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N-Acetylcysteine relieving hydrogen peroxide-induced damage in granulosa cells of sheep. n -乙酰半胱氨酸减轻过氧化氢诱导的绵羊颗粒细胞损伤。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-03-30 DOI: 10.1080/19336918.2025.2484182
Hao Chen, Jine Wang, Bingzhu Zhao, Yahua Yang, Chongfa Yang, Zhijie Zhao, Xiaona Ding, Yang Li, Taojie Zhang, Zhaxi Yingpai, Shengdong Huo
{"title":"N-Acetylcysteine relieving hydrogen peroxide-induced damage in granulosa cells of sheep.","authors":"Hao Chen, Jine Wang, Bingzhu Zhao, Yahua Yang, Chongfa Yang, Zhijie Zhao, Xiaona Ding, Yang Li, Taojie Zhang, Zhaxi Yingpai, Shengdong Huo","doi":"10.1080/19336918.2025.2484182","DOIUrl":"10.1080/19336918.2025.2484182","url":null,"abstract":"<p><p>Sheep ovarian granulosa cells (GCs) play a unique role in the ovary. Damage to GCs can affect the normal development of oocytes. The oxidative stress model was constructed by H<sub>2</sub>O<sub>2</sub>to study the biological changes. Specifically, pathological characteristic was assessed by immunohistochemistry (IHC), while signaling pathway was studied using western blot, quantitative RT-PCR, and immunofluorescence. Theresults showed that the oxidative damage model was successfully constructed by 200 μmol/LH<sub>2</sub>O<sub>2</sub> for 12 h. NAC can protect the proliferation of GCs under H<sub>2</sub>O<sub>2</sub>-induced oxidative stress and reduce apoptosis. It can also promote the secretion of E<sub>2</sub> and P<sub>4</sub> by GCs and reduce the inflammatory response of GCs. NAC can enhance the expression of NRF2, PI3K and Akt. These findings suggest that NAC alleviates H<sub>2</sub>O<sub>2</sub>-induced oxidative stress injury through NRF2/PI3K/AKT signaling pathways. Provide ideas for studying the poor quality of mammalian oocytes.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2484182"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Influences of physical stimulations on the migration and differentiation of Schwann cells involved in peripheral nerve repair. 物理刺激对参与周围神经修复的雪旺细胞迁移和分化的影响。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-01-16 DOI: 10.1080/19336918.2025.2450311
Qingyan Sun, Xiaodan Mu, Qi Gao, Juncheng Wang, Min Hu, Huawei Liu
{"title":"Influences of physical stimulations on the migration and differentiation of Schwann cells involved in peripheral nerve repair.","authors":"Qingyan Sun, Xiaodan Mu, Qi Gao, Juncheng Wang, Min Hu, Huawei Liu","doi":"10.1080/19336918.2025.2450311","DOIUrl":"10.1080/19336918.2025.2450311","url":null,"abstract":"<p><p>Peripheral nerve injury repair has always been a research concern of scientists. At the tissue level, axonal regeneration has become a research spotlight in peripheral nerve repair. Through transplantation of autologous nerve grafts or other emerging biomaterials functional recovery after facial nerve injury is not ideal in clinical scenarios. Great strides have been made to improve facial nerve repair at the micro-cellular level. Physical stimulation techniques can trigger Schwann cells (SCs) to migrate and differentiate into cells required for peripheral nerve repair. Classified by the sources of physical stimulations, SCs repair peripheral nerves through galvanotaxis, magnetotaxis and durotaxis. This article summarized the activation, directional migration and differentiation of SCs induced by physical stimulations, thus providing new ideas for the research of peripheral nerve repair.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2450311"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Acyl-CoA dehydrogenase long chain acts as a tumor-suppressive factor in lung adenocarcinoma progression. 酰基辅酶a脱氢酶长链在肺腺癌进展中作为肿瘤抑制因子。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-04-22 DOI: 10.1080/19336918.2025.2495676
Tingju Wei, Guowei Fu, Junjie Zhao, Fengan Cao, Danfeng Guo
