Journal of Molecular Cell Biology最新文献_第6页

Fam3C alters Golgi apparatus morphology and function in triple negative breast cancer. Fam3C改变三阴性乳腺癌的高尔基体形态和功能。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-04-29 DOI: 10.1093/jmcb/mjaf042

Annamarie C Dalton, Elisabeth R M Rochel, William S Streitfeld, Cécile Fréreux, Breege V Howley, Philip H Howe

{"title":"Fam3C alters Golgi apparatus morphology and function in triple negative breast cancer.","authors":"Annamarie C Dalton, Elisabeth R M Rochel, William S Streitfeld, Cécile Fréreux, Breege V Howley, Philip H Howe","doi":"10.1093/jmcb/mjaf042","DOIUrl":"10.1093/jmcb/mjaf042","url":null,"abstract":"Fam3C, also known as ILEI, is an established regulator of the epithelial-to-mesenchymal transition (EMT) and breast cancer stem cell phenotypes. Multiple cancer cell models and orthotopic animal model experiments have demonstrated a role for Fam3C in tumor progression and metastasis. Here, we establish Fam3C's impact on triple negative breast cancer (TNBC) patients and genetically engineered mouse models of spontaneous breast cancer tumor progression. Though Fam3C is a known secreted protein, we discovered its retention in the Golgi apparatus through anchoring of its signal peptide into the membrane before its signal peptide and pro-peptide are processed and removed. While retained in the Golgi apparatus, Fam3C affects the overall morphology of the organelle and its biological functions, including alterations in protein secretion and invasive potential. Expanding our knowledge of the biological mechanisms behind EMT will help develop therapies to specifically target cells with increased metastatic potential in TNBC.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13198017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145541067","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

Posttranslational modifications in regulating Notch signaling pathway and tumor angiogenesis: from molecular mechanisms to therapeutic applications. 调节Notch信号通路和肿瘤血管生成的翻译后修饰：从分子机制到治疗应用。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-04-29 DOI: 10.1093/jmcb/mjaf051

Jiaan Wang, Meng Zhang, Donglai Wang

{"title":"Posttranslational modifications in regulating Notch signaling pathway and tumor angiogenesis: from molecular mechanisms to therapeutic applications.","authors":"Jiaan Wang, Meng Zhang, Donglai Wang","doi":"10.1093/jmcb/mjaf051","DOIUrl":"10.1093/jmcb/mjaf051","url":null,"abstract":"Tumorigenesis exhibits complex interactions with the vascular system. Targeting angiogenesis represents an emerging strategy for remodeling the tumor microenvironment. The Notch signaling pathway, a key regulatory mechanism, orchestrates tumor angiogenesis by modulating endothelial cell differentiation and vascular homeostasis. However, the clinical translation of Notch-targeted therapies is limited by severe toxicities due to lack of tissue specificity. Posttranslational modifications (PTMs) chemically regulate protein functions, thereby influencing multiple signaling cascades, including Notch signaling. Notably, Notch-associated PTMs are essential for signal transduction integrity. Some types of PTMs, such as glycosylation and ubiquitination, are the core for maintaining the integrity of the Notch signaling pathway. Dysfunctional Notch-related PTMs disrupt signal fidelity and drive pathological angiogenesis. This review systematically explores (i) crosstalk between Notch signaling and tumor angiogenesis, (ii) regulatory roles of PTMs on Notch molecules in tumor angiogenesis, and (iii) therapeutic potential of targeting Notch-related PTMs for anti-angiogenic strategies in tumor. We aim to elucidate the molecular nexus of PTMs-Notch-angiogenesis in tumor progression. Furthermore, we discuss therapeutic challenges in modulating Notch signaling pathway-dependent PTMs within tumor angiogenesis, focusing on critical barriers to their clinical translation in oncology.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13228142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687445","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

