Cellular and Molecular Life Sciences最新文献

{"title":"MicroRNA-34a-5p induces cell cycle arrest and leads to spermatogenesis failure by targeting CDC25A.","authors":"Meina Lin, Ziyan Shi, Xinren Chen, Xiang Ni, Yu Sui, Huan Li, Changji Guan, Zhiying Tian, Miao Jiang, Jingyi Jiang, Tingchao Guo, Yongping Lu","doi":"10.1007/s00018-025-05738-1","DOIUrl":"https://doi.org/10.1007/s00018-025-05738-1","url":null,"abstract":"<p><p>Non-obstructive azoospermia (NOA) is among the most severe type of male infertility, which is characterized by the absence of sperm in the ejaculate of affected individuals. The underlying causes of NOA remain largely unidentified, leading to a dearth of effective clinical interventions. This study aimed to explore a potential biomarker for NOA, and to elucidate the underlying mechanisms involved. The RNA-sequencing of the testis tissue revealed that miR-34a-5p increased, while CDC25A mRNA decreased in NOA patients compared to obstructive azoospermia (OA) controls. RT-qPCR confirmed that miR-34a-5p was upregulated in the seminal plasma of NOA patients compared to healthy individuals, demonstrating its potential as a discriminatory marker for distinguishing between NOA and healthy individuals. The dual-luciferase assay demonstrated that miR-34a-5p directly targets CDC25A and inhibits the cell proliferation of TM4, GC-1 and GC-2 cells by arresting the cell cycle at the G1 phase. Both in vitro and in vivo experiments, the overexpression of miR-34a-5p led to a reduction in the level of CDC25A and CCNB1, accompanied by an elevation in the level of CDK1 phosphorylation. In mice overexpressing miR-34a-5p, the testicular size, testicular organ coefficient, total epididymal sperm count and motility were significantly decreased, the structure of seminiferous tubules was disrupted, and the abnormal tubules was significantly increased. In summary, miR-34a-5p causes cell cycle arrest by targeting CDC25A, inhibiting the expression of CDC25A and CCNB1, preventing the dephosphorylation of CDK1, which ultimately leads to male spermatogenic failure. The miR-34a-5p level in seminal plasma may have potential value for the diagnosis of NOA.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"212"},"PeriodicalIF":6.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"4-octyl itaconate reduces human NLRP3 inflammasome constitutive activation with the cryopyrin-associated periodic syndrome p.R262W, p.D305N and p.T350M variants.","authors":"Cristina Molina-Lopez, Laura Hurtado-Navarro, Luke A J O'Neill, Pablo Pelegrin","doi":"10.1007/s00018-025-05699-5","DOIUrl":"10.1007/s00018-025-05699-5","url":null,"abstract":"<p><p>Cryopyrin-associated periodic syndrome (CAPS) is a condition characterized by dominant genetic variants in the NLRP3 gene, which lead to the formation of constitutively active inflammasomes. These inflammasomes play a crucial role in CAPS patients' inflammatory episodes, these being primarily driven by the production of interleukin (IL)-1b. Although treatment with IL-1 blockers is effective for CAPS, some patients develop refractory responses and adverse reactions to these therapies. Consequently, there is a need for novel treatments for CAPS patients. Promising candidates are the derivatives of itaconate, which have been shown to impair NLRP3 inflammasome activation and IL-1β release in blood mononuclear cells from CAPS patients. In this study, we provide insight into the inhibitory mechanisms by which the itaconate derivative 4-octyl itaconate (4-OI) acts on NLRP3 that has different gain-of-function mutations (p.R262W, p.D305N and p.T350M) associated with CAPS. Notably, 4-OI effectively blocks the basal auto-activation of the inflammasome formed by NLRP3 p.R262W, p.D305N and p.T350M variants, which in turn reduces caspase-1 activation, gasdermin D processing, and IL-18 release. Furthermore, after lipopolysaccharide priming of macrophages, 4-OI also decreases IL-1β gene expression and release. Overall, 4-OI impairs CAPS-associated inflammasome function at multiple levels, meaning that therapeutic agents based on itaconate could be a promising therapeutic approach to managing inflammatory episodes in CAPS patients carrying p.R262W, p.D305N or p.T350M variants.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"209"},"PeriodicalIF":6.