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Crystal structures of Aspergillus oryzae exo-β-(1,3)-glucanase reveal insights into oligosaccharide binding, recognition, and hydrolysis 黑曲霉外β-(1,3)-葡聚糖酶的晶体结构揭示了寡糖的结合、识别和水解过程。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-24 DOI: 10.1002/1873-3468.15045
Barnava Banerjee, Chinmay K. Kamale, Abhishek B. Suryawanshi, Subrata Dasgupta, Santosh Noronha, Prasenjit Bhaumik
{"title":"Crystal structures of Aspergillus oryzae exo-β-(1,3)-glucanase reveal insights into oligosaccharide binding, recognition, and hydrolysis","authors":"Barnava Banerjee,&nbsp;Chinmay K. Kamale,&nbsp;Abhishek B. Suryawanshi,&nbsp;Subrata Dasgupta,&nbsp;Santosh Noronha,&nbsp;Prasenjit Bhaumik","doi":"10.1002/1873-3468.15045","DOIUrl":"10.1002/1873-3468.15045","url":null,"abstract":"<p>Exo-β-(1,3)-glucanases are promising enzymes for use in the biofuel industry as they hydrolyse sugars such as laminarin, a major constituent of the algal cell wall. This study reports structural and biochemical characterizations of <i>Aspergillus oryzae</i> exo-β-(1,3)-glucanase (AoBgl) belonging to the GH5 family. Purified AoBgl hydrolyses β-(1,3)-glycosidic linkages of the oligosaccharide laminaritriose and the polysaccharide laminarin effectively. We have determined three high-resolution structures of AoBgl: (a) the apo form at 1.75 Å, (b) the complexed form with bound cellobiose at 1.73 Å and (c) the glucose-bound form at 1.20 Å. The crystal structures, molecular dynamics simulation studies and site-directed mutagenesis reveal the mode of substrate binding and interactions at the active site. The results also indicate that AoBgl effectively hydrolyses trisaccharides and higher oligosaccharides. The findings from our structural and biochemical studies would aid in rational engineering efforts to generate superior AoBgl variants and similar GH5 enzymes for their industrial use.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 1","pages":"53-73"},"PeriodicalIF":3.5,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497592","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}
引用次数: 0
RETRACTION: Role of the PDK1–PKB–GSK3 Pathway in Regulating Glycogen Synthase and Glucose Uptake in the Heart 回归：PDK1-PKB-GSK3 通路在调节心脏糖原合成酶和葡萄糖摄取中的作用。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-24 DOI: 10.1002/1873-3468.15044
{"title":"RETRACTION: Role of the PDK1–PKB–GSK3 Pathway in Regulating Glycogen Synthase and Glucose Uptake in the Heart","authors":"","doi":"10.1002/1873-3468.15044","DOIUrl":"10.1002/1873-3468.15044","url":null,"abstract":"<p><b>RETRACTION</b>: A. Mora, K. Sakamoto, E. J. McManus, and D. R. Alessi, “Role of the PDK1–PKB–GSK3 Pathway in Regulating Glycogen Synthase and Glucose Uptake in the Heart,” <i>FEBS Letters</i> 579, no. 17 (2005): 3632–3638, https://doi.org/10.1016/j.febslet.2005.05.040.</p><p>The above article, published online on 06 June 2005 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Michael Brunner; FEBS Press; and John Wiley and Sons Ltd. The journal was contacted by a representative of the research integrity group at the authors' institute, since an institutional investigation revealed inappropriate splicing and duplication of image sections within Fig. 2A, B and Fig. 3A. Consequently, the conclusions of the paper are substantially compromised, and the institute has recommended the paper to be retracted. The editors of the journal agree with the retraction based on the institutional investigation.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 23","pages":"2939"},"PeriodicalIF":3.5,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497670","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}
引用次数: 0
Substrate recognition by the 4-hydroxytryptamine kinase PsiK in psilocybin biosynthesis 迷幻药生物合成过程中 4-羟色胺激酶 PsiK 的底物识别。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-24 DOI: 10.1002/1873-3468.15042
Kai Rogge, Tobias Johannes Wagner, Dirk Hoffmeister, Bernhard Rupp, Sebastiaan Werten
