Journal of cellular biochemistry最新文献

{"title":"RETRACTION: Phytosomal-curcumin Antagonizes Cell Growth and Migration, Induced by Thrombin Through AMP-Kinase in Breast Cancer","authors":"","doi":"10.1002/jcb.30656","DOIUrl":"10.1002/jcb.30656","url":null,"abstract":"<p><b>RETRACTION</b>: M. Hashemzehi, R. Behnam-Rassouli, S. M. Hassanian, M. Moradi-Binabaj, R. Moradi-Marjaneh, F. Rahmani, H. Fiuji, M. Jamili, M. Mirahmadi, N. Boromand, M. Piran, M. Jafari, A. Sahebkar, A. Avan, and M. Khazaei, “Phytosomal-curcumin Antagonizes Cell Growth and Migration, Induced by Thrombin Through AMP-Kinase in Breast Cancer,” <i>Journal of Cellular Biochemistry</i> 119, no. 7 (2018): 5996–6007, https://doi.org/10.1002/jcb.26796.</p><p>The above article, published online on 30 March 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, possible duplication of Western Blot bands was identified within Figure 5. The raw data provided by the authors upon request did not address the concerns, as clear evidence of image manipulation and fabrication was detected. Consequently, the article is being retracted, as the editors have lost confidence in the integrity of the presented data and deem the conclusions invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30656","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390756","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":"Lnc-Pim1 Promotes Neurite Outgrowth and Regeneration of Neuron-Like Cells Following ACR-Induced Neuronal Injury","authors":"He Li,&nbsp;Ruo yu Jiang,&nbsp;Ya jie Tang,&nbsp;Cong Ling,&nbsp;Fang Liu,&nbsp;Jia jun Xu","doi":"10.1002/jcb.30659","DOIUrl":"10.1002/jcb.30659","url":null,"abstract":"<div>\u0000 \u0000 <p>Decreased regenerative capacity of central nervous system neurons is the main cause for failure of damaged neuron regeneration and functional recovery. Long noncoding RNAs (lncRNAs) are abundant in mammalian transcriptomes, and many time- and tissue-specific lncRNAs are thought to be closely related to specific biological functions. The promoting effect of Pim-1 gene on neural differentiation and regeneration has been documented, but the effect and mechanism of its neighbor gene Lnc-Pim1 in regulating the response of central neurons to injury remain unclear. RT-PCR in this study demonstrated that the expression of Lnc-Pim1 was upregulated in acrylamide (ACR)-induced neuronal injury. FISH and nucleus-cytoplasmic assay demonstrated that Lnc-Pim1 was mainly expressed in the neuron cytoplasm, with a small amount in the nucleus. Western blot analysis proved that Lnc-Pim1 overexpression induced by the lentivirus vector could promote neurite outgrowth in Neuro-2a cells by activating the Erk1/2 signal pathway, and improve neurite regeneration of injured neurons by upregulating GAP-43 and β-Ⅲ tubulin protein expression. However, silencing Lnc-Pim1 expression by interfering RNA could effectively downregulate the GAP-43 and β-Ⅲ tubulin protein expression, and inhibit neurite growth of neurons. In addition, CHIRP-MS was performed to identify several potential targets of Lnc-Pim1 involved in the regulation of neurite regeneration of injured neurons. In conclusion, our study demonstrated that Lnc-Pim1 is a potential lnc-RNA, playing an important role in regulating central nerve regeneration.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380939","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":"Biochemical Properties of Synaptic Proteins Are Dependent on Tissue Preparation: NMDA Receptor Solubility Is Regulated by the C-Terminal Tail","authors":"Sehoon Won,&nbsp;Colin L. Sweeney,&nbsp;Katherine W. Roche","doi":"10.1002/jcb.30664","DOIUrl":"10.1002/jcb.30664","url":null,"abstract":"<p>Synaptic proteins are essential for neuronal development, synaptic transmission, and synaptic plasticity. The postsynaptic density (PSD) is a membrane-associated structure at excitatory synapses, which is composed of a huge protein complex. To understand the interactions and functions of PSD proteins, researchers have employed a variety of imaging and biochemical approaches including sophisticated mass spectrometry. However, the field is lacking a systematic comparison of different experimental conditions and how they might influence the study of the PSD interactome isolated from various tissue preparations. To evaluate the efficiency of several common solubilization conditions, we isolated receptors, scaffolding proteins, and adhesion molecules from brain tissue or primary cultured neurons or human forebrain neurons differentiated from induced pluripotent stem cells (iPSCs). We observed some striking