FEBS LettersPub Date : 2025-05-27DOI: 10.1002/1873-3468.70082
{"title":"RETRACTION: Sialic Acids Acquired by Pseudomonas aeruginosa Are Involved in Reduced Complement Deposition and Siglec Mediated Host-Cell Recognition.","authors":"","doi":"10.1002/1873-3468.70082","DOIUrl":"https://doi.org/10.1002/1873-3468.70082","url":null,"abstract":"<p><strong>Retraction: </strong>B. Khatua, A. Ghoshal, K. Bhattacharya, C. Mandal, B. Saha, P.R. Crocker, and C. Mandal, \"Sialic Acids Acquired by Pseudomonas Aeruginosa Are Involved in Reduced Complement Deposition and Siglec Mediated Host-Cell Recognition,\" FEBS Letters 584, no. 3 (2010): 555-561, https://doi.org/10.1016/j.febslet.2009.11.087. The above article, published online on 27 November 2009 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Michael Brunner; the Federation of European Biochemical Societies; and John Wiley & Sons Ltd. UK. The retraction has been agreed due to concerns raised by a third party. Further investigation revealed the unattributed duplication of nearly all of the data presented in Figures 1 and 2 from Figures 2 and 3 from a now-retracted article by the same authors (DOI: 10.1128/IAI.01083-08). In addition, there is duplication of data within the MALDI-TOF-MS data in Figure 3b and within the flow cytometry-based binding assay data in Figure 5. These concerns undermine the journal's confidence in the results and conclusions presented. Therefore, the parties agree that the article must be retracted.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157542","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 : 2025-05-27DOI: 10.1002/1873-3468.70081
Kevin Assoumou, Sofia Papadogkonaki, Itziar Muneta-Arrate, Miriam Stoeber
{"title":"Mechanisms governing GPCR anterograde transport.","authors":"Kevin Assoumou, Sofia Papadogkonaki, Itziar Muneta-Arrate, Miriam Stoeber","doi":"10.1002/1873-3468.70081","DOIUrl":"https://doi.org/10.1002/1873-3468.70081","url":null,"abstract":"<p><p>G protein-coupled receptors (GPCRs) constitute the largest family of human membrane proteins. GPCRs recognize diverse extracellular stimuli and activate intracellular signaling cascades that regulate key physiological processes such as neurotransmission and cardiovascular function. The controlled transport of nascent GPCRs from the endoplasmic reticulum (ER) via the Golgi apparatus to the cell surface critically determines the cellular responsiveness to incoming ligands. Here, we present a comprehensive overview of the cellular mechanisms and motif-driven interactions with regulatory proteins that orchestrate GPCR folding, post-translational modifications, and vesicular transport along the secretory pathway. We highlight signaling cues that can modulate the anterograde transport and specialized mechanisms that deliver biosynthetic GPCRs to dendrites and axons in neurons. Furthermore, we discuss that many disease-causing GPCR mutants exhibit aberrant intracellular retention, which can be rescued by pharmacological strategies that stabilize misfolded GPCRs. Finally, we highlight insights into the agonist-driven signaling of biosynthetic GPCRs in secretory organelles. This review covers the complex roles of anterograde transport in controlling GPCR function and emerging possibilities to target the underlying mechanisms in disease.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157540","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":"Characterization of molecular mechanisms of CaMKKα/1 oligomerization.","authors":"Shun Uenoyama, Hayato Nitta, Satomi Ohtsuka, Masaki Magari, Futoshi Suizu, Hiroshi Tokumitsu","doi":"10.1002/1873-3468.70078","DOIUrl":"https://doi.org/10.1002/1873-3468.70078","url":null,"abstract":"<p><p>Calcium/calmodulin-dependent protein kinase kinase (CaMKK) is an activating kinase for calcium/calmodulin-dependent protein kinase type 1 (CaMKI), calcium/calmodulin-dependent protein kinase type IV (CaMKIV), RAC-alpha serine/threonine-protein kinase (PKB), and AMP-activated protein kinase (AMPK) that has been reported to form an active oligomer in cells. Glutathione S-transferase (GST) pulldown assay from the extracts of COS-7 cells expressing GST- and His<sub>6</sub>-CaMKKα/1 mutants showed that the C-terminal region containing the autoinhibitory and calmodulin (CaM)-binding sequence (residues 438-463) is required for CaMKKα/1 homo-oligomerization. This was confirmed by the fact that the GST-CaMKKα/1 C-terminal domain (residues 435-505) directly interacted with EGFP-CaMKKα/1 residues 435-505 as well as with wild-type CaMKKα/1. Notably, once oligomerized in cells, CaMKKα/1 is neither exchangeable between the oligomeric complexes nor dissociated by Ca<sup>2+</sup>/CaM binding. These results support stable oligomerization of CaMKK in the cells by intermolecular self-association of its C-terminal region containing a regulatory domain.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141909","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 : 2025-05-21DOI: 10.1002/1873-3468.70069
Lison Cancade-Veyre, Arthur Louche, Francine C A Gérard, Laurent Terradot, Suzana P Salcedo
