International Journal of Biochemistry & Cell Biology最新文献

{"title":"Metabolic perturbations associated with hIAPP-induced insulin resistance in skeletal muscles: Implications to the development of type 2 diabetes","authors":"Arya R. Naik ,&nbsp;Shreyada N. Save ,&nbsp;Soumya S. Sahoo ,&nbsp;Saurabh S. Yadav ,&nbsp;Ashutosh Kumar ,&nbsp;Jeetender Chugh ,&nbsp;Shilpy Sharma","doi":"10.1016/j.biocel.2024.106665","DOIUrl":"10.1016/j.biocel.2024.106665","url":null,"abstract":"<div><div>The human islet amyloid polypeptide (hIAPP) tends to misfold and self-assemble to form amyloid fibrils, which has been associated with the loss of function and viability of pancreatic β-cells in type 2 diabetes mellitus (T2DM). The role of hIAPP in the development of insulin resistance (a hallmark of T2DM) in skeletal muscles – the major sites for glucose utilization – needs further investigation. Even though, insulin-resistant conditions have been known to stimulate hIAPP aggregation, the events that lead to the development of insulin resistance due to hIAPP aggregation in skeletal muscles remain unidentified. Here, we have attempted to identify metabolic perturbations in L6 myotubes that were exposed to increasing concentrations of recombinant hIAPP for different time durations. It was observed that hIAPP exposure was associated with increased mitochondrial and cellular ROS levels, loss in mitochondrial membrane potential and viability of the myotubes. Metabolomic investigations of hIAPP-treated myotubes revealed significant perturbations in o-phosphocholine, sn-glycero-3-phosphocholine and dimethylamine levels (p &lt; 0.05). Therefore, we anticipate that defects in glycerophospholipid metabolism and the associated oxidative stress and membrane damage may play key roles in the development of insulin resistance due to protein misfolding in skeletal muscles. In summary, the perturbed metabolites and their pathways have not only the potential to be used as early biomarkers to predict the onset of insulin resistance and T2DM but also as therapeutic targets for the effective management of the same.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106665"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revisiting serotonin’s role in spatial memory: A call for sensitive analytical approaches","authors":"Paulina Kazmierska-Grebowska ,&nbsp;Witold Żakowski ,&nbsp;Dorota Myślińska ,&nbsp;Ravindra Sahu ,&nbsp;Maciej M. Jankowski","doi":"10.1016/j.biocel.2024.106663","DOIUrl":"10.1016/j.biocel.2024.106663","url":null,"abstract":"<div><div>The serotonergic system is involved in various psychiatric and neurological conditions, with serotonergic drugs often used in treatment. These conditions frequently affect spatial memory, which can serve as a model of declarative memory due to well-known cellular components and advanced methods that track neural activity and behavior with high temporal resolution. However, most findings on serotonin's effects on spatial learning and memory come from studies lacking refined analytical techniques and modern approaches needed to uncover the underlying neuronal mechanisms. This In Focus review critically investigates available studies to identify areas for further exploration. It finds that well-established behavioral models could yield more insights with modern tracking and data analysis approaches, while the cellular aspects of spatial memory remain underexplored. The review highlights the complex role of serotonin in spatial memory, which holds the potential for better understanding and treating memory-related disorders.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106663"},"PeriodicalIF":3.4,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142315079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High glucose induces DNA methyltransferase 1 dependent epigenetic reprogramming of the endothelial exosome proteome in type 2 diabetes","authors":"Sampara Vasishta ,&nbsp;Shruthi Ammankallu ,&nbsp;Ganesha Poojary ,&nbsp;Sarah Michael Gomes ,&nbsp;Kailash Ganesh ,&nbsp;Shashikiran Umakanth ,&nbsp;Prashanth Adiga ,&nbsp;Dinesh Upadhya ,&nbsp;Thottethodi Subrahmanya Keshava Prasad ,&nbsp;Manjunath B. Joshi","doi":"10.1016/j.biocel.2024.106664","DOIUrl":"10.1016/j.biocel.2024.106664","url":null,"abstract":"<div><div>In response to hyperglycemia, endothelial cells (ECs) release exosomes with altered protein content and contribute to paracrine signalling, subsequently leading to vascular dysfunction in type 2 diabetes (T2D). High glucose reprograms DNA methylation patterns in various cell/tissue types, including ECs, resulting in pathologically relevant changes in cellular and extracellular proteome. However, DNA methylation-based proteome reprogramming in endothelial exosomes and associated pathological implications in T2D are not known. Hence, in the present study, we used Human umbilical vein endothelial cells (HUVECs), High Fat Diet (HFD) induced diabetic mice (C57BL/6) and clinical models to understand epigenetic basis of exosome proteome regulation in T2D pathogenesis . Exosomes were isolated by size exclusion chromatography and subjected to tandem mass tag (TMT) labelled quantitative proteomics and bioinformatics analysis. Immunoblotting was performed to validate exosome protein signature in clinically characterized individuals with T2D. We observed ECs cultured in high glucose and aortic ECs from HFD mouse expressed elevated DNA methyltransferase1 (DNMT1) levels. Quantitative proteomics of exosomes isolated from ECs treated with high glucose and overexpressing DNMT1 showed significant alterations in both protein levels and post translational modifications which were aligned to T2D associated vascular functions. Based on ontology and gene-function-disease interaction analysis, differentially expressed exosome proteins such as Thrombospondin1, Pentraxin3 and Cystatin C related to vascular complications were significantly increased in HUVECs treated with high glucose and HFD animals and T2D individuals with higher levels of glycated hemoglobin. These proteins were reduced upon treatment with 5-Aza-2’-deoxycytidine. Our study shows epigenetic regulation of exosome proteome in T2D associated vascular complications.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106664"},"PeriodicalIF":3.4,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001560/pdfft?md5=09356ee9f592b8107927607f95021599&pid=1-s2.0-S1357272524001560-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142299984","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}

{"title":"PIAS1 S510G variant acts as a genetic modifier of spinocerebellar ataxia type 3 by selectively impairing mutant ataxin-3 proteostasis","authors":"Yi-Ching Chang ,&nbsp;Yao-Chou Tsai ,&nbsp;En-Cheng Chang ,&nbsp;Yu-Chien Hsu ,&nbsp;Yi-Ru Huang ,&nbsp;Yan-Hua Lee ,&nbsp;Yu-Shuen Tsai ,&nbsp;Yin-Quan Chen ,&nbsp;Yi-Chung Lee ,&nbsp;Yi-Chu Liao ,&nbsp;Jean-Cheng Kuo ,&nbsp;Ming-Tsan Su ,&nbsp;Ueng-Cheng Yang ,&nbsp;Yijuang Chern ,&nbsp;Tzu-Hao Cheng","doi":"10.1016/j.biocel.2024.106662","DOIUrl":"10.1016/j.biocel.2024.106662","url":null,"abstract":"<div><div>Dysregulated protein homeostasis, characterized by abnormal protein accumulation and aggregation, is a key contributor to the progression of neurodegenerative disorders such as Huntington's disease and spinocerebellar ataxia type 3 (SCA3). Previous studies have identified <em>PIAS1</em> gene variants in patients with late-onset SCA3 and Huntington's disease. This study aims to elucidate the role of <em>PIAS1</em> and its S510G variant in modulating the pathogenic mechanisms of SCA3. Through <em>in vitro</em> biochemical analyses and <em>in vivo</em> assays, we demonstrate that PIAS1 stabilizes both wild-type and mutant ataxin-3 (ATXN3). The <em>PIAS1</em> S510G variant, however, selectively reduces the stability and SUMOylation of mutant ATXN3, thereby decreasing its aggregation and toxicity while maintaining the stability of wild-type ATXN3. This effect is mediated by a weakened interaction with the SUMO-conjugating enzyme UBC9 in the presence of mutant ATXN3. In Drosophila models, downregulation of dPIAS1 resulted in reduced levels of mutant ATXN3 and alleviated associated phenotypes, including retinal degeneration and motor dysfunction. Our findings suggest that the <em>PIAS1</em> S510G variant acts as a genetic modifier of SCA3, highlighting the potential of targeting SUMOylation as a therapeutic strategy for this disease.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106662"},"PeriodicalIF":3.4,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001547/pdfft?md5=ee2968809e055b854132c73ad3383723&pid=1-s2.0-S1357272524001547-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142262019","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}

{"title":"Unveiling the role of taurine and SLC6A6 in tumor immune evasion: Implications for gastric cancer therapy","authors":"Jianqiao Shentu,&nbsp;Xinming Su,&nbsp;Yueqi Yu,&nbsp;Shiwei Duan","doi":"10.1016/j.biocel.2024.106661","DOIUrl":"10.1016/j.biocel.2024.106661","url":null,"abstract":"<div><p>Metabolic changes are key drivers of tumor progression. Understanding how metabolic reprogramming promotes tumor development and identifying key metabolic activities are essential for improving tumor diagnosis and treatment. Among the numerous transporters in the body, solute carriers (SLCs) are particularly significant, often overexpressed in cancer cells to meet the tumor's demand for nutrients and energy. While the role of SLCs in nutrient absorption within the gastrointestinal tract is well-established, their specific role in gastric cancer (GC) remains unclear. Recently, Xiaodi Zhao's team investigated the critical role of taurine and its transporter, SLC6A6, in anti-tumor immunity and clinical outcomes. Notably, this research marks the first instance of taurine exhibiting a dual role. It promotes tumor growth in immunodeficient mice while inhibiting it in immunocompetent mice. The study found that taurine exerts its anti-cancer effects by modulating CD8⁺ T cells rather than directly inhibiting tumor cells, revealing the SP1-SLC6A6 axis as a key mechanism behind chemotherapy-induced immune evasion. Our work further explored the potential, advantages, and challenges of using taurine and SLC6A6 as biomarkers and therapeutic targets in gastric cancer. We aim to underscore their importance in both basic research and clinical applications, providing valuable insights and guidance for future investigations.