FEBS Letters最新文献

{"title":"miRNA-29 regulates epidermal and mesenchymal functions in skin repair","authors":"Lalitha Thiagarajan,&nbsp;Rosa Sanchez-Alvarez,&nbsp;Chiho Kambara,&nbsp;Poojitha Rajasekar,&nbsp;Yuluang Wang,&nbsp;François Halloy,&nbsp;Jonathan Hall,&nbsp;Hans-Jürgen Stark,&nbsp;Iris Martin,&nbsp;Petra Boukamp,&nbsp;Svitlana Kurinna","doi":"10.1002/1873-3468.70051","DOIUrl":"10.1002/1873-3468.70051","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <p>MicroRNAs (miRNAs) control organogenesis in mammals by inhibiting translation of mRNA. Skin is an excellent model to study the role of miRNAs in epidermis and the mesenchyme. Previous research demonstrated miRNA-29 family functions in skin; however, the mRNA targets and the downstream mechanisms of miRNA-29-mediated regulation are missing. We used the miRNA crosslinking and immunoprecipitation method to find direct targets of miRNA-29 in keratinocytes and fibroblasts from human skin. miRNA-29 inhibition using modified antisense oligonucleotides in 2D and 3D cultures of keratinocytes and fibroblasts enhanced cell-to-matrix adhesion through autocrine and paracrine mechanisms of miRNA-29-dependent tissue growth. We reveal a full transcriptome of human keratinocytes with enhanced adhesion to the matrix, which supports regeneration of the epidermis and is regulated by miRNA-29.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <div>\u0000 \u0000 <div>\u0000 \u0000 <h3>Impact statement</h3>\u0000 <p>The functions of small, therapeutically targetable microRNA molecules identified in our study can provide a new approach to improve wound healing by restoring and enhancing the inner molecular mechanisms of a cell and its surrounding matrix. We also provide a plethora of new mRNA targets for follow-up studies of cell adhesion and extracellular matrix formation in humans.</p>\u0000 </div>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 12","pages":"1795-1817"},"PeriodicalIF":3.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143988814","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":"Social context prevents heat hormetic effects against mutagens during fish development.","authors":"Lauric Feugere, Claudio Silva De Freitas, Adam Bates, Kenneth B Storey, Pedro Beltran-Alvarez, Katharina C Wollenberg Valero","doi":"10.1002/1873-3468.70047","DOIUrl":"https://doi.org/10.1002/1873-3468.70047","url":null,"abstract":"<p><p>Since stress can be transmitted to congeners via social metabolites, it is paramount to understand how the social context of abiotic stress influences aquatic organisms' responses to global changes. Here, we integrated the transcriptomic and phenotypic responses of zebrafish embryos to a UV damage/repair assay following scenarios of heat stress, its social context and their combination. Heat stress preceding UV exposure had a hormetic effect through the cellular stress response and DNA repair, rescuing and/or protecting embryos from UV damage. However, experiencing heat stress within a social context negated this molecular hormetic effect and lowered larval fitness. We discuss the molecular basis of interindividual chemical transmission within animal groups as another layer of complexity to organisms' responses to environmental stressors.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958240","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":"Correction to “Versican V2 isoform enhances angiogenesis by regulating endothelial cell activities and fibronectin expression”","authors":"","doi":"10.1002/1873-3468.70046","DOIUrl":"10.1002/1873-3468.70046","url":null,"abstract":"<p>\u0000 <span>Weining Yang</span>, <span>Albert J. Yee</span>. <span>Versican V2 isoform enhances angiogenesis by regulating endothelial cell activities and fibronectin expression</span>. <i>FEBS Letters</i> <span>2013</span>; <span>587</span>: <span>185</span>-<span>192</span>. https://doi.org/10.1016/j.febslet.2012.11.023\u0000 </p><p>In Fig. 3B of the published article, the two vector images (5x and 20x) are of the same vector sample 5 days after co-culture. The four V2 images (5x, 20x, 20x, 20x) are of the same V2 sample 5 days after co-culture. This was intentional, with the multiple images included to show readers more detail of the cell–cell interaction. This corrigendum has been published to amend the figure legend to make this clear. The amended figure legend is shown below.</p><p><b>Figure 3</b></p><p>Expression versican V2 promotes cell–cell interaction and tube-like structure formation. (A) V2- and vector-transfected cells were co-cultured with endothelial cells EOMA at a 1:1 ratio. After 5 days, the co-cultured cells were photographed. The V2 cells displayed higher capacities in interaction with EOMA cells than the control cells. As a result, there was closed contact between the V2 and EOMA cells compared with the control cells; (B) V2- and vector-transfected cells were co-cultured with YPEN endothelial cells at a ratio of 1:1. After 5 days, the co-cultured cells were photographed. The two vector images are of a single sample. The four V2 images (one at 5x magnification, and the other three at 20x magnification) are also of a single sample. YPEN cells could mix well with V2 expressing U87 cells, but not the control cells; (C) V2- and vector-transfected cells were mixed with YPEN cells and inoculated in Matrigel, followed by examination of tube formation. The YPEN cells formed complex tube-like structures when mixed with the V2 cells, but not with the control cells; (D) typical photographs of tube-like structures are shown; (E) V2- and vector-transfected cells were mixed with EOMA cells for tube formation assay. Similarly, the EOMA cells formed complex tube-like structures when mixed with the V2 cells, but not with the control cells.