{"title":"NSUN2-mediated GATM m5C methylation regulates creatine metabolism to drive mitochondrial fission and promote renal fibrosis.","authors":"Xiaoguo Suo, Mengmeng Zhang, Qi Zhu, Qichao Luo, Fang Wang, Qinglin Ge, Lijin Peng, Jutao Yu, Jie Wei, Chao Hou, Minglu Ji, Danfeng Zhang, Linhui Wu, Zhijuan Wang, Chao Li, Xin Chen, Sai Zhu, Shuaishuai Xie, Yu-Hang Dong, Peng Chen, Chen Yang, Juan Jin, FeiXavier Chen, Jianan Wang, Xiaoming Meng","doi":"10.1016/j.celrep.2026.117253","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117253","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is increasing globally, presenting a critical health challenge. Renal fibrosis, the main pathological feature of CKD, is poorly understood and lacks targeted therapies. Here, we reveal that 5-methylcytosine (m5C) RNA methylation, primarily mediated by methyltransferase NSUN2, is significantly upregulated in renal fibrosis. Reduction of m5C RNA methylation levels upon NSUN2 loss attenuates fibrosis responses in cells, and specific knockout of NSUN2 in renal tubular epithelial cells alleviates renal fibrosis in several disease models. Mechanistically, NSUN2 methylates and stabilizes glycine amidinetransferase (GATM) mRNA. GATM exacerbates mitochondrial fission not only by directly binding to Drp1 but also through its product creatine, collectively driving the progression of renal fibrosis. We subsequently identify an inhibitor of NSUN2 that mitigates the progression of renal fibrosis. Collectively, our study demonstrates that targeting NSUN2-mediated m5C methylation of GATM mRNA therapeutically offers a promising strategy to slow the progression of CKD.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117253"},"PeriodicalIF":6.9,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-15DOI: 10.1016/j.celrep.2026.117260
Shengnan Zheng, Zhikai Chen, Lingyun Nie, Wenyue Liu, Yaqian Zhang, Kai Jiang, Xing Liu, Chao Xu, Xuebiao Yao, Chuanhai Fu
{"title":"The endoplasmic reticulum protein Erg28 restrains Mto1-Mto2-γ-TuSC-mediated microtubule assembly.","authors":"Shengnan Zheng, Zhikai Chen, Lingyun Nie, Wenyue Liu, Yaqian Zhang, Kai Jiang, Xing Liu, Chao Xu, Xuebiao Yao, Chuanhai Fu","doi":"10.1016/j.celrep.2026.117260","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117260","url":null,"abstract":"<p><p>Interphase microtubule arrays play critical roles in a variety of cellular functions, including the spatial organization and distribution of the endoplasmic reticulum (ER). However, the role of the ER in regulation of microtubule assembly remains poorly characterized. Here, we identify Erg28, a conserved transmembrane protein localized to the ER, as a key factor that inhibits microtubule assembly. Biochemical analyses demonstrate that Erg28 physically interacts with the microtubule assembly-promoting factors-the Mto1-Mto2 complex and the γ-tubulin small complex (γ-TuSC)-and significantly attenuates the binding of γ-TuSC to the Mto1-Mto2 complex. Additionally, microscopic analyses show that Erg28 inhibits microtubule assembly mediated by Mto1-Mto2 complex and γ-TuSC in vitro. The cytosolic N-terminal region of Erg28 is indispensable for its inhibitory activity. Moreover, erg28 deletion leads to excessive microtubule assembly, causing nuclear shape deformation. These findings provide insights into the regulatory mechanism by which the ER influences microtubule cytoskeleton organization.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117260"},"PeriodicalIF":6.9,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-15DOI: 10.1016/j.celrep.2026.117268
Dongfa Wang, Liangliang He, Chunmei Zong, Xuan Zhou, Hanyan Feng, Baolin Zhao, Shaoli Zhou, Liling Yang, Qing Wu, Weiyue Zhao, Xiaomin Ji, Quanzi Bai, Jing Yang, Dan Wang, Weiguang Du, Yanping Wang, Chonghui Duan, Jianghua Chen
