FEBS LettersPub Date : 2025-09-17DOI: 10.1002/1873-3468.70160
{"title":"EXPRESSION OF CONCERN: TIEG1 Induces Apoptosis Through Mitochondrial Apoptotic Pathway and Promotes Apoptosis Induced by Homoharringtonine and Velcade.","authors":"","doi":"10.1002/1873-3468.70160","DOIUrl":"https://doi.org/10.1002/1873-3468.70160","url":null,"abstract":"","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-17DOI: 10.1002/1873-3468.70163
Matteo Oliverio, Duncan E Wright
{"title":"The art of the graphical abstract-a visual approach to scientific storytelling.","authors":"Matteo Oliverio, Duncan E Wright","doi":"10.1002/1873-3468.70163","DOIUrl":"https://doi.org/10.1002/1873-3468.70163","url":null,"abstract":"<p><p>In an increasingly competitive research landscape, the graphical abstract has emerged as a vital tool for enhancing visibility and communicating scientific findings. Each element in a graphical abstract helps convey the essence of a research article in the form of a visual story. By distilling complex studies into an engaging and accessible format, these visual guides help readers quickly grasp key insights. Here, we explore the essential components of an effective graphical abstract, covering principles of design, colour theory and text usage. Additionally, we discuss various tools and services available to researchers seeking to create impactful, high-quality graphical abstracts to enhance the visibility and reach of their work.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-17DOI: 10.1002/1873-3468.70167
{"title":"RETRACTION: Breast Cancer Cell Survival Signal is Affected by Bergapten Combined With an Ultraviolet Irradiation.","authors":"","doi":"10.1002/1873-3468.70167","DOIUrl":"https://doi.org/10.1002/1873-3468.70167","url":null,"abstract":"<p><strong>Retraction: </strong>M. L. Panno , F. Giordano , F. Mastroianni , M. G. Palma, V. Bartella, A. Carpino , S. Aquila , and S. Andò, \"Breast Cancer Cell Survival Signal is Affected by Bergapten Combined With an Ultraviolet Irradiation,\" FEBS Letters 584, no. 11 (2010): 2321-2326, https://doi.org/10.1016/j.febslet.2010.04.001. The above article, published online on 04 April 2010 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Michael Brunner; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation prompted by concerns raised by a third party. The investigation identified inappropriate duplications of image sections in Figures 2A, 2B, and 2C; Figure 3B; as well as in Supplementary Figures S1B, S1C, and S2A. The authors' explanation and the data provided by the authors-pertaining to a different set of experiments conducted under the same treatment conditions-were found to be insufficient to resolve these concerns. The extent and nature of the inconsistencies identified in the published figures raised significant concerns regarding the data. As a result, the editors no longer have confidence in the integrity of the presented data and consider the study's conclusions to be compromised. The authors do not agree with this retraction.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-16DOI: 10.1002/1873-3468.70169
Giuseppe Ranieri, Andrea Lapucci, Giuseppe Orsomando, Nadia Raffaelli, Alberto Chiarugi, Daniela Buonvicino
{"title":"Cancer cell death induced by the NAD antimetabolite Vacor discloses the antitumor potential of SARM1.","authors":"Giuseppe Ranieri, Andrea Lapucci, Giuseppe Orsomando, Nadia Raffaelli, Alberto Chiarugi, Daniela Buonvicino","doi":"10.1002/1873-3468.70169","DOIUrl":"https://doi.org/10.1002/1873-3468.70169","url":null,"abstract":"<p><p>In a previous study, we showed that the NAD antimetabolite Vacor is metabolized by two enzymes implicated in the NAD salvage pathway-to Vacor mononucleotide (VMN) by nicotinamide phosphoribosyltransferase (NAMPT) and, in turn, to Vacor adenine dinucleotide (VAD) by nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2)-leading to NAD depletion and antitumor activity. Recent findings in neurons show that VMN activates SARM1, a NAD glycohydrolase, triggering NAD depletion and degeneration. In this study, we report that altering NMNAT2 levels did not affect Vacor-induced NAD depletion or cell death. In contrast, SARM1 expression alone was sufficient to induce Vacor sensitivity. Further, we report that cancer cells sense the abnormal expression of SARM1 and readily induce the expression of NMNAT2. Overall, the data underscore the antitumor potential of pharmacological approaches aimed at activating SARM1.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-16DOI: 10.1002/1873-3468.70170
Cristina Gómez-Navarro, Julia Hansen
