{"title":"Epigenetic control of cell identities from epiblast to gastrulation.","authors":"Katrin M Schüle, Simone Probst","doi":"10.1111/febs.70024","DOIUrl":"https://doi.org/10.1111/febs.70024","url":null,"abstract":"<p><p>Epigenetic modifications of chromatin are essential for the establishment of cell identities during embryogenesis. Between embryonic days 3.5-7.5 of murine development, major cell lineage decisions are made that discriminate extraembryonic and embryonic tissues, and the embryonic primary germ layers are formed, thereby laying down the basic body plan. In this review, we cover the contribution of dynamic chromatin modifications by DNA methylation, changes of chromatin accessibility, and histone modifications, that in combination with transcription factors control gene expression programs of different cell types. We highlight the differences in regulation of enhancer and promoter marks and discuss their requirement in cell lineage specification. Importantly, in many cases, lineage-specific targeting of epigenetic modifiers is carried out by pioneer or master transcription factors, that in sum mediate the chromatin landscape and thereby control the transcription of cell-type-specific gene programs and thus, cell identities.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Stress exposure in the mdx mouse model of Duchenne muscular dystrophy provokes a widespread metabolic response.","authors":"Erynn E Johnson, James M Ervasti","doi":"10.1111/febs.70029","DOIUrl":"10.1111/febs.70029","url":null,"abstract":"<p><p>Duchenne muscular dystrophy is a severe neuromuscular wasting disease that is caused by a primary defect in dystrophin protein and involves organism-wide comorbidities such as cardiomyopathy, metabolic and mitochondrial dysfunction, and nonprogressive cognitive impairments. Physiological stress exposure in the mdx mouse model of Duchenne muscular dystrophy results in phenotypic abnormalities that include locomotor inactivity, hypotension, and increased morbidity. Severe and lethal stress susceptibility in mdx mice corresponds to metabolic dysfunction in several coordinated metabolic pathways within dystrophin-deficient skeletal muscle, as well as prolonged elevation in mdx plasma corticosterone levels that extends beyond the wild-type (WT) stress response. Here, we performed a targeted mass spectrometry-based plasma metabolomics screen focused on biological stress pathways in healthy and dystrophin-deficient mdx mice exposed to mild scruff stress. One-third of the stress-relevant metabolites interrogated displayed significant elevation or depletion in mdx plasma after scruff stress and were restored to WT levels by skeletal muscle-specific dystrophin expression. The metabolic pathways of mdx mice altered by scruff stress are associated with regulation of the hypothalamic-pituitary-adrenal axis, locomotor tone, neurocognitive function, redox metabolism, cellular bioenergetics, and protein catabolism. Our data suggest that a mild stress triggers an exaggerated, multi-system metabolic response in mdx mice.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Binary protein interactome mapping of the Giardia lamblia proteasome lid reveals extra proteasomal functions of GlRpn11.","authors":"Ankita Das, Atrayee Ray, Nibedita Ray Chaudhuri, Soumyajit Mukherjee, Shubhra Ghosh Dastidar, Alok Ghosh, Sandipan Ganguly, Kuladip Jana, Srimonti Sarkar","doi":"10.1111/febs.70027","DOIUrl":"https://doi.org/10.1111/febs.70027","url":null,"abstract":"<p><p>The assembly of the 26S proteasome, a multi-subunit complex for regulated protein turnover, proceeds via the formation of intermediates. Giardia lamblia does not encode proteasome regulatory subunit Rpn12 or proteasome complex subunit Sem1, two proteins crucial for assembling the proteasome lid. To understand how the interactions between the giardial proteasome lid subunits may have changed to compensate for their absence, we used yeast two-hybrid to generate a binary interactome map of Giardia's lid subunits. Most interactions within the Giardia lid are stronger than Saccharomyces cerevisiae lid, which may compensate for Rpn12 and Sem1 absence. A notable exception was the weaker interaction between the two non-ATPase lid subunits, GlRpn11 and GlRpn8, compared to the strong interaction between yeast orthologs Rpn11 and Rpn8. The Rpn11-Rpn8 dimer provides a platform for lid assembly. Their interaction involves the insertion of a methionine residue of Rpn11 into a hydrophobic pocket of Rpn8. Molecular modeling indicates that GlRpn8's pocket is wider, reconciling the experimental observation of its weak interaction with GlRpn11. This weaker interaction may have evolved to support proteasome-independent functions of GlRpn11, which localizes to multiple subcellular regions, including the mitosomes, where other proteasome subunits cannot be detected. Functional complementation in yeast shows that GlRpn11 can influence mitochondrial function and distribution. Together these observations show that GlRpn11 functions at the mitosome. Thus, this parasite's proteasome lid has a simpler subunit architecture than that of yeast with structural attributes to support dual functionalities for GlRpn11. Such parasite-specific proteasome features provide opportunities for controlling parasite transmission.