FEBS LettersPub Date : 2026-08-24Epub Date: 2026-08-02DOI: 10.1002/1873-3468.70426
{"title":"RETRACTION: MicroRNA-106b Regulates the Tumor Suppressor RUNX3 in Laryngeal Carcinoma Cells","authors":"","doi":"10.1002/1873-3468.70426","DOIUrl":"10.1002/1873-3468.70426","url":null,"abstract":"<p><b>RETRACTION</b>: Y. Xu, K. Wang, W. Gao, C. Zhang, F. Huang, S. Wen and B. Wang, “MicroRNA-106b Regulates the Tumor Suppressor RUNX3 in Laryngeal Carcinoma Cells,” <i>FEBS Letters</i> 587, no. 19 (2013): 3166-3174, https://doi.org/10.1016/j.febslet.2013.05.069.</p><p>The above article, published online on 01 August 2013 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Michael Brunner; the Federation of European Biochemical Societies; and John Wiley & Sons Ltd. The retraction has been agreed following concerns raised by a third party. An investigation identified a duplication between the Hep2, miR-106b ASO band and the Hep2, Mimics-NC band in Figure 2D. A further duplication was identified between the TU-212 GAPDH bands in Figure 2D and ASO/Control GAPDH bands in Figure 3E. In addition, the ASO/Control TU-212 panel in Figure 3D is duplicated with the pCMV6/Control TU-212 panel in Figure 4D. Finally, the real-time PCR results in Figure 6A are duplicated with those shown in Figure 6B. The authors did not respond to requests from the integrity team to comment on the concerns or provide original data. The editors therefore consider the results and conclusions to be compromised. The authors did not respond to our notice of retraction.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 16","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70426","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663727","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}
{"title":"Differential recruitment of acetylcholine vesicle pools by electrical stimulation and KCl depolarization in cholinergic nerve terminals","authors":"Ikunobu Muramatsu, Junsuke Uwada, Itsumi Nagai-Arakawa, Noriyuki Matsukawa, Takayoshi Masuoka","doi":"10.1002/1873-3468.70385","DOIUrl":"10.1002/1873-3468.70385","url":null,"abstract":"<p>Depolarizing stimuli regulate acetylcholine (ACh) storage and release via distinct synaptic vesicle pools in cholinergic terminals, but the mechanisms remain unclear. Here, we examined the effects of preliminary depolarization on choline uptake, ACh synthesis, and release in rat striatal segments using [<sup>3</sup>H]choline incorporation and [<sup>3</sup>H]ACh release assays. Preliminary KCl depolarization significantly increased functional high-affinity choline transporter-1 (CHT1) availability, enhancing subsequent [<sup>3</sup>H]choline uptake, [<sup>3</sup>H]ACh synthesis, and release. In contrast, preliminary electrical stimulation selectively increased evoked [<sup>3</sup>H]ACh release without affecting choline uptake or tissue ACh content. These results suggest that electrical stimulation primarily mobilizes vesicles from the readily releasable pool (RRP) and recycling pool, whereas KCl depolarization additionally recruits vesicles from the reserve pool and may directly trigger ACh release.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 16","pages":"2320-2333"},"PeriodicalIF":3.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249817","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 : 2026-08-24Epub Date: 2026-07-25DOI: 10.1002/1873-3468.70415
Barry Halliwell
{"title":"The therapeutic opportunities and pitfalls of using iron ion chelators to treat neurodegenerative diseases","authors":"Barry Halliwell","doi":"10.1002/1873-3468.70415","DOIUrl":"10.1002/1873-3468.70415","url":null,"abstract":"<p>There is considerable evidence that iron accumulation in the affected brain regions plays a role in the pathology of neurodegenerative diseases, probably because of the ability of iron ions to promote oxidative damage to important biomolecules, such as DNA, RNA, proteins and lipids (leading to lipid peroxidation). Yet recent clinical trials of iron ion-chelating agents in human neurodegenerative diseases have given unimpressive results, in several cases making the diseases worse. In using iron chelators, it is important to remember the basics of their redox chemistry, which could explain their lack of therapeutic effects. This issue is explored here, and the potential of iron ion chelation in the treatment of neurodegeneration is critically evaluated.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"600 16","pages":"2219-2225"},"PeriodicalIF":3.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70415","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590907","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}
FEBS LettersPub Date : 2026-08-21DOI: 10.1002/1873-3468.70439
Claudia E Ramirez Bustamante, Robert Sharp, Pradip K Saha, Elizabeth S Anaya, Elizabeth L Lieu, Evelyn L de Groot, Pooja Patel, Mi Jeong Heo, Aaron R Cox, Kang Ho Kim, Sean M Hartig