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106661"},"PeriodicalIF":3.4,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142172564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-146b-5p/FDFT1 mediates cisplatin sensitivity in bladder cancer by redirecting cholesterol biosynthesis to the non-sterol branch","authors":"Nurul Amniyyah Azhar ,&nbsp;Yogaambikai Paramanantham ,&nbsp;W M Farhan Syafiq B W M Nor ,&nbsp;Nur Akmarina B. M. Said","doi":"10.1016/j.biocel.2024.106652","DOIUrl":"10.1016/j.biocel.2024.106652","url":null,"abstract":"<div><p>Chemotherapy against muscle-invasive bladder cancer is increasingly challenged by the prevalence of chemoresistance. The cholesterol biosynthesis pathway has garnered attention in studies of chemoresistance, but conflicting clinical and molecular findings necessitate a clearer understanding of its underlying mechanisms. Recently, we identified farnesyl-diphosphate farnesyltransferase 1 (FDFT1)—the first specific gene in this pathway—as a tumor suppressor and chemoresistance modulator. Raman spectroscopy revealed higher levels of FDFT1-related metabolites in chemotherapy-sensitive bladder cancer tissue compared to resistant tissue; however, this observation lacks mechanistic insight. FDFT1 expression was reduced in our cisplatin-resistant bladder cancer cells (T24R) compared to parental cisplatin-sensitive cells (T24). Using functional knockdown and ectopic overexpression in T24/T24R cells, we mechanistically demonstrate the pathway through which FDFT1 mediates cisplatin sensitivity in bladder cancer cells. Bioinformatics analysis and rescue experiments showed that microRNA-146b-5p directly targets and downregulates FDFT1, reducing the cisplatin sensitivity of T24 cells, which can be restored by forced FDFT1 expression. Further investigation into the downstream cholesterol pathway revealed that FDFT1 suppression redirects its substrate toward the non-sterol branch of the pathway, as evidenced by the upregulation of non-sterol branch-associated genes and a reduced total cholesterol level in the sterol branch. Since the non-sterol pathway leads to the prenylation of isoprenoids and activation of Ras and Rho family proteins involved in cancer progression and chemoresistance, our findings suggest that redirection of the cholesterol biosynthesis pathway is a key mechanism underlying FDFT1-mediated cisplatin resistance in bladder cancer. The miR-146b-5p/FDFT1 axis represents a promising target for overcoming chemoresistance in bladder cancer.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106652"},"PeriodicalIF":3.4,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142243467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"QSOX1 exerts anti-inflammatory effects in sepsis-induced acute lung injury: Regulation involving EGFR phosphorylation mediated M1 polarization of macrophages","authors":"Wenjia Tong ,&nbsp;Conglei Song ,&nbsp;Danqun Jin ,&nbsp;Min Li ,&nbsp;Zimei Cheng ,&nbsp;Guoping Lu ,&nbsp;Bin Yang ,&nbsp;Fang Deng","doi":"10.1016/j.biocel.2024.106651","DOIUrl":"10.1016/j.biocel.2024.106651","url":null,"abstract":"<div><p>Sepsis is a systemic inflammatory response caused by an infection, which can easily lead to acute lung injury. Quiescin Q6 sulfhydryl oxidase 1 (QSOX1) is a sulfhydryl oxidase involved in oxidative stress and the inflammatory response. However, there are few reports on the role of QSOX1 in sepsis-induced acute lung injury (SALI). In this study, mice model of SALI was constructed by intraperitoneal injection with lipopolysaccharide (LPS). The increased inflammatory response and lactate dehydrogenase activity in bronchoalveolar lavage fluid (BALF) indicated successful modeling. Increased QSOX1 expression was both observed in lung tissues and lung macrophages of sepsis mice accompanied by increased polarization of M1-type macrophages. To explore the role of QSOX1 in the SALI, lentivirus containing QSOX1-specific overexpression or knockdown vectors were used to change QSOX1 expression in LPS-treated RAW264.7 cells. QSOX1 suppressed LPS-induced M1 polarization and further inhibited inflammatory response in RAW264.7 cells. Interestingly, the phosphorylation of epidermal growth factor receptor (EGFR), the promoter of M1 polarization in macrophages, was found to be downregulated upon QSOX1 overexpression in RAW264.7 cells. Mechanically, the binding of QSOX1 to EGFR protein promoted EGFR ubiquitination and degradation, thereby down-regulating EGFR phosphorylation. Moreover, inhibiting EGFR expression or its phosphorylation restored the impact of QSOX1 silencing on M1 polarization and inflammation in the LPS-treated RAW264.7 cells. In summary, QSOX1 may exert anti-inflammatory effects in SALI by inhibiting EGFR phosphorylation-mediated M1 macrophage polarization. This presented a potential target for the treatment and prevention of SALI.