Journal of cellular biochemistry最新文献

{"title":"RETRACTION: Activation of Akt/PDK Signaling in Macrophages Upon Binding of Receptor-Recognized Forms of α2-Macroglobulin to Its Cellular Receptor: Effect of Silencing the CREB Gene","authors":"","doi":"10.1002/jcb.70044","DOIUrl":"https://doi.org/10.1002/jcb.70044","url":null,"abstract":"<p><b>RETRACTION</b>: U. K. Misra, and S. V. Pizzo, “Activation of Akt/PDK Signaling in Macrophages Upon Binding of Receptor-Recognized Forms of α2-Macroglobulin to Its Cellular Receptor: Effect of Silencing the CREB Gene,” <i>Journal of Cellular Biochemistry</i> 93, no. 5 (2004): 1020–1032, https://doi.org/10.1002/jcb.20233.</p><p>The above article, published online on 9 September 2004 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.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. Specifically, duplication of image elements has been detected between Figures 2A and 5A, within Figure 3 and between Figures 3 and 4B, and between Figures 4A and 6. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624740","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":"RETRACTION: Loss of Cell Surface TFII-I Promotes Apoptosis in Prostate Cancer Cells Stimulated With Activated α2-Macroglobulin*","authors":"","doi":"10.1002/jcb.70047","DOIUrl":"https://doi.org/10.1002/jcb.70047","url":null,"abstract":"<p><b>RETRACTION:</b> U. K. Misra, Y. M. Mowery, G. Gawdi, and S. V. Pizzo, “Loss of Cell Surface TFII-I Promotes Apoptosis in Prostate Cancer Cells Stimulated With Activated α2-Macroglobulin*,” <i>Journal of Cellular Biochemistry</i> 112, no. 6 (2011): 1685–1695, https://doi.org/10.1002/jcb.23083</p><p>The above article, published online on 24 February 2011 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. Specifically, duplication of image elements has been detected between Figures 1A and 3, and within Figure 3. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144624742","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":"Correction to “Role of VPS39, a Key Tethering Protein for Endolysosomal Trafficking and Mitochondria–Lysosome Crosstalk, in Health and Disease”","authors":"","doi":"10.1002/jcb.70041","DOIUrl":"10.1002/jcb.70041","url":null,"abstract":"<p>H. Li, W. Gong, W. Sun, Y. Yao, and Y. Han, “Role of VPS39, a Key Tethering Protein for Endolysosomal Trafficking and Mitochondria-Lysosome Crosstalk, in Health and Disease,” <i>Journal of Cellular Biochemistry</i> 125, no. 11 (2024): e30396, https://doi.org/10.1002/jcb.30396.</p><p>In the article, there is an error in the citation numbering starting from the second paragraph of Section 4.1. The reference numbers in the text do not match the final reference list, and similar discrepancies occur in Table 2.</p><p>We apologize for this error.</p><p>Correction to “Role of VPS39, A Key Tethering Protein for Endolysosomal Trafficking And Mitochondria–Lysosome Crosstalk, in Health and Disease”</p><p>The reference numbers in Table 2 have also been corrected in the same way as the text. Each reference number has been increased by 2 to match the correct reference numbers, as follows:</p><p>“88” has been changed to “90”; “89” has been changed to “91”; “90” has been changed to “92”; “91” has been changed to “93”; “92” has been changed to “94”; “93” has been changed to “95”; “94” has been changed to “96”; “95” has been changed to “97”; “96” and “97” have been changed to “98” and “99”; “98” has been changed to “100”; “99” has been changed to “101”; “100” and “101” have been changed to “102” and “103”; “102” has been changed to “104”; “102-104” has been changed to “104–106”; “105” has been changed to “107”; “106” has been changed to “108.”</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567483","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":"The Multifaceted Influence of Beta-Hydroxybutyrate on Autophagy, Mitochondrial Metabolism, and Epigenetic Regulation","authors":"Sajad Ehtiati,&nbsp;Behzad Hatami,&nbsp;Seyyed Hossein Khatami,&nbsp;Kiarash Tajernarenj,&nbsp;Saeed Abdi,&nbsp;Majid Sirati-Sabet,&nbsp;Seyyed Amir Hossein Ghazizadeh Hashemi,&nbsp;Reyhane Ahmadzade,&nbsp;Nastran Hamed,&nbsp;Marziyeh Goudarzi,&nbsp;Fatemeh Namvarjah,&nbsp;Melika Hajimohammadebrahim-Ketabforoush,&nbsp;Abbas Tafakhori,&nbsp;Vajiheh Aghamollaii,&nbsp;Saeed Karima","doi":"10.1002/jcb.70050","DOIUrl":"https://doi.org/10.1002/jcb.70050","url":null,"abstract":"<div>\u0000 \u0000 <p>Beta-hydroxybutyrate (BHB), a key ketone body produced during fatty acid metabolism, plays critical roles in various