Journal of Cellular Physiology最新文献

{"title":"RETRACTION: Molecular Insights Into Development of Trichoderma Interfusants for Multistress Tolerance Enhancing Antagonism Against Sclerotium rolfsii Sacc","authors":"","doi":"10.1002/jcp.70050","DOIUrl":"https://doi.org/10.1002/jcp.70050","url":null,"abstract":"<p><b>RETRACTION</b>: Hirpara, D. G., H. P. Gajera, A. K. Patel, Z. A. Katakpara, and B. A. Golakiya, “Molecular Insights Into Development of Trichoderma Interfusants for Multistress Tolerance Enhancing Antagonism Against <i>Sclerotium rolfsii</i> Sacc.” <i>Journal of Cellular Physiology</i> 234, no. 5 (2019): 7368–7383. https://doi.org/10.1002/jcp.27496.</p><p>The above article, published online on 28 October 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath, and Wiley Periodicals LLC. A third party notified the journal of image duplications within Figure 2 of this article: Fu 9(a) had been re-used as Fu 21(a) and Fu 22 (12 DAI) had been re-used as Fu 23 (12 DAI). The third party also indicated that the Fu 21(a)/Fu 21(a) image had been re-used in another article by some of the same authors (Hirpara and Gajera [2018]; https://doi.org/10.1016/j.meegid.2018.09.005) and that all images describe different experimental conditions. Lastly, the third party also found evidence of duplicated datapoints within Table 1. An investigation by the publisher confirmed the duplication of images within Figure 8 and also found evidence of duplication and resizing of cellular sections between the Fu 21 and Fu 28 images in Figure S1.</p><p>The authors responded to an inquiry by the publisher and provided what was labeled as original data. The authors confirmed that the FU 21 image in Figure 2 had been reused in another article but stated that the image was intended to provide background information on the purity of the fusant culture and that the duplication does not influence the results. The authors also confirmed the duplications of images in Figure 2 as well as the duplication in Figure S1, but they did not provide the original images for these experiments for verification by the publisher. A review of the original data found several duplicated datapoints that were not adequately explained and that some values reported in the original data did not match those in the published article.</p><p>The retraction has been agreed to because of discrepancies between the published data and the original data, as well as the duplication of images within this article and with another published article, which fundamentally compromises the editors’ confidence in the conclusions presented in the article. The authors disagree with the retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144100619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiolipin Dysregulation in Glioblastoma—Effects on Mitochondrial Function Tumor Cell Death and Sensitivity to Mitochondria-Targeting Drugs","authors":"Jean-Jacques Hunter,&nbsp;Luis Del Valle,&nbsp;Francesca Peruzzi,&nbsp;Krzysztof Reiss","doi":"10.1002/jcp.70045","DOIUrl":"https://doi.org/10.1002/jcp.70045","url":null,"abstract":"<div>\u0000 \u0000 <p>Biological systems do not exist in isolation. Analogous to the intricate design of a spider web, the metabolic adaptations propagated by glioblastoma cells are interlaced, creating a “defense mechanism” that increases the likelihood of mutagenesis and proliferation, while mitigating stress-induced tumor cell death and immune evasion. Previous studies have observed the role of cardiolipin (CL) in the electron transport chain (ETC) function and several other intracellular signaling pathways. Our review provides a synopsis of the existing knowledge about CL in glioblastoma and its complex relationship with metabolic reprogramming at the subcellular level. Through a meticulous examination of CL defects due to its biogenesis and stress-induced modifications, we seek to elucidate the multifaceted connections between aberrant CL variants and the metabolic alterations that underlie glioblastoma progression. A comprehensive grasp of these mechanisms could provide future direction in designing chemotherapeutic agents that selectively target glioblastoma, are less harmful to normal cells, and therefore, may extend patient survival.