The inwardly rectifying potassium channel KCNJ12 regulates the stemness of hepatocellular carcinoma cells through the Wnt/β-catenin pathway. 内整流钾通道KCNJ12通过Wnt/β-catenin通路调控肝癌细胞的干性。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-04-29 DOI: 10.1093/jmcb/mjaf048

Zihan Zhao, Mixue Bai, Shan Wang, Yangqianwen Zhang, Shuowu Liu, Meiyu Bao, Shuang Lu, Dan Cao, Siyun Shen, Lili Xie, Hongyang Wang, Lei Chen

{"title":"The inwardly rectifying potassium channel KCNJ12 regulates the stemness of hepatocellular carcinoma cells through the Wnt/β-catenin pathway.","authors":"Zihan Zhao, Mixue Bai, Shan Wang, Yangqianwen Zhang, Shuowu Liu, Meiyu Bao, Shuang Lu, Dan Cao, Siyun Shen, Lili Xie, Hongyang Wang, Lei Chen","doi":"10.1093/jmcb/mjaf048","DOIUrl":"10.1093/jmcb/mjaf048","url":null,"abstract":"Emerging evidence implicates tumor stemness features-characterized by self-renewal capacity, microenvironment adaptability, and immune evasion mechanisms-as critical determinants of therapeutic resistance and recurrence in hepatocellular carcinoma (HCC). KCNJ12, an inward rectifier potassium channel, has shown electrophysiological functions in cardiomyocytes; however, its oncogenic potential and the role in hepatocarcinogenesis involving cancer stemness regulation remain unexplored. This study systematically characterizes the KCNJ12-mediated molecular pathway driving HCC tumorigenicity. Lentiviral-mediated overexpression and knockdown models with functional assessments revealed KCNJ12's critical role in maintaining cancer cell self-renewal capacity. Mechanistic studies using cycloheximide chase assays, Wnt pathway modulators (LiCl, SKL2001, and salinomycin), and protein interaction analyses demonstrated that KCNJ12 stabilizes β-catenin through the physical interaction with lipoprotein receptor-associated protein 6 (LRP6), disrupting AXIN/APC/GSK-3β complex assembly and subsequent proteasomal degradation. The nuclear β-catenin accumulation drives TCF/LEF-dependent transcriptional activation and thus enhances the self-renewal capacity of HCC cells. Our findings establish KCNJ12 as a novel Wnt/β-catenin regulator and propose dual therapeutic strategies against HCC-mediated chemoresistance: pharmacological suppression of KCNJ12 channel activity and targeted disruption of KCNJ12-LRP6 protein interactions. This mechanistic framework advances our understanding of stemness regulation in HCC and provides feasible targets for developing next-generation anti-HCC therapies.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13198016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145654519","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

Comments on 'BAF60a-dependent chromatin remodeling preserves β-cell function and contributes to the therapeutic benefits of GLP-1R agonists'. “baf60a依赖性染色质重塑保留β细胞功能，有助于GLP-1R激动剂的治疗效果”。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-04-03 DOI: 10.1093/jmcb/mjaf044

Qingqian Wu, Yue Gao, Zhuo-Xian Meng

引用次数: 0

Canonical Wnt signaling affects calcium homeostasis in serum-treated AC16 cells through MLN-mediated SERCA2a regulation. 典型Wnt信号通过mln介导的SERCA2a调控影响血清处理的AC16细胞的钙稳态。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-04-03 DOI: 10.1093/jmcb/mjaf050