{"title":"Brucella NyxA and NyxB dimerization enhances effector function during infection.","authors":"Lison Cancade-Veyre, Arthur Louche, Francine C A Gérard, Laurent Terradot, Suzana P Salcedo","doi":"10.1002/1873-3468.70069","DOIUrl":"https://doi.org/10.1002/1873-3468.70069","url":null,"abstract":"<p><p>Brucella abortus is the cause of one of the most prevalent zoonoses worldwide. We have recently discovered two translocated effectors, NyxA and NyxB, that contribute to the late stages of the infectious cycle. Although their structure was solved, the importance of their interactions and dimeric states remains unknown. We found that NyxA and NyxB directly interact and that their dimerization is essential for their function during infection. We show that monomeric forms of the Nyx effectors still interact with their host cellular target, the deSUMOylase sentrin-specific protease 3 (SENP3) but are less able than the dimers to delocalize SENP3 from the nucleoli. This study provides new insights into the intra- and inter-effector molecular interactions during Brucella pathogenesis.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110091","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":"Structural insights into the binding of human TGIF1 with SMAD2 MH2 domain.","authors":"Heng Zhou, Zheyu Xu, Yue Xiong, Yuanyuan Zhang, Runchen Li, Xiaoling He, Rui Hu, Jiang Zhu, Yunhuang Yang, Maili Liu","doi":"10.1002/1873-3468.70073","DOIUrl":"https://doi.org/10.1002/1873-3468.70073","url":null,"abstract":"<p><p>Homeobox protein TGIF1 plays crucial roles in human development and body functions, partly by functioning as a corepressor in TGFβ signaling pathway. TGIF1 interacts with the MH2 domain of SMAD2 and is subsequently recruited to SMAD-binding elements to repress TGFβ-responsive gene expression. Here, through NMR titration, HDX-MS, and AlphaFold3 modeling, we reveal that a vertebrate-conserved short motif (I302-L310) of TGIF1 binds to a groove on the surface of SMAD2-MH2. The TGIF1-binding sites of SMAD2 overlap with those for its coactivators. BiFC assays verified that α2-β8 loop of SMAD2-MH2 plays a key role in binding to TGIF1. This study provides structural insight into the mechanism by which TGIF1 acts as a corepressor of SMAD2, probably through competing with coactivators for binding.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110122","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 : 2025-05-21DOI: 10.1002/1873-3468.70072
Laura Magdalena Jordt, Manuela Gellert, Finja Zelms, Sander Bekeschus, Christopher Horst Lillig
{"title":"The thioredoxin-like and one glutaredoxin domain are required to rescue the iron-starvation phenotype of HeLa GLRX3 knock out cells.","authors":"Laura Magdalena Jordt, Manuela Gellert, Finja Zelms, Sander Bekeschus, Christopher Horst Lillig","doi":"10.1002/1873-3468.70072","DOIUrl":"https://doi.org/10.1002/1873-3468.70072","url":null,"abstract":"<p><p>Glutaredoxin 3 (Grx3) is a multidomain protein (Trx-GrxA-GrxB) with a Trx-like domain and two Grx domains containing a CGFS motif for binding Fe2S2 clusters. To study the function of these domains, HeLa cells with GLRX3 knockout were generated via CRISPR/Cas. The knockout activated iron-regulatory protein 1, indicating iron starvation due to impaired iron metabolism. Transfection with constructs encoding wild-type or individual domains showed that only the Trx-GrxA construct could rescue the phenotype, matching the effect of full-length Grx3. The specific role of the second Grx domain in human Grx3, absent in simpler eukaryotes such as yeast, remains unclear. While the individual domains are insufficient to rescue the knockout of full-length Grx3, the Trx-GrxA module is functionally critical. Impact statement Glutaredoxin 3 (Grx3) contains a Trx-like domain and two Grx domains. The importance of the domains in higher eukaryotes has not previously been addressed in physiological or cellular contexts. Here, we report GLRX3 knockout results in activation of iron regulatory protein 1, and a Trx-GrxA construct could rescue the phenotype.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119301","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 : 2025-05-21DOI: 10.1002/1873-3468.70077
Jenny P Berrío, Otto Kalliokoski
{"title":"Fraudulent studies are undermining the reliability of systematic reviews: on the prevalence of problematic images in preclinical depression studies.","authors":"Jenny P Berrío, Otto Kalliokoski","doi":"10.1002/1873-3468.70077","DOIUrl":"https://doi.org/10.1002/1873-3468.70077","url":null,"abstract":"<p><p>Systematic reviews are considered by many to constitute the highest level of scientific evidence. However, the methods used in a systematic review for combining information from multiple studies are predicated on all of the reports being truthful. For a systematic review of preclinical studies of depression, we found that potentially fraudulent studies-studies featuring problematic images suggestive of gross error or manipulation-were both common and capable of biasing our findings. The prevalence of problematic studies (we had concerns with 19% of all studies with images) and our inability to find a simple pattern for identifying them undermine systematic reviews within our research field. We suspect that this is symptomatic of a broader problem that needs immediate addressing.