physiological and pathological conditions. Synthesized in the liver through ketogenesis, BHB serves as an essential energy substrate during glucose deprivation, supporting survival by efficiently utilizing fat reserves. It crosses the blood-brain barrier, providing energy for neuronal function, enhancing cognitive processes such as learning and memory, and offering neuroprotection by modulating synaptic plasticity and neurotransmitter levels. BHB's impact extends to cellular pathways, including autophagy, mitochondrial biogenesis, and epigenetic regulation. By modulating autophagy, BHB ensures mitochondrial integrity and function through intricate molecular pathways involving AMPK, mTOR, PINK1/Parkin, and others. This regulation plays vital roles in neurodegenerative diseases, metabolic disorders, cancer, and cardiovascular diseases, reducing oxidative stress and preventing cellular dysfunction. Epigenetically, BHB acts as an endogenous histone deacetylase inhibitor, inducing beneficial histone modifications that enhance cellular resilience and stress responses. This epigenetic influence is crucial in conditions like diabetes and cancer, aiding insulin secretion, protecting pancreatic beta cells, and impacting cancer cell gene expression and survival. Furthermore, BHB's therapeutic potential is evident in its ability to improve mitochondrial function across various tissues, including neurons, muscle, and liver. By enhancing mitochondrial respiration, reducing oxidative stress, and altering metabolic pathways, BHB mitigates conditions such as ICU-acquired weakness, nonalcoholic fatty liver disease, and cardiovascular diseases. BHB's modulation of autophagy and epigenetic regulation underscores its comprehensive role in cellular homeostasis and health across multiple physiological contexts, providing a foundation for future therapeutic strategies.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 6","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514958","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":"Sweet Science: Exploring the Impact of Fructose and Glucose on Brown Adipocyte Differentiation Using Optical Diffraction Tomography","authors":"Pooja Anantha,&nbsp;Xiangdong Wu,&nbsp;Salaheldeen Elsaid,&nbsp;Piyush Raj,&nbsp;Junkai Hu,&nbsp;Ishan Barman,&nbsp;Sui Seng Tee","doi":"10.1002/jcb.70052","DOIUrl":"https://doi.org/10.1002/jcb.70052","url":null,"abstract":"<p>The thermogenic capacity of brown adipose tissue (BAT) has garnered much attention for its potential to regulate systemic energy balance. BAT depot size and function need to be tightly regulated to prevent loss of metabolic homeostasis due to energy dissipation via non-shivering thermogenesis. While adipocyte-intrinsic mechanisms controlling thermogenesis are critical, an increasing appreciation for the role of the BAT microenvironment is emerging. For example, changes in circulating hexoses due to dietary intake have shown to impact BAT function. Here, we show that murine BAT preadipocytes metabolism is impacted when fructose is used as the sole carbon source. Similarly, differentiation medium containing only fructose yield mature adipocytes with fewer lipid droplets, with a concomitant decrease in adipogenic genes. These deficiencies are also observed in human BAT preadipocytes, where cutting-edge optical imaging modalities show a decrease in total cell mass and lipid mass in fructose-only medium. Taken together, the metabolic microenvironment significantly impacts BAT growth and function, with implications for the role of diets potentially mitigating the efficacy of BAT-targeted therapies.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 6","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514954","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":"Machine Learning Models and Structure-Based Antibacterial Drug Discovery of the Key ABC Transporter Maltose-Binding Protein A","authors":"Anupama Binoy,&nbsp;Ratul Bhowmik,&nbsp;Preena S. Parvathy,&nbsp;C. Gopi Mohan","doi":"10.1002/jcb.70049","DOIUrl":"https://doi.org/10.1002/jcb.