{"title":"Partial depletion of plasminogen activator inhibitor-1 decreases subcutaneous fat cell hypertrophy and liver cholesterol in high-fat-fed female mice.","authors":"Claudia E Ramirez Bustamante, Robert Sharp, Pradip K Saha, Elizabeth S Anaya, Elizabeth L Lieu, Evelyn L de Groot, Pooja Patel, Mi Jeong Heo, Aaron R Cox, Kang Ho Kim, Sean M Hartig","doi":"10.1002/1873-3468.70439","DOIUrl":"10.1002/1873-3468.70439","url":null,"abstract":"<p><p>Higher levels of plasminogen activator inhibitor-1 (PAI-1) circulate in the blood of people with obesity and predict hyperlipidemia and metabolic dysfunction-associated steatotic liver disease in studies predominantly conducted in women. To understand the roles of PAI-1 in women with obesity, we generated inducible whole-body PAI-1-depleted female mice (Pai-1<sup>i-KD</sup>). After high-fat diet feeding, Pai-1<sup>i-KD</sup> and littermate controls did not differ in body weight or energy balance. However, Pai-1<sup>i-KD</sup> females accumulated smaller inguinal WAT adipocytes. Spectral flow cytometry revealed reduced adipocyte progenitors and macrophages in inguinal WAT. Pai-1<sup>i-KD</sup> mice also exhibited decreased liver cholesterol. These preclinical findings argue that elevated PAI-1 alters subcutaneous adipose tissue biology and contributes to pathogenic phenotypes of obesity.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790139","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":"Ligand-dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry.","authors":"Ririn Rahmala Febri, Ayaka Nagasato-Ichikawa, Keita Iida, Shuhei Kimura, Akira Imamoto, Mariko Okada","doi":"10.1002/1873-3468.70440","DOIUrl":"https://doi.org/10.1002/1873-3468.70440","url":null,"abstract":"<p><p>ErbB ligands activate distinct receptor dimers that regulate cell proliferation, but how they influence cell-cycle commitment remains unclear. Here, we show that EGF and HRG induce different modes of G1/S progression in ErbB2-amplified BT474 breast cancer cells. Unexpectedly, HRG, despite activating the more potent ErbB2-ErbB3 heterodimer, failed to accelerate G1/S progression; instead, EGF promoted earlier passage through the restriction point and faster S-phase entry. Mechanistically, EGF drove rapid and coordinated cell-cycle progression through ERK-FOS signaling, whereas HRG induced sustained MYC activity, elevated transcriptional heterogeneity, and caused extensive rewiring of cell-cycle regulatory networks. Together, these findings reveal that ligand-specific ErbB signaling controls not only the timing of cell-cycle entry but also the transcriptional architecture that governs proliferative fate decisions.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790192","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 : 2026-08-20DOI: 10.1002/1873-3468.70445
Konstancja Gałat, Natalia Rzepka, Aleksandra A Kołodziejczyk
{"title":"The impact of aging on the gut-liver axis in health and disease.","authors":"Konstancja Gałat, Natalia Rzepka, Aleksandra A Kołodziejczyk","doi":"10.1002/1873-3468.70445","DOIUrl":"https://doi.org/10.1002/1873-3468.70445","url":null,"abstract":"<p><p>Aging is a complex biological process characterized by gradual impairment of organ function and increased susceptibility to disease. Among the systems most affected, the gut and liver are particularly important because of their role in metabolism, detoxification, and immune regulation. These two organs are closely connected through the portal vein and bile ducts, enabling continuous, bidirectional communication that coordinates homeostasis. Understanding how gut-liver communication changes with age is therefore critical, as even subtle alterations over time can have widespread effects on overall physiology and the progression of age-related disorders. In this review, we examine current knowledge on how aging shapes gut and liver physiology, highlighting changes in microbial composition, barrier function, and hepatic metabolism. We then discuss how sex influences the gut-liver axis during aging. Finally, we explore how disruptions in the gut-liver axis contribute to the development of age-related conditions.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790179","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 : 2026-08-19DOI: 10.1002/1873-3468.70431
Terry M Bricker, Laurie K Frankel
