Cellular and Molecular Life Sciences最新文献_第9页

LRRK2 kinase modulates glucose-stimulated insulin secretion via RAB8 phosphorylation and ciliogenesis. LRRK2激酶通过RAB8磷酸化和纤毛发生调节葡萄糖刺激的胰岛素分泌。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-17 DOI: 10.1007/s00018-025-05810-w

Nevia Dule, Algerta Marku, Alessandra Galli, Francesca Pischedda, Adriano Lama, Michela Castagna, Paola Marciani, Federico Bertuzzi, Giovanni Piccoli, Carla Perego

{"title":"LRRK2 kinase modulates glucose-stimulated insulin secretion via RAB8 phosphorylation and ciliogenesis.","authors":"Nevia Dule, Algerta Marku, Alessandra Galli, Francesca Pischedda, Adriano Lama, Michela Castagna, Paola Marciani, Federico Bertuzzi, Giovanni Piccoli, Carla Perego","doi":"10.1007/s00018-025-05810-w","DOIUrl":"10.1007/s00018-025-05810-w","url":null,"abstract":"Leucine-rich repeat kinase 2 (LRRK2) encodes a multidomain protein whose mutations have been identified as genetic risk factors for Parkinson's disease (PD), an age-related neurodegenerative disorder. Outside the nervous system, LRRK2 is expressed in multiple tissues, including the endocrine pancreas, but its role here is unknown. Using pharmacological and molecular approaches, we show that LRRK2 kinase activity regulates stimulated insulin secretion by influencing secretory granule trafficking. The PD-associated LRRK2 mutant G2019S, characterized by enhanced kinase activity, increases the basal insulin release in complementary in vitro models and affects the metabolic profile in transgenic mice. Mechanistically, we demonstrate that LRRK2 kinase activity influences the formation of the primary cilium, an antenna-like structure acting as signaling platform to regulate hormones secretion. Specifically, LRRK2 phosphorylates RAB8 in a glucose-dependent manner, facilitating its recruitment to the primary cilium. These findings identify LRRK2 as a regulator of insulin secretion in pancreatic β-cells. Given the role of insulin signaling and glucose homeostasis in the nervous system, our data suggest that LRRK2 may also contribute to PD development through peripheral action.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"276"},"PeriodicalIF":6.2,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658582","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}

引用次数: 0

Integrative proteomics and metabolomics analyses reveals the regulation of autophagy and ferroptosis by RAB10 through Slc37a2/mTOR pathway in breast cancer. 综合蛋白质组学和代谢组学分析揭示RAB10通过Slc37a2/mTOR途径调控乳腺癌自噬和铁凋亡。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-14 DOI: 10.1007/s00018-025-05788-5

Yuxin Ji, Ruonan Li, Guohui Tang, Yuhan Xiao, Ruyin Ye, Jiwen Shi, Chenchen Geng, Ruorong Ran, Chengle Zhu, Wenrui Wang, Changjie Chen, Qingling Yang

