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Knockdown of RFC4 inhibits cell proliferation of oral squamous cell carcinoma in vitro and in vivo RFC4基因下调对口腔鳞状细胞癌细胞增殖的抑制作用。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-13 DOI: 10.1002/2211-5463.13929
Pengyue You, Di Wang, Zheng Liu, Shuzhen Guan, Ning Xiao, Haotian Chen, Xin Zhang, Lichuan Wu, Guizhen Wang, Haitao Dong
{"title":"Knockdown of RFC4 inhibits cell proliferation of oral squamous cell carcinoma in vitro and in vivo","authors":"Pengyue You,&nbsp;Di Wang,&nbsp;Zheng Liu,&nbsp;Shuzhen Guan,&nbsp;Ning Xiao,&nbsp;Haotian Chen,&nbsp;Xin Zhang,&nbsp;Lichuan Wu,&nbsp;Guizhen Wang,&nbsp;Haitao Dong","doi":"10.1002/2211-5463.13929","DOIUrl":"10.1002/2211-5463.13929","url":null,"abstract":"<p>Oral squamous cell carcinoma (OSCC) is the one of the most common types of malignant tumor found in the head and neck area. Replication factor C subunit 4 (RFC4), an oncogene active in various human cancers, has been rarely studied in OSCC. In the present study, bioinformatics analysis identified RFC4 as a potential key target in OSCC progression. Additional experiments showed that RFC4 expression was significantly higher in OSCC tumor tissues than in normal tissues. Knockdown of RFC4 led to G2/M phase cell cycle arrest and inhibited the proliferation of OSCC cells both <i>in vitro</i> and <i>in vivo</i>. High RFC4 expression in OSCC tumors was linked to increased levels of MET, along with reduced levels of CD274 and CD160. Overall, the present study reveals that RFC4 may play a pivotal role in OSCC tumorigenesis and could serve as a potential predictive marker for the efficacy of immunotherapy.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 2","pages":"346-358"},"PeriodicalIF":2.8,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13929","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Evaluation of binding activities of a putative lipoprotein LIC_13355 of Leptospira spp. 钩端螺旋体脂蛋白LIC_13355结合活性的评价。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13942
Igor R. M. Silva, Maria B. Takahashi, Aline F. Teixeira, Ana L. T. O. Nascimento
{"title":"Evaluation of binding activities of a putative lipoprotein LIC_13355 of Leptospira spp.","authors":"Igor R. M. Silva,&nbsp;Maria B. Takahashi,&nbsp;Aline F. Teixeira,&nbsp;Ana L. T. O. Nascimento","doi":"10.1002/2211-5463.13942","DOIUrl":"10.1002/2211-5463.13942","url":null,"abstract":"<p>Pathogenic <i>Leptospira</i> is the etiological cause of the zoonotic life-threatening infection called leptospirosis. The disease is spread worldwide with higher risk in tropical regions. Although leptospirosis represents a burden to the health of humans and animals, the pathogenic mechanisms of <i>Leptospira</i> infection are yet to be clarified. Leptospirosis infection is multifactorial, involving functionally redundant proteins with the capability to invade, disseminate, and escape the host's immune response. In this work, we describe a putative lipoprotein encoded by the gene LIC_13355, genome annotated as hypothetical of unknown function. The coding sequence is conserved among pathogenic <i>Leptospira</i> spp. with high percentage of coverage and identity. The recombinant protein, rLIC_13355, was expressed in <i>Escherichia coli</i> host system in its insoluble form. The circular dichroism spectrum of the refolded protein showed it containing a mixture of secondary structures. rLIC_13355 interacts with extracellular matrix (ECM) component laminin and binds plasminogen (PLG), generating plasmin (PLA), thus possibly participating during the adhesion and dissemination processes. The rLIC_13355 has the ability to interact with Ea.hy926 and HMEC-1 endothelial cells either in monolayer or suspension. The binding of rLIC_13355 with monolayer cells is dose-dependent on protein concentration. Taken together, our data suggest that this is presumably an adhesion lipoprotein that may play diverse roles in host–<i>Leptospira</i> interactions by mediating the interaction with host components and with endothelial cell.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"447-461"},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13942","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Using TECHnology to predict the future of biomedical education 利用技术预测生物医学教育的未来。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13953