{"title":"Mentoring to cultivate female talent in science.","authors":"Cristina Gómez-Navarro, Julia Hansen","doi":"10.1002/1873-3468.70170","DOIUrl":"https://doi.org/10.1002/1873-3468.70170","url":null,"abstract":"<p><p>Women in science face external barriers and internal challenges, such as the 'stereotype threat', which can lead to self-limiting practices. To help students overcome these, Cristina Goméz-Navarro, a professor and member of the gender equality commission at IFIMAC Madrid, set up a female mentoring program. Here, she outlines objectives and cornerstones of this program, unexpected outcomes, and tips for others who plan to set up similar systems.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diacylglycerol kinase ε depletion suppresses LPS-stimulated NF-κB activation and reduces free radical-induced DNA damage.","authors":"Akiko Ozawa, Tomoyuki Nakano, Toshiaki Tanaka, Yasukazu Hozumi, Ken Iseki, Kaoru Goto","doi":"10.1002/1873-3468.70164","DOIUrl":"https://doi.org/10.1002/1873-3468.70164","url":null,"abstract":"<p><p>The diacylglycerol kinase (DGK) family regulates lipid-mediated signaling machinery. The present study examined how DGKε depletion affects lipopolysaccharide (LPS)-mediated inflammatory responses at the cellular and organismal levels. In the early phase, DGKε-deficient cells showed reduced phosphorylation levels of Akt and NF-κB p65 subunit. In the animal model of endotoxin shock, DGKε-deficient mice showed full survival (100%) at 24 h after LPS administration, compared to the wild-type mice survival rate of 53%. In this setting, TNF-α and iNOS, the NF-κB-inducible inflammatory genes, were downregulated in DGKε-deficient liver. Furthermore, free radical-mediated cytotoxicity as evaluated by 8-OHdG staining was significantly lower in the liver. Results suggest that DGKε depletion suppresses the NF-κB pathway, thereby conferring resistance to endotoxin shock in mice. Impact statement We examined how DGKε depletion affects LPS-mediated inflammatory responses. At the cellular level, NF-κB signaling was attenuated in DGKε-deficient cells. DGKε-deficient mice were less vulnerable to endotoxin shock than the wild-type. Our results suggest DGKε depletion promotes suppression of the NF-κB pathway, thereby conferring resistance to endotoxin shock in mice.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Imeglimin attenuates liver fibrosis by inhibiting vesicular ATP release from hepatic stellate cells.","authors":"Seiji Nomura, Lixiang Wang, Nao Hasuzawa, Ayako Nagayama, Sawako Moriyama, Kenji Ashida, Yoshinori Moriyama, Masatoshi Nomura, Ken Yamamoto","doi":"10.1002/1873-3468.70166","DOIUrl":"https://doi.org/10.1002/1873-3468.70166","url":null,"abstract":"<p><p>The protective effects of imeglimin, a recently approved antidiabetic agent, against liver fibrosis have not been previously evaluated. In this study, we demonstrated that 8-week administration of imeglimin attenuated immune cell infiltration and reduced collagen deposition, improving fibrosis stage in a thioacetamide-induced murine model. Further analyses focusing on hepatic stellate cells (HSCs), the primary effector cells in fibrogenesis, revealed decreased expression of α-smooth muscle actin and desmin, markers of HSC activation. Mechanistically, a clinically relevant low concentration (10 μm) of imeglimin reduced intracellular vesicular ATP accumulation and subsequently suppressed ATP release from HSCs in vitro. These findings suggest that imeglimin may exert anti-inflammatory and antifibrotic effects by inhibiting vesicular ATP release and ATP-mediated purinergic signaling. Impact statement At clinically relevant doses, imeglimin inhibits vesicular ATP release from hepatic stellate cells, reducing inflammatory infiltration and fibrotic collagen accumulation. These findings support its evaluation as a combined metabolic and antifibrotic therapy for MASLD and other chronic liver conditions.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-13DOI: 10.1002/1873-3468.70155
Michael Beer, Philip Hinchliffe, Marko Hanževački, Christopher R Bethel, Catherine L Tooke, Marc W Van der Kamp, Krisztina M Papp-Wallace, Robert A Bonomo, Stuart Shapiro, Adrian J Mulholland, James Spencer
