FEBS Open Bio最新文献

{"title":"Professor Stuart John Ferguson (29 September 1949–25 April 2024)","authors":"Julie M. Stevens","doi":"10.1002/2211-5463.13943","DOIUrl":"https://doi.org/10.1002/2211-5463.13943","url":null,"abstract":"<p>We reflect with great fondness and admiration on the life and work of Stuart Ferguson, following his passing earlier this year at the age of 74. He was an internationally distinguished scientist who leaves a significant legacy. He was a dedicated long-term member of the Editorial Board of <i>FEBS Letters</i> and more recently on the Board of <i>FEBS Open Bio</i>, where he was a founding member and a vital contributor to its formation.</p><p>Born in the UK, Stuart attended the University of Oxford as an undergraduate in Chemistry, where he was awarded a first-class degree. He completed his PhD under the supervision of the renowned scientist George Radda, who also passed away recently. Stuart took up a lectureship at the University of Birmingham, where he met and published with Tina George; they later married and had two sons, Robin and George. He returned in 1985 to Oxford to St Edmund Hall, as the William R Miller Tutorial Fellow in Biochemistry. Stuart built a productive multidisciplinary research group in Oxford, with numerous national and international collaborations, and in 1997, he was awarded the title of Professor of Biochemistry. His legacy is marked by exceptional contributions to both research and education in the field of bioenergetics: the very fundamental principles of how energy flows in living systems.</p><p>His research discoveries were wide-ranging and impacted many areas of biology. It happens that Stuart's very first publication (of hundreds) was in <i>FEBS Letters</i> in 1972, an NMR study on lysozyme, as was his second paper on one of his favourite protein complexes, ATP synthase.</p><p>ATP synthase is central to bioenergetics as it produces ATP, driven by a gradient of ions across membranes. It is a large, multicomponent complex, the mechanism of which took years to elucidate. Stuart conducted a number of key studies on ATP synthase, including a critical early observation using a chemical modification experiment. Modification of only one of the three ATP synthesising components inhibited the entire complex, showing that the three sites were not operating independently. This experiment underpinned the so-called binding change mechanism, for which Boyer later received a Nobel Prize in Chemistry. With the respect and recognition of the community, Stuart went on to become a thought leader on the subject, notably on P/O ratios, and the intriguing variety of subunits in the c-rings of the ATPases from different organisms, as detailed structural information became available.</p><p>The enzymology of the nitrogen cycle was a significant area of study for Stuart's group and the subject of many collaborations for much of his career. The context for Stuart's interest in the bacterium <i>Paracoccus denitrificans</i> was that it is a close relative of the bacterial progenitor of our own mitochondria (a discovery made nearby in Oxford's Botany Department). Mitochondria are known to be remnants of bacteria that colonised our ancestral ce","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"14 12","pages":"1932-1933"},"PeriodicalIF":2.8,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13943","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142762171","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":"FXR activation reduces the formation of macrophage foam cells and atherosclerotic plaque, possibly by down regulating hepatic lipase in macrophages","authors":"Qiang Gu,&nbsp;Jia Liu,&nbsp;Li Li Shen","doi":"10.1002/2211-5463.13925","DOIUrl":"10.1002/2211-5463.13925","url":null,"abstract":"<p>Macrophages are the most important immune cells affecting the formation of atherosclerotic plaque. Nevertheless, the mechanisms that promote formation of foamy macrophages during atherogenesis remain poorly understood. This study explored the effects of Farnesoid X receptor (FXR) and hepatic lipase (HL, encoded by <i>LIPC</i>) on atherogenesis, particularly in foamy macrophage formation. A luciferase reporter assay indicated that FXR could bind to the <i>LIPC</i> promoter and inhibit <i>LIPC</i> transcription. FXR agonist GW4064 decreased HL expression, foam cell formation, and increased the expression of FXR downstream genes and polarization to M2 in ox-LDL-induced THP-1 and U937 foam cells. In addition, GW4064 exerted anti-atherosclerotic effects in ApoE^−/− mice, manifested as decreased serum cholesterol and triglyceride levels, and alleviated atherosclerotic plaque formation. Collectively, FXR exerted anti-atherosclerotic effects, possibly by negatively regulating HL expression in macrophages.