FEBS Journal最新文献

{"title":"Author response for \"Acetylation of the influenza A virus polymerase subunit PA in the N-terminal domain positively regulates its endonuclease activity\"","authors":"D. Hatakeyama, M. Shoji, Seiryo Ogata, Takeshi Masuda, M. Nakano, Tsugunori Komatsu, A. Saitoh, Kyoko Makiyama, Hazuki Tsuneishi, Asuka Miyatake, Mizuki Takahira, Erin Nishikawa, A. Ohkubo, T. Noda, Y. Kawaoka, S. Ohtsuki, T. Kuzuhara","doi":"10.1111/FEBS.16123/V2/RESPONSE1","DOIUrl":"https://doi.org/10.1111/FEBS.16123/V2/RESPONSE1","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89800792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review for \"Identification of a small molecule splicing inhibitor targeting UHM domains\"","authors":"H. Arthanari","doi":"10.1111/febs.16199/v2/review1","DOIUrl":"https://doi.org/10.1111/febs.16199/v2/review1","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78849643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author response for \"Resurrection and characterization of ancestral CYP11A1 enzymes\"","authors":"Philip Hartz, Silja J. Strohmaier, Basma M. EL‐Gayar, Ammar Abdulmughni, M. Hutter, F. Hannemann, E. Gillam, R. Bernhardt","doi":"10.1111/FEBS.16054/V2/RESPONSE1","DOIUrl":"https://doi.org/10.1111/FEBS.16054/V2/RESPONSE1","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89195800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review for \"Interaction mechanism of endogenous PP2A inhibitor protein ENSA with PP2A\"","authors":"Miquel Pons","doi":"10.1111/febs.16150/v1/review2","DOIUrl":"https://doi.org/10.1111/febs.16150/v1/review2","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85537916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review for \"Conformational Switches and Redox Properties of the Colon Cancer‐Associated Human Lectin ZG16\"","authors":"C. Rademacher","doi":"10.1111/FEBS.16044/V1/REVIEW2","DOIUrl":"https://doi.org/10.1111/FEBS.16044/V1/REVIEW2","url":null,"abstract":"","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77900936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenic postzygotic mosaicism in the tyrosine receptor kinase pathway: potential unidentified human disease hidden away in a few cells.","authors":"Irene Tiemann-Boege, Theresa Mair, Atena Yasari, Michal Zurovec","doi":"10.1111/febs.15528","DOIUrl":"10.1111/febs.15528","url":null,"abstract":"<p><p>Mutations occurring during embryonic development affect only a subset of cells resulting in two or more distinct cell populations that are present at different levels, also known as postzygotic mosaicism (PZM). Although PZM is a common biological phenomenon, it is often overlooked as a source of disease due to the challenges associated with its detection and characterization, especially for very low-frequency variants. Moreover, PZM can cause a different phenotype compared to constitutional mutations. Especially, lethal mutations in receptor tyrosine kinase (RTK) pathway genes, which exist only in a mosaic state, can have completely new clinical manifestations and can look very different from the associated monogenic disorder. However, some key questions are still not addressed, such as the level of mosaicism resulting in a pathogenic phenotype and how the clinical outcome changes with the development and age. Addressing these questions is not trivial as we require methods with the sensitivity to capture some of these variants hidden away in very few cells. Recent ultra-accurate deep-sequencing approaches can now identify these low-level mosaics and will be central to understand systemic and local effects of mosaicism in the RTK pathway. The main focus of this review is to highlight the importance of low-level mosaics and the need to include their detection in studies of genomic variation associated with disease.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8247027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38275798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-catenin regulates FOXP2 transcriptional activity via multiple binding sites.","authors":"Gesa Richter,&nbsp;Tianshu Gui,&nbsp;Benjamin Bourgeois,&nbsp;Chintan N Koyani,&nbsp;Peter Ulz,&nbsp;Ellen Heitzer,&nbsp;Dirk von Lewinski,&nbsp;Boudewijn M T Burgering,&nbsp;Ernst Malle,&nbsp;Tobias Madl","doi":"10.1111/febs.15656","DOIUrl":"https://doi.org/10.1111/febs.15656","url":null,"abstract":"<p><p>The transcription factor forkhead box protein P2 (FOXP2) is a highly conserved key regulator of embryonal development. The molecular mechanisms of how FOXP2 regulates embryonal development, however, remain elusive. Using RNA sequencing, we identified the Wnt signaling pathway as key target of FOXP2-dependent transcriptional regulation. Using cell-based assays, we show that FOXP2 transcriptional activity is regulated by the Wnt coregulator β-catenin and that β-catenin contacts multiple regions within FOXP2. Using nuclear magnetic resonance spectroscopy, we uncovered the molecular details of these interactions. β-catenin contacts a disordered FOXP2 region with α-helical propensity via its folded armadillo domain, whereas the intrinsically disordered β-catenin N terminus and C terminus bind to the conserved FOXP2 DNA-binding domain. Using RNA sequencing, we confirmed that β-catenin indeed regulates transcriptional activity of FOXP2 and that the FOXP2 α-helical motif acts as a key regulatory element of FOXP2 transcriptional activity. Taken together, our findings provide first insight into novel regulatory interactions and help to understand the intricate mechanisms of FOXP2 function and (mis)-regulation in embryonal development and human diseases. DATABASE: Expression data are available in the GEO database under the accession number GSE138938.