{"title":"Integrative proteomics and metabolomics analyses reveals the regulation of autophagy and ferroptosis by RAB10 through Slc37a2/mTOR pathway in breast cancer.","authors":"Yuxin Ji, Ruonan Li, Guohui Tang, Yuhan Xiao, Ruyin Ye, Jiwen Shi, Chenchen Geng, Ruorong Ran, Chengle Zhu, Wenrui Wang, Changjie Chen, Qingling Yang","doi":"10.1007/s00018-025-05788-5","DOIUrl":"10.1007/s00018-025-05788-5","url":null,"abstract":"Breast cancer (BC) is the most prevalent and highly heterogeneous malignancy affecting females worldwide, and its development is closely linked to metabolic reprogramming. In this study, label-free quantification (LFQ) was used to analyze the protein expression in exosomes secreted by BC drug-resistant cells, identifying RAS-associated binding protein (RAB) 10 as the most significantly upregulated protein. RAB10, a member of the small GTPase family with complex biological functions, is highly expressed in BC and is associated with poor prognosis. In this study, we mainly utilized mouse breast cancer 4T-1 cells (wild-type control cells) and tumor-induced 4T-1 cells (isolated from mouse in situ tumor tissues to simulate the phenotype of the in vivo tumor microenvironment), and on this basis, conducted in vitro functional verification and in vivo tumorigenesis experiments. A comprehensive multi-omics analysis, including metabolomics and proteomics, following RAB10 knockdown, demonstrated the crucial role of RAB10 in regulating central carbon metabolism, which is essential for autophagy and ferroptosis in BC cells. Our study further confirmed that RAB10 mediates metabolic reprogramming in BC cells by regulating the Slc37a2/mTOR pathway, leading to enhanced autophagy and inhibition of ferroptosis. This comprehensive multi-omics analysis elucidated the key molecular and regulatory mechanisms underlying RAB10-induced metabolic reprogramming in tumors, providing potential new therapeutic targets and biomarkers for prognostic assessment in BC treatment.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"275"},"PeriodicalIF":6.2,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625492","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}

引用次数: 0

Correction: A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication. 纠正：抗病毒防御的双刃剑：ATG7结合骰子促进病毒复制。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-12 DOI: 10.1007/s00018-025-05762-1

Yaotang Wu, Yang Wu, Chenlu Wang, Ningna Xiong, Wenxin Ji, Mei Fu, Junpeng Zhu, Zhixin Li, Jian Lin, Qian Yang

引用次数: 0

Natriuretic peptides as novel regulators of dendritic cells-mediated inflammation. 利钠肽作为树突状细胞介导的炎症的新调节剂。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-11 DOI: 10.1007/s00018-025-05769-8

Giorgia Manni, Estevao Carlos Silva Barcelos, Doriana Ricciuti, Benedetta Pieroni, Marco Gargaro, Giulia Mencarelli, Hans Acha-Orbea, Vincenzo Nicola Talesa, Letizia Mezzasoma, Francesca Fallarino

{"title":"Natriuretic peptides as novel regulators of dendritic cells-mediated inflammation.","authors":"Giorgia Manni, Estevao Carlos Silva Barcelos, Doriana Ricciuti, Benedetta Pieroni, Marco Gargaro, Giulia Mencarelli, Hans Acha-Orbea, Vincenzo Nicola Talesa, Letizia Mezzasoma, Francesca Fallarino","doi":"10.1007/s00018-025-05769-8","DOIUrl":"10.1007/s00018-025-05769-8","url":null,"abstract":"Natriuretic Peptides (NPs), including atrial (ANP) and brain (BNP) types, exert pleiotropic effects in regulating immune responses via the Natriuretic Peptide Receptor-1 (NPR1), expressed across various immune cells. While NPs are established inhibitors of inflammasome activation and IL-1β secretion in human monocytes, their role in dendritic cells (DCs)-key regulators of innate and adaptive immunity-remains unclear. Inflammasome activation in DCs can yield both protective and detrimental outcomes depending on the context of the disease, suggesting that modulating this pathway could offer a promising pharmacological strategy for controlling immune responses. This study explored the regulation of the NLRP3 inflammasome by NPs in two conventional DC subsets: cDC1 and cDC2. We found that both subsets express basal levels of the NPR1 receptor, which increase under inflammatory conditions. Additionally, cDCs themselves produce ANP and BNP during inflammation. Although both subsets express basal levels of NLRP3 inflammasome proteins, cDC2 display a more robust NLRP3/IL-1β activation in response to LPS + ATP stimulation compared to cDC1. Notably, the NPs/NPR1 axis suppresses NLRP3 activation more effectively in the cDC2 subset by acting at translational and post-translational levels. These findings highlight NPs as a novel mechanism for controlling the inflammatory phenotype of cDCs and underscores NPs/NPR1 axis as therapeutic target for immune modulation of DC subsets.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"273"},"PeriodicalIF":6.2,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607625","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}