{"title":"Acyl-CoA dehydrogenase long chain acts as a tumor-suppressive factor in lung adenocarcinoma progression.","authors":"Tingju Wei, Guowei Fu, Junjie Zhao, Fengan Cao, Danfeng Guo","doi":"10.1080/19336918.2025.2495676","DOIUrl":"https://doi.org/10.1080/19336918.2025.2495676","url":null,"abstract":"<p><p>This study investigated the role of long-chain acyl-CoA dehydrogenase (ACADL) in lung adenocarcinoma (LUAD). ACADL was significantly downregulated in human LUAD tissues compared to normal lung tissues. In vitro, ectopic expression of ACADL in murine LLC cells decreased cell viability, migration, and invasion, while ACADL knockdown exhibited the opposite effect. <i>In vivo</i>, ACADL overexpression impeded tumor growth and metastasis. Mechanistically, ACADL hindered tumor progression by inducing cell cycle arrest, promoting apoptosis, and suppressing the epithelial-mesenchymal transition (EMT) process. These findings suggest ACADL acts as a tumor suppressor in LUAD progression.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2495676"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Knockdown of HGH1 in breast cancer cell lines can inhibit the viability, invasion and migration of tumor cells. 在乳腺癌细胞系中敲低HGH1可抑制肿瘤细胞的活力、侵袭和迁移。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2024-12-18 DOI: 10.1080/19336918.2024.2442349
Zeyu Wang, Taiyuan Liu, Kang He, Longyun Wang, Xiaoxuan Ma, Zhaoyun Yang, Yingchao Zhang, Lijing Zhao
{"title":"Knockdown of HGH1 in breast cancer cell lines can inhibit the viability, invasion and migration of tumor cells.","authors":"Zeyu Wang, Taiyuan Liu, Kang He, Longyun Wang, Xiaoxuan Ma, Zhaoyun Yang, Yingchao Zhang, Lijing Zhao","doi":"10.1080/19336918.2024.2442349","DOIUrl":"10.1080/19336918.2024.2442349","url":null,"abstract":"<p><strong>Background: </strong>Research on the function of HGH1 in breast cancer remains lacking.</p><p><strong>Methods: </strong>TCGAand GEO (GSE45827) datasets investigated discrepancies in HGH1 expression in BC. An aggregate of 106 clinical samples were gathered through immunohistochemistry, KM curves were drawn for prognostic analysis, and the function of HGH1 of BC was predicted. Finally, the effects of HGH1 knockdown on MDA-MB-231 and MCF-7 BC cells were verified via CCK8, invasion, wound healing and colony formation assays.</p><p><strong>Results: </strong>HGH1 is highly expressed in BC and is linked to unfavorable prognosis. HGH1 overexpression is connected to keratinization and the cell cycle and is closely related to ER and PR expression and tumor stage in BC patients. Knocking down HGH1 in BC cells inhibited the viability, invasion and migration.</p><p><strong>Conclusion: </strong>Knockdown of HGH1 in breast cancer cell lines can inhibit the viability, invasion and migration of tumor cells.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"1-14"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11657051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Advancing in vitro cell migration studies: a review of open-source analytical platforms for cancer and wound healing research. 推进体外细胞迁移研究：癌症和伤口愈合研究的开源分析平台综述。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-04-16 DOI: 10.1080/19336918.2025.2488116
Abhayraj S Joshi
{"title":"Advancing in vitro cell migration studies: a review of open-source analytical platforms for cancer and wound healing research.","authors":"Abhayraj S Joshi","doi":"10.1080/19336918.2025.2488116","DOIUrl":"https://doi.org/10.1080/19336918.2025.2488116","url":null,"abstract":"<p><p>A single cell or cell population exhibits the fundamental phenomenon of cell migration during developmental processes or disease progression. Vast literature suggests that, <i>in vitro</i> 2-dimensional or 3-dimensional cell migration assay is one of the most commonly used assays in cancer, wound healing research, and developmental biology research. The data obtained from this assay are often analyzed using various proprietary or open-source programs. Proprietary software are costly and not always accessible to everyone. Whereas the open-source programs are free, easy to access, and user friendly. However, not all researchers are aware of these open-source programs. Despite the increasing availability of these programs, many researchers still rely on proprietary software, due to a lack of comparative analyses and practical guidance on their implementation. Hence, this review aims to provide insights into these open-source tools and serves as a practical guide to both biologists and computational researchers for their specific analytical needs.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2488116"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12006941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Brief biology and pathophysiology of Tekt bundles. Tekt束的生物学和病理生理学简介。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-02-13 DOI: 10.1080/19336918.2025.2465421