Robert A. Harris, Hasan Kazdağlı
{"title":"Using TECHnology to predict the future of biomedical education","authors":"Robert A. Harris,&nbsp;Hasan Kazdağlı","doi":"10.1002/2211-5463.13953","DOIUrl":"10.1002/2211-5463.13953","url":null,"abstract":"<p>Biomedical research is currently benefiting from a technological revolution in which multiple forms of omics are permitting unprecedented characterization of molecular pathways. Likewise, medical device and Ai-assisted technologies now make diagnoses and medical imaging more accurate. The field of education is also starting to embrace how technology can promote pedagogical development and student learning. But how will this landscape look like in 2050? With the premise that collaboration will be central to teaching and learning practices, that Together, Everything Can Happen (TECH), we examine the emerging trends and innovations in biomedical education, exploring how they will influence the field's evolution and shape future teaching practices in the coming years.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"48-55"},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A white paper from the FEBS Education and Training Conference: challenges, opportunities, and action plans for transforming molecular life sciences education FEBS教育与培训会议白皮书:分子生命科学教育转型的挑战、机遇和行动计划。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13916
Ly Villo, Nino Sincic, Luciane V. Mello, Manuel Joao Costa, Didier Picard, Francesco Malatesta, Jerka Dumic, Ferhan G. Sagin
{"title":"A white paper from the FEBS Education and Training Conference: challenges, opportunities, and action plans for transforming molecular life sciences education","authors":"Ly Villo,&nbsp;Nino Sincic,&nbsp;Luciane V. Mello,&nbsp;Manuel Joao Costa,&nbsp;Didier Picard,&nbsp;Francesco Malatesta,&nbsp;Jerka Dumic,&nbsp;Ferhan G. Sagin","doi":"10.1002/2211-5463.13916","DOIUrl":"10.1002/2211-5463.13916","url":null,"abstract":"<p>The inaugural FEBS Education and Training Conference (ETC) was held in Türkiye, in 2024. This first-ever Molecular Life Sciences Education Conference in Europe was organized by the FEBS Education and Training Committee and it was a groundbreaking event that brought together educators and scientists to explore how to enhance education and training in molecular life sciences. The conference explored a wide range of critical themes, for example—digital revolution, active learning and student engagement, multidisciplinary teaching and learning, transitions and inclusivity in education, students' self-assessment, and self-regulated learning. The discussions and presentations underscored the pressing need for transformation in how academics and researchers approach teaching and learning. Such shift is driven by rapid technological advancements, societal shifts, and the evolving demands of the scientific landscape. This document synthesizes key insights, discussions, and recommendations from the conference and proposes actionable strategies for all stakeholders in the field—institutions, educators and students—to address current challenges in education and training in molecular life sciences.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"11-20"},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin 阿霉素诱导胃肠道细胞衰老的δ -9去饱和酶降低。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-10 DOI: 10.1002/2211-5463.13945
Valentina De Nunzio, Emanuela Aloisio Caruso, Matteo Centonze, Giuliano Pinto, Miriam Cofano, Ilenia Saponara, Maria Notarnicola
