{"title":"Inhibiting UPF1 methylation enhances tumor immunotherapy sensitivity by reducing nonsense-mediated mRNA decay.","authors":"Shengyu Zhu, Yucong Bai, Dongjing Zhang, Changsheng Huang, Xu Qian, Pengcheng Li, Tianci Xie, Qi Wu, Anyi Liu, Tong Zhu, Wangshuo Yang, Xiaowei She, Mao Li, Zejun Rao, Siqi Chen, Lang Liu, Chengxin Yu, Xiang Liu, Guihua Wang, Guangyong Zhang, Junbo Hu","doi":"10.1016/j.celrep.2025.115919","DOIUrl":"10.1016/j.celrep.2025.115919","url":null,"abstract":"<p><p>Nonsense-mediated mRNA decay (NMD) is a conserved RNA surveillance mechanism. Inhibition of NMD leads to increased expression of tumor neoantigens encoded by genes with premature termination codons (PTCs), thereby enhancing tumor immunogenicity. In this study, we find that protein levels of up-frameshift protein 1 (UPF1), a key factor in the NMD pathway, show significant differences in clinical tumor samples of microsatellite-stable (MSS) and microsatellite-unstable (MSI) colorectal cancer (CRC). UPF1 protein levels negatively regulate tumor immunogenicity and sensitivity to anti-PD-1 therapy in MSS and MSI CRC mouse models. Mechanistically, asymmetric di-methylation of UPF1 R433 by protein arginine methyltransferase 4 inhibits the autophagic degradation of UPF1, and inhibiting UPF1 R433 methylation can weaken NMD, thus increasing the immunogenicity and anti-PD-1 sensitivity of CRC, regardless of MSS or MSI status. Our study highlights the potential of combination strategies in CRC immunotherapy, promising to expand the beneficiaries of immunotherapy and provide insights for new therapeutic targets.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115919"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504876","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 : 2025-07-22Epub Date: 2025-06-24DOI: 10.1016/j.celrep.2025.115896
Stefano Secchia, Vera Beilinson, Xiaoting Chen, Melanie Gucwa, Lee A Denson, Emily R Miraldi, Matthew T Weirauch, Kohta Ikegami
{"title":"Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence.","authors":"Stefano Secchia, Vera Beilinson, Xiaoting Chen, Melanie Gucwa, Lee A Denson, Emily R Miraldi, Matthew T Weirauch, Kohta Ikegami","doi":"10.1016/j.celrep.2025.115896","DOIUrl":"10.1016/j.celrep.2025.115896","url":null,"abstract":"<p><p>Depletion of growth factors and nutrients induces cellular quiescence, which often accompanies transcriptional silencing and chromatin compaction. Paradoxically, such depletion occurs in pathological microenvironments in which fibroblasts are activated to orchestrate tissue remodeling. The relationship between fibroblast activation and growth factor and nutrient depletion remains unclear. Here, we report that serum depletion in cell culture, a model for growth factor and nutrient depletions, extensively activates transcription in fibroblasts despite inducing quiescence. Activated genes were enriched for extracellular matrix (ECM) structural components and proteases. ECM-related transcription accompanied the activation of putative distal enhancers but not promoters. The activated putative enhancers were enriched for non-coding variants associated with inflammatory bowel disease (IBD) risk, suggesting an alteration in the ECM-remodeling gene regulatory network in IBD. This study implicates nutrient and growth factor depletion in activating the ECM-remodeling gene program in fibroblasts, challenging the prevailing view linking such depletion to transcriptional dormancy.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115896"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494907","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":"VCPIP1 potentiates innate immune responses by non-catalytically reducing the ubiquitination of IRAK1/2.","authors":"Liyan Lou, Jiangyun Shen, Jianzhao Zhang, Fuqi Mei, Deyu Deng, Deqi Wang, Yanqi Xu, Kangmin Chen, Baoli Cheng, Jinghua Liu, Xu Wang","doi":"10.1016/j.celrep.2025.115931","DOIUrl":"10.1016/j.celrep.2025.115931","url":null,"abstract":"<p><p>The host innate immune system is efficiently activated after recognizing microbial components, such as lipopolysaccharide (LPS), by Toll-like receptors (TLRs). However, the molecular basis for the regulation of TLR-mediated signaling remains poorly understood. Here, we report that valosin containing protein interacting protein 1 (VCPIP1), a deubiquitinating enzyme, acts as a critical positive regulator of TLR4 signaling. TLR4 activation induces the upregulation and nuclear-to-cytoplasmic translocation of VCPIP1. The cytoplasmic VCPIP1 interacts with interleukin-1 receptor-associated kinase 1 and 2 (IRAK1/2) and maintains IRAK1/2 protein levels by reducing their degradation through the ubiquitin-proteasome system. Instead of directly deubiquitinating IRAK1/2 through the enzymatic activity, VCPIP1 blocks the K48 ubiquitination of IRAK1/2 in a non-catalytic manner. Ablation of VCPIP1 significantly attenuates LPS-induced inflammatory gene expression in macrophages. Consistently, VCPIP1-deficient mice are less susceptible to sepsis. Thus, this work reveals an essential role of VCPIP1 in TLR4 signaling and suggests that VCPIP1 may become a potential therapeutic target for inflammatory diseases.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115931"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526534","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 : 2025-07-22Epub Date: 2025-06-25DOI: 10.1016/j.celrep.2025.115913
Patricia Favaro, David R Glass, Luciene Borges, Reema Baskar, Avery Lam, Warren Reynolds, Daniel Ho, Trevor Bruce, Dmitry Tebaykin, Thomas Koehnke, Vanessa M Scanlon, Ilya Shestopalov, Sean C Bendall
