophy.Methods: In this investigation, vagal ES, characterized by its wireless, battery-free, and fully implantable nature, was utilized to treat cardiac hypertrophy. The vagus nerve at the stimulation site was carefully embedded within an envelope, sealed securely using multiple bioabsorbable sutures. Subsequently, a cardiac hypertrophy model was induced in rats via abdominal aortic coarctation for four weeks. A comprehensive array of experimental techniques was employed, encompassing qRT-PCR, Western blotting, transmission electron microscopy, HE staining, WGA staining, Masson’s staining, immunohistochemistry, and immunofluorescence.Results: The findings of this investigation demonstrated that ES markedly attenuates cardiac hypertrophy. Metabolomic analysis revealed a notable reduction in lactate levels within myocardial tissue following ES. Proteomic analysis of myocardial tissues indicated a substantial decrease in the expression of autophagy and mitophagy-related proteins after ES. Additionally, ChIP-seq results identified BCL2 interacting protein 3 (Bnip3) as a binding partner for H3K18 lactylation (H3K18la), exploring its role in modulating mitophagy. Mechanistically, it was shown that ES reduced lactate accumulation through the upregulation of monocarboxylate transporter 4 (MCT4) by decreasing norepinephrine (NE) levels. Furthermore, ES reversed cardiac hypertrophy by diminishing H3K18la levels, thus inhibiting BNIP3 protein expression.Conclusion: Continuous ES effectively reduces intracellular lactate by lowering NE levels within myocardial tissue, inhibiting mitophagy mediated by H3K18la.This pathway assists in diminishing cardiac hypertrophy, emphasizing the critical involvement of the afferent vagal pathway in regulating cardiac hype…
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详细内容（全部4条）

1. 随着年龄增长，一种隐匿的免疫回路可能导致危险的炎症。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、inflammation
• 📝 描述：Aging immune cells may be sabotaging the body from within. Researchers found that macrophages produce a protein that locks them into a chronic inflammatory state, making infections like sepsis more deadly in older adults. Turning off this signal reduced inflammation and improved survival in older models. The findings hint at future treatments that could dial back harmful immune overreactions.
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2. 一种天然抗衰老分子可能有助于恢复阿尔茨海默病患者的记忆力。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging、Alzheimer
• 📝 描述：Researchers have found that a natural aging-related molecule can repair key memory processes affected by Alzheimer’s disease. The compound improves communication between brain cells and restores early memory abilities that typically fade first. Because it already exists in the body and declines with age, boosting it may offer a safer way to protect the brain. The discovery hints at a new strategy for slowing cognitive ageing before severe damage sets in.
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3. 结肠僵硬可能是年轻成年人罹患癌症的诱因之一

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Chronic inflammation may be quietly reshaping the colon and making it more vulnerable to early-onset colorectal cancer. Scientists found that colon tissue in younger patients was stiffer, even in areas that appeared healthy, suggesting these changes may happen before cancer develops. Lab experiments showed that cancer cells grow faster in rigid environments.
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4. 科学家揭示了癌症如何隐藏在人们的视线中

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Pancreatic cancer may evade the immune system using a clever molecular trick. Researchers found that the cancer-driving protein MYC also suppresses immune alarm signals, allowing tumors to grow unnoticed. When this immune-shielding ability was disabled in animal models, tumors rapidly collapsed. The findings point to a new way to expose cancer to the body’s own defenses without harming healthy cells.
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