{"title":"Substrate recognition by the 4-hydroxytryptamine kinase PsiK in psilocybin biosynthesis","authors":"Kai Rogge,&nbsp;Tobias Johannes Wagner,&nbsp;Dirk Hoffmeister,&nbsp;Bernhard Rupp,&nbsp;Sebastiaan Werten","doi":"10.1002/1873-3468.15042","DOIUrl":"10.1002/1873-3468.15042","url":null,"abstract":"<p>Psilocybin, the natural hallucinogen from <i>Psilocybe</i> (magic) mushrooms, is a highly promising drug candidate for the treatment of depression and several other mental health conditions. Biosynthesis of psilocybin from the amino acid <span>l-</span>tryptophan involves four strictly sequential modifications. The third of these, ATP-dependent phosphorylation of the intermediate 4-hydroxytryptamine, is catalysed by PsiK. Here we present a crystallographic analysis and a structure-based mutagenesis study of this kinase, providing insight into its mode of substrate recognition. The results of our work will support future bioengineering efforts aimed at generating variants of psilocybin with enhanced therapeutic properties.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 3","pages":"447-455"},"PeriodicalIF":3.5,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497671","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}
引用次数: 0
Mapping the sclerostin–LRP4 binding interface identifies critical interaction hotspots in loops 1 and 3 of sclerostin 绘制硬骨蛋白-LRP4 结合界面图，确定硬骨蛋白环 1 和环 3 中的关键相互作用热点。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-23 DOI: 10.1002/1873-3468.15033
Svetlana Katchkovsky, Reut Meiri, Shiran Lacham-Hartman, Yaron Orenstein, Noam Levaot, Niv Papo
{"title":"Mapping the sclerostin–LRP4 binding interface identifies critical interaction hotspots in loops 1 and 3 of sclerostin","authors":"Svetlana Katchkovsky,&nbsp;Reut Meiri,&nbsp;Shiran Lacham-Hartman,&nbsp;Yaron Orenstein,&nbsp;Noam Levaot,&nbsp;Niv Papo","doi":"10.1002/1873-3468.15033","DOIUrl":"10.1002/1873-3468.15033","url":null,"abstract":"<p>The interaction of sclerostin (Scl) with the low-density lipoprotein receptor-related protein 4 (LRP4) leads to a marked reduction in bone formation by inhibiting the Wnt/β-catenin pathway. To characterize the Scl–LRP4 binding interface, we sorted a combinatorial library of Scl variants and isolated variants with reduced affinity to LRP4. We identified Scl single-mutation variants enriched during the sorting process and verified their reduction in affinity toward LRP4—a reduction that was not a result of changes in the variants' secondary structure or stability. We found that Scl positions K75 (loop 1) and V136 (loop 3) are critical hotspots for binding to LRP4. Our findings establish the foundation for targeting these hotspots for developing novel therapeutic strategies to promote bone formation.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 3","pages":"316-329"},"PeriodicalIF":3.5,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497594","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}
引用次数: 0
Expression and function of interferon lambda receptor 1 variants. 干扰素λ受体1变体的表达和功能。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-22 DOI: 10.1002/1873-3468.15041
Laura A Novotny, Eric G Meissner
{"title":"Expression and function of interferon lambda receptor 1 variants.","authors":"Laura A Novotny, Eric G Meissner","doi":"10.1002/1873-3468.15041","DOIUrl":"10.1002/1873-3468.15041","url":null,"abstract":"<p><p>Lambda interferons (IFNLs) provide critical host defense against pathogens encountered at mucosal surfaces. In humans, IFNL signaling is regulated in part by low and cell-type restricted expression of the lambda interferon receptor 1 protein with expression restricted primarily to epithelial cells located at mucosal surfaces. This review will examine the evidence suggesting a role for IFNLR1 transcriptional variants in mediating cell responsiveness to IFNL ligand exposure and regulation of pathway activity.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461343","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}
引用次数: 0
Solving the protein folding problem… 解决蛋白质折叠问题....
