Biology of the Cell最新文献

{"title":"Editorial for the “Cell Energetics & Cell Mechanics” themed issues","authors":"René Marc Mège, Geri Kreitzer","doi":"10.1111/boc.202400026","DOIUrl":"10.1111/boc.202400026","url":null,"abstract":"","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 5","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140142739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Testicular niche repair after gonadotoxic treatments: Current knowledge and future directions","authors":"Amirhossein Mohammadi,&nbsp;Zahra Bashiri,&nbsp;Sara Rafiei,&nbsp;Hamidreza Asgari,&nbsp;Ronak Shabani,&nbsp;SeyedJamal Hosseini,&nbsp;Morteza Koruji","doi":"10.1111/boc.202300123","DOIUrl":"10.1111/boc.202300123","url":null,"abstract":"<p>The testicular niche, which includes the germ cells, somatic cells, and extracellular matrix, plays a crucial role in maintaining the proper functions of the testis. Gonadotoxic treatments, such as chemotherapy and radiation therapy, have significantly improved the survival rates of cancer patients but have also been shown to have adverse effects on the testicular microenvironment. Therefore, repairing the testicular niche after gonadotoxic treatments is essential to restore its function. In recent years, several approaches, such as stem cell transplantation, gene therapy, growth factor therapy, and pharmacological interventions have been proposed as potential therapeutic strategies to repair the testicular niche. This comprehensive review aims to provide an overview of the current understanding of testis damage and repair mechanisms. We will cover a range of topics, including the mechanism of gonadotoxic action, repair mechanisms, and treatment approaches. Overall, this review highlights the importance of repairing the testicular niche after gonadotoxic treatments and identifies potential avenues for future research to improve the outcomes for cancer survivors.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cells flowing to attain functionality","authors":"Martín G. Bellino","doi":"10.1111/boc.202300120","DOIUrl":"10.1111/boc.202300120","url":null,"abstract":"<p>Unraveling the fundamental biological processes underpinning cell functions and behavior remains a key challenge. Researchers working on cell biological processes might want to take a look at microscale cell flow as functionality genesis. This Commentary provides an outlook on how cell-microcirculation interplay promises to lead to exciting insights into the cell biology complexity.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diosgenyl glucosamine conjugates increase pro-apoptotic and selective activities in cancer cell lines","authors":"Martínez Mata Sergio Iván,&nbsp;Escobar Sánchez María Luisa,&nbsp;López Muñoz Hugo,&nbsp;Hilario Martínez Jazmín Ciciolil,&nbsp;Sandoval Ramírez Jesús,&nbsp;Aparicio Sánchez Uriel Yair,&nbsp;Sánchez Sánchez Luis","doi":"10.1111/boc.202300052","DOIUrl":"10.1111/boc.202300052","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>Antiproliferative and apoptotic activities have been attributed to the phytosteroid diosgenin ((25R)-spirost-5-en-3β-ol; <b>1</b>). It is known that combining glucose with two rhamnoses (the chacotrioside framework) linked to diosgenin increases its apoptotic activity. However, the effects of diosgenin glucosamine glycosides on different cancer cell types and cell death have not been entirely explored.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>This study reports the antiproliferative, cytotoxic, and apoptotic activities of diosgenin and its glycosylated derivative ((25R)-spirost-5-en-3β-yl β-D-glucopyranoside; <b>2</b>). It also explores the effects of two diosgenin glucosamine derivates, diosgenin 2-acetamido-2-deoxy-β-D-glucopyranoside (<b>3</b>), and diosgenin 2-amino-2-deoxy-β-D-glucopyranoside hydrochloride (<b>4</b>), on different cancer cell lines. We found that all the compounds affected proliferative activity with minimal toxicity. In addition, all cancer cell lines showed morphological and biochemical characteristics corresponding to an apoptotic process. Apoptotic cell death was higher in all cell lines treated with compounds <b>2</b>, <b>3</b> and <b>4</b> than in those treated with diosgenin. Moreover, compounds <b>3</b> and <b>4</b> induced apoptosis better than compounds <b>1</b> and <b>2</b>. These results suggest that combining glucosamine with modified glucosamine attached to diosgenin has a greater apoptotic effect than diosgenin or its glycosylated derivative (compound <b>2</b>). Furthermore, diosgenin and the abovementioned glycosides had a selective effect on tumour cells since the proliferative capacity of human lymphocytes, keratinocytes (HaCaT) and epithelial cells (CCD841) was not significantly affected.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Altogether, these results demonstrate that diosgenin glucosamine compounds exert an antiproliferative effect on cancer cell lines and induce apoptotic effects more efficiently than diosgenin alone without affecting non-tumour cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>This study evidences the pro-apoptotic and selective activities of diosgenyl glucosamine compounds in cancer cell lines.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139970866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lamin A K97E leads to NF-κB-mediated dysfunction of inflammatory responses in dilated cardiomyopathy","authors":"Duhita Sengupta,&nbsp;Kaushik Sengupta","doi":"10.1111/boc.202300094","DOIUrl":"10.1111/boc.202300094","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>Lamins are type V intermediate filament proteins underlying the inner nuclear membrane which provide structural rigidity to the nucleus, tether the chromosomes, maintain nuclear homeostasis, and remain dynamically associated with developmentally regulated regions of the genome. A large number of mutations particularly in the LMNA gene encoding lamin A/C results in a wide array of human diseases, collectively termed as laminopathies. Dilated Cardiomyopathy (DCM) is one such laminopathic cardiovascular disease which is associated with systolic dysfunction of left or both ventricles leading to cardiac arrhythmia which ultimately culminates into myocardial infarction.