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"De Novo Protein Synthesis Occurs Through the Cytoplasmic Translation Machinery in Mammalian Spermatozoa","authors":"Pedro O. Corda,&nbsp;Joana Vieira Silva,&nbsp;Catarina R. Almeida,&nbsp;Philippe Pierre,&nbsp;Margarida Fardilha","doi":"10.1002/jcp.70038","DOIUrl":"https://doi.org/10.1002/jcp.70038","url":null,"abstract":"<div>\u0000 \u0000 <p>The current hypothesis suggests that translation occurs in capacitated spermatozoa through mitochondrial ribosomes. Mitochondrial translation has several particularities, which rise some questions about how mitochondrial ribosomes can ensure sperm translation activity. Here, we aimed to elucidate if cytoplasmic translation occurs in mammalian spermatozoa. A bioinformatic workflow was performed to identify translation-related proteins in human spermatozoa and their association with cytoplasmic translation. The surface sensing of translation (SUnSET) method was used to measure translation activity in capacitated human and bovine spermatozoa. Two translation inhibitors, cycloheximide (CHX, cytoplasmic) and <span>D</span>-chloramphenicol (<span>D</span>-CP, mitochondrial) were used to identify which ribosomes were active in sperm. To spot newly synthesized proteins, puromycin-peptides were immunoprecipitated and analysed by mass spectrometry. A second approach was performed using translation inhibitors and analysing the sperm proteome by mass spectrometry. Bioinformatic analysis revealed that human spermatozoa possess 510 translation proteins, which were enriched for cytoplasmic mRNA translation. CHX decreased translation activity in mammalian sperm, whereas no effect was observed after D-CP treatment. Nine proteins were immunoprecipitated and identified as newly synthesized in capacitated bovine spermatozoa. CHX and <span>D</span>-CP decreased the level of 22 proteins that were replaced, or de novo translated during capacitation. New proteins were associated with relevant processes for sperm physiology. Both translation inhibitors decreased sperm rapid progressive motility and increased sperm immotility. Our results proved sperm translation occurs through cytoplasmic translation machinery in capacitated bovine and human spermatozoa. These results also support that sperm translation is required during capacitation to produce relevant proteins for sperm functions.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144074698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: MicroRNA-29a-3p Regulates Abdominal Aortic Aneurysm Development and Progression via Direct Interaction With PTEN","authors":"","doi":"10.1002/jcp.70043","DOIUrl":"https://doi.org/10.1002/jcp.70043","url":null,"abstract":"<p><b>RETRACTION</b>: Zhou, Y., Wang, M., Zhang, J., Xu, P., and Wang, H. 2020. “MicroRNA-29a-3p Regulates Abdominal Aortic Aneurysm Development and Progression via Direct Interaction With PTEN.” <i>Journal of Cellular Physiology</i> 235, no. 12: 9414–9423, https://doi.org/10.1002/jcp.29746.</p><p>The above article, published online on 7 May 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. Following an investigation by the publisher, it was determined that this article was accepted solely on the basis of a compromised peer review process. The editor has therefore decided to retract the article. The authors did not respond to requests for comment.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lysosomal Repair in Health and Disease","authors":"Jinrui Xun,&nbsp;Jay Xiaojun Tan","doi":"10.1002/jcp.70044","DOIUrl":"https://doi.org/10.1002/jcp.70044","url":null,"abstract":"<p>Lysosomes are essential organelles degrading a wide range of substrates, maintaining cellular homeostasis, and regulating cell growth through nutrient and metabolic signaling. A key vulnerability of lysosomes is their membrane permeabilization (LMP), a process tightly linked to diseases including aging, neurodegeneration, lysosomal storage disorders, and cardiovascular disease. Research progress in the past few years has greatly improved our understanding of lysosomal repair mechanisms. Upon LMP, cells activate multiple membrane remodeling processes to restore lysosomal integrity, such as membrane invagination, tubulation, lipid patching, and membrane stabilization. These repair pathways are critical in preserving cellular stress tolerance and preventing deleterious inflammation and cell death triggered by lysosomal damage. This review focuses on the expanding mechanistic insights of lysosomal repair, highlighting its crucial role in maintaining cellular health and the implications for disease pathogenesis and therapeutic strategies.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2 Infection Reactivates HIV-1 Replication From Latency in U1 Cells","authors":"Xue Wang,&nbsp;Weichun Tang,&nbsp;Jiangqin Zhao,&nbsp;Zhiping Ye2,&nbsp;Hang Xie,&nbsp;Indira Hewlett","doi":"10.1002/jcp.70049","DOIUrl":"https://doi.org/10.1002/jcp.