differences in solubility. We found that N-methyl-<span>d</span>-aspartate receptors (NMDARs) and PSD-95 are relatively insoluble in brain tissue, cultured neurons, and human forebrain neurons compared to α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptors (AMPARs) or SAP102. In general, synaptic proteins were more soluble in primary neuronal cultures and human forebrain neurons compared to brain tissue. Interestingly, NMDARs are relatively insoluble in HEK293T cells suggesting that insolubility does not directly represent the synaptic fraction but rather it is related to a detergent-insoluble fraction such as lipid rafts. Surprisingly, truncation of the intracellular carboxyl-terminal tail (C-tail) of NMDAR subunits increased NMDAR solubility in HEK293T cells. Our findings show that detergent, pH, and temperature are important for protein preparations to study PSD protein complexes, and NMDAR solubility is regulated by its C-tail, thus providing a technical guide to study synaptic interactomes and subcellular localization of synaptic proteins.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380937","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":"KDM4B Histone Demethylase Inhibition Attenuates Tumorigenicity of Malignant Melanoma Cells by Overriding the p53-Mediated Tumor Suppressor Pathway","authors":"Arif Ul Hasan,&nbsp;Satoshi Serada,&nbsp;Sachiko Sato,&nbsp;Mami Obara,&nbsp;Sho Hirata,&nbsp;Yukako Nagase,&nbsp;Yukiko Kondo,&nbsp;Eiichi Taira","doi":"10.1002/jcb.30643","DOIUrl":"10.1002/jcb.30643","url":null,"abstract":"<div>\u0000 \u0000 <p>Despite significant advances in the treatment of cutaneous melanoma (hereafter melanoma), the prognosis remains less favorable due to therapeutic resistance, which is presumably linked to epigenetic dysregulation. We hypothesized that the histone lysine demethylase KDM4B could play a pivotal role in controlling therapy-resistant melanoma. To validate our hypothesis, we retrieved RNA sequencing data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) program and observed upregulation of <i>KDM4B</i> in both primary and metastatic melanoma, which was associated with poor survival. To explore its role, we used murine B16, human SK-MEL-5, and G-361 melanoma cells as in vitro models of melanoma. We found that KDM4B inhibition using NCGC00244536 increased global levels of H3K9me3 and downregulated the expressions of cell cycle progression–related genes <i>Cdk1</i>, <i>Cdk4</i>, <i>Ccnb1</i>, and <i>Ccnd1</i>. Moreover, genetic ablation of <i>KDM4B</i> or its chemical inhibition using NCGC00244536 reduced p53 production by upregulating MDM2, which enhances the proteolytic degradation of p53. Interestingly, despite the reduction of p53, these interventions augmented apoptosis and senescence-induced cell death by activating pathways downstream of p53, as evidenced by reduced levels of pro-survival Bcl-2 and Bcl-xL proteins and increased production of pro-apoptotic cleaved caspase-3, caspase-7, <i>Bax</i>, and the senescence inducer <i>Cdkn1a</i>. Compared to the FDA-approved anti-melanoma agent dacarbazine, NCGC00244536 exhibited more pronounced cytotoxic and antiproliferative effects in melanoma cells. Importantly, NCGC00244536 demonstrated minimal cytotoxicity to low <i>Kdm4b</i>-expressing mouse embryonic fibroblasts. In conclusion, our findings suggest that KDM4B inhibition can override the antitumor effect of p53, and potentially serve as a therapeutic strategy for melanoma.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365367","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":"RETRACTION: Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma","authors":"","doi":"10.1002/jcb.30650","DOIUrl":"10.1002/jcb.30650","url":null,"abstract":"<p><b>RETRACTION:</b> Z. Zhao, T. Liang, and S. Feng,<b> </b>“Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma,” <i>Journal of Cellular Biochemistry</i> 120, no. 7 (2019): 11510-11516, https://doi.org/10.1002/jcb.28430.</p><p>The above article, published online on 20 February 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, image elements in Figure 4 were found to have been previously published in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. The authors have been informed of the decision of retraction but unavailable for a final confirmation.