{"title":"The AP2 transcription factor LF1 coordinates auxin signaling and LFY/FLO pathway to control leaflet number determination in soybean.","authors":"Dongfa Wang, Liangliang He, Chunmei Zong, Xuan Zhou, Hanyan Feng, Baolin Zhao, Shaoli Zhou, Liling Yang, Qing Wu, Weiyue Zhao, Xiaomin Ji, Quanzi Bai, Jing Yang, Dan Wang, Weiguang Du, Yanping Wang, Chonghui Duan, Jianghua Chen","doi":"10.1016/j.celrep.2026.117268","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117268","url":null,"abstract":"<p><p>Compound leaves initiate as simple primordia, with LFY/FLO orthologs orchestrating subsequent leaflet initiation. Although several LFY/FLO repressors have been identified, the activating mechanisms remain unknown. Here, we investigate the soybean dominant mutant Lf1, which exhibits five palmately arranged leaflets. LF1 encodes an AP2 transcription factor homologous to Arabidopsis DRN/DRNL and is specifically expressed in incipient and developing leaflet primordia. LF1 binds to GCC-box motifs, enabling autoregulation and activating downstream targets GmLFYa&b-key regulators of leaflet initiation. The Lf1 mutation substitutes Asp with Gly in the AP2 domain, enhancing its regulatory activity. Consequently, Lf1 and GmLFYa&b expression is upregulated and ectopic in early leaflet primordia, triggering extra leaflet formation. Auxin upregulates the endogenous LF1 transcription but suppresses the activity of the exogenous LF1 promoter in ProLF1:GUS reporter lines, suggesting a context-dependent role for auxin in modulating LF1 expression. Therefore, LF1 mechanistically links auxin signaling with the LFY/FLO pathway during compound leaf development.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117268"},"PeriodicalIF":6.9,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-15DOI: 10.1016/j.celrep.2026.117266
Felipe A M Otsuka, Ingemar André
{"title":"Effects of single synonymous substitutions on fold efficiency demonstrate the influence of rare codons and protein structure.","authors":"Felipe A M Otsuka, Ingemar André","doi":"10.1016/j.celrep.2026.117266","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117266","url":null,"abstract":"<p><p>Codon sequences can influence proteins to misfold during cotranslational folding. Here, we develop an in vivo assay in E. coli to comprehensively study the impact of single synonymous substitutions on protein folding efficiency and apply it to the N-terminal domain of ddlA. By mapping the influence of codons along the sequence, we show that codon identity can substantially influence folding efficiency in a manner depending on structure and topology. We found that a cluster of codons in the N-terminal domain strongly impacts ddlA folding. Further analysis revealed that substitutions to rarer codons generally lead to increased folding efficiency. Consistent with this, an mRNA composed exclusively of rare codons yields higher expression and folding efficiency than one containing only commons codons. Our results highlight the importance of rare codons in cotranslational folding and the relationship between codon sequence and protein structure.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117266"},"PeriodicalIF":6.9,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-15DOI: 10.1016/j.celrep.2026.117180
Daniel L V Bader, Claudia T Flynn, Oleksandr Kalyuzhniy, Gabriel Ozorowski, Martin M Corcoran, Alison Burns, Pilar Altman, Romy Rouzeau, Troy Sincomb, Alessia Liguori, Monica L Fernández-Quintero, Johannes R Loeffler, Jonathan L Torres, Hannah L Turner, Erik Georgeson, Amelia Zhou, Hannah Voic, Sue Goo, Lara Shahin, Iszac Burton, Mengyu Wu, Robyn L Stanfield, Saman Eskandarzadeh, Danny Lu, Nushin Alavi, Nicole Phelps, Ryan Tingle, Katherine McKenney, John Youhanna, Sonya Amirzehni, Torben Schiffner, Jon M Steichen, Dennis R Burton, Ian A Wilson, Gunilla B Karlsson Hedestam, Elise Landais, Jeong Hyun Lee, Devin Sok, Christopher A Cottrell, Andrew B Ward, William R Schief
{"title":"Structural and immunogenetic signatures guide CD4-mimetic HIV vaccine development.","authors":"Daniel L V Bader, Claudia T Flynn, Oleksandr Kalyuzhniy, Gabriel Ozorowski, Martin M Corcoran, Alison Burns, Pilar Altman, Romy Rouzeau, Troy Sincomb, Alessia Liguori, Monica L Fernández-Quintero, Johannes R Loeffler, Jonathan L Torres, Hannah L Turner, Erik Georgeson, Amelia Zhou, Hannah Voic, Sue Goo, Lara Shahin, Iszac Burton, Mengyu Wu, Robyn L Stanfield, Saman Eskandarzadeh, Danny Lu, Nushin Alavi, Nicole Phelps, Ryan Tingle, Katherine McKenney, John Youhanna, Sonya Amirzehni, Torben Schiffner, Jon M Steichen, Dennis R Burton, Ian A Wilson, Gunilla B Karlsson Hedestam, Elise Landais, Jeong Hyun Lee, Devin Sok, Christopher A Cottrell, Andrew B Ward, William R Schief","doi":"10.1016/j.celrep.2026.117180","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117180","url":null,"abstract":"<p><p>HIV vaccine strategies include aims to elicit broadly neutralizing antibodies (bnAbs) targeting the CD4-binding site, that are derived from immunoglobulin heavy-chain variable