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ARIES domains: functional signaling units of type I interferon responses.","authors":"Lauren M Landau, Jonathan C Kagan","doi":"10.1111/febs.70023","DOIUrl":"https://doi.org/10.1111/febs.70023","url":null,"abstract":"<p><p>The innate immune system relies on a network of signaling proteins classified by shared domains, which serve as functional units that orchestrate inflammatory and host defensive activities. Within type I interferon (IFN) responses, the stimulator of interferon genes protein (STING), mitochondrial antiviral-signaling protein (MAVS), Toll-IL-1 receptor-resistance protein domain-containing adapter-inducing interferon-β (TRIF), Toll-like receptor adapter interacting with SLC15A4 on the lysosome (TASL), insulin receptor tyrosine kinase substrate protein of 53 kDa (IRSp53), and GEM interacting protein (GMIP) utilize a conserved pLxIS motif to recruit IRF family transcription factors. Notably, the pLxIS motif functions within a larger signaling unit, which is referred to here as an Activator of Interferon Expression via a pLxIS motif (ARIES) domain. ARIES domains consist of the pLxIS motif and adjacent kinase activation motifs that together drive IFN responses. This review explores how ARIES domains promote immune responses via shared and distinct signaling mechanisms, protein localization, and regulation of metabolic shifts, underscoring their evolutionary conservation and critical role in host defense.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Timur A Khasanov, Konstantin S Mineev, Aleksandr P Kalinovskii, Yuliya V Korolkova, Victor A Palikov, Yulia A Palikova, Igor A Dyachenko, Sergey A Kozlov, Yaroslav A Andreev, Dmitry I Osmakov
{"title":"Sea anemone Cys-ladder peptide Ms13-1 induces a pain response as a positive modulator of acid-sensing ion channel 1a.","authors":"Timur A Khasanov, Konstantin S Mineev, Aleksandr P Kalinovskii, Yuliya V Korolkova, Victor A Palikov, Yulia A Palikova, Igor A Dyachenko, Sergey A Kozlov, Yaroslav A Andreev, Dmitry I Osmakov","doi":"10.1111/febs.70032","DOIUrl":"https://doi.org/10.1111/febs.70032","url":null,"abstract":"<p><p>Acid-sensing ion channel 1a (ASIC1a) is involved in processes associated with fear, learning, and neurodegeneration within the central nervous system. However, ASIC1a is also abundant in the peripheral nervous system, where its role is still poorly understood, largely due to the lack of selective ligands. In this study, we present the discovery of the first selective positive allosteric modulator for ASIC1a, isolated from the sea anemone Metridium senile. The active compound, a peptide named Ms13-1, features a novel type of fold named 'Cys-ladder'. Ms13-1 exhibits high affinity and selectivity for ASIC1a, enhancing channel activation in response to a broad range of acidic stimuli (pH 6.9-5.5) without altering the proton affinity for the channel. Moreover, injection of Ms13-1 into the hind paw of mice provokes robust and long-lasting pain-related behavior, which is significantly attenuated by a selective ASIC1 antagonist. The discovery of this novel selective positive allosteric modulator opens up new perspectives to investigate the role of ASIC1a in various physiological processes.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Estrogen synthesized in the central nervous system enhances MC4R expression and reduces food intake.","authors":"Takanori Hayashi, Kanako Kumamoto, Tatsuya Kobayashi, Xinfeng Hou, Shizuko Nagao, Nobuhiro Harada, Shinichiro Honda, Yohei Shimono, Eiji Nishio","doi":"10.1111/febs.17426","DOIUrl":"https://doi.org/10.1111/febs.17426","url":null,"abstract":"<p><p>Estrogen is synthesized throughout various tissues in the body, and its production is regulated by the rate-limiting enzyme aromatase (encoded by the Cyp19a1 gene). Notably, aromatase is also expressed in central nervous system cells, allowing for localized estrogen synthesis in regions such as the hypothalamus. Estrogens produced within these neurons are referred to as neuroestrogens. In this study, we investigated the role of neuroestrogens in the regulation of appetite through modulation of hypothalamic pathways in OVX, ArKO, and aromatase-restored mice. Estrogen suppresses appetite by influencing the expression of appetite-regulating peptides, including POMC and NPY, via MC4R. We explored the direct effects of neuroestrogens, independent from ovarian estrogen, on appetite suppression and the underlying molecular mechanisms. We monitored body weight and food intake and evaluated the expression of Cyp19a1, Mc4r, and other appetite-related genes. Our findings indicate that OVX and ArKO mice exhibited increased body weight and food consumption, which correlated with altered expression of Mc4r and Cyp19a1. Conversely, restoration of Cyp19a1 expression in a neuron specific manner significantly decreased food intake and increased Mc4r expression in the hypothalamus. Furthermore, neuroestrogens enhanced leptin responsiveness. Our results imply that neuroestrogens likely contribute to appetite regulation and may be relevant for body weight reduction.