Jun Yin, Min Liu, Xiao Wang, Hongming Miao, Wenjuan He, Wei Liu, Zhongying Yu, Qinghua Zhang, Jialian Bai, Yimei Cheng, Bing Ni
{"title":"Brief biology and pathophysiology of Tekt bundles.","authors":"Jun Yin, Min Liu, Xiao Wang, Hongming Miao, Wenjuan He, Wei Liu, Zhongying Yu, Qinghua Zhang, Jialian Bai, Yimei Cheng, Bing Ni","doi":"10.1080/19336918.2025.2465421","DOIUrl":"10.1080/19336918.2025.2465421","url":null,"abstract":"<p><p>Tektins, a family of microtubule-stabilizing proteins, are critical for cilia and flagella assembly in mammals. They maintain doublet microtubule stability and ciliary/flagellar motility. Loss of Tekt1-5 causes microtubule instability, impaired motility, and diseases like infertility, retinal degeneration, Mainzer-Saldino syndrome, and diabetic nephropathy. Pathophysiological stimuli regulate Tektin expression through transcriptional, posttranscriptional, translational, and posttranslational modifications. This review summarizes the latest findings on Tektin functions and their role in diseases.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2465421"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11834534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Dual implication of endothelial adhesion molecules in tumor progression and cancer immunity. 内皮粘附分子在肿瘤进展和癌症免疫中的双重作用。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2025-03-12 DOI: 10.1080/19336918.2025.2472308
Louis-Emmanuel Chriqui, Sabrina Cavin, Jean Yannis Perentes
{"title":"Dual implication of endothelial adhesion molecules in tumor progression and cancer immunity.","authors":"Louis-Emmanuel Chriqui, Sabrina Cavin, Jean Yannis Perentes","doi":"10.1080/19336918.2025.2472308","DOIUrl":"10.1080/19336918.2025.2472308","url":null,"abstract":"<p><p>Adhesion molecules are proteins expressed at the surface of various cell types. Their main contribution to immunity is to allow the infiltration of immune cells in an inflamed site. In cancer, adhesion molecules have been shown to promote tumor dissemination favoring the development of metastasis. While adhesion molecule inhibition approaches were unsuccessful for cancer control, their importance for the generation of an immune response alone or in combination with immunotherapies has gained interest over the past years. Currently, the balance of adhesion molecules for tumor promotion/inhibition is unclear. Here we review the role of selectins, intercellular adhesion molecules (ICAM) and vascular cell adhesion molecules (VCAM) from the perspective of the dual contribution of adhesion molecules in tumor progression and immunity.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"2472308"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11913389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Orosomucoid 1 interacts with S100A12 and activates ERK signalling to expedite the advancement of bladder cancer. Orosomucoid 1与S100A12相互作用，激活ERK信号，加速膀胱癌的进展。
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2025-12-01 Epub Date: 2024-12-07 DOI: 10.1080/19336918.2024.2434209
Zhe Liu, Xiaofeng Pu