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytes at the heart of sleep: from genes to network dynamics.","authors":"Félix Bellier, Augustin Walter, Laure Lecoin, Fréderic Chauveau, Nathalie Rouach, Armelle Rancillac","doi":"10.1007/s00018-025-05671-3","DOIUrl":"10.1007/s00018-025-05671-3","url":null,"abstract":"<p><p>Astrocytes have transcended their role from mere structural scaffolds to pivotal regulators of neural circuitry and sleep-wake dynamics. The strategic proximity of their fine processes to blood vessels and synapses positions them as key players in neurobiology, contributing to the tripartite synapse concept. Gap-junction proteins also enable astrocytes to form an extensive network interacting with neuronal assemblies to influence sleep physiology. Recent advances in genetic engineering, neuroimaging and molecular biology have deepened our understanding of astrocytic functions. This review highlights the different mechanisms by which astrocytes regulate sleep, notably through transcriptomic and morphological changes, as well as gliotransmission, whereby intracellular calcium (Ca²⁺) dynamics plays a significant role in modulating the sleep-wake cycle. In vivo optogenetic stimulation of astrocytes indeed induces ATP release, which is subsequently degraded into adenosine, modulating neuronal excitability in sleep-wake regulatory brain regions. Astrocytes also participate in synaptic plasticity, potentially modulating sleep-associated downscaling, a process essential for memory consolidation and preventing synaptic saturation. Although astrocytic involvement in synaptic maintenance is well supported, the precise molecular mechanisms linking these processes to sleep regulation remain to be elucidated. By highlighting astrocytes' multiple roles in sleep physiology, these insights deepen our understanding of sleep mechanisms and pave the way for improving sleep quality.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"207"},"PeriodicalIF":6.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant downregulation of Y-box binding protein 1 expression impairs the cell cycle in an m⁵C-dependent manner in human granulosa cells from patients with primary ovarian insufficiency.","authors":"Qichao Chen, Sisi Wang, Min Zhang, Yu Xiang, Qingqing Chen, Zhekun Li, Yang Song, Long Bai, Yimin Zhu","doi":"10.1007/s00018-025-05709-6","DOIUrl":"10.1007/s00018-025-05709-6","url":null,"abstract":"<p><p>Y-box binding protein 1 (YBX1) has been reported to play a role in human granulosa cell (GC) dysfunction by binding with long noncoding RNAs in patients with primary ovarian insufficiency (POI). 5-Methylcytosine (m⁵C) methylation is an abundant RNA epigenetic modification that is widely present in eukaryotic RNAs. However, whether YBX1, an important m⁵C reader, whether YBX1 participates in POI in an m⁵C- dependent manner remains unknown. Here, we demonstrated that the expression levels of YBX1 were decreased in GCs from patients with biochemical POI. YBX1 knockdown in a human granulosa cell line (KGN) impaired cell proliferation by preventing the G1 to S transition in the cell cycle. Conversely, YBX1 overexpression promoted the KGN cell proliferation. Integrated analysis of the transcriptome and m⁵C methylome profiles revealed that in human GCs, knockdown of YBX1 expression destabilized cell cycle-associated transcripts in an m⁵C-dependent manner, resulting in cell cycle arrest. Our results provide new insights of the pathogenesis of POI, revealing an alternative molecular mechanism in which YBX1 participates in human GC dysfunction by affecting the stability of cell cycle-associated genes in an m⁵C-dependent manner and thereby modulating GC proliferation.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"206"},"PeriodicalIF":6.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory metabolite 7α,25-OHC promotes TIMP1 expression in COVID-19 monocytes through synergy effect of SMARCC1/JUND/H3K27ac.","authors":"Ying Feng, Zheng Wu, Kefan Hu, Shenzhen Yuan, Jun Li, Yi Wang, Zhongyi Wang, Han Yang, Zhi-Hui Luo, Jingjiao Zhou","doi":"10.1007/s00018-025-05721-w","DOIUrl":"10.1007/s00018-025-05721-w","url":null,"abstract":"<p><p>Chromatin remodeling factors are involved in the inflammatory responses, contributing to tissue damage and multi-organ dysfunction in COVID-19 patients. However, the underlying mechanisms remain unclear. In this study, high-dimensional analyses of single-cell RNA sequencing and single-cell ATAC sequencing data revealed increased chromatin accessibility at the promoters or enhancers of the pro-inflammatory cytokine tissue inhibitor of metalloproteinase-1 (TIMP1), as well as altered gene transcription profiles in monocytes from COVID-19 patients. Motif enrichment and positive regulators analyses identified SMARCC1, the core subunit of the chromatin remodeling complex, and the transcription factor JUND as positive regulators to co-modulate TIMP1 expression. In-vitro experiments, co-immunoprecipitation and chromatin immunoprecipitation (ChIP)-qPCR, and others, demonstrated the collaboration of SMARCC1 and JUND. Increased 7α,25-dihydroxycholesterol (7α,25-OHC) enhanced SMARCC1-JUND interactions to co-regulate TIMP1 expression. Further investigation indicated that 7α,25-OHC promoted the expression of SMARCC1 and its co-localization with H3K27ac, which involved in the expression of TIMP1 and inflammatory responses. Our study highlights the critical roles of SMARCC1 and JUND in COVID-19 inflammation, and offers the potential targets for the prevention and treatment of COVID-19.