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Renato X Santos, Sophie H Lee, Richard Lofthouse, Valeria Melis, Lianne Robinson, Michael Leith, Eline Dreesen, Paul Armstrong, Thomas Vorley, Elizabeth A Goatman, Claire Hull, Gernot Riedel, Claude M Wischik, Charles R Harrington
{"title":"Hydromethylthionine sustains truncated tau-dependent inflammation-lowering effects in mouse brain.","authors":"Renato X Santos, Sophie H Lee, Richard Lofthouse, Valeria Melis, Lianne Robinson, Michael Leith, Eline Dreesen, Paul Armstrong, Thomas Vorley, Elizabeth A Goatman, Claire Hull, Gernot Riedel, Claude M Wischik, Charles R Harrington","doi":"10.1111/febs.70021","DOIUrl":"https://doi.org/10.1111/febs.70021","url":null,"abstract":"<p><p>Tauopathies are a heterogeneous mixture of neurodegenerative disorders, including Alzheimer's disease and frontotemporal dementia (FTD), characterised by the accumulation of tau filaments in brain tissue. Tau protein aggregation is inhibited by hydromethylthionine (HMT), an effect that appeared to be prevented in clinical trials for subjects already receiving acetylcholinesterase inhibitors or memantine. Since neuroinflammatory responses are associated with tauopathies, we investigated the effect of HMT on the brain immune response and inflammatory status in line 66 (L66) mice, an FTD-like model overexpressing human tau, in the presence of memantine. We determined whether HMT (5 and 15 mg·kg<sup>-1</sup>), either singly or combined with memantine (20 mg·kg<sup>-1</sup>), would have a sustained impact on neuroinflammation following the cessation of drug administration. The levels of core tau fragments in L66<sup>+/-</sup> mice (P301S/G335D-hTau) were decreased in a dose-dependent manner 12 weeks after the last administration of HMT, an effect that was not affected by memantine. HMT lowered the levels of tumour necrosis factor alpha (TNF-α), thus favouring an environment conducive to neuronal protection and repair. HMT sustained increased microglial reactivity after its discontinuation, which may assist in the removal of tau aggregates, but co-administration with memantine prevented the HMT-sustained activation of microglia. These findings indicate that HMT has a beneficial effect in reducing neuroinflammation that accompanies a decrease in the accumulation of truncated tau species and that these benefits are not susceptible to interference by memantine. In turn, the nature of drug interference between HMT and memantine seems to be independent of tau and related to microglia reactivity.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Genetic and functional dissection of the glutamate-proline pathway reveals a shortcut for glutamate catabolism in Leishmania.","authors":"Gustavo Daniel Campagnaro, Angela Kaysel Cruz","doi":"10.1111/febs.70030","DOIUrl":"https://doi.org/10.1111/febs.70030","url":null,"abstract":"<p><p>Trypanosomatids are early-divergent eukaryotes that have adapted to parasitism. During their life cycles, these parasites switch between a mammalian and an invertebrate host, and the ability to adapt their metabolism to different nutritional sources is instrumental for their success. In the invertebrate host, these protists have access to high amounts of amino acids and efficiently utilise it for energy production. Proline is a particularly efficient energy source for trypanosomes. Glutamate is also efficiently used by Trypanosoma cruzi and can be converted into proline as part of the glutamate-proline pathway prior to its intramitochondrial catabolism. By employing a series of genetic modifications and functional analysis, we show here that Leishmania parasites, the causative agents of leishmaniases, can utilise proline, glutamate and glutamine as energy sources, and although these parasites possess all the genes necessary for the biosynthesis of proline from glutamate, this pathway has, at best, limited function, with at least one of its components (pyrroline-5-carboxylate reductase) assuming divergent functions in different life cycle stages of the parasite. In fact, we show that the catabolism of glutamate is independent of proline biosynthesis and the former is most likely directly imported into the mitochondrion and catabolised to recover the cellular redox metabolism and increase mitochondrial membrane potential. Moreover, our data suggest a relevant role for glutamate dehydrogenase in nutritional stress response in Leishmania. These findings highlight relevant differences in amino acid metabolism between Trypanosoma and Leishmania and suggest a diversification in amino acid metabolic pathways within Trypanosomatidae.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhexi Chi, Van Quan Do, Rukhsana Kausar, Hyun Kyung Kim, Nga Thi Thanh Nguyen, Truc Phan Hoang Le, Jungwoo Lee, In-Jeoung Baek, Sang-Wook Lee, Jae Hyung Kim, Sang Yoon Lee