Ang Li, Yuanyuan Shen, Zhenyan Li, Wenyu Jiang, Jie Su, Xiaomin Song, Lin Li

{"title":"Canonical Wnt signaling affects calcium homeostasis in serum-treated AC16 cells through MLN-mediated SERCA2a regulation.","authors":"Ang Li, Yuanyuan Shen, Zhenyan Li, Wenyu Jiang, Jie Su, Xiaomin Song, Lin Li","doi":"10.1093/jmcb/mjaf050","DOIUrl":"10.1093/jmcb/mjaf050","url":null,"abstract":"The canonical Wnt/β-catenin pathway critically regulates cardiac calcium homeostasis, yet its interplay with microenvironmental factors remains unclear. This study reveals that fetal bovine serum (FBS) treatment alters Wnt-mediated calcium dynamics in AC16 cardiomyocytes. While Wnt activation elevates cytosol calcium in serum-free conditions, FBS supplementation reverses this response: Wnt inhibitors (SFRP2, XAV939, and LF3) induce cytosol calcium accumulation, while the activators (LiCl and Wnt3a) lose efficacy. Mechanistically, FBS ablates RyR2 expression, uncoupling calcium-induced calcium release. Consequently, calcium handling shifts to SERCA2a-dependent regulation. We identify myoregulin (MLN) as a pivotal effector of Wnt/β-catenin signaling, with Wnt inhibition upregulating MLN to suppress SERCA2a activity. MLN knockdown (90% suppression) abolishes the effects of Wnt inhibitors on SERCA2a function and calcium distribution patterns. RyR2 reconstitution in FBS-treated cells restores calcium release but not Wnt activation responses, confirming the dominant role of MLN. Crucially, a combination of RyR2 overexpression and MLN depletion fully restores Wnt-calcium responses, phenocopying serum-free conditions. Our work establishes a serum-dependent regulatory axis where Wnt/β-catenin signaling maintains calcium homeostasis by repressing MLN, thereby preserving SERCA2a function. This FBS-induced shift mirrors pathological adaptations in heart failure, positioning MLN as a therapeutic target for calcium-handling disorders.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13093114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687453","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

NAMPT improves high-fat diet-induced nonalcoholic fatty liver disease (NAFLD) via the SIRT1-C/EBPβ-STEAP4-NRF2 axis. NAMPT通过SIRT1-C/ ebp - β- steap4 - nrf2轴改善高脂肪饮食诱导的非酒精性脂肪性肝病（NAFLD）。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-04-03 DOI: 10.1093/jmcb/mjaf045

Jingwu Zhao, Qinjin Li, Yi Wang, Bingbing Liu, Sisi Gui, Yazhen Zheng, Xiaodong Chen

{"title":"NAMPT improves high-fat diet-induced nonalcoholic fatty liver disease (NAFLD) via the SIRT1-C/EBPβ-STEAP4-NRF2 axis.","authors":"Jingwu Zhao, Qinjin Li, Yi Wang, Bingbing Liu, Sisi Gui, Yazhen Zheng, Xiaodong Chen","doi":"10.1093/jmcb/mjaf045","DOIUrl":"10.1093/jmcb/mjaf045","url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is a prevalent chronic condition, yet therapeutic targets remain elusive. Nicotinamide phosphoribosyl transferase (NAMPT) and six-transmembrane epithelial antigen of the prostate 4 (STEAP4) are integral regulators in various metabolic disorders. This study investigates the role and molecular mechanisms of NAMPT in NAFLD pathogenesis. We found that inhibiting NAMPT or silent information regulator 1 (SIRT1) exacerbates liver steatosis and impairs hepatic antioxidant defenses in high-fat diet (HFD)-induced obese mice, while reducing STEAP4 expression in liver tissues, suggesting that NAMPT and SIRT1 are pivotal in NAFLD progression and may regulate STEAP4. The role of NAMPT in SIRT1 expression involves nicotinamide adenine dinucleotide synthesis. Our results indicate that inhibiting SIRT1's deacetylase activity impairs CCAAT/enhancer-binding protein β (C/EBPβ) deacetylation and consequently its function. Additionally, STEAP4, previously identified as a C/EBPβ target, can upregulate the expression and nuclear translocation of NF-E2-related factor 2 (NRF2) to combat oxidative stress in NAFLD. This study confirms that NAMPT ameliorates NAFLD via the SIRT1-C/EBPβ-STEAP4-NRF2 signaling axis in HFD-induced obese mice, proposing a novel strategy for the prevention and treatment of NAFLD.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13108263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649012","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