genes 1-2 (V<sub>H</sub>1-2) and 1-46 (V<sub>H</sub>1-46). Here, we present an integrated analysis of V<sub>H</sub>1-46 bnAbs, including in vitro functional studies, cryo-electron microscopy structures of two V<sub>H</sub>1-46 bnAbs (1-23 and 9-71) complexed with envelope trimers, and comprehensive structural and immunogenetic analyses, to help guide vaccine design. We show that V<sub>H</sub>1-46-derived bnAbs use diverse light-chain variable (V<sub>K</sub>/V<sub>L</sub>) genes and LCDR3 lengths commonly found in human antibody repertoires, which generate unique LCDR3 signatures that influence both the antibody paratope and approach angle. We identify three V<sub>H</sub>1-46 bnAb classes, 1B2530 (V<sub>L</sub>1-47), CH235 (V<sub>K</sub>3-15), and 561 (V<sub>K</sub>3-20), with the 561 class further subdivided into types I and II. Our findings indicate that V<sub>H</sub>1-46 priming immunogens should be tailored to each bnAb class, with 561-class bnAbs presenting optimal targets for germline-targeting vaccine design.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117180"},"PeriodicalIF":6.9,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-13DOI: 10.1016/j.celrep.2026.117176
Marta Ballester, Anita Kurilla, Yifan Dai, Leire Bergara-Muguruza, Katarzyna Radke, H Carlo Maurer, Elisa Espinet, Kristina Høj, Aida Marisch-Delgado, Philip A Seymour, Saynab Omar, Charlotte Vestrup Rift, Jane Hasselby, Pia Klausen, Peter Vilmann, Ainara Castellanos-Rubio, Izortze Santin, Albin Sandelin, Luis Arnes
{"title":"Regulatory elements in the Sox9 locus license the initiation of pancreatic ductal adenocarcinoma.","authors":"Marta Ballester, Anita Kurilla, Yifan Dai, Leire Bergara-Muguruza, Katarzyna Radke, H Carlo Maurer, Elisa Espinet, Kristina Høj, Aida Marisch-Delgado, Philip A Seymour, Saynab Omar, Charlotte Vestrup Rift, Jane Hasselby, Pia Klausen, Peter Vilmann, Ainara Castellanos-Rubio, Izortze Santin, Albin Sandelin, Luis Arnes","doi":"10.1016/j.celrep.2026.117176","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117176","url":null,"abstract":"<p><p>Cellular plasticity enables tissue regeneration but can be hijacked by oncogenic programs. In the pancreas, Kras acts on tissue-specific enhancers to lock regeneration into a pro-inflammatory state that drives cancer initiation. Enhancer transcription, an early event during cell state transitions, generates long noncoding RNAs (lncRNAs) that influence transcription and genome organization, yet their roles in pancreatic regeneration remain unclear. We profiled epithelial lncRNAs and their targets during pancreatic ductal adenocarcinoma (PDAC) precursor formation, focusing on those transcribed from enhancers near cell identity regulators. LINC00673, expressed from a Sox9-associated super-enhancer during development, is reactivated in PDAC. Conditional deletion of LINC00673 accelerates acinar-to-ductal metaplasia resolution and impairs PDAC initiation. Moreover, LINC00673 harbors a variant associated with PDAC risk. In addition, our data are consistent with a contribution of transcribed super-enhancers to long-range gene regulation during pancreatic cancer initiation. These findings reveal a regulatory layer linking developmental enhancer activity, cellular plasticity, and pancreatic disease progression.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117176"},"PeriodicalIF":6.9,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Structural mechanism of 3'3'-cGAMP-induced filamentation and phospholipid hydrolysis by CapV in bacterial antiphage defense.","authors":"Yun Lv, Sheng Liu, Qihai Wang, Jing Zhu, Yingxiang Hou, Haiyan Xu, Deyan Zhu, Yu Liu, Jing Wu, Changxin Wu, Guijun Shang, Hongxiang Lou, Defen Lu, Huiqing Yuan, Deyu Zhu","doi":"10.1016/j.celrep.2026.117261","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117261","url":null,"abstract":"<p><p>The cyclic-oligonucleotide-based antiphage signaling system (CBASS) protects bacteria from phage infection. In Vibrio cholerae, phage infection activates CD-NTase DncV to produce 3'3'-cGAMP, which triggers phospholipase CapV to degrade phosphatidylethanolamine and phosphatidylglycerol, the major phospholipids in the inner-membranes, thereby inducing cell death. However, how 3'3'-cGAMP activates CapV was unclear. Here we present crystal structures of inactive Acinetobacter baumannii CapV in apo and 3'3'-cGAMP-bound forms, along with cryo-EM structures of activated CapV-3'3'-cGAMP complex, with or without substrate dioleoylphosphatidyl-ethanolamine (DOPE). Apo-CapV forms symmetric dimers in a \"closed\" state. 