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>Generating new and efficient drugs through machine learning-assisted quantitative structure–activity relationships (ML-QSAR) has become a promising strategy for addressing multidrug-resistant gram-negative bacterial infections. We developed robust ML-QSAR models using Genetic Function Approximation (GFA), Support Vector Machine (SVM), and Artificial Neural Network (ANN) methods to predict the activity of experimentally known quinoline-based MsbA inhibitors, aiming to create more effective antibacterial drugs. The ML models were built using eight significant molecular descriptors: B09[N-Cl], CATS3D_04_AA, F06[N-O], G2i, molecular weight (MW), Mor04p, VE1sign_B(s), and VE1sign_Dz(i), along with 279 molecular fingerprints to predict the MsbA inhibition activity of quinoline-based compounds. The molecular descriptor-based SVM model achieved an R² of 0.9891 and a q² cross-validation correlation of 0.9388. In contrast, the molecular fingerprint-based SVM model had an R² of 0.9981 and a q² cross-validation correlation of 0.7584, making it the best-performing model. The robustness of these developed models was further validated through various internal, external, and applicability domain analyses. The most active compounds identified in this data set, compounds 31 and 40, were subsequently used to generate 62 new quinoline-based compounds. Additionally, three modelled quinoline-based inhibitors, M28, N7, and N23, demonstrated excellent bioactivity, binding affinity, and pharmacokinetic profiles. To support further research, the fingerprint-based ML-QSAR model is available as a web application, MsbA-Pred (https://msba-mohan-amrita.streamlit.app/), which allows users to predict MsbA inhibitory activity from any device.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 6","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514959","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":"Purinergic Receptor P2Y2 Activity Prevents DNA Damage in CCl4-Induced Hepatic Fibrosis","authors":"Erandi Velázquez-Miranda,&nbsp;Ana Patricia Juárez-Mercado,&nbsp;Esperanza Mata-Martínez,&nbsp;María Guadalupe Ramírez-Ledesma,&nbsp;Adriana González-Gallardo,&nbsp;María Eugenia Ramos-Aguilar,&nbsp;Olivia Vázquez-Martínez,&nbsp;Mauricio Díaz-Muñoz,&nbsp;Francisco G. Vázquez-Cuevas","doi":"10.1002/jcb.70042","DOIUrl":"https://doi.org/10.1002/jcb.70042","url":null,"abstract":"<p>DNA damage is one of the key processes that underlie hepatic fibrosis, and its progression could lead to the development of neoplastic events and ultimately hepatocarcinoma. Tissue injury, including DNA damage, can involve the activation of purinergic signaling. It has been shown that P2Y2 receptor signaling is exacerbated during hepatic fibrosis. Little is known, however, about the roles played by P2Y2 receptor in the processes involved in fibrosis. In this study, we used CCl₄ treatment to induce a reversible hepatic fibrosis, and by using a microarray assay we observed an upregulation of transcripts related to the DNA damage repair of double strand breaks (DNA-dr-dsb) after P2Y2 receptor stimulation in primary cultures of hepatocytes from fibrotic mice. The transcriptional data were confirmed demonstrating an UTP-promoted reduction in the number of γH2AX+ positive cells in etoposide-treated fibrotic primary hepatocytes. Furthermore, HIF-1α, a known transcription factor that drives P2Y2 receptor expression, showed a significant increase upon CCl₄ treatment, especially within the perivascular zones. Chemical activation of HIF-1α by CoCl₂ in fibrotic hepatocytes promoted a partial protection against increased levels of γH2AX induced by etoposide, as well as an evident enhancement in the intracellular calcium response induced by UTP in fibrotic hepatocytes, suggesting a regulatory role of this transcriptional factor on the effect of P2Y2 receptor on DNA-dr-dbs response. This regulation was also investigated pharmacologically by activating or blocking the signaling from either P2Y2 receptor or HIF-1α. Our work, in summary, shows a novel relationship between P2Y2 receptor-dependent purinergic signaling and DNA-dr-dbs in hepatic fibrosis.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 6","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144255809","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":"Energy-Dependent Phosphate and Acid Transport for Bone Formation and Resorption","authors":"Irina L. Tourkova,&nbsp;Deborah J. Nelson,&nbsp;Paul H. Schlesinger,&nbsp;Harry C. Blair","doi":"10.1002/jcb.70039","DOIUrl":"https://doi.org/10.1002/jcb.70039","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Bone formation and resorption are mediated by an epithelial-like cell layer on bone. Formation or resorption requires active transport that depends on aerobic glycolysis, ATP, and acid transport. Metabolic activity of bone cells during matrix formation or removal is so high that the cells autolyze rapidly