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this work, we have unraveled the epigenetic landscape to address the regulation of gene expression in mouse myoblast cell line in the context of the missense mutation LMNA 289A&lt;G (Lys97Glu) that is found in DCM-afflicted patient with severe symptoms. Significant changes in H3-specific epigenetic modifications indicated a dysregulation in transcription machinery which was investigated by RNA sequencing analysis. The major pathways involved in IL-17 signaling, cellular response to interferon-beta and gamma, cytokine production, and related pathways are found to be downregulated. Analysis of the promoter sequences of the genes in the abovementioned pathways led us to the master regulator NF-κB and its regulatory network.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We report here for the first time that there is a significant downregulation of the NF-κB pathway, which has been implicated in cardio-protection elsewhere.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>This provides a new pathophysiological explanation that correlates an LMNA mutation and dilated cardiomyopathy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139970867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"To squeeze or not: Regulation of cell size by mechanical forces in development and human diseases","authors":"Aurore Claude-Taupin,&nbsp;Nicolas Dupont","doi":"10.1111/boc.202200101","DOIUrl":"10.1111/boc.202200101","url":null,"abstract":"<p>Physical constraints, such as compression, shear stress, stretching and tension play major roles during development and tissue homeostasis. Mechanics directly impact physiology, and their alteration is also recognized as having an active role in driving human diseases. Recently, growing evidence has accumulated on how mechanical forces are translated into a wide panel of biological responses, including metabolism and changes in cell morphology. The aim of this review is to summarize and discuss our knowledge on the impact of mechanical forces on cell size regulation. Other biological consequences of mechanical forces will not be covered by this review. Moreover, wherever possible, we also discuss mechanosensors and molecular and cellular signaling pathways upstream of cell size regulation. We finally highlight the relevance of mechanical forces acting on cell size in physiology and human diseases.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.202200101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138497734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DDX5 enhances HIF-1 activity by promoting the interaction of HIF-1α with HIF-1β and recruiting the resulting heterodimer to its target gene loci","authors":"Yukari Shirai,&nbsp;Tatsuya Suwa,&nbsp;Minoru Kobayashi,&nbsp;Sho Koyasu,&nbsp;Hiroshi Harada","doi":"10.1111/boc.202300077","DOIUrl":"10.1111/boc.202300077","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>Cancer cells acquire malignant characteristics and therapy resistance by employing the hypoxia-inducible factor 1 (HIF-1)-dependent adaptive response to hypoxic microenvironment in solid tumors. Since the underlying molecular mechanisms remain unclear, difficulties are associated with establishing effective therapeutic strategies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We herein identified DEAD-box helicase 5 (DDX5) as a novel activator of HIF-1 and found that it enhanced the heterodimer formation of HIF-1α and HIF-1β and facilitated the recruitment of the resulting HIF-1 to its recognition sequence, hypoxia-response element (HRE), leading to the expression of a subset of cancer-related genes under hypoxia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study reveals that the regulation of HIF-1 recruitment to HRE is an important regulatory step in the control of HIF-1 activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>The present study provides novel insights for the development of strategies to inhibit the HIF-1-dependent expression of cancer-related genes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138457637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomics analysis identifies the ribosome associated coiled-coil domain-containing protein-124 as a novel interaction partner of nucleophosmin-1","authors":"Gamze Çakırca,&nbsp;Merve Tuzlakoğlu Öztürk,&nbsp;Pelin Telkoparan-Akillilar,&nbsp;Ömer Güllülü,&nbsp;Agit Çetinkaya,&nbsp;Uygar Halis Tazebay","doi":"10.1111/boc.202300049","DOIUrl":"10.1111/boc.202300049","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>Coiled-coil domain-containing protein-124 (Ccdc124) is a conserved eukaryotic ribosome-associated RNA-binding protein which is involved in resuming ribosome activity after stress-related translational shutdown. Ccdc124 protein is also detected at cellular localizations devoid of ribosomes, such as the centrosome, or the cytokinetic midbody, but its translation-independent cellular function is currently unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>By using an unbiased LC-MS/MS-based proteomics approach in human embryonic kidney (HEK293) cells, we identified novel Ccdc124 partners and mapped the cellular organization of interacting proteins, a subset of which are known to be involved in nucleoli biogenesis and function. We then identified a novel interaction between the cancer-associated multifunctional nucleolar marker nucleophosmin (Npm1) and Ccdc124, and we characterized this interaction both in HEK293 (human embryonic kidney) and U2OS (osteosarcoma) cells. As expected, in both types of cells, Npm1 and Ccdc124 proteins colocalized within the nucleolus when assayed by immunocytochemical methods, or by monitoring the localization of green fluorescent protein-tagged Ccdc124.