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30650","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347403","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":"EXPRESSION OF CONCERN: Ap1 Mediates uPA/uPAR Induced FUT4 Expression and Trophoblast Invasion","authors":"","doi":"10.1002/jcb.30657","DOIUrl":"10.1002/jcb.30657","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: Q. Zheng, Y. Yang, X. Cui, D. Zhang, S. Liu, and Q. Yan, “AP1 Mediates uPA/uPAR Induced FUT4 Expression and Trophoblast Invasion,” <i>Journal of Cellular Biochemistry</i> 119, no. 8 (2018): 6442-6451, https://doi.org/10.1002/jcb.26648.</p><p>This Expression of Concern is for the above article, published online on 26 December 2017 in Wiley Online Library (wileyonlinelibrary.com), has been issued by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals, LLC.</p><p>The Expression of Concern has been agreed due to concerns raised by third parties regarding the data presented in the article. Specifically, overlaps have been detected in the invasion assay images between the “uPAR+c-Fos siRNA” and “uPAR+TIIA” groups in Figure 5C. Further investigation by the publisher revealed additional overlaps in the migration assay images between the “uPAR+SP600125” and “uPAR+TIIA” groups in the same figure. The authors explained that these overlaps occurred due to errors during the figure assembly and provided revised images to correct the mistakes. However, the replacement images provided by the authors failed to reproduce the results of the originally published images. Consequently, the journal has decided to issue this Expression of Concern to inform and alert readers.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30657","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347401","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":"A Novel Assay Reveals the Early Setting-Up of Membrane Repair Machinery in Human Skeletal Muscle Cells","authors":"Léna d'Agata,&nbsp;Phoebe Rassinoux,&nbsp;Céline Gounou,&nbsp;Flora Bouvet,&nbsp;Dounia Bouragba,&nbsp;Kamel Mamchaoui,&nbsp;Anthony Bouter","doi":"10.1002/jcb.30662","DOIUrl":"10.1002/jcb.30662","url":null,"abstract":"<p>Defect in membrane repair contributes to the development of muscular dystrophies such as limb girdle muscular dystrophy (LGMD) type R2 or R12. Nevertheless, many other muscular dystrophies may also result from a defect in this process. Identifying these pathologies requires the development of specific methods to inflict sarcolemma damage on a large number of cells and rapidly analyze their response. We adapted a protocol hitherto used to study the behavior of cancer cells to mechanical constraint. This method is based on forcing the passage of cells through a thin needle, which induces shear stress. Due to size considerations, this method requires working with mononuclear muscle cells instead of myotubes or muscle fibers. Although functional sarcolemma repair was thought to be restricted to myotubes and muscle fibers, we show here that 24h-differentiated myoblasts express a complete machinery capable of addressing membrane damage. At this stage, muscle cells do not yet form myotubes, revealing that the membrane repair machinery is set up early throughout the differentiation process. When submitted to the shear-stress assay, these cells were observed to repair membrane damage in a Ca²⁺-dependent manner, as previously reported. We show that this technique is able to identify the absence of membrane resealing in muscle cells from patient suffering from LGMDR2. The proposed technique provides therefore a suitable method for identifying cellular dysregulations in membrane repair of dystrophic human muscle cells.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347399","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":"Assessing the Inhibitory Potential of Pregnenolone Sulfate on Pentraxin 3 in Diabetic Kidney Disease: A Molecular Docking and Simulation Study","authors":"Soumik Das,&nbsp;Gnanasambandan Ramanathan","doi":"10.1002/jcb.30661","DOIUrl":"10.1002/jcb.30661","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetic Kidney Disease (DKD), a frequent consequence of diabetes, has substantial implications for both morbidity and mortality rates, prompting the exploration of new metabolic biomarkers due to limitations in current methods like creatinine and albumin measurements. Pentraxin 3 (PTX3) shows promise for assessing renal inflammation in DKD. This study investigates how DKD metabolites could influence PTX3 expression through molecular docking, ADMET profiling, and dynamic simulation. Network and pathway analyses were conducted to explore metabolite interactions with DKD genes and their contributions to DKD pathogenesis. Thirty-three DKD-associated metabolites were screened, using pentoxifylline (PEN) as a reference. The pharmacokinetic properties of these compounds