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 2","pages":"311-323"},"PeriodicalIF":2.8,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13925","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727413","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 role of fibromodulin in myocardial fibrosis in a diabetic cardiomyopathy rat model","authors":"Xiyan Dai,&nbsp;Fan Yang,&nbsp;Dongping Chen,&nbsp;Lu Yang,&nbsp;Zhihui Dong,&nbsp;Can Chen,&nbsp;Jianmin Xiao","doi":"10.1002/2211-5463.13935","DOIUrl":"10.1002/2211-5463.13935","url":null,"abstract":"<p>Diabetic cardiomyopathy (DCM) is pathologically characterized by excessive deposition of extracellular matrix proteins, leading to myocardial fibrosis. Fibromodulin (Fmod) plays a crucial role in the pathogenesis of fibrotic diseases. However, the role and mechanism of Fmod in DCM-related myocardial fibrosis remain unclear. In the present study, we established a DCM rat model and an <i>in vitro</i> model of rat primary cardiac fibroblasts (RPCFs) exposed to high glucose. We assessed mRNA and protein expression levels of Col1a1, Col3a1, α-SMA and Fmod in both models. <i>Fmod</i>-overexpressing (ov-Fmod) and <i>Fmod</i>-knockdown (si-Fmod) rat cardiac fibroblasts (RCFs) were generated. Subsequently, whole RNA sequencing was conducted on ov-Fmod RCFs. The gene <i>Col15a1</i> was evaluated in the DCM rat and all cell models. The correlation between plasma levels of Fmod and Col15a1 in DCM rat models was assessed. Transcription and protein levels of Fmod, Col1a1, Col3a1 and α-SMA were significantly elevated in DCM rat hearts and RPCFs. In ov-Fmod RCFs, fibrosis markers were similarly increased, except for Col3a1, which decreased. The Col1a1/Col3a1 ratio was elevated. Conversely, knocking down Fmod yielded opposite results. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that Fmod participates in multiple fibrosis-related pathways, affecting Col15a1. Expression of <i>Col15a1</i> was significantly decreased in all models, compared to controls, except in si-Fmod RCFs. Importantly, Col15a1 and Fmod in plasma exhibited an inverse relationship in DCM. In summary, Fmod is implicated in DCM, with <i>Fmod</i> overexpression downregulating Col15a1 and increasing the Col1a1/Col3a1 ratio. This mechanism may influence diastolic heart failure in DCM by modulating myocardial stiffness and elasticity.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"436-446"},"PeriodicalIF":2.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13935","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727416","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":"Alcohol induces α2-6sialo mucin O-glycans that kill U937 macrophages mediated by sialic acid-binding immunoglobulin-like lectin 7 (Siglec 7)","authors":"Pi-Wan Cheng,&nbsp;Vishwanath-Reddy Hothpet,&nbsp;Ganapati Bhat,&nbsp;Kristina Bailey,&nbsp;Lei Li,&nbsp;Derrick R. Samuelson","doi":"10.1002/2211-5463.13919","DOIUrl":"10.1002/2211-5463.13919","url":null,"abstract":"<p>Alcohol misuse increases infections and cancer fatalities, but mechanisms underlying its toxicity are ill-defined. We show that alcohol treatment of human tracheobronchial epithelial cells leads to inactivation of giantin-mediated Golgi targeting of glycosylation enzymes. Loss of core 2 <i>N</i>-acetylglucosaminyltransferase 1, which uses only giantin for Golgi targeting, coupled with shifted targeting of other glycosylation enzymes to Golgi matrix protein 130-Golgi reassembly stacking protein 65, the site normally used by core 1 enzyme, results in loss of sialyl Lewis x and increase of sialyl Lewis a and α2-6sialo mucin O-glycans. The α2-6sialo mucin O-glycans induced by alcohol cause death of U937 macrophages mediated by sialic acid-binding immunoglobulin-like lectin 7. These results provide a mechanistic insight into the cause of the toxic effects of alcohol and might contribute to the development of therapies to alleviate its toxicity.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"165-179"},"PeriodicalIF":2.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142727406","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":"Effect of Cordyceps militaris extract containing cordycepin on the adipogenesis and lipolysis of adipocytes","authors":"Kazuya Kusama,&nbsp;Kodai Oka,&nbsp;Yumi Yashiro,&nbsp;Kanoko Yoshida,&nbsp;Hiroaki Miyaoka,&nbsp;Kazuhiro Tamura","doi":"10.1002/2211-5463.13930","DOIUrl":"10.1002/2211-5463.13930","url":null,"abstract":"<p>Obesity, a global health concern, results from an energy imbalance leading to lipid accumulation. In the present study, <i>Cordyceps militaris</i> extract (CM) and its primary component, cordycepin, were investigated to characterize their potential effects on adipogenesis and lipolysis. Treatment with CM or cordycepin reduced lipid droplets and increased hormone-sensitive lipase activation in 3T3-L1 cells. In a diabetic obese mouse model, CM and cordycepin lowered serum low-density lipoprotein/very low-density lipoprotein levels and reduced oxidative stress and cell senescence markers. Thus, cordycepin inhibits preadipocyte differentiation and promotes lipolysis, which may serve as a novel obesity treatment. Further studies, including clinical trials, are required to validate the clinical potential of cordycepin.