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"208"},"PeriodicalIF":6.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic changes in neuroendocrine neoplasms.","authors":"Chunhua Hu, Lingyi Chen, Yi Ding, Mujie Ye, Qiyun Tang","doi":"10.1007/s00018-025-05656-2","DOIUrl":"10.1007/s00018-025-05656-2","url":null,"abstract":"<p><p>Neuroendocrine neoplasms (NENs) are a group of highly heterogeneous neoplasms originating from neuroendocrine cells with a gradually increased incidence. Metabolic change is one of the recognized markers of tumor progression, which has been extensively and systematically studied in other malignant tumors. However, metabolic change in NENs has been relatively poorly studied, and systematic reviews are lacking. We reviewed the relationship between metabolic changes and NENs from the aspects of glucose metabolism, lipid metabolism, metabolic syndrome, amino acid metabolism and metabolomics, and discussed the potential therapeutic strategies of metabolic changes for NENs.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"205"},"PeriodicalIF":6.2,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12084448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of CMIP contributes to preeclampsia development by impairing trophoblast function via the PDE7B-cAMP pathway.","authors":"Yina Li, Xinjing Yan, Haiyang Yu, Yuanbo Zhou, Yongrui Gao, Xinyuan Zhou, Yujie Yuan, Yangnan Ding, Qianqian Shi, Yang Fang, Hongmei Du, Enwu Yuan, Xin Zhao, Linlin Zhang","doi":"10.1007/s00018-025-05726-5","DOIUrl":"10.1007/s00018-025-05726-5","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia (PE) is one of the leading causes of perinatal maternal and fetal morbidity and mortality, but its precise mechanism remains elusive. Previous research has suggested that c-Maf-inducible protein (CMIP) is abnormally expressed in PE pathophysiology. Therefore, we aimed to explore the potential role of CMIP and its downstream molecules in PE.</p><p><strong>Methods: </strong>Multiplex immunofluorescence and immunohistochemical assays were conducted on preeclamptic placentas. Functional analysis of CMIP was performed in HTR-8/SVneo cells through transfection experiments in which either CMIP was overexpressed or downregulated. RNA sequencing was utilized to identify the molecular pathways downstream of CMIP. The impact of hypoxia on CMIP levels was assessed in three different types of trophoblast cells. The therapeutic efficacy of CMIP was evaluated in an N(ω)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE.</p><p><strong>Results: </strong>CMIP expression was downregulated in extrachorionic trophoblasts (EVTs) and syncytiotrophoblasts (STBs) in preeclamptic placentas. This downregulation of CMIP in trophoblast cells disrupts cell proliferation, migration, invasion, and angiogenesis by upregulating the PDE7B-cAMP pathway, while elevated CMIP levels enhance these cellular functions. Hypoxia reduced CMIP expression in all three types of trophoblast cells. Moreover, in a rat model of PE, supplementation with CMIP alleviated hypertension and increased fetal weight and number.</p><p><strong>Conclusions: </strong>Our study demonstrates for the first time that the CMIP-PDE7B-cAMP pathway contributes to PE development by influencing trophoblast function. The signaling pathway proteins involved in PE induced by CMIP may provide new clues to the occurrence of PE and new targets for future PE therapy.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"203"},"PeriodicalIF":6.2,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPI-anchorless prion disease is sensitive to oxidative stress and shows potential for treatment with edaravone, based on iPS-derived neuron study.","authors":"Kosuke Matsuzono, Hiroyuki Honda, Takafumi Mashiko, Reiji Koide, Eiji Sakashita, Hitoshi Endo, Tetsuyuki Kitamoto, Shigeru Fujimoto","doi":"10.1007/s00018-025-05698-6","DOIUrl":"10.1007/s00018-025-05698-6","url":null,"abstract":"<p><p>Only a few reports have generated induced pluripotent stem cells from patients with prion diseases, making it important to conduct translational studies using cells derived from individuals with prion protein (PRNP) mutations. In this study, we established induced pluripotent stem cells from a patient with a glycosylphosphatidylinositol-anchorless PRNP mutation (Y162X), which leads to abnormal deposits of prion protein in various organs. While no