{"title":"Mechanistic basis for inhibition of the extended-spectrum β-lactamase GES-1 by enmetazobactam and tazobactam.","authors":"Michael Beer, Philip Hinchliffe, Marko Hanževački, Christopher R Bethel, Catherine L Tooke, Marc W Van der Kamp, Krisztina M Papp-Wallace, Robert A Bonomo, Stuart Shapiro, Adrian J Mulholland, James Spencer","doi":"10.1002/1873-3468.70155","DOIUrl":"https://doi.org/10.1002/1873-3468.70155","url":null,"abstract":"<p><p>β-Lactamase-catalysed hydrolysis is the primary form of β-lactam antibiotic resistance in Gram-negative bacteria. The penicillanic acid sulfone (PAS) enmetazobactam is thought to inhibit extended-spectrum β-lactamases (ESBLs) by fragmentation of an initial acyl-enzyme to form an active-site lysinoalanine cross link. We investigate interactions of enmetazobactam and its congener tazobactam with GES-1, an ESBL with structural features of carbapenem-hydrolysing β-lactamases. Crystal structures show different breakdown products of the two inhibitors covalently bound to the catalytic Ser70, assigned using quantum mechanics/molecular mechanics (QM/MM) calculations. We find no evidence for lysinoalanine formation, with mass spectrometry indicating active enzyme regeneration, behaviour previously observed for carbapenem-hydrolysing enzymes, but not ESBLs. This work establishes that PAS inhibitors interact with diverse β-lactamases by differing mechanisms, which should inform development of future compounds.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145052647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-12DOI: 10.1002/1873-3468.70161
Audrey Inge Schytz Andersen-Civil, Marine Mantel, Julia Soh, Serge Mostowy, Sylvia Brugman, Gilles Claude Vanwalleghem
{"title":"Novel and unscrutinized immune entities of the zebrafish gut.","authors":"Audrey Inge Schytz Andersen-Civil, Marine Mantel, Julia Soh, Serge Mostowy, Sylvia Brugman, Gilles Claude Vanwalleghem","doi":"10.1002/1873-3468.70161","DOIUrl":"https://doi.org/10.1002/1873-3468.70161","url":null,"abstract":"<p><p>The zebrafish model offers a unique opportunity to study gut immunity due to its diverse applicability within several fields of research, combined with an evolutionarily conserved immune system, transparency, and genetic tractability. This review highlights recent advances in understudied immune cell types in the zebrafish gut, emphasizing their potential to illuminate immune processes of the vertebrate immune system. The biological function of the gut is highly conserved in zebrafish, which makes them a relevant model to study intestinal immune cells with advanced molecular and imaging techniques that enable in vivo visualization of immune mechanisms and cell trajectories. Rodent and pig models have successfully contributed to our understanding of many aspects of the immune system, while zebrafish have so far been underestimated in their potential role in furthering our knowledge in this field. We suggest how future study directions can help elucidate the complex nature of gut immunity and highlight similarities between mammalian and zebrafish immune systems. Provided that immune cell functions are conserved, zebrafish can offer great opportunities for translational studies and have an important impact in improving human health.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
FEBS LettersPub Date : 2025-09-12DOI: 10.1002/1873-3468.70157
Deeksha Sugunan, Piero R Bianco, K Neelakanteshwar Patil
{"title":"Functional implications of arginine-121 in RuvA oligomerisation and RuvAB-mediated branch migration in the Gram-positive Listeria monocytogenes.","authors":"Deeksha Sugunan, Piero R Bianco, K Neelakanteshwar Patil","doi":"10.1002/1873-3468.70157","DOIUrl":"https://doi.org/10.1002/1873-3468.70157","url":null,"abstract":"<p><p>In prokaryotes, the RuvAB complex drives Holliday junction (HJ) branch migration, but the relative importance of RuvA tetramers versus octamers remains debatable and unexplored in Gram-positive bacteria. In this study, we aimed to determine whether RuvA from Listeria monocytogenes (LmRuvA) is active as a tetramer or octamer in branch migration. We identified arginine-121 as being critical for the formation of the tetramer-tetramer interface. Mutation of arginine-121 to aspartate results in a protein that exists in a dimer to tetramer equilibrium in solution (unlike other octamer-deficient mutants from earlier studies), binds to the HJ as a tetramer only, interacts poorly with RuvB, and cannot catalyse branch migration. Collectively, these findings suggest that the ability of LmRuvA to bind HJs as an octamer is critical to branch migration. Impact statement The study highlights the role of DNA repair protein RuvA in Gram-positive Listeria monocytogenes, demonstrating that its mutation at arginine-121 leads to branch migration deficiency. Hence, targeting RuvA offers a promising therapeutic strategy to slow down the development processes of antibiotic resistance in deadly foodborne pathogens of public concern.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}