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 2","pages":"335-345"},"PeriodicalIF":2.8,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13930","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686399","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":"Protein crystallization and structure determination at room temperature in the CrystalChip","authors":"Petr Pachl,&nbsp;Léna Coudray,&nbsp;Romain Vincent,&nbsp;Léa Nilles,&nbsp;Hélène Scheer,&nbsp;Christophe Ritzenthaler,&nbsp;Adéla Fejfarová,&nbsp;Pavlína Řezáčová,&nbsp;Sylvain Engilberge,&nbsp;Claude Sauter","doi":"10.1002/2211-5463.13932","DOIUrl":"10.1002/2211-5463.13932","url":null,"abstract":"<p>The production of high-quality crystals is a key step in crystallography in general, but control of crystallization conditions is even more crucial in serial crystallography, which requires sets of crystals homogeneous in size and diffraction properties. This protocol describes the implementation of a simple and user-friendly microfluidic device that allows both the production of crystals by the counter-diffusion method and their <i>in situ</i> analysis by serial crystallography. As an illustration, the whole procedure is used to determine the crystal structure of three proteins from data collected at room temperature at a synchrotron radiation source.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"532-541"},"PeriodicalIF":2.8,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13932","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686401","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":"Interrogating stonefish venom: small molecules present in envenomation caused by Synanceia spp.","authors":"Silvia Luiza Saggiomo,&nbsp;Steve Peigneur,&nbsp;Jan Tytgat,&nbsp;Norelle L. Daly,&nbsp;David Thomas Wilson","doi":"10.1002/2211-5463.13926","DOIUrl":"10.1002/2211-5463.13926","url":null,"abstract":"<p>The stonefish <i>Synanceia verrucosa</i> and <i>Synanceia horrida</i> are arguably the most venomous fish species on earth and the culprits of severe stings in humans globally. Investigation into the venoms of these two species has mainly focused on protein composition, in an attempt to identify the most medically relevant proteins, such as the lethal verrucotoxin and stonustoxin components. This study, however, focused on medically relevant small molecules, and through nuclear magnetic resonance, mass spectroscopy, and fractionation techniques, we discovered and identified the presence of three molecules new to stonefish venom, namely γ-aminobutyric acid (GABA), choline and <i>0</i>-acetylcholine, and provide the first report of GABA identified in a fish venom. Analysis of the crude venoms on human nicotinic acetylcholine receptors (nAChRs) and a GABA_A receptor (GABA_AR) showed <i>S. horrida</i> venom could activate neuronal (α7) and adult muscle-type (α1β1δε) nAChRs, while both crude <i>S. horrida</i> and <i>S. verrucosa</i> venoms activated the GABA_AR (α1β2γ2). Cytotoxicity studies in immunologically relevant cells (human PBMCs) indicated the venoms possess cell-specific cytotoxicity and analysis of the venom fractions on Na⁺ channel subtypes involved in pain showed no activity. This work highlights the need to further investigate the small molecules found in venoms to help understand the mechanistic pathways of clinical symptoms for improved treatment of sting victims, in addition to the discovery of potential drug leads.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"399-414"},"PeriodicalIF":2.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13926","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675544","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":"Unique pharmacological properties of etrasimod among S1P receptor modulators","authors":"Ibragim Gaidarov,&nbsp;H. Kiyomi Komori,&nbsp;Dariusz T. Stepniak,&nbsp;Karin Bruinsma,&nbsp;Huong Dang,&nbsp;Xiaohua Chen,&nbsp;Todd Anthony,&nbsp;Joel Gatlin,&nbsp;Lisa Karimi-Naser,&nbsp;Anh-Tuan Ton,&nbsp;Tim Indersmitten,&nbsp;Paul E. Miller,&nbsp;Andre Ghetti,&nbsp;Najah Abi-Gerges,&nbsp;David Unett,&nbsp;Hussien Al-Shamma,&nbsp;Christopher J. Rabbat,&nbsp;Catherine Crosby,&nbsp;John W. Adams","doi":"10.1002/2211-5463.13907","DOIUrl":"10.1002/2211-5463.13907","url":null,"abstract":"<p>Etrasimod (ADP334) is an oral, once-daily, selective sphingosine 1-phosphate (S1P)_1,4,5 receptor modulator for the treatment of moderately to severely active ulcerative colitis and in development for the treatment of immune-mediated inflammatory diseases. Interaction between S1P and its five receptor subtypes (S1P₁–S1P₅) plays a role in several physiologic systems, including the cardiovascular and immune systems. Since differences in S1PR binding and downstream intracellular signaling could contribute to distinct profiles of drug efficacy and safety, we directly compared the S1P_1–5 selectivity profile of etrasimod to three marketed S1PR modulators: fingolimod, ozanimod, and siponimod. Using both heterologous expression systems and human umbilical vein endothelial cells that spontaneously express S1P₁, we profiled key S1P₁ downstream signaling pathways and found that etrasimod