abnormal intracellular prion protein deposits were observed in the neurons differentiated from PRNP Y162X induced pluripotent stem cells, extracellular PrP aggregates secretions were significantly increased, and these cells were significantly more sensitive to oxidative stress compared to control cells. Utilizing this PRNP Y162X iPSC-derived neuron model, we discovered that edaravone reduced the sensitivity of PRNP Y162X cells to oxidative stress. Following this finding, we treated a PRNP Y162X patient with edaravone for two years, which successfully suppressed indicators of disease progression. Our study demonstrates that the pathology of the glycosylphosphatidylinositol-anchorless PRNP mutation is associated with oxidative stress and highlights the potential of induced pluripotent stem cell technology in identifying novel treatments for rare prion diseases.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"202"},"PeriodicalIF":6.2,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taurolidine inhibits influenza virus infection and prevents influenza-induced cytokine storm, vasoconstriction and lung damage.","authors":"Chaoxiang Lv, Jin Guo, Rongbo Luo, Yuanguo Li, Bingshuo Qian, Xiaopan Zou, Tiecheng Wang, Beilei Shen, Weiyang Sun, Yuwei Gao","doi":"10.1007/s00018-025-05636-6","DOIUrl":"https://doi.org/10.1007/s00018-025-05636-6","url":null,"abstract":"<p><p>Influenza virus causes worldwide outbreaks and seasonal epidemics, posing a severe threat to public health and social development. Effective prevention and treatment of influenza infections remain major challenge for global healthcare. In this study, we observed that taurolidine effectively inhibited the proliferation of several human or animal influenza virus strains and protected mice from lethal-infection. Taurolidine treatment decreased the viral titer in the lungs of infected mice, reduced the ratio of immune cells, and alleviated lung pathology. Additionally, taurolidine treatment attenuated the rise of blood pressure, pulse wave velocity, and pulmonary aortic thickness in a mouse model for influenza virus infection. We also found that taurolidine significantly decreased intracellular Ca²⁺ concentration and effectively alleviated pulmonary artery vasoconstriction during influenza virus infection. Mechanistically, we observed that vascular smooth muscle contraction signaling pathway was significantly enriched, and taurolidine inhibited the activation of the MLCK/p-MLC pathway. Taking together, these findings confirm the effectiveness of taurolidine as an antiviral agent and highlight its important roles in mitigating host immune cell infiltration and vasoconstriction induced by influenza virus infection.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"201"},"PeriodicalIF":6.2,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-126-5p protects from URSA via inhibiting Caspase-1-dependent pyroptosis of trophoblast cells.","authors":"Xiaoxiao Zhu, Ke Xu, Shuang Ai, Yingjie Zhang, Chu Chu, Ran Wei, Shufeng Gao, Lu Liu, Wei Li, Yunhong Zhang, Siambi Kikete, Xinkui Liu, Zhen Zhang, Xia Li","doi":"10.1007/s00018-025-05713-w","DOIUrl":"10.1007/s00018-025-05713-w","url":null,"abstract":"<p><p>Unexplained recurrent spontaneous abortion (URSA) is a distressing pregnancy complication that seriously threat to women's reproductive health. Trophoblast pyroptosis was involved in the occurrence of URSA, but the potential mechanism remains unclear. In this work, we found CASP1 transcription and the level of pyroptosis were significantly elevated in the villous tissues of URSA patients. Suppression of cell pyroptosis by Gasdermin-D (GSDMD) or Caspase-1 inhibitors can reduce embryo resorption rate of URSA mice, while Caspase-1 over-expression in normal pregnant (NP) mice can aggravate embryo resorption. Meanwhile, a pronounced decline in the expression of microRNA-126-5p (miR-126-5p) was found in URSA patients, which was inversely related to CASP1 expression. Over-expression of miR-126-5p restrained trophoblast pyroptosis via inhibiting Caspase-1/GSDMD signaling pathway by direct binding to 3'-UTR of CASP1. Moreover, experiments in vivo substantiated that up-regulation of miR-126-5p effectively suppressed Caspase-1-mediated pyroptosis in placental tissue and significantly reduced embryo resorption rate. Collectively, these results underscored that diminished miR-126-5p expression plays a crucial role in URSA by enhancing trophoblast pyroptosis through activating Caspase-1/GSDMD signaling pathway. As a result, miR-126-5p shows significant promise as a possible biomarker for diagnosis and treatment of URSA.</p>","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"204"},"PeriodicalIF":6.2,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}