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106651"},"PeriodicalIF":3.4,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142227053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microtubules and cardiovascular diseases: insights into pathology and therapeutic strategies","authors":"Qiaomin Wu ,&nbsp;Yanli Wang ,&nbsp;Jinfeng Liu,&nbsp;Xuanke Guan,&nbsp;Xing Chang,&nbsp;Zhiming Liu,&nbsp;Ruxiu Liu","doi":"10.1016/j.biocel.2024.106650","DOIUrl":"10.1016/j.biocel.2024.106650","url":null,"abstract":"<div><p>Microtubules, complex cytoskeletal structures composed of tubulin proteins in eukaryotic cells, have garnered recent attention in cardiovascular research. Investigations have focused on the post-translational modifications of tubulin, including acetylation and detyrosination. Perturbations in microtubule homeostasis have been implicated in various pathological processes associated with cardiovascular diseases such as heart failure, ischemic heart disease, and arrhythmias. Thus, elucidating the intricate interplay between microtubule dynamics and cardiovascular pathophysiology is imperative for advancing preventive and therapeutic strategies. Several natural compounds have been identified to potentially modulate microtubules, thereby exerting regulatory effects on cardiovascular diseases. This review synthesizes current literature to delineate the roles of microtubules in cardiovascular diseases and assesses the potential of natural compounds in microtubule-targeted therapies.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"175 ","pages":"Article 106650"},"PeriodicalIF":3.4,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001420/pdfft?md5=6303e5d7ef334e5755c8488b0c002f42&pid=1-s2.0-S1357272524001420-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141583","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}

{"title":"Cell-cell fusion in cancer: The next cancer hallmark?","authors":"Paulameena V. Shultes ,&nbsp;Davis T. Weaver ,&nbsp;Dagim S. Tadele ,&nbsp;Rowan J. Barker-Clarke ,&nbsp;Jacob G. Scott","doi":"10.1016/j.biocel.2024.106649","DOIUrl":"10.1016/j.biocel.2024.106649","url":null,"abstract":"<div><p>In this review, we consider the role of cell-cell fusion in cancer development and progression through an evolutionary lens. We begin by summarizing the origins of fusion proteins (fusogens), of which there are many distinct classes that have evolved through convergent evolution. We then use an evolutionary framework to highlight how the persistence of fusion over generations and across different organisms can be attributed to traits that increase fitness secondary to fusion; these traits map well to the expanded hallmarks of cancer. By studying the tumor microenvironment, we can begin to identify the key selective pressures that may favor higher rates of fusion compared to healthy tissues. The paper concludes by discussing the increasing number of research questions surrounding fusion, recommendations for how to answer them, and the need for a greater interest in exploring cell fusion and evolutionary principles in oncology moving forward.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"175 ","pages":"Article 106649"},"PeriodicalIF":3.4,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142074433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent technical advances in cellular cryo-electron tomography","authors":"Tianyu Zheng ,&nbsp;Shujun Cai","doi":"10.1016/j.biocel.2024.106648","DOIUrl":"10.1016/j.biocel.2024.106648","url":null,"abstract":"<div><p>Understanding the in situ structure, organization, and interactions of macromolecules is essential for elucidating their functions and mechanisms of action. Cellular cryo-electron tomography (cryo-ET) is a cutting-edge technique that reveals in situ molecular-resolution architectures of macromolecules in their lifelike states. It also provides insights into the three-dimensional distribution of macromolecules and their spatial relationships with various subcellular structures. Thus, cellular cryo-ET bridges the gap between structural biology and cell biology. With rapid advancements, this technique achieved substantial improvements in throughput, automation, and resolution. This review presents the fundamental principles and methodologies of cellular cryo-ET, highlighting recent developments in sample preparation, data collection, and image processing. We also discuss emerging trends and potential future directions. As cellular cryo-ET continues to develop, it is set to play an increasingly vital role in structural cell biology.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"175 ","pages":"Article 106648"},"PeriodicalIF":3.4,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142057129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}