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-20 DOI: 10.1002/1873-3468.15043
Roy D. Sleator
{"title":"Solving the protein folding problem…","authors":"Roy D. Sleator","doi":"10.1002/1873-3468.15043","DOIUrl":"10.1002/1873-3468.15043","url":null,"abstract":"<p>The protein folding problem was, to paraphrase Churchill, ‘<i>A riddle wrapped in a mystery inside an enigma’</i>. The <i>riddle</i>, in this context, was the folding code; what interactions at the amino acid level are driving the folding process? The <i>mystery</i> was the kinetic question (Levinthal's paradox); how does the folding process occur so quickly (typically in timescales ranging from μS to mS)? Finally, the <i>enigma</i> represents the computational problem of developing approaches to predict the final folded sate of a protein given only its amino acid sequence. Herein, I trace the path to solving this riddle wrapped in a mystery inside an enigma.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 23","pages":"2831-2835"},"PeriodicalIF":3.5,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461346","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}
引用次数: 0
Platycodin D reduces PD-L1 levels by inhibiting LXR-β activity and combines with nintedanib to enhance the tumor-killing effect of T cells Platycodin D通过抑制LXR-β活性来降低PD-L1水平，并与nintedanib联用，增强T细胞的肿瘤杀伤效果。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-20 DOI: 10.1002/1873-3468.15034
Jin Lei, Xue-Wei Cao, Peng-Fei Li, Jian Zhao, Fu-Jun Wang
{"title":"Platycodin D reduces PD-L1 levels by inhibiting LXR-β activity and combines with nintedanib to enhance the tumor-killing effect of T cells","authors":"Jin Lei,&nbsp;Xue-Wei Cao,&nbsp;Peng-Fei Li,&nbsp;Jian Zhao,&nbsp;Fu-Jun Wang","doi":"10.1002/1873-3468.15034","DOIUrl":"10.1002/1873-3468.15034","url":null,"abstract":"<p>Most tumors are resistant to programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) checkpoint inhibitors, which may be due to impaired antigen presentation resulting from the downregulation of major histocompatibility complex class I (MHC-I) expression on tumor cells. We observed that platycodin D (PD), polygalacin D, and platycodin D2, which are plant-derived triterpenoid saponins, significantly reduced PD-L1 levels. RNA sequencing and the PharmMapper database analysis identified liver X receptor β (LXR-β) as a potential PD target. Further studies showed that PD reduces PD-L1 levels by binding to LXR-β and inhibiting LXR-β activity. Coadministration of PD and nintedanib, known to upregulate MHC-I expression, enhanced tumor recognition and killing by T cells. This study provides new insights into PD applications and mechanisms.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 24","pages":"3053-3070"},"PeriodicalIF":3.5,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461345","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}
引用次数: 0
YAP1 modulation of primary cilia-mediated ciliogenesis in 2D and 3D prostate cancer models YAP1 在二维和三维前列腺癌模型中对原发性纤毛介导的纤毛生成的调节。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-18 DOI: 10.1002/1873-3468.15029
Yingbo Guo, Mathilde Dupart, Marie Irondelle, Pascal Peraldi, Frederic Bost, Nathalie M. Mazure
{"title":"YAP1 modulation of primary cilia-mediated ciliogenesis in 2D and 3D prostate cancer models","authors":"Yingbo Guo,&nbsp;Mathilde Dupart,&nbsp;Marie Irondelle,&nbsp;Pascal Peraldi,&nbsp;Frederic Bost,&nbsp;Nathalie M. Mazure","doi":"10.1002/1873-3468.15029","DOIUrl":"10.1002/1873-3468.15029","url":null,"abstract":"<p>The primary cilium, a non-motile organelle present in most human cells, plays a crucial role in detecting microenvironmental changes and regulating intracellular signaling. Its dysfunction is linked to various diseases, including cancer. We explored the role of ciliated cells in prostate cancer by using Gefitinib and Jasplakinolide compounds to induce ciliated cells in both normal and tumor-like prostate cell lines. We assessed GLI1 and IFT20 expression and investigated YAP1 protein's role, which is implicated in primary cilium regulation. Finally, we examined these compounds in 3D cell models, aiming to simulate <i>in vivo</i> conditions. Our study highlights YAP1 as a potential target for novel genetic models to understand the primary cilium's role in mediating resistance to anticancer treatments.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 24","pages":"3071-3086"},"PeriodicalIF":3.5,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461349","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}