after cell death. Mineralization of bone matrix uses import of phosphate by sodium-phosphate cotransport, supported by the Na⁺/K⁺ ATPase. Glucose is the main energy source; ATP is exported to generate phosphate for hydroxyapatite in the bone matrix. Mechanism of export is not established, but phosphate is generated at least in part via phosphatase/pyrophosphatase activity including the tissue nonspecific alkaline phosphatase (TNAP) and ectonucleotide pyrophosphatase/phosphodiesterase 2 (ENPP2). Ca²⁺ is imported by paracellular transport. Protons, generated in producing hydroxyapatite, are exported by apical H⁺/Cl⁻ exchangers ClC3 and ClC5, and basolateral Na⁺/H⁺ exchange. In bone resorption, ATP-dependent acid transport, the reverse of acid transport in bone formation, is essential. This uses the vacuolar-type H⁺ATPase linked to Cl⁻ transport via a ClC family H⁺/Cl⁻ exchanger, ClC7, and a Cl⁻ channel. Other transporters contributing include carbonic anhydrase and chloride-bicarbonate exchange to replace H⁺ equivalents exported for bone resorption.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> New and Noteworthy</h3>\u0000 \u0000 <p>This focused short review considers the relationship of oxidative phosphorylation to acid transport in bone formation and resorption, processes with very high metabolic activity for storage or removal of phosphate, calcium and acid equivalents.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 5","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171947","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":"RETRACTION: Leptin Induces Matrix Metalloproteinase 7 Expression to Promote Ovarian Cancer Cell Invasion by Activating ERK and JNK Pathways","authors":"","doi":"10.1002/jcb.70036","DOIUrl":"https://doi.org/10.1002/jcb.70036","url":null,"abstract":"<p><b>RETRACTION:</b> A. Ghasemi, S. I. Hashemy, M. Aghaei, and M. Panjehpour, “Leptin Induces Matrix Metalloproteinase 7 Expression to Promote Ovarian Cancer Cell Invasion by Activating ERK and JNK Pathways,” <i>Journal of Cellular Biochemistry</i> 119, no. 2 (2018): 2333–2344, https://doi.org/10.1002/jcb.26396.</p><p>The above article, published online on 8 September 2017 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. Specifically, overlapping areas between the panels showing the “Lep+SP600125” and “Lep+PD098059” groups in SKOV3 cells have been detected within Figure 4. Additionally, the publisher's further investigation revealed duplication of the GAPDH bands in Figure 1A,D. The authors have acknowledged errors in figure compilation of Figure 4 and provided the corrected image corresponding to SKOV3 cells treated with Lep+PD098059. However, they did not provide the raw data underlying the experiments shown in Figure 1. In light of the multiple inaccuracies and the authors' failure to address the concerns related to Figure 1, the editors have lost confidence in the integrity of the whole body of data and consider the conclusions of the article to be unreliable. As a result, the article is retracted. The authors have been informed of the retraction decision and disagree with it.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 5","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135535","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":"RETRACTION: Exploring the Effect of Inhibitor AKB-9778 on VE-PTP by Molecular Docking and Molecular Dynamics Simulation","authors":"","doi":"10.1002/jcb.70037","DOIUrl":"https://doi.org/10.1002/jcb.70037","url":null,"abstract":"<p><b>RETRACTION</b>: W.-S. Liu, R.-R. Wang, Y.-Z. Sun, W.-Y. Li, H.-L. Li, C.-L. Liu, Y. et al., “Exploring the Effect of Inhibitor Akb-9778 on Ve-Ptp by Molecular Docking and Molecular Dynamics Simulation,” <i>Journal of Cellular Biochemistry</i> 120, no. 10 (2019): 17015–17029, https://doi.org/10.1002/jcb.28963.</p><p>The above article, published online on 24 May 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. The retraction has been agreed upon following concerns raised by a third party that the authors used the protein crystal structure PDB ID: 3O4U (https://www.rcsb.org/structure/3O4U) to explore the interaction between VE-PTP and AKB-9778. However, PDB ID: 3O4U corresponds to HePTP and not VE-PTP. The authors admit they inadvertently selected the incorrect crystal structure and agree to retract this article.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 5","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135536","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}