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>The global impact of COVID-19, caused by SARS-CoV-2, has infected millions, including those with HIV-1. However, it is unclear if SARS-CoV-2 affects HIV-1 reactivation from latency. Here, we used the U1 cell line to explore how SARS-CoV-2 infection affects HIV-1 reactivation from latency, employing real-time PCR assays and Western blot analysis. Our results show higher levels of HIV-1 RNA after SARS-CoV-2 infection. Importantly, we noticed enhanced reactivation of HIV-1 replication in cells infected with viruses carrying a deletion of amino acids R₆₈₂, R₆₈₃, A₆₈₄ (RRAΔ) in the spike (S) protein, compared to infections with viruses carrying the wild-type S protein. This is involvement of host transcription factors like NFAT, NF-κB p65, Ap-1, and Sp-1, which facilitate HIV production via TCR-related pathways. Additionally, activation of p-TEFb pathways enhances transcription elongation, upregulates Jak/Stat pathways, leading to increased viral replication, while TLR pathways impact the host immune response. Furthermore, RRAΔ showed increased apoptotic activity through both extrinsic and intrinsic apoptotic signaling pathways compared to wild-type SARS-CoV-2. These indicate that SARS-CoV-2 infection could revive HIV-1 replication from latency. The deletion of amino acids R₆₈₂R₆₈₃A₆₈₄ in the viral S protein might regulate further HIV-1 replication and apoptotic conditions, potentially benefiting HIV-1 survival.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mg2+ Supplementation Mitigates Metabolic Deficits Associated With TRPM7 Disruption","authors":"Severin Boulassel,&nbsp;Pascale C. F. Schreier,&nbsp;Anna M. Melyshi,&nbsp;Johanna Berger,&nbsp;Peter S. Reinach,&nbsp;Katharina Jacob,&nbsp;Ingrid Boekhoff,&nbsp;Andreas Breit,&nbsp;Timo D. Müller,&nbsp;Susanna Zierler,&nbsp;Thomas Gudermann,&nbsp;Noushafarin Khajavi","doi":"10.1002/jcp.70042","DOIUrl":"https://doi.org/10.1002/jcp.70042","url":null,"abstract":"<p>Transient receptor potential channel subfamily M member 7 (TRPM7) regulates cellular and systemic Mg²⁺ homeostasis through its channel domain and induces protein phosphorylation via its kinase domain. We recently found that mice with selective deletion of <i>Trpm7</i> in β-cells develop glucose intolerance and declines in insulin secretion, primarily due to the impaired enzymatic activity of this protein. Accumulating evidence suggests that Mg²⁺ supplementation effectively mitigates the detrimental effects of TRPM7 disruption in various cell types. However, the impact of Mg²⁺ supplementation on metabolic impairments caused by TRPM7 inactivation remains unclear. In the present study, we found that Mg²⁺ supplementation significantly ameliorates glucose intolerance observed in high-fat-fed TRPM7 kinase-deficient mice (<i>Trpm7</i>^<i>R/R</i>). However, our ex vivo analysis of islets isolated from <i>Trpm7</i>^<i>R/R</i> mice revealed that Mg²⁺ supplementation does not enhance glucose-induced insulin secretion. Instead, the improvement appears to be partially driven by enhanced insulin sensitivity and increased β-cell proliferation. The pharmacological analysis in MIN6 cells showed that inhibiting TRPM7 with either NS8593 or VER155008 disrupts β-cell proliferation. These effects mimicked the phenotype seen in <i>Trpm7</i>^<i>R/R</i> mice. We attribute this impairment to diminished ERK1/2 signaling, which suppressed PDX1 expression, while Mg²⁺ supplementation in vitro partially restored ERK1/2 phosphorylation levels. Collectively, Mg²⁺ supplementation enhances glucose metabolism in <i>Trpm7</i>^<i>R/R</i> mice and mitigates the ERK1/2 signaling disruptions and proliferation arrest induced by TRPM7 inactivation in vitro. These findings provide compelling evidence that Mg²⁺ supplementation can reverse the adverse metabolic and cellular phenotypes associated with the loss of TRPM7 function.