{"title":"HDAC6 inhibition upregulates endothelial SOD3 expression via Sp1 acetylation and attenuates angiotensin II-induced hypertension.","authors":"Zhexi Chi, Van Quan Do, Rukhsana Kausar, Hyun Kyung Kim, Nga Thi Thanh Nguyen, Truc Phan Hoang Le, Jungwoo Lee, In-Jeoung Baek, Sang-Wook Lee, Jae Hyung Kim, Sang Yoon Lee","doi":"10.1111/febs.70026","DOIUrl":"https://doi.org/10.1111/febs.70026","url":null,"abstract":"<p><p>Extracellular superoxide dismutase (SOD3) plays an important role in maintaining vascular redox homeostasis by eliminating superoxides. The angiotensin II (AngII) peptide mediates vasoconstriction in part via reactive oxygen species (ROS) but has pathologic effects when elevated in adults. Histone deacetylase 6 (HDAC6) modulates the acetylation of non-histone substrates and is associated with hypertensive disorders. Here, we investigated the potential regulation of SOD3 by HDAC6 in human aortic endothelial cells (HAECs) and its implications for AngII-induced oxidative stress and hypertension. HDAC6 inhibition (via the specific inhibitor tubastatin A (TubA), gene knockdown, or a deacetylase activity-deficient mutant) significantly increased SOD3 protein and mRNA expression but did not affect SOD1 or SOD2 protein levels. Conversely, AngII downregulated SOD3 levels and increased ROS and superoxide levels; these effects were antagonized by TubA. We confirmed that the transcription factor Sp1 mediates TubA-induced as well as basal SOD3 expression. Notably, TubA strongly augmented Sp1 acetylation at lysine 703, which activated Sp1 binding to the proximal SOD3 promoter region and, consequently, SOD3 expression. Alternatively, AngII decreased Sp1 acetylation, and TubA-mediated SOD3 induction was reduced upon overexpression of an acetylation-resistant Sp1 mutant (K703R) compared to that by the wild-type protein. Consistent with these findings, aortic SOD3 expression was significantly higher in HDAC6-deficient mice than in wild-type mice. Moreover, AngII infusion-mediated blood pressure elevation was reduced in HDAC6-deficient mice compared with that in wild-type mice. Collectively, our results suggest that HDAC6 inhibition leads to SOD3 upregulation by enhancing Sp1 acetylation in HAECs, thereby mitigating AngII-induced oxidative stress and hypertension.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sadia Fida Ullah, Mislav Oreb, Eckhard Boles, Vaibhav Srivastava, Verena Seidl-Seiboth, Bernhard Seiboth, Lisa Kappel
{"title":"N-acetylglucosamine sensing in the filamentous soil fungus Trichoderma reesei.","authors":"Sadia Fida Ullah, Mislav Oreb, Eckhard Boles, Vaibhav Srivastava, Verena Seidl-Seiboth, Bernhard Seiboth, Lisa Kappel","doi":"10.1111/febs.70015","DOIUrl":"https://doi.org/10.1111/febs.70015","url":null,"abstract":"<p><p>N-acetylglucosamine (GlcNAc) is involved in diverse signaling pathways in dimorphic yeasts and bacteria and is related to morphogenetic switching, mating, stress, virulence, and cell death. Recently, GlcNAc has been shown to promote plant growth by shaping the bacterial soil community. However, the role of GlcNAc sensing in filamentous soil fungi has not been investigated. By using Trichoderma reesei as a model organism, we show here that GlcNAc impacts the expression of around 2100 genes. Carbohydrate metabolism, amino acid metabolism, and secondary metabolism were the three most strongly affected classes of eukaryotic orthologous groups (KOG classes). Two key regulators of GlcNAc catabolism, the NDT80 domain-containing transcriptional regulator RON1, and a GlcNAc sensor, NGS1, are needed for differential regulation of two-thirds of these genes. In silico structural modeling of NGS1 identified a domain with homology to the GCN5-related histone acetyltransferase from Candida albicans, which serves as a GlcNAc catabolism regulator and GlcNAc sensor. Finally, we characterized the third regulator of GlcNAc sensing in T. reesei, which is the highly specific GlcNAc transporter N-acetylglucosamine transporter (NGT1). Using a deletion mutant of ngt1, we demonstrate that GlcNAc has to enter the cell to activate the GlcNAc catabolic gene expression. Interestingly, in contrast to dimorphic yeasts, the pathways for defense and pathogenicity seem to be induced in T. reesei by external GlcNAc. Given the ancestral role of Trichoderma spp. in the fungal kingdom and the highly conserved GlcNAc catabolism cluster that includes their regulators in many species of fungi, we propose a regulatory network for GlcNAc sensing in soil fungi.</p>","PeriodicalId":94226,"journal":{"name":"The FEBS journal","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}