引用次数: 0

Organoids as powerful models of endometrium epithelium in transcriptomic, cellular and functional mimicry. 类器官是子宫内膜上皮在转录组学、细胞学和功能模拟中的强大模型。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-07 DOI: 10.1007/s00018-025-05807-5

Martina Ciprietti, Celine Bueds, Hugo Vankelecom, Joris Vriens

{"title":"Organoids as powerful models of endometrium epithelium in transcriptomic, cellular and functional mimicry.","authors":"Martina Ciprietti, Celine Bueds, Hugo Vankelecom, Joris Vriens","doi":"10.1007/s00018-025-05807-5","DOIUrl":"10.1007/s00018-025-05807-5","url":null,"abstract":"Organoids have emerged as revolutionary biomimetic systems that offer a physiologically relevant in vitro model to study the specific tissue or organ of origin. In the field of female reproductive biology, endometrial organoids have proven their high value in the exploration of intricate physiological processes of the endometrium such as hormonal differentiation (decidualization) and embryo-receptivity, as well as to understand the pathophysiology of diseases associated with endometrial deficits. Moreover, organoid-based adhesion models have emerged as appropriate in vitro platform that faithfully reproduces the receptive endometrium. These in vitro models offer new tools to explore the molecular mechanisms of the early embryo-endometrium interaction and to bypass the barrier of ethical restrictions. This review highlights recent advances in the endometrial research domain, focusing on endometrial epithelial organoid models that closely replicate the cellular, transcriptomic and functional characteristics of the native tissue. A comprehensive overview of the transcriptomic changes during the menstrual cycle is provided, as well as of the detailed comparison between the different cell populations of the endometrium and the endometrial organoid model. Here, we provide evidence that endometrial organoids mimic the native endometrial tissue and offer relevant tools to advance our understanding of endometrial (patho)biology, enabling us to gain insights into molecular pathways.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"272"},"PeriodicalIF":6.2,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574867","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}

引用次数: 0

HUWE1 is involved in Sertoli cell polarity establishment by ubiquitination mediated degradation of WT1. HUWE1通过泛素化介导的WT1降解参与支持细胞极性的建立。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-03 DOI: 10.1007/s00018-025-05779-6

Bowen Liu, Mengyue Wang, Changhuo Cen, Zhiming Shen, Jiayi Li, Xiuhong Cui, Xudong Zhao, Min Chen, Fei Gao

{"title":"HUWE1 is involved in Sertoli cell polarity establishment by ubiquitination mediated degradation of WT1.","authors":"Bowen Liu, Mengyue Wang, Changhuo Cen, Zhiming Shen, Jiayi Li, Xiuhong Cui, Xudong Zhao, Min Chen, Fei Gao","doi":"10.1007/s00018-025-05779-6","DOIUrl":"10.1007/s00018-025-05779-6","url":null,"abstract":"HUWE1, a member of HECT E3 ubiquitin ligase family, is implicated in a variety of cellular processes. Recent studies find that HUWE1 also plays critical roles in germ cell development and inactivation of HUWE1 causes germ cell loss in both male and female mice. In this study, we found that Huwe1 was also highly expressed in testicular Sertoli cells. Inactivation of Huwe1 in Sertoli cells resulted in loss of cell polarity, which in turn caused germ cells loss and male infertility. Further study revealed that dysregulation in the expression of cytoskeletal and adhesion-related molecules, as well as a significant increase in EMT-related trans-factors SNAI1&2 in Huwe1-deficient Sertoli cells. Intriguingly, the protein level of WT1 was significantly increased in Huwe1-deficient Sertoli cells, and overexpression of Wt1 in Sertoli cells also caused the defects in spermatogenesis which was consistent with Huwe1 CKO mouse model. Furthermore, the defect of spermatogenesis in Huwe1 CKO mice was partially rescued by deleting one allele of Wt1 gene. Mechanistic studies revealed that WT1 interacts with HUWE1 protein and it could be ubiquitinated by HUWE1. Our study demonstrates that HUWE1 is involved in the establishment of Sertoli cell polarity mainly by regulating the protein level of WT1 gene.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"271"},"PeriodicalIF":6.2,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559354","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}