{"title":"Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin","authors":"Valentina De Nunzio,&nbsp;Emanuela Aloisio Caruso,&nbsp;Matteo Centonze,&nbsp;Giuliano Pinto,&nbsp;Miriam Cofano,&nbsp;Ilenia Saponara,&nbsp;Maria Notarnicola","doi":"10.1002/2211-5463.13945","DOIUrl":"10.1002/2211-5463.13945","url":null,"abstract":"<p>The condition of cellular senescence has specific features, including an altered lipid metabolism. Delta-9 desaturase (Δ9) catalyzes the conversion of saturated fatty acids, such as palmitic acid and stearic acid, into their monounsaturated forms, palmitoleic and oleic acid, respectively. Δ9 activity is important for most lipid functions, such as membrane fluidity, lipoprotein metabolism and energy storage. The present study aimed to investigate differences in the expression of Δ9 in senescence-induced pancreatic (MIA-PaCa-2 and PANC-1) and hepatic (Hepa-RG and HLF) cancer cell lines. Cellular senescence was induced by growing cells in the presence of the chemotherapic drug doxorubicin. Senescence status was determined by the senescence-associated beta-galactosidase activity assay kit combined with the p21 and senescence associated secretory phenotype protein assay. Δ9 was downregulated in all senescence-induced cell lines compared to control cells, in both the lipidomic analysis and when measuring protein levels via western blotting. Hence, our findings demonstrate that the study of membrane lipid composition and the expression levels of Δ9 could potentially form the basis for future applications investigating the state of cellular senescence.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"462-473"},"PeriodicalIF":2.8,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13945","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione mediates the effect of ROS-enhanced PI3K/Akt/mTOR pathway on autophagy in breast cancer 2-十二烷基-6-甲氧基环己-2,5-二烯-1,4-二酮介导ros增强的PI3K/Akt/mTOR通路对乳腺癌自噬的影响。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-09 DOI: 10.1002/2211-5463.13940
Linqian Chen, Meifeng Chen, Yan Xie, Yuyan Zhang, Shutian Mo, Yongfei He, Tianyi Liang, Yuan Liao, Renbin Huang, Guodong Huang, Chuangye Han, Thi Thai Hoa Pham
{"title":"2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione mediates the effect of ROS-enhanced PI3K/Akt/mTOR pathway on autophagy in breast cancer","authors":"Linqian Chen,&nbsp;Meifeng Chen,&nbsp;Yan Xie,&nbsp;Yuyan Zhang,&nbsp;Shutian Mo,&nbsp;Yongfei He,&nbsp;Tianyi Liang,&nbsp;Yuan Liao,&nbsp;Renbin Huang,&nbsp;Guodong Huang,&nbsp;Chuangye Han,&nbsp;Thi Thai Hoa Pham","doi":"10.1002/2211-5463.13940","DOIUrl":"10.1002/2211-5463.13940","url":null,"abstract":"<p>Several studies have suggested a potential antitumor effect of 2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD). To further understand the mechanism of action of this compound, we investigated its effect on the phosphatidylinositol-3-kinase (PI3K)/serine–threonine kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. We show that DMDD application significantly inhibited the proliferation of breast cancer cell lines MDA-MB-231 and ER-α positive MCF-7. Furthermore, DMDD application resulted in increased intracellular reactive oxygen species (ROS) levels, apoptosis and autophagy, whereas it downregulated the expression of PI3K, Akt and mTOR mRNA and proteins, and increased the expression of LC3II/I and p62 proteins. In a mouse breast cancer xenograft model, DMDD inhibited tumor growth. Expression analyses suggest that ROS levels were higher in DMDD treated tumor tissues, whereas immunohistochemical analyses suggest that apoptotic cells were more prevalent in the DMDD treated group compared to the control group. Taken together, our results suggest that the molecular mechanism of action of DMDD may involve the enhancement of breast cancer autophagy through the PI3K/Akt/mTOR signaling pathway by mediating ROS expression.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"474-489"},"PeriodicalIF":2.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13940","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: LKB1 Suppresses Androgen Synthesis in a Mouse Model of Hyperandrogenism via IGF-1 Signaling 撤回:LKB1通过IGF-1信号抑制高雄激素血症小鼠模型中的雄激素合成。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13948