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/febs.15656","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38682243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular self-cannibalism helps immune cells fight the flu.","authors":"Joshua Luke Postoak,&nbsp;Guan Yang,&nbsp;Lan Wu,&nbsp;Luc Van Kaer","doi":"10.1111/febs.15641","DOIUrl":"https://doi.org/10.1111/febs.15641","url":null,"abstract":"<p><p>CD4 T cells are critical for generating protective immune responses to infection with influenza virus. Although most CD4 T cells react with peptides from extracellular sources, many react with peptides from viral particles synthesized inside cells; however, the pathways employed for processing the latter antigens remain uncertain. Deng et al. provide evidence for a role of autophagy, a cellular self-eating process, in this unconventional antigen processing route, with potential implications for the development of influenza virus vaccines.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/febs.15641","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38792351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influenza A virus infection-induced macroautophagy facilitates MHC class II-restricted endogenous presentation of an immunodominant viral epitope.","authors":"Jieru Deng,&nbsp;Chunni Lu,&nbsp;Chuanxin Liu,&nbsp;Sara Oveissi,&nbsp;W Douglas Fairlie,&nbsp;Erinna F Lee,&nbsp;Pamuk Bilsel,&nbsp;Hamsa Puthalakath,&nbsp;Weisan Chen","doi":"10.1111/febs.15654","DOIUrl":"https://doi.org/10.1111/febs.15654","url":null,"abstract":"<p><p>CD4⁺ T cells recognize peptides presented by major histocompatibility complex class II molecules (MHC-II). These peptides are generally derived from exogenous antigens. Macroautophagy has been reported to promote endogenous antigen presentation in viral infections. However, whether influenza A virus (IAV) infection-induced macroautophagy also leads to endogenous antigen presentation through MHC-II is still debated. In this study, we show that IAV infection leads to endogenous presentation of an immunodominant viral epitope NP_311-325 by MHC-II to CD4⁺ T cells. Mechanistically, such MHC-II-restricted endogenous IAV antigen presentation requires de novo protein synthesis as it is inhibited by the protein synthesis inhibitor cycloheximide, and a functional ER-Golgi network as it is totally blocked by Brefeldin A. These results indicate that MHC-II-restricted endogenous IAV antigen presentation is dependent on de novo antigen and/or MHC-II synthesis, and transportation through the ER-Golgi network. Furthermore, such endogenous IAV antigen presentation by MHC-II is enhanced by TAP deficiency, indicating some antigenic peptides are of cytosolic origin. Most importantly, the bulk of such MHC-II-restricted endogenous IAV antigen presentation is blocked by autophagy inhibitors (3-MA and E64d) and deletion of autophagy-related genes, such as Beclin1 and Atg7. We have further demonstrated that in dendritic cells, IAV infection prevents autophagosome-lysosome fusion and promotes autophagosome fusion with MHC class II compartment (MIIC), which likely promotes endogenous IAV antigen presentation by MHC-II. Our results provide strong evidence that IAV infection-induced autophagosome formation facilitates endogenous IAV antigen presentation by MHC-II to CD4⁺ T cells. The implication for influenza vaccine design is discussed.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/febs.15654","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25571059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum response factor-cofactor interactions and their implications in disease.","authors":"John Oloche Onuh,&nbsp;Hongyu Qiu","doi":"10.1111/febs.15544","DOIUrl":"https://doi.org/10.1111/febs.15544","url":null,"abstract":"<p><p>Serum response factor (SRF), a member of the Mcm1, Agamous, Deficiens, and SRF (MADS) box transcription factor, is widely expressed in all cell types and plays a crucial role in the physiological function and development of diseases. SRF regulates its downstream genes by binding to their CArG DNA box by interacting with various cofactors. However, the underlying mechanisms are not fully understood, therefore attracting increasing research attention due to the importance of this topic. This review's objective is to discuss the new progress in the studies of the molecular mechanisms involved in the activation of SRF and its impacts in physiological and pathological conditions. Notably, we summarized the recent studies on the interaction of SRF with its two main types of cofactors belonging to the myocardin families of transcription factors and the members of the ternary complex factors. The knowledge of these mechanisms will create new opportunities for understanding the dynamics of many traits and disease pathogenesis especially, cardiovascular diseases and cancer that could serve as targets for pharmacological control and treatment of these diseases.</p>","PeriodicalId":12261,"journal":{"name":"FEBS Journal","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/febs.15544","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38343706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}