NAD+ subcellular partitioning mediated by miR-183 and miR-96 regulates muscle stem cell differentiation. miR-183和miR-96介导的NAD+亚细胞分配调节肌肉干细胞分化。

IF 5.9 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-03-31 DOI: 10.1093/jmcb/mjag015

Mei Ma, Ruisen Ma, Zhuoyang Li, Siyi Shen, Wenqing Kong, Tianyuan Qiu, Zhoumin Niu, Jingjing Chen, Yuting Wu, Yan Li, Zi-Bing Jin, Yuying Li, Hao Ying

{"title":"NAD+ subcellular partitioning mediated by miR-183 and miR-96 regulates muscle stem cell differentiation.","authors":"Mei Ma, Ruisen Ma, Zhuoyang Li, Siyi Shen, Wenqing Kong, Tianyuan Qiu, Zhoumin Niu, Jingjing Chen, Yuting Wu, Yan Li, Zi-Bing Jin, Yuying Li, Hao Ying","doi":"10.1093/jmcb/mjag015","DOIUrl":"https://doi.org/10.1093/jmcb/mjag015","url":null,"abstract":"The intracellular abundance of NAD+, a vital metabolic cofactor, critically influences muscle stem cell (MuSC) function. However, the spatial regulation of NAD+ and its impact on MuSC function remain unclear. In this study, we demonstrated that the loss of miR-183 and miR-96 leads to inefficient skeletal muscle regeneration upon injury and triggers premature differentiation of MuSC-derived primary myoblasts. The underlying mechanism involves miRNA-mediated regulation through targeting SLC25A51, a mitochondrial transporter for NAD+ that elevates mitochondrial NAD+ while reducing cytoplasmic NAD+ levels. Our results suggest that the reduction in cytoplasmic NAD+ diminishes SIRT1-mediated deacetylation, increasing H4K16ac at the promoters of myogenic genes to promote differentiation. Concurrently, the mitochondrial NAD+ accumulation stimulates the tricarboxylic acid cycle, leading to elevated levels of ATP and citrate. These metabolites allosterically activate the ACLY pathway, which in turn increases acetyl-CoA production, thereby supplying acetyl groups for H4K16ac. Furthermore, SIRT3 knockdown impaired myogenic differentiation and attenuated the increased levels of both ATP and acetyl-CoA in miR-183/96-deficient cells, suggesting that the elevated mitochondrial NAD+ also enhances differentiation via SIRT3-mediated regulation of mitochondrial metabolism and acetyl-CoA production. Our work establishes miR-183 and miR-96 as critical regulators of epigenetic-metabolic networks that influence MuSC differentiation through subcellular partitioning of NAD+, ensuring proper regeneration timing.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581610","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}

引用次数: 0

Cyclin B3 dsRNA Orchestrate Meiotic Progression in Porcine Oocytes. 细胞周期蛋白B3 dsRNA调控猪卵母细胞减数分裂进程。

IF 5.9 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-03-24 DOI: 10.1093/jmcb/mjag014

Yanlong Zhu, Xi-Qing Jiang, Shuang Gao, Chen-Yuan Zhang, Hongshuang Xie, Qingbo Yang, Zi-Hao Wang, Zhuang Chai, Zhonghua Liu, Jing-Tao Sun, Tianyao He, Jiaqiang Wang, Jun-Xue Jin