引用次数: 0
Feedback regulation of retinaldehyde reductase DHRS3, a critical determinant of retinoic acid homeostasis 视黄醛还原酶 DHRS3 的反馈调节是视黄酸平衡的关键因素。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-17 DOI: 10.1002/1873-3468.15038
Parisa Varshosaz, Catherine O'Connor, Alexander R. Moise
{"title":"Feedback regulation of retinaldehyde reductase DHRS3, a critical determinant of retinoic acid homeostasis","authors":"Parisa Varshosaz,&nbsp;Catherine O'Connor,&nbsp;Alexander R. Moise","doi":"10.1002/1873-3468.15038","DOIUrl":"10.1002/1873-3468.15038","url":null,"abstract":"<p>Retinoic acid is crucial for vertebrate embryogenesis, influencing anterior-posterior patterning and organogenesis through its interaction with nuclear hormone receptors comprising heterodimers of retinoic acid receptors (RARα, β, or γ) and retinoid X receptors (RXRα, β, or γ). Tissue retinoic acid levels are tightly regulated since both its excess and deficiency are deleterious. Dehydrogenase/reductase 3 (DHRS3) plays a critical role in this regulation by converting retinaldehyde to retinol, preventing excessive retinoic acid formation. Mutations in <i>DHRS3</i> can result in embryonic lethality and congenital defects. This study shows that mouse <i>Dhrs3</i> expression is responsive to vitamin A status and is directly regulated by the RAR/RXR complex through <i>cis</i>-regulatory elements. This highlights a negative feedback mechanism that ensures retinoic acid homeostasis.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 3","pages":"340-351"},"PeriodicalIF":3.5,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461344","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}
引用次数: 0
The autophagy initiation factor ATG13 mRNA is stabilized by the RNA-binding protein YBX3 自噬启动因子 ATG13 mRNA 由 RNA 结合蛋白 YBX3 稳定。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-10-16 DOI: 10.1002/1873-3468.15035
Liva Pfuhler, Silina Awad, William Skipper, Jeremy Lavietes, Thomas Sah, Kayla Ho, Radha Ivanova, Amy Cooke
{"title":"The autophagy initiation factor ATG13 mRNA is stabilized by the RNA-binding protein YBX3","authors":"Liva Pfuhler,&nbsp;Silina Awad,&nbsp;William Skipper,&nbsp;Jeremy Lavietes,&nbsp;Thomas Sah,&nbsp;Kayla Ho,&nbsp;Radha Ivanova,&nbsp;Amy Cooke","doi":"10.1002/1873-3468.15035","DOIUrl":"10.1002/1873-3468.15035","url":null,"abstract":"<p>Autophagy, a highly conserved form of cellular recycling, is essential for cellular homeostasis. Its dysregulation has been linked to neurodegenerative diseases and various cancers, including breast cancer. We set out to determine if the RNA-binding protein (RBP) YBX3 regulates autophagy mRNAs, as previous findings suggest YBX3 depletion reduces distinct autophagy transcripts. We found that YBX3 interacts with and stabilizes the mRNA of the autophagy initiation factor <i>ATG13</i> in HeLa, which in turn increases ATG13 protein expression. We have shown that this requires the 3′ untranslated region (UTR) of <i>ATG13</i> and occurs in other human cell lines, including HEK293, HepG2, and HCT116. Together, our data suggest a novel regulatory role for YBX3 of autophagy initiation through posttranscriptional control of <i>ATG13</i> mRNA stability.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 1","pages":"89-99"},"PeriodicalIF":3.5,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461347","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}
引用次数: 0
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