引用次数: 0

Cell division cycle protein 42-driven activation of the MKK3/6-p38 signaling pathway participates in cardiac remodeling in mice. 细胞分裂周期蛋白42驱动的MKK3/6-p38信号通路激活参与小鼠心脏重构。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-03 DOI: 10.1007/s00018-025-05743-4

Ke Wen, Lin Xie, Quan-Wen Liu, Guan-Hui Yu, Xu-Hui Qiao, Yu-Chun Huang, Lu Wang, Xin Li, Li-Dan Wen, Xiao-Lei Wang, Jing He, Xin-Yu Xiao, Xiao-Xiao Zhao, Ling-Fang Wang, Hong-Bo Xin, Ke-Yu Deng

{"title":"Cell division cycle protein 42-driven activation of the MKK3/6-p38 signaling pathway participates in cardiac remodeling in mice.","authors":"Ke Wen, Lin Xie, Quan-Wen Liu, Guan-Hui Yu, Xu-Hui Qiao, Yu-Chun Huang, Lu Wang, Xin Li, Li-Dan Wen, Xiao-Lei Wang, Jing He, Xin-Yu Xiao, Xiao-Xiao Zhao, Ling-Fang Wang, Hong-Bo Xin, Ke-Yu Deng","doi":"10.1007/s00018-025-05743-4","DOIUrl":"10.1007/s00018-025-05743-4","url":null,"abstract":"Cell division cycle protein 42 (Cdc42) is a member of the Rho GTPase subfamily that serves as a signal mediating factor in cell cycle division, cytoskeleton arrangement, cell polarization, membrane trafficking and signal transduction. However, the role of Cdc42 in cardiac remodeling, including hypertrophy and fibrosis, remains controversial. This study aimed to clarify the role and underlying mechanism of Cdc42 in cardiac remodeling. Cardiac Cdc42 knockout (Cdc42CKO) mice were generated by crossing Cdc42loxP/loxP mice with MLC2v-Cre mice. Mouse cardiac remodeling models were induced by subcutaneous administration of AngII (1500 ng/kg/min) for 7 days or transverse aortic constriction (TAC) for 2 or 8 weeks. Our results showed that cardiac Cdc42 deletion significantly suppressed AngII- or TAC-induced cardiac hypertrophy and fibrosis and improved cardiac function in mice. Cdc42CKO or specific inhibition of Cdc42, markedly inhibited Ang II-mediated activation of the MKK3/6-p38 cascade in the heart and in isolated newborn/adult mouse cardiomyocytes or H9c2 cells. Furthermore, Cdc42 overexpression increased the surface area and hypertrophic gene expression in myocytes, whereas ML141 (a Cdc42 inhibitor) and SB203580 (a p38 inhibitor) specifically decreased p38 activation and hypertrophy in Cdc42-overexpressing or AngII-induced hypertrophic cardiomyocytes, indicating that p38 is a downstream effector of Cdc42 in cardiac hypertrophy. Taken together, our results demonstrated that Cdc42 is a key driver of cardiac remodeling via activation of the p38 signaling pathway.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"269"},"PeriodicalIF":6.2,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559353","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}

引用次数: 0

Aquaglyceroporin-7 ameliorates sorafenib resistance and immune evasion in hepatocellular carcinoma through inhibition of lipid accumulation. Aquaglyceroporin-7通过抑制脂质积累改善肝细胞癌索拉非尼耐药和免疫逃避。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-03 DOI: 10.1007/s00018-025-05801-x