{"title":"Oxidative modification of the D1 residue <sup>332</sup>H during photoinactivation drives photosystem II turnover.","authors":"Terry M Bricker, Laurie K Frankel","doi":"10.1002/1873-3468.70431","DOIUrl":"https://doi.org/10.1002/1873-3468.70431","url":null,"abstract":"<p><p>Photosystem II (PS II) is a water-plastoquinone oxidoreductase. This photosystem has a short half-life (< 1 h) which is driven by repair of oxidative damage to the D1 protein. Reactive oxygen species (ROS) produced by the photosystem under stress conditions oxidatively modify key residues, which trigger the sequential disassembly of the photosystem. We hypothesize that the principal target for ROS damage of D1 is <sup>332</sup>His. This residue is a ligand to Mn1 of the Mn<sub>4</sub>CaO<sub>5</sub> cluster and is the first residue exhibiting oxidative modification during photoinactivation. Recently, cryo-EM studies indicate that PS II monomers containing oxidatively modified <sup>332</sup>His lose their manganese clusters and the extrinsic proteins associated with the photosystem, both hallmarks of the earliest stages of PS II turnover/repair.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790136","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 : 2026-08-19DOI: 10.1002/1873-3468.70436
Yunkyeong Lee, Mingming Tong, Anna L Gloyn
{"title":"Autophagy and mitophagy in pancreatic β-cell homeostasis and their involvement in diabetes pathophysiology.","authors":"Yunkyeong Lee, Mingming Tong, Anna L Gloyn","doi":"10.1002/1873-3468.70436","DOIUrl":"https://doi.org/10.1002/1873-3468.70436","url":null,"abstract":"<p><p>Autophagy is an evolutionarily conserved cellular quality control pathway that responds to the metabolic state of the cell, and its dysregulation has been broadly associated with metabolic disorders like diabetes mellitus. Among different types of autophagy, mitophagy or the selective autophagic clearance of dysfunctional mitochondria has emerged as particularly relevant in pancreatic β-cell biology and its pathophysiology. Recent advances in functional genomics and animal studies implicate the autophagy/mitophagy pathway components as effector transcripts at diabetes risk loci, providing a new rationale for investigation of genetic determinants of autophagy/mitophagy in β cells. In this review, we take a β-cell centric perspective to examine the evidence for autophagy/mitophagy across four clinically relevant diabetes categories (type 1, type 2, gestational, and monogenic diabetes) and discuss the functional significance and complexity of these pathways in β-cell failure.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790209","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 : 2026-08-19DOI: 10.1002/1873-3468.70444
Sara De Bragança, Eline L Jansen, Jorine M Eeftens
{"title":"Synergistic perspectives-How single-molecule biophysics complement biochemical understanding.","authors":"Sara De Bragança, Eline L Jansen, Jorine M Eeftens","doi":"10.1002/1873-3468.70444","DOIUrl":"https://doi.org/10.1002/1873-3468.70444","url":null,"abstract":"<p><p>Single-molecule biophysical techniques enable the study of biological systems by directly observing individual molecules and events, rather than measuring population averages. These approaches reveal transient states, rare events, conformational dynamics, and subpopulations that are often obscured in biochemical assays. The application of single-molecule methods has been limited by technical complexity and the need for specialized instrumentation. Recent standardization of protocols, methodologies, and platforms has lowered these barriers, enabling broader adoption and promoting interdisciplinary collaborations that facilitate integration into biochemical research. In this review, we discuss how ensemble biochemistry and single-molecule approaches are complementary, outline commonly used single-molecule techniques, and illustrate their relevance through two representative case studies: chromatin organization by SMC complexes and pathway choice during DNA double-strand break repair.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790174","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":"Divergent effects of copper and cisplatin on the endocytic trafficking of copper transporter-1.","authors":"Mainak Chakraborty, Swastika Dey, Sumanta Kar, Arnab Gupta","doi":"10.1002/1873-3468.70441","DOIUrl":"https://doi.org/10.1002/1873-3468.70441","url":null,"abstract":"<p><p>Cisplatin (CDDP), a widely used chemotherapeutic agent, enters mammalian cells through high-affinity copper transporter CTR1. We found that copper preloading reduces CDDP cytotoxicity, supporting a shared uptake mechanism for copper and cisplatin. CDDP-induced CTR1 endocytosis requires both the amino-terminal His-Met motifs and the conserved 150MXXM154 pore-motif, similar to copper-mediated transport. Following internalization, CTR1 is routed through VPS35-positive endosomes and ultimately targeted to lysosomes. However, unlike copper, CDDP suppresses local recycling of CTR1 to plasma membrane and delays its lysosomal delivery. While copper promotes rapid lysosomal clearance of CTR1, CDDP results in prolonged intracellular trafficking. Additionally, CDDP enhances lysosomal size and cathepsin activity, indicating lysosomal activation. These findings reveal distinct mechanisms underlying CTR1-mediated cisplatin uptake and its impact on lysosomal physiology.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790197","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}