{"title":"Cyclin B3 dsRNA Orchestrate Meiotic Progression in Porcine Oocytes.","authors":"Yanlong Zhu, Xi-Qing Jiang, Shuang Gao, Chen-Yuan Zhang, Hongshuang Xie, Qingbo Yang, Zi-Hao Wang, Zhuang Chai, Zhonghua Liu, Jing-Tao Sun, Tianyao He, Jiaqiang Wang, Jun-Xue Jin","doi":"10.1093/jmcb/mjag014","DOIUrl":"https://doi.org/10.1093/jmcb/mjag014","url":null,"abstract":"Cyclin B3 (CCNB3) plays a critical regulatory role in mammalian meiosis. Studies in mice have demonstrated that CCNB3 interacts with CDK1 to modulate the activity of MPF, thereby driving meiotic progression. However, the functional mechanisms of CCNB3 in porcine oocytes remain unclear. In this study, we reveal for the first time that knockdown of CCNB3 in porcine oocytes induces meiotic arrest at metaphase I, accompanied by impaired degradation of cyclin B1 and securin. Further investigation identifies that the antisense long non-coding RNA CCNB3-AS forms a double-stranded RNA (dsRNA) structure with the CCNB3 mRNA, significantly enhancing its stability by resisting PAT1 homolog 1 (PATL1)-mediated degradation. Mechanistically, CCNB3-AS interacts with the scaffold protein Vimentin (VIM). Structural analysis reveals that VIM binds to the PAT1 domain of PATL1 and is capable of influencing the ability of CNOT7, the core subunit of the CCR4-NOT complex, to bind to PATL1, ultimately maintaining stable CCNB3 mRNA expression. Our study elucidates the molecular mechanism by which the CCNB3-AS/CCNB3 dsRNA duplex cooperates with VIM and PATL1 to collectively regulate meiosis in porcine oocytes. Furthermore, we reveal the non-canonical role of VIM in mRNA degradation, providing new theoretical support for understanding the mechanisms underlying porcine oocyte meiosis.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504111","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}

引用次数: 0

In vitro oogenesis and parthenogenetic development of chicken female germ cells. 鸡雌性生殖细胞的体外卵发生和孤雌发育。

IF 5.9 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-03-20 DOI: 10.1093/jmcb/mjag013

Yuxiao Ma, Changhao Yu, Jiahui Wei, Feiyi Wang, Qing Sun, Jingui Hao, Zimo Zhu, Pengxiang Zhao, Guiyu Zhu

{"title":"In vitro oogenesis and parthenogenetic development of chicken female germ cells.","authors":"Yuxiao Ma, Changhao Yu, Jiahui Wei, Feiyi Wang, Qing Sun, Jingui Hao, Zimo Zhu, Pengxiang Zhao, Guiyu Zhu","doi":"10.1093/jmcb/mjag013","DOIUrl":"https://doi.org/10.1093/jmcb/mjag013","url":null,"abstract":"In vitro reconstruction of gametogenesis is an important research direction in germ cell biology and assisted reproduction. While substantial progress has been made in the in vitro oogenesis of mammalian germ cells, analogous approaches in avian species remain unexplored. In this study, we investigated the capacity of chicken primordial germ cells (PGCs) and oogonial stem cells (OSCs) to differentiate into oocyte-like cells in vitro. Under meiotic induction with retinoic acid and vitamin C, both PGCs and OSCs initiated meiosis but arrested at the prophase I stage. Subsequent exposure to follicle-stimulating hormone, human chorionic gonadotropin, and progesterone facilitated the resumption of meiosis, leading to the formation of secondary oocytes. Next, parthenogenetic activation experiments showed that these germ cell-derived secondary oocytes were capable of undergoing cleavage and developing into blastomeres. Furthermore, in the aged and stopped-laying ovaries, OSCs retained the proliferation ability but lost their differentiation potential to increase the risk of germ cell tumor. The current in vitro oogenesis system enabled evaluation of healthy and compromised oocytes in avian species. This study not only provides direct evidence for the in vitro recapitulation of oogenesis in birds but also offers new avenues for preserving female germ cells and mass production of chicken oocytes.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147486342","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}

引用次数: 0

A high-throughput method for quantifying relative telomere length in single cells in situ combined with live-cell imaging. 一种高通量的方法，定量相对端粒长度在单细胞原位结合活细胞成像。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-03-19 DOI: 10.1093/jmcb/mjaf046

Qingyang Sun, Zhengzhi Zou, Mingwei Min

引用次数: 0