Guangsi He, Wenzhu Shao, Weifei Wang, Lu Sun, Beibei Gao, Jie Wei

{"title":"Aquaglyceroporin-7 ameliorates sorafenib resistance and immune evasion in hepatocellular carcinoma through inhibition of lipid accumulation.","authors":"Guangsi He, Wenzhu Shao, Weifei Wang, Lu Sun, Beibei Gao, Jie Wei","doi":"10.1007/s00018-025-05801-x","DOIUrl":"10.1007/s00018-025-05801-x","url":null,"abstract":"Sorafenib, a multikinase inhibitor targeting cell growth and angiogenesis, was approved for advanced unresectable hepatocellular carcinoma (HCC) in 2007. This investigation aims to elucidate the involvement of aquaglyceroporin-7 (AQP7) in regulating sorafenib resistance (SR) in HCC. AQP7 was downregulated in HCC-SR cells. AQP7 upregulation inhibited lipid accumulation, enhanced the sorafenib sensitivity of SR cells, and improved immune evasion. TBX19 protein was elevated in HCC-SR cells, and TBX19 repressed AQP7 transcription by binding to its promoter. E3-ubiquitin ligase MGRN1 was reduced in HCC, and its overexpression promoted TBX19 degradation. MGRN1 overexpression enhanced AQP7 and improved SR and immune evasion in HCC, which was reversed by TBX19 overexpression. Mouse HCC cells Hepa1-6 were used to construct an orthotopic tumor model and to analyze the effects of AQP7 and MGRN1 expression on the in vivo antitumor effects of Sorafenib, lipid accumulation in tumor tissues, and immune cell infiltration. MGRN1 silencing in Hepa1-6 cells induced sorafenib resistance and created an immunosuppressive tumor microenvironment, which was repressed by AQP7 upregulation. In conclusion, MGRN1 loss in HCC-SR cells blocked TBX19 degradation and strengthened TBX19-mediated AQP7 repression, leading to immune evasion. Targeting this signaling might offer a promising therapeutic strategy to overcome SR in HCC.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"270"},"PeriodicalIF":6.2,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559352","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}

引用次数: 0

NSD proteins in anti-tumor immunity and their therapeutic targeting by protein degraders. NSD蛋白在抗肿瘤免疫中的作用及其蛋白降解物的靶向治疗作用。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-06-30 DOI: 10.1007/s00018-025-05806-6

Suresh Chava, Narendra Wajapeyee

{"title":"NSD proteins in anti-tumor immunity and their therapeutic targeting by protein degraders.","authors":"Suresh Chava, Narendra Wajapeyee","doi":"10.1007/s00018-025-05806-6","DOIUrl":"10.1007/s00018-025-05806-6","url":null,"abstract":"Chromatin modifiers, owing to their enzymatic activities and frequent overexpression or hyperactivation in cancer, have emerged as promising therapeutic targets. Among these, the nuclear receptor-binding SET domain (NSD) family of proteins catalyzes lysine methylation-a key histone post-translational modification that is implicated in diverse biological processes, primarily through the regulation of transcription. Previous studies have demonstrated that NSD proteins are often overexpressed, mutated, or involved in chromosomal translocations in both hematologic malignancies and solid tumors, thereby regulating tumor initiation and progression. Motivated by these insights, a range of NSD-targeting agents, including targeted protein degraders such as proteolysis-targeting chimeras (PROTACs), have been developed and have exhibited notable anti-cancer activities. In this review, we provide an overview of the NSD family of protein, highlighting their roles in regulating anti-tumor immunity and their implications for immunotherapy response and resistance. We further assess the current landscape of NSD-targeted protein degrader-based therapeutics and their potential utility as anti-cancer agents.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"268"},"PeriodicalIF":6.2,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526612","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}

引用次数: 0

SOX3 facilitates granulosa cell proliferation and suppresses cell apoptosis through modulating PI3K/AKT pathway by targeting SPP1. SOX3通过靶向SPP1调控PI3K/AKT通路，促进颗粒细胞增殖，抑制细胞凋亡。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-06-30 DOI: 10.1007/s00018-025-05797-4

Rui Cai, Cong Li, Wenhui Shi, Fenfen Xie, Mengmeng Fan, Hao Zhang, Zhuang Liu, Yuanhua Chen, Qiang Hong

引用次数: 0