were evaluated through molecular docking and ADMET profiling. Molecular dynamics simulations over 200 ns assessed the stability of PTX3 (apo), the PRE-PTX3 complex, and PEN-PTX3 across multiple parameters. Cytoscape identified 1082 nodes and 1381 edges linking metabolites with DKD genes. KEGG pathway analysis underscored PTX3's role in inflammation. Molecular docking revealed pregnenolone sulfate (PRE) with the highest binding affinity (−6.25 kcal/mol), followed by hydrocortisone (−6.03 kcal/mol) and 2-arachidonoylglycerol (−5.92 kcal/mol), compared to PEN (−5.35 kcal/mol). ADMET profiling selected PRE for dynamic simulation alongside PEN. Analysis of RMSD, RMSF, RG, SASA, H-bond, PCA, FEL, and MM-PBSA indicated stable complex behavior over time. Our findings suggest that increasing PRE levels could be beneficial in managing DKD, potentially through isolating PRE from fungal sources, synthesizing it as dietary supplements, or enhancing endogenous PRE synthesis within the body.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347400","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":"RETRACTION: MiR-125a Suppresses Malignancy of Multiple Myeloma by Reducing the Deubiquitinase USP5","authors":"","doi":"10.1002/jcb.30628","DOIUrl":"10.1002/jcb.30628","url":null,"abstract":"<p><b>RETRACTION:</b> L. Wu, C. Zhang, M. Chu, Y. Fan, L. Wei, Z. Li, Y. Yao, and W. Zhuang, “MiR-125a Suppresses Malignancy of Multiple Myeloma by Reducing the Deubiquitinase USP5,” <i>Journal of Cellular Biochemistry</i> 121, no. 1 (2020): 642-650, https://doi.org/10.1002/jcb.29309.</p><p>The above article, published online on 26 August 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.</p><p>The retraction has been agreed upon the authors' request. In the following investigation performed by the journal, several inconsistencies between results presented and experimental methods described were found. Specifically, the experimental methods were found to lack or have unavailable supporting data, making the experiments not comprehensible nor reproducible to readers. Additionally, evidence of editing was found in the Western Blot images presented in the article. The authors were unable to provide comprehensive raw data upon request. Accordingly, the conclusions of this article are considered invalid by the editors.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30628","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347402","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":"Septins: Structural Insights, Functional Dynamics, and Implications in Health and Disease","authors":"Aurosikha Das,&nbsp;Ambarish Kunwar","doi":"10.1002/jcb.30660","DOIUrl":"10.1002/jcb.30660","url":null,"abstract":"<div>\u0000 \u0000 <p>Septins are a class of proteins with diverse and vital roles in cell biology. Structurally, they form hetero-oligomeric complexes and assemble into filaments, contributing to the organization of cells. These filaments act as scaffolds, aiding in processes like membrane remodeling, cytokinesis, and cell motility. Functionally, septins are essential to cell division, playing essential roles in cytokinetic furrow formation and maintaining the structural integrity of the contractile ring. They also regulate membrane trafficking and help organize intracellular organelles. In terms of physiology, septins facilitate cell migration, phagocytosis, and immune responses by maintaining membrane integrity and influencing cytoskeletal dynamics. Septin dysfunction is associated with pathophysiological conditions. Mutations in septin genes have been linked to neurodegenerative diseases, such as hereditary spastic paraplegias, underscoring their significance in neuronal function. Septins also play a role in cancer and infectious diseases, making them potential targets for therapeutic interventions. Septins serve as pivotal components of intracellular signaling networks, engaging with diverse proteins like kinases and phosphatases. By modulating the activity of these molecules, septins regulate vital cellular pathways. This integral role in signaling makes septins central to orchestrating cellular responses to environmental stimuli. This review mainly focuses on the human septins, their structural composition, regulatory functions, and implication in pathophysiological conditions underscores their importance in fundamental cellular biology. Moreover, their potential as therapeutic targets across various diseases further emphasizes their significance.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347413","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}