{"title":"Orosomucoid 1 interacts with S100A12 and activates ERK signalling to expedite the advancement of bladder cancer.","authors":"Zhe Liu, Xiaofeng Pu","doi":"10.1080/19336918.2024.2434209","DOIUrl":"10.1080/19336918.2024.2434209","url":null,"abstract":"<p><p>The research endeavors to expound the role of ORM1 in bladder cancer (BCa) and the implied response mechanism. RT-qPCR and Western blotting examined ORM1 and S100A12 expression. Functional experiments assessed the cellular phenotypes. HDOCK and Co-IP confirmed the interaction of ORM1 and S100A12. Western blotting tested apoptosis- and ERK signaling-associated proteins. ORM1 and S100A12 were abundant in the BCa cells. ORM1 or S100A12 loss impaired cell proliferation, migration, and invasion, and aggravated cell apoptosis. ORM1 interacted with S100A12. ORM1 knockdown down-regulated S100A12 expression and inactivated ERK signaling.S100A12 overexpression or ERK activator reversed the impacts of ORM1 interference on ERK signaling and BCa cells. ORM1 mightdrive BCa via binding to S100A12 and activating ERK signaling.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"19 1","pages":"1-11"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Fe3O4 nanoparticles containing gambogic acid inhibit metastasis in colorectal cancer via the RORB/EMILIN1 axis. 含有甘草酸的Fe3O4纳米粒子通过RORB/EMILIN1轴抑制结直肠癌转移
IF 3.3 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-11-13 DOI: 10.1080/19336918.2024.2427585
Xiaodong Fan, Chunyang Lv, Meiling Xue, Peng Meng, Xiaoping Qian
{"title":"Fe<sub>3</sub>O<sub>4</sub> nanoparticles containing gambogic acid inhibit metastasis in colorectal cancer via the RORB/EMILIN1 axis.","authors":"Xiaodong Fan, Chunyang Lv, Meiling Xue, Peng Meng, Xiaoping Qian","doi":"10.1080/19336918.2024.2427585","DOIUrl":"10.1080/19336918.2024.2427585","url":null,"abstract":"<p><p>This research aims to study the effect of magnetic nanoparticles of Fe3O4 (MNP Fe3O4) containing gambogic acid (GA-MNP Fe3O4) on colorectal cancer (CRC). MNP Fe3O4 enhanced the antitumor effect of GA by inhibiting the malignant behavior of CRC cells. RORB was a target of GA, and GA activated RORB expression to inhibit metastasis of CRC. Knockdown of RORB impaired the effect of GA-MNP Fe3O4 on CRC metastasis. EMILIN1 was a target of RORB, and RORB promoted transcription of EMILIN1. Overexpression of EMILIN1 reversed the effect of knockdown of RORB on GA-MNP Fe3O4 and inhibited metastasis in CRC. These findings revealed that MNP Fe3O4 enhanced the antitumor effect of GA and activated RORB to promote EMILIN1 transcription and inhibit CRC metastasis.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"38-53"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Knockdown of PIK3R6 impedes the onset and advancement of clear cell renal cell carcinoma. 敲除 PIK3R6 会阻碍透明细胞肾细胞癌的发生和发展。
IF 3.2 3区 生物学
Cell Adhesion & Migration Pub Date : 2024-12-01 Epub Date: 2024-06-03 DOI: 10.1080/19336918.2024.2353920
Jia Yang, Xiaoni Zhong, Xiaoling Gao, Wenyi Xie, Yaokai Chen, Yuanjiang Liao, Peilin Zhang
{"title":"Knockdown of PIK3R6 impedes the onset and advancement of clear cell renal cell carcinoma.","authors":"Jia Yang, Xiaoni Zhong, Xiaoling Gao, Wenyi Xie, Yaokai Chen, Yuanjiang Liao, Peilin Zhang","doi":"10.1080/19336918.2024.2353920","DOIUrl":"10.1080/19336918.2024.2353920","url":null,"abstract":"<p><p>In this research, we investigated the role of PIK3R6, a regulatory subunit of PI3Kγ, known for its tumor-promoting properties, in clear cell renal cell carcinoma (CCRCC). Utilizing the UALCAN website, we found PIK3R6 upregulated in CCRCC, correlating with lower survival rates. We compared PIK3R6 expression in CCRCC tumor tissues and adjacent normal tissues using immunohistochemistry. Post RNA interference-induced knockdown of PIK3R6 in 786-O and ACHN cell lines, we performed CCK-8, colony formation, Edu staining, flow cytometry, wound healing, and transwell assays. Results showed that PIK3R6 silencing reduced cell proliferation, migration, and invasion, and induced G0/G1 phase arrest and apoptosis. Molecular analysis revealed decreased CDK4, Cyclin D1, N-cadherin, Vimentin, Bcl-2, p-PI3K and p-AKT, with increased cleaved caspase-3, Bax, and E-cadherin levels in CCRCC cells. Moreover, inhibiting PIK3R6 hindered tumor growth. These findings suggest a significant role for PIK3R6 in CCRCC cell proliferation and metastasis, presenting it as a potential therapeutic target.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"18 1","pages":"1-12"},"PeriodicalIF":3.2,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141236410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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