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 10","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975351","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":"The Saccharomyces cerevisiae amino acid transporter Lyp1 has a broad substrate spectrum","authors":"Foteini Karapanagioti,&nbsp;Sebastian Obermaier,&nbsp;Dirk J. Slotboom,&nbsp;Bert Poolman","doi":"10.1002/1873-3468.70044","DOIUrl":"10.1002/1873-3468.70044","url":null,"abstract":"<p>The main mediators for the amino acid uptake in <i>Saccharomyces cerevisiae</i> are the permeases belonging to the yeast amino acid transporter family. Recently, we discovered that members of this family support growth on more amino acids than previously described. Here we study the substrate spectrum of Lyp1, the main transporter responsible for the uptake of lysine in yeast. We show that overexpressed Lyp1 supports growth on alanine, asparagine, leucine, methionine, phenylalanine, serine, and valine when these are provided as the sole source of nitrogen to a strain severely deficient for the uptake of amino acids. We show that alanine and serine compete with lysine for the common transport system, albeit with much lower affinity. Thus, Lyp1 has a much broader substrate spectrum than previously thought, which may be true for many amino acid transporters.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 11","pages":"1609-1621"},"PeriodicalIF":3.5,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989128","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":"The cytoskeletal control of B cell receptor and integrin signaling in normal B cells and chronic lymphocytic leukemia.","authors":"Abhishek Pethe, Tanja Nicole Hartmann","doi":"10.1002/1873-3468.70045","DOIUrl":"https://doi.org/10.1002/1873-3468.70045","url":null,"abstract":"<p><p>B cells migrate within lymphoid organs during maturation and activation, processes orchestrated by the interplay between B cell receptor (BCR) signaling and microenvironmental cues. Integrins act as mechanoreceptors, linking BCR activation to cytoskeletal remodeling, facilitating immune synapse formation, antigen recognition, and extraction. BCR activation models describe receptor clustering and mechanical changes within the antigen-BCR complex. Upon activation, immune synapses form, enabling antigen extraction and downstream signaling. Integrins stabilize these synapses, amplify BCR signaling, and modulate BCR positioning via actin reorganization. In chronic lymphocytic leukemia (CLL), aberrant BCR signaling and integrins are major players in leukemic cell homing, prognosis, and therapy resistance. In this review, we summarize the current understanding of the interplay of BCR mechanics and B cell localization, with a particular focus on communication between BCR signaling and integrin-mediated processes via actin dynamics. We give insights into normal B cell biology and then outline aspects typical to CLL.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998526","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":"The power of microRNA regulation-insights into immunity and metabolism.","authors":"Stefania Oliveto, Nicola Manfrini, Stefano Biffo","doi":"10.1002/1873-3468.70039","DOIUrl":"https://doi.org/10.1002/1873-3468.70039","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are a prominent class of small non-coding RNAs that control gene expression. This comprehensive review explores the intricate roles of miRNAs in metabolism and immunity, as well as the emerging field of immunometabolism. The core of this work delves into the functional and regulatory capabilities of miRNAs, examining their complex influence on glucose and lipid metabolism, as well as their pivotal roles in shaping T-cell development and function. Specifically, this review addresses how miRNAs orchestrate the complex interaction between cellular metabolic processes and immune responses, underscoring the essential nature of these small regulatory molecules in maintaining homeostasis. Finally, we examine the emerging role of Artificial Intelligence (AI) in miRNA research, focusing on how machine learning techniques are revolutionizing the identification and validation of potential miRNA biomarkers. By integrating these diverse aspects, this review underscores the multifaceted roles of miRNAs in biological processes and their significant potential in advancing biomedical research and clinical applications.