had similar potency to the other tested S1PR modulators in promoting β-arrestin recruitment and S1P₁ internalization. However, etrasimod was notably less potent than other S1PR modulators in assays measuring S1P₁-mediated G protein activation (GTPγS binding and cAMP inhibition). Relatively lower potency of etrasimod in inducing G protein signaling corresponded to significantly diminished activation of human cardiac G protein-coupled inwardly rectifying potassium channels when compared to ozanimod. Together with pharmacokinetic properties, this pharmacologic profile of etrasimod may contribute to the positive benefit risk profile of etrasimod observed during the phase III ELEVATE UC 52 and ELEVATE UC 12 trials in patients with moderately to severely active ulcerative colitis.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"108-121"},"PeriodicalIF":2.8,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675549","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":"Structural analysis of an Asterias rubens peptide indicates the presence of a disulfide-directed β-hairpin fold","authors":"Rozita Takjoo,&nbsp;David T. Wilson,&nbsp;Justine Le Quilliec,&nbsp;Casey A. Schmidt,&nbsp;Guangzu Zhao,&nbsp;Michael J. Liddell,&nbsp;Naeem Y. Shaikh,&nbsp;Kartik Sunagar,&nbsp;Alex Loukas,&nbsp;Michael J. Smout,&nbsp;Norelle L. Daly","doi":"10.1002/2211-5463.13931","DOIUrl":"10.1002/2211-5463.13931","url":null,"abstract":"<p>Sea stars are an abundant group of marine invertebrates that display remarkably robust regenerative capabilities throughout all life stages. Numerous proteins and peptides have been identified in a proteome study on the coelomic fluid (biofluid) of the common sea star <i>Asterias rubens</i>, which appear to be involved with the wound-healing response in the organism. However, the three-dimensional structure and function of several of these injury-responsive peptides, including the peptide KASH2, are yet to be investigated. Here, we show that the KASH2 peptide adopts a disulfide-directed β-hairpin fold (DDH). The DDH motif appears to be evolutionarily related to the inhibitor cystine knot motif, which is one of the most widespread disulfide-rich peptide folds. The DDH motif was originally thought to be restricted to arachnids, but our study suggests that as a result of convergent evolution it could also have originated in sea stars. Although the widely conserved DDH fold has potential cross-phyla wound-healing capacity, we have shown that KASH2 does not enhance the proliferation of human fibroblasts, a simple method for wound-healing re-epithelialisation screening. Therefore, additional research is necessary to determine the role of KASH2 in the sea stars.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 3","pages":"415-426"},"PeriodicalIF":2.8,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13931","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675546","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":"Making teamwork work: enhancing teamwork and assessment in higher education","authors":"Nigel Francis,&nbsp;Connie Pritchard,&nbsp;Zoe Prytherch,&nbsp;Stephen Rutherford","doi":"10.1002/2211-5463.13936","DOIUrl":"10.1002/2211-5463.13936","url":null,"abstract":"<p>The ability to work in teams is one of the most sought-after graduate skills by employers. However, team-based learning activities, and especially team-based assessments, are commonly disliked (even actively avoided) by students. Team-based assessments are often problematic for students, mostly due to logistical problems and interpersonal difficulties. These difficulties often lead to dissatisfaction with the process and poor satisfaction responses in quality assessments of their teaching. This review takes a four-way approach to evaluate current approaches to team assessment aimed at enhancing student engagement, satisfaction and learning gain. Firstly, we identify why team-based activity is so important to include in our overall pedagogy in Higher Education. Secondly, we examine evidence from the literature on students' reactions to team-based activities (especially focusing on assessment) and the reasons for both positive and negative perceptions. The third focus is on identifying the root of the problem from a pedagogic perspective and highlighting the deficiencies in approaches to team-based activities that might lead to negative student perceptions. Finally, we discuss examples from the literature of where team-based learning and assessment activities have been successful. Approaches to team-based activities need to be more proactive and supportive so that students understand the dynamics of teams, how to plan team-based activities, and how to deal with interpersonal issues positively and productively. Team-based learning is arguably the least well-taught element of our curricula, yet it is important and straightforward to address.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"35-47"},"PeriodicalIF":2.8,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647206","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}