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nestin(+)- and Nestin(−)-Ventricular Cardiomyocytes Reenter the Cell Cycle In Vitro but Are Reciprocally Regulated in the Partial Apex-Resected 7-Day Neonatal Rat Heart","authors":"Adrien Aubry,&nbsp;Mariana Kebbe,&nbsp;Patrice Naud,&nbsp;Louis Villeneuve,&nbsp;Charles Alexandre Leblanc,&nbsp;Angelino Calderone","doi":"10.1002/jcp.70040","DOIUrl":"https://doi.org/10.1002/jcp.70040","url":null,"abstract":"<p>The 1-day-old neonatal rat heart contains two subpopulations of ventricular cardiomyocytes (NNVMs) that reenter the cell cycle in vitro and in vivo distinguished by the absence or de novo expression of the intermediate filament protein nestin. Furthermore, de novo nestin expression in NNVMs directly facilitated cell cycle reentry and elicited a morphological migratory phenotype. Previous studies have reported that ventricular cardiomyocytes failed to reenter the cell cycle following damage to the 7-day-old rodent heart. The present study tested the hypothesis that cell cycle reentry of one or both of the NNVM subpopulations of 7-day-old neonatal rat pups was compromised in vitro and/or in vivo following cardiac damage. Three-day treatment of 7-day-old NNVMs with the protein kinase C activator phorbol 12,13-dibutyrate and the serine/threonine p38α/β MAPK kinase inhibitor SB203580 facilitated cell cycle reentry into the S phase and G₂–M phase of the cell cycle. Two distinct subpopulations of 7-day NNVMs reentered the cell cycle, and the predominant subpopulation was distinguished by de novo nestin expression. Three days following the sham-operation of 7-day-old neonatal rat hearts, cell cycle reentry was detected exclusively in NNVMs lacking nestin expression. Partial apex resection of 7-day-old neonatal rat hearts led to the de novo appearance of nestin⁽⁺⁾-NNVMs preferentially bordering the damaged region and a subpopulation reentered the S-phase and G₂–M phase of the cell cycle in the absence of p38α/β MAPK inhibition. By contrast, cell cycle reentry of nestin⁽⁻⁾-NNVMs identified adjacent to the apex-resected region was significantly reduced. These data highlight the disparate in vivo regulation of the two subpopulations of NNVMs following damaged to the 7-day-old neonatal rat heart and reaffirm the premise that targeting the subpopulation of nestin⁽⁺⁾-ventricular cardiomyocytes identified in the ischemically damaged adult mammalian heart represents a plausible first step to initiate cell cycle reentry.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “Taurine Improves Low-Level Inorganic Arsenic-Induced Insulin Resistance by Activating PPARγ-mTORC2 Signalling and Inhibiting Hepatic Autophagy”","authors":"","doi":"10.1002/jcp.70015","DOIUrl":"https://doi.org/10.1002/jcp.70015","url":null,"abstract":"<p>Gao, N., Yao, X., Jiang, L., et al. 2019. “Taurine Improves Low-Level Inorganic Arsenic-Induced Insulin Resistance by Activating PPARγ-mTORC2 Signalling and Inhibiting Hepatic Autophagy. <i>Journal of Cellular Physiology</i> 234, no. 4: 5143–5152. https://doi.org/10.1002/jcp.27318</p><p>An incorrect PAS staining image for the 1 mg/L iAs3+ group in Figure 1i was used inadvertently during compilation. The corrected figure is shown below.</p><p>We apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143866040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “The Effect of lncRNA-ARAP1-AS2/ARAP1 on High Glucose-Induced Cytoskeleton Rearrangement and Epithelial–Mesenchymal Transition in Human Renal Tubular Epithelial Cells”","authors":"","doi":"10.1002/jcp.70041","DOIUrl":"https://doi.org/10.1002/jcp.70041","url":null,"abstract":"<p>Li, L., L. Xu, S. Wen, Y. Yang, X. Li, and Q. Fan. 2020. “The Effect of lncRNA-ARAP1-AS2/ARAP1 on High Glucose-Induced Cytoskeleton Rearrangement and Epithelial-Mesenchymal Transition in Human Renal Tubular Epithelial Cells.” <i>Journal of Cellular Physiology</i> 235, no. 7–8: 5787–5795. https://10.1002/jcp.29512.</p><p>Figure 3d was mistakenly replaced with an incorrect version, here is the picture to be corrected.</p><p></p><p><b>Figure 3d</b></p><p>During the image processing, due to my oversight, the image for the ARAP1-shRNA-NG group was mistakenly used for the NG group. This error occurred entirely because of my carelessness in data organization and image labeling, and I deeply regret it. I take full responsibility for this mistake. I understand that such an error may significantly affect the accuracy of the research findings, mislead readers, and compromise the credibility of the article. Therefore, I sincerely apologize for any negative consequences this may have caused.</p><p>To rectify this issue, I have carefully reviewed all the raw data and identified the correct images. The new images are consistent with the original experimental results, and we have confirmed that they do not affect the conclusions of the article.</p><p>Once again, I sincerely apologize for this mistake. I will take this as a serious lesson to exercise greater diligence in my future research to prevent similar occurrences.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}