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110117","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":"Binding mechanism of adenylate kinase-specific monobodies.","authors":"Ibuki Nakamura, Hiroshi Amesaka, Satoshi Nagao, Naoki Orito, Shigeru Negi, Shun-Ichi Tanaka, Takashi Matsuo","doi":"10.1002/1873-3468.70076","DOIUrl":"https://doi.org/10.1002/1873-3468.70076","url":null,"abstract":"<p><p>Monobodies are synthetic antibody-mimetic proteins that regulate enzyme functions through protein-protein interactions. In this study, we investigated the binding mechanisms of monobodies to adenylate kinase (Adk). Calorimetric and X-ray crystallographic analyses revealed that CL-1, a monobody specific for the CLOSED form of Adk, binds to the CORE domain of Adk in an enthalpy-driven manner, forming several hydrogen bonds and a cation-π interaction at the protein interface, without perturbing the Adk backbone. In contrast, OP-4, an OPEN-form-specific monobody, exhibited entropy-driven binding. <sup>1</sup>H-<sup>15</sup>N 2D nuclear magnetic resonance (NMR), <sup>31</sup>P-NMR, and calorimetric studies revealed conformational perturbations to Adk by OP-4, while substrate access remained intact. The different thermodynamic and structural effects between the monobodies highlight the diverse binding mechanisms among monobodies.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119300","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 : 2025-05-19DOI: 10.1002/1873-3468.70071
Marta Sampietro, Marco Cellani, Cristina Scielzo
{"title":"B cell mechanobiology in health and disease: emerging techniques and insights into therapeutic responses.","authors":"Marta Sampietro, Marco Cellani, Cristina Scielzo","doi":"10.1002/1873-3468.70071","DOIUrl":"https://doi.org/10.1002/1873-3468.70071","url":null,"abstract":"<p><p>Cells sense physical cues from their environment and convert them into biochemical responses through mechanotransduction. Unlike solid tumours, the role of such forces in haematological cancers is underexplored. In this context, immune cells experience dynamic mechanical stimuli as they migrate, extravasate and home to specific tissues. Understanding how these forces shape B-cell function and malignancy represents a groundbreaking area of research. This review examines the key mechanosensory pathways and molecules involved in lymphocyte mechanotransduction, beginning with mechanosensory proteins at the plasma membrane, followed by intracellular signal propagation through the cytoskeleton, eventually highlighting the nucleus as a 'signal actuator'. Subsequently, we cover some measurement approaches and advanced systems to investigate tumour biomechanics, highlighting their application in the context of B cells. Finally, we focus on the implications of mechanobiology in leukaemia, identifying molecules involved in B-cell malignancies that could serve as potential 'mechano-targets' for personalised therapies. This review emphasises the need to understand how lymphocytes generate, sense and respond to mechanical stimuli, which could open avenues for future biomedical innovations. Impact statement Our review is particularly valuable in highlighting the underexplored role of mechanobiology in B cell function and malignancies, while also discussing emerging techniques that can advance this research area. It bridges mechanotransduction, immunology, and cancer biology in a way that will be of interest to researchers across these three main fields.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093006","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 : 2025-05-19DOI: 10.1002/1873-3468.70068
Pratik Dasgupta, Shankar Prasad Kanaujia
{"title":"Biophysical characterization of a putative antimicrobial peptide-binding protein of Escherichia coli highlights its dual functionality.","authors":"Pratik Dasgupta, Shankar Prasad Kanaujia","doi":"10.1002/1873-3468.70068","DOIUrl":"https://doi.org/10.1002/1873-3468.70068","url":null,"abstract":"<p><p>Antimicrobial peptides (AMPs) disrupt the integrity of the bacterial membrane, ultimately leading to their death. In counter-defense, pathogens are reported to have developed systems such as the sensitivity to antimicrobial peptides (Sap) transport system that evade the action of AMPs and sequester essential micronutrients. However, recent contrasting reports cloud the functional prospects of the Sap system. Hence, this study aimed to characterize the Escherichia coli Sap (EcSap) transport system using biophysical techniques. The results obtained from various approaches suggested the binding of heme to the substrate-binding component (EcSapA) of the EcSap system. Further, this study suggests the interaction of EcSapA with the AMP protamine. In summary, the findings of this study suggest the dual ligand-binding ability of EcSapA. Impact statement The present study reports the functional prospects of the enigmatic substrate-binding protein SapA of E. coli. This analysis highlights the essentiality of the intra-protein disulfide bonds in maintaining the structural integrity of EcSapA. Further, biophysical studies of EcSapA highlight its dual ligand binding propensity, earmarking it as a drug target.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093028","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}