3'3'-cGAMP binding drives lateral polymerization of dimers into filament assembly, inducing an \"open\" state that exposes the active site and substrate-binding cleft. DOPE binding further shifts CapV to an \"ajar\" state, where a Y-shaped cleft positions DOPE for hydrolysis via a conserved Ser/Asp catalytic dyad. This 3'3'-cGAMP-induced filamentation mirrors activation mechanisms of TIR-STING, TIR-SAVED, and mammalian STING, revealing a conserved signaling pattern across immune systems.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117261"},"PeriodicalIF":6.9,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-13DOI: 10.1016/j.celrep.2026.117223
Hayk Mnatsakanyan, Alessandro Sammarco, Abigail Hewett, Rami Awwad, Elie Roumieh, Caline Pechdimaljian, Cagri Cakici, Caroline M Spangler, Yana Azar, Richa Pradhan, Baolong Su, Kevin J Williams, Steven J Bensinger, Christian E Badr
{"title":"SCD1 and SCD5 modulate PARP-dependent DNA repair via fatty acid desaturation in glioblastoma.","authors":"Hayk Mnatsakanyan, Alessandro Sammarco, Abigail Hewett, Rami Awwad, Elie Roumieh, Caline Pechdimaljian, Cagri Cakici, Caroline M Spangler, Yana Azar, Richa Pradhan, Baolong Su, Kevin J Williams, Steven J Bensinger, Christian E Badr","doi":"10.1016/j.celrep.2026.117223","DOIUrl":"10.1016/j.celrep.2026.117223","url":null,"abstract":"<p><p>Glioblastoma (GBM) relies on fatty acid metabolism for aggressive growth. This study identifies stearoyl-CoA desaturase-5 (SCD5), a brain-enriched isoform, as a critical driver of glioblastoma stem cell (GSC) maintenance and genomic stability. While SCD1's role in GBM is well-established, our research reveals that SCD5 plays a non-redundant role by preferentially desaturating C18:0 and uniquely remodeling sphingolipids. Genetic silencing of SCD5 disrupts the cell cycle, impairs DNA repair, and triggers parthanatos-a form of cell death caused by PARP1 hyperactivation. Mechanistically, loss of SCD activity or saturated fatty acid accumulation triggers PARP1 hyperactivation and subsequent degradation, depleting RAD51 to compromise homologous recombination and induce parthanatos. These findings uncover a lipid-mediated vulnerability in GBM, linking fatty acid desaturation to PARP1-dependent genome integrity. Targeting SCD5 may offer a therapeutic strategy to eliminate therapy-resistant GSCs and enhance the efficacy of genotoxic or immunotherapeutic interventions.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117223"},"PeriodicalIF":6.9,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2026-04-13DOI: 10.1016/j.celrep.2026.117258
Rob van der Kammen, Or Yakov, Shinyeong Ju, Ferhat Alkan, Onno B Bleijerveld, Cheolju Lee, William James Faller, Yuval Malka
{"title":"RNA dicing promotes the expression of an oncogenic JAK1 isoform.","authors":"Rob van der Kammen, Or Yakov, Shinyeong Ju, Ferhat Alkan, Onno B Bleijerveld, Cheolju Lee, William James Faller, Yuval Malka","doi":"10.1016/j.celrep.2026.117258","DOIUrl":"https://doi.org/10.1016/j.celrep.2026.117258","url":null,"abstract":"<p><p>The translation of an mRNA transcript is traditionally thought to be limited to its open reading frames (ORFs). However, recent findings reveal a more complex reality in which the proteome vastly exceeds transcriptome limits. Here, we demonstrate that JAK1 mRNA can be cleaved into a truncated, uncapped form with a shorter ORF, leading to the translation of the JH1 kinase domain independently of other domains, a process we term \"RNA dicing.\" Canonical and diced JAK1 variants differently impact cell proliferation and tumorigenesis, with the balance of these isoforms altered in tumorigenesis and in response to IFN-γ. Analyzing JAK1 nonsense mutations in endometrial tumors reveals that mutations inhibit the tumor-suppressive functions of canonical JAK1 while enhancing the oncogenic diced JH1 domain. This results in a better response to the JAK1 inhibitor momelotinib, highlighting RNA dicing's role in patient stratification. Our findings show that RNA dicing diversifies mRNA products, significantly impacting biological functions.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"45 4","pages":"117258"},"PeriodicalIF":6.9,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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