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999019","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":"C-terminal anchor endolysins—proposing a third class of tailed bacteriophage endolysins","authors":"Elina Cernooka,&nbsp;Nikita Zrelovs,&nbsp;Andris Kazaks","doi":"10.1002/1873-3468.70042","DOIUrl":"10.1002/1873-3468.70042","url":null,"abstract":"<p>Endolysins—enzymes produced by tailed bacteriophages to degrade bacterial cell walls—have traditionally been classified as canonical or signal-anchor-release (SAR) endolysins. However, analysis of expanding viral (meta)genomic data has revealed a third class, which we designate as C-terminal anchor (CTA) endolysins. These enzymes feature an N-terminal enzymatic domain, a C-terminal transmembrane domain, and typically lack signal sequences, distinguishing them from SAR endolysins. CTA endolysins span all known enzymatic activities and exhibit diverse architectures, though most have a single transmembrane helix and an N-out, C-in topology, consistent with periplasmic activity. While their functional mechanisms remain to be elucidated, our findings suggest that CTA endolysins are nearly as prevalent as SAR endolysins and represent a distinct, previously unrecognized branch of the endolysin world.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 11","pages":"1499-1508"},"PeriodicalIF":3.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981363","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":"Identification of novel small molecule inhibitors of ETS transcription factors","authors":"Shaima Abdalla,&nbsp;Zary Forghany,&nbsp;Jin Ma,&nbsp;Johan G. Hollander,&nbsp;Ruta Nachane,&nbsp;Karoly Szuhai,&nbsp;Pancras C. W. Hogendoorn,&nbsp;Peter ten Dijke,&nbsp;Dipen Shah,&nbsp;David A. Baker","doi":"10.1002/1873-3468.70040","DOIUrl":"10.1002/1873-3468.70040","url":null,"abstract":"<p>The evolutionarily conserved E-Twenty-Six (ETS) family of transcription factors acts downstream of major signal transduction pathways and plays a pivotal role in tissue development and maintenance. Importantly, their function is frequently corrupted in a substantial proportion of tumour types, and they are also indispensable for angiogenic sprouting, a hallmark of cancer, which is essential for fuelling tumour enlargement and dissemination. Consequently, targeting aberrant ETS activity could potentially represent a precise and effective means by which to block tumour growth. Here, we present proof-of-principle high-throughput screens and an initial characterization of candidate hits, as a methodological and conceptual framework for the identification of novel ETS transcription factor inhibitors, which may ultimately lead to new therapeutic avenues for treating cancer.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 12","pages":"1733-1748"},"PeriodicalIF":3.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970427","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":"Septin2 regulates ARHGAP25-mediated suppression of lamellipodia formation and cell spreading","authors":"Tomoe Tamura,&nbsp;Emi Umekawa,&nbsp;Mamiko Mori,&nbsp;Mayuko Otsuki,&nbsp;Yoshio Shibagaki,&nbsp;Seisuke Hattori,&nbsp;Takeyuki Sugawara,&nbsp;Koji Saito,&nbsp;Yasutaka Ohta","doi":"10.1002/1873-3468.70041","DOIUrl":"10.1002/1873-3468.70041","url":null,"abstract":"<p>Rho family small GTPases are key regulators of the actin cytoskeletal organization that controls cell morphology, but the regulatory mechanism of Rho small GTPase activity is not fully understood. Here we identified septin2, a component of the septin cytoskeleton, as an interacting protein of ARHGAP25, a GTPase-activating protein for Rho small GTPase Rac, in mammalian cells. ARHGAP25 colocalized with septin2 at lamellipodia, which are actin filament-rich protrusions. Overexpression of ARHGAP25 suppressed Rac-dependent lamellipodia formation and cell spreading, and ARHGAP25-mediated suppression was restored by depletion of septin2. Forced expression of septin2 enhanced ARHGAP25-mediated suppression of cell spreading, and septin2-enhanced suppression was restored by the depletion of ARHGAP25. These results suggest that septin2 controls cell morphology by regulating the function of ARHGAP25.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 11","pages":"1582-1594"},"PeriodicalIF":3.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958309","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":"Fanzors, a family of eukaryotic RNA-guided DNA endonucleases","authors":"Kaiyi Jiang,&nbsp;Jonathan S. Gootenberg,&nbsp;Omar O. Abudayyeh","doi":"10.1002/1873-3468.70038","DOIUrl":"10.1002/1873-3468.70038","url":null,"abstract":"<p>Fanzor proteins represent the first confirmed family of RNA-guided DNA endonucleases in eukaryotes. Originally identified in 2013 as TnpB homologs, Fanzors remained functionally uncharacterized until 2023, when three independent research groups demonstrated their activity as programmable nucleases. Comprehensive bioinformatic analysis revealed over 3000 unique Fanzor sequences across diverse eukaryotic phyla and viruses. Fanzors share core mechanisms with their prokaryotic counterparts, utilizing a RuvC domain for DNA cleavage and requiring a Fanzor RNA (ωRNA) for targeting. However, they exhibit distinctive features, including diverse target adjacent motif preferences, extended ωRNA structure, and RuvC domain rearrangements. The eukaryotic origins of Fanzors make them promising tools for mammalian genome editing, with initial studies demonstrating successful editing in human cells without extensive engineering.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 8","pages":"1089-1093"},"PeriodicalIF":3.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771808","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}