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The nucleolar localization of Ccdc124 was impaired when Npm1 translocates from the nucleolus to the nucleoplasm in response to treatment with the DNA-intercalator and Topo2 inhibitor chemotherapeutic drug doxorubicin. Npm1 is critically involved in maintaining genomic stability by mediating various DNA-repair pathways, and over-expression of Npm1 or specific <i>NPM1</i> mutations have been previously associated with proliferative diseases, such as acute myelogenous leukemia, anaplastic large-cell lymphoma, and solid cancers originating from different tissues.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>Identification of Ccdc124 as a novel interaction partner of Nmp1 within the frame of molecular mechanisms involving nucleolar stress-sensing and DNA-damage response is expected to provide novel insights into the biology of cancers associated with aberrations in <i>NPM1</i>.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.202300049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138457638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liproxstatin-1 alleviates cartilage degradation by inhibiting chondrocyte ferroptosis in the temporomandibular joint","authors":"Bei Cheng,&nbsp;Jun Zhang,&nbsp;Qinhao Shen,&nbsp;Zheyi Sun,&nbsp;Yingwei Luo,&nbsp;Yu Hu","doi":"10.1111/boc.202300042","DOIUrl":"10.1111/boc.202300042","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Bground Information</h3>\u0000 \u0000 <p>Ferroptosis contributes to temporomandibular joint osteoarthritis (TMJOA) lesion development and is still poorly understood.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this study, we used different TMJOA animal models to examine whether ferroptosis was related to disease onset in TMJOA induced by monosodium iodoacetate (MIA), IL-1β, occlusion disorder (OD), and unilateral anterior crossbite (UAC). Immunohistochemical staining and Western blot analysis were used to detect ferroptosis- and cartilage degradation-related protein expression. Our results revealed reduced levels of the ferroptosis-related protein GPX4 in the cartilage layer, but the levels of ACSL4 and P53 were increased in the condyle. Injection of the ferroptosis inhibitor liproxstatin-1 (Lip-1) effectively decreased ACSL4, P53 and TRF expression. In vitro, IL-1β reduced cartilage extracellular matrix expression in mandibular condylar chondrocytes (MCCs). Lip-1 maintained the morphology and function of mitochondria and ameliorated the exacerbation of lipid peroxidation and reactive oxygen species (ROS) production induced by IL-1β.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These results suggest that chondrocyte ferroptosis plays an important role in the development and progression of TMJOA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>Inhibiting condylar chondrocyte ferroptosis could be a promising therapeutic strategy for TMJOA.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"116 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71420340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytic phagocytosis of myelin debris and reactive characteristics in vivo and in vitro","authors":"Xiaohui Li,&nbsp;Zhibin Ding,&nbsp;Kexin Liu,&nbsp;Qing Wang,&nbsp;Lijuan Song,&nbsp;Zhi Chai,&nbsp;Jiezhong Yu,&nbsp;Dong Ma,&nbsp;Baoguo Xiao,&nbsp;Cungen Ma","doi":"10.1111/boc.202300057","DOIUrl":"10.1111/boc.202300057","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>Persistent myelin debris can inhibit axonal regeneration, thereby hindering remyelination. Effective removal of myelin debris is essential to eliminate the interference of myelin debris in oligodendrocyte progenitor cell (OPC) activation, recruitment to demyelinating sites and/or differentiation into mature oligodendrocytes (OLs). In addition to microglia, it has been reported that astrocytic phagocytosis of myelin debris is a feature of early demyelination.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In the present study, astrocytes effectively phagocytized myelin debris in vitro and in vivo. On the 5th day after injecting myelin debris into the brain, astrocytes were enriched in the area injected with myelin debris compared with microglia, and their ability to engulf myelin debris was stronger than that of microglia. When exposed to myelin debris, astrocytes phagocytizing myelin debris triggered self-apoptosis, accompanied by the activation of NF-κB, down-regulation of Nrf2, and the increase of ciliary neurotrophic factor (CNTF) and basic fibroblast growth factor (bFGF). However, the activation of astrocytic NF-κB did not influence the inflammatory cytokines IL-1β, IL-6, and TNF-α, and the anti-inflammatory factor IL-10. The proliferation of astrocytes and mobilization of OPCs in the subventricular zone were elevated on the 5th day after intracerebral injection of myelin debris.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The results suggested that myelin phagocytosis of astrocytes should help improve the microenvironment and promote myelin regeneration by increasing CNTF and bFGF within the central nervous system.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>However, the molecular interaction of astrocytes acting as phagocytes remains to be further explored. Therefore, an improvement of astrocytes to phagocytize myelin debris may be a promising treatment measure to prevent demyelination and promote remyelination in MS and other diseases with prominent myelin injury.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"115 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2023-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49673909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}