{"title":"RETRACTION: LKB1 Suppresses Androgen Synthesis in a Mouse Model of Hyperandrogenism via IGF-1 Signaling","authors":"","doi":"10.1002/2211-5463.13948","DOIUrl":"10.1002/2211-5463.13948","url":null,"abstract":"<p><b>RETRACTION</b>: Y. Xu, Y. Gao, Z. Huang, Y. Zheng, W. Teng, D. Zheng, and X. Zheng, “LKB1 Suppresses Androgen Synthesis in a Mouse Model of Hyperandrogenism via IGF-1 Signaling,” <i>FEBS Open Bio</i> 9, no. 10 (2019): 1817-1825, https://doi.org/10.1002/2211-5463.12723.</p><p>The above article, published online on 12 September 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 1C, 1H) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"525"},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13948","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: NGF Protects Neuroblastoma Cells Against β-Amyloid-Induced Apoptosis via the Nrf2/HO-1 pathway 结论:NGF通过Nrf2/HO-1途径保护神经母细胞瘤细胞免受β-淀粉样蛋白诱导的凋亡。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13950
{"title":"RETRACTION: NGF Protects Neuroblastoma Cells Against β-Amyloid-Induced Apoptosis via the Nrf2/HO-1 pathway","authors":"","doi":"10.1002/2211-5463.13950","DOIUrl":"10.1002/2211-5463.13950","url":null,"abstract":"<p><b>RETRACTION</b>: R. Su, W. Su, and Q. Jiao, “NGF Protects Neuroblastoma Cells Against β-Amyloid-Induced Apoptosis via the Nrf2/HO-1 pathway,” <i>FEBS Open Bio</i> 9, no. 12 (2019): 2063-2071, https://doi.org/10.1002/2211-5463.12742.</p><p>The above article, published online on 01 November 2019, in Wiley Online Library (wileyonlinelibrary.com), and its correction (https://doi.org/10.1002/2211-5463.12782) has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 2A, 3A, 5A and 6E) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 5","pages":"888"},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13950","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: MicroRNA-498 Reduces the Proliferation and Invasion of Colorectal Cancer Cells via Targeting Bcl-2 撤回:MicroRNA-498通过靶向Bcl-2抑制结直肠癌细胞的增殖和侵袭。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13949
{"title":"RETRACTION: MicroRNA-498 Reduces the Proliferation and Invasion of Colorectal Cancer Cells via Targeting Bcl-2","authors":"","doi":"10.1002/2211-5463.13949","DOIUrl":"10.1002/2211-5463.13949","url":null,"abstract":"<p><b>RETRACTION</b>: T. Wang, L. Ma, W. Li, L. Ding, and H. Gao, “MicroRNA-498 Reduces the Proliferation and Invasion of Colorectal Cancer Cells via Targeting Bcl-2,” <i>FEBS Open Bio</i> 10, no. 1 (2020): 168-175, https://doi.org/10.1002/2211-5463.12767.</p><p>The above article, published online on 17 December 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 3A and B, 5E and F) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 5","pages":"887"},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13949","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: XBP1 Inhibits Mesangial Cell Apoptosis in Response to Oxidative Stress via the PTEN/AKT Pathway in Diabetic Nephropathy 回顾:XBP1通过PTEN/AKT通路抑制糖尿病肾病中氧化应激反应中的系膜细胞凋亡。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13947
{"title":"RETRACTION: XBP1 Inhibits Mesangial Cell Apoptosis in Response to Oxidative Stress via the PTEN/AKT Pathway in Diabetic Nephropathy","authors":"","doi":"10.1002/2211-5463.13947","DOIUrl":"10.1002/2211-5463.13947","url":null,"abstract":"<p><b>RETRACTION</b>: Y. Wang, Z. He, Q. Yang, and G. Zhou, “XBP1 Inhibits Mesangial Cell Apoptosis in Response to Oxidative Stress via the PTEN/AKT Pathway in Diabetic Nephropathy,” <i>FEBS Open Bio</i> 9, no. 7 (2019): 1249-1258, https://doi.org/10.1002/2211-5463.12655.</p><p>The above article, published online on 02 June 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 1C-F, 3A and C) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"524"},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13947","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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