{"title":"Quantification of intrinsic regulatory factors refines human hematopoietic progenitor definitions and reveals early erythroid lineage priming.","authors":"Patricia Favaro, David R Glass, Luciene Borges, Reema Baskar, Avery Lam, Warren Reynolds, Daniel Ho, Trevor Bruce, Dmitry Tebaykin, Thomas Koehnke, Vanessa M Scanlon, Ilya Shestopalov, Sean C Bendall","doi":"10.1016/j.celrep.2025.115913","DOIUrl":"10.1016/j.celrep.2025.115913","url":null,"abstract":"<p><p>Hematopoietic stem and progenitor cell (HSPC) transplantation is an essential therapy for hematological conditions, but finer definitions of human HSPC subsets with associated function could enable better tuning of grafts and more routine, lower-risk application. To deeply phenotype HSPCs, following a screen of 328 antigens, we quantified 41 surface proteins and functional regulators on millions of CD34<sup>+</sup> and CD34<sup>-</sup> cells, spanning four primary hematopoietic tissues: bone marrow, mobilized peripheral blood, cord blood, and fetal liver. We propose more granular definitions of HSPC subsets and present detailed differentiation trajectories of erythroid and myeloid lineages. These aspects of our revised human hematopoietic model are validated with corresponding epigenetic analysis, in vitro clonal differentiation assays, and an in vivo cell tracing model. Overall, we demonstrate the utility of using molecular regulators as surrogates for cellular identity and functional potential, providing a framework for description, prospective isolation, and cross-tissue comparison of HSPCs in humans.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115913"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511614","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 : 2025-07-22Epub Date: 2025-06-19DOI: 10.1016/j.celrep.2025.115855
Jolien J E van Hooff, Maximilian W D Raas, Eelco C Tromer, Laura Eme
{"title":"Repeated duplications and losses shaped SMC complex evolution from archaeal ancestors to modern eukaryotes.","authors":"Jolien J E van Hooff, Maximilian W D Raas, Eelco C Tromer, Laura Eme","doi":"10.1016/j.celrep.2025.115855","DOIUrl":"10.1016/j.celrep.2025.115855","url":null,"abstract":"<p><p>Across life, structural maintenance of chromosomes (SMC) complexes organize chromosomes. While most prokaryotes have one, eukaryotes usually possess four (condensin I, condensin II, cohesin, and SMC5/6), shaping their considerably larger genomes. Although essential, SMC complexes differ among model eukaryotes, suggesting underexplored diversity. Here, we reconstruct eukaryotic SMC complex evolution, revealing that the last eukaryotic common ancestor (LECA) had all four complexes, supporting a sophisticated LECA. Subsequently, condensin II was lost at least 30 times, making it one of the most frequently lost eukaryotic machineries. Moreover, multiple SMC complex components are more ancient and widespread than previously appreciated. Tracing prokaryotic origins, we propose that the SMC complex was already duplicated in the Thaumarchaeota-Aigarchaeota-Crenarchaeota-Korarchaeota (TACK) and Asgard archaeal ancestor, suggesting sophisticated chromosome organization in eukaryotes' archaeal ancestor. Gene duplications further expanded the eukaryotic SMC complex inventory, highlighting their significance in establishing eukaryotic complexity. Altogether, our work suggests major shifts in genome organization throughout eukaryote history.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115855"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336362","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 : 2025-07-22Epub Date: 2025-06-23DOI: 10.1016/j.celrep.2025.115876
Nicolas Chiaruttini, Carlo Castoldi, Linda Maria Requie, Carmen Camarena-Delgado, Beatrice Dal Bianco, Johannes Gräff, Arne Seitz, Bianca A Silva
{"title":"ABBA+BraiAn, an integrated suite for whole-brain mapping, reveals brain-wide differences in immediate-early genes induction upon learning.","authors":"Nicolas Chiaruttini, Carlo Castoldi, Linda Maria Requie, Carmen Camarena-Delgado, Beatrice Dal Bianco, Johannes Gräff, Arne Seitz, Bianca A Silva","doi":"10.1016/j.celrep.2025.115876","DOIUrl":"10.1016/j.celrep.2025.115876","url":null,"abstract":"<p><p>Unbiased characterization of whole-brain cytoarchitecture is crucial for understanding brain function, requiring precise mapping of 2D histological sections onto 3D brain atlases. We introduce two software tools to facilitate this process: Aligning Big Brains and Atlases (ABBA), designed to streamline the precise and efficient registration of 2D sections to 3D reference atlases, and BraiAn, an integrated suite for multi-marker automated segmentation, whole-brain statistical analysis, and data visualization. Combining these tools, we conducted a comprehensive comparative study of the whole-brain expression of three widely used immediate-early genes (IEGs)-cFos, Arc, and NPAS4-across three memory-related behavioral conditions. Our findings reveal significant differences in their distribution and induction patterns, suggesting that these IEGs offer complementary, rather than equivalent, information about neural activity across brain regions and activity states.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115876"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144483339","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 : 2025-07-22Epub Date: 2025-06-25DOI: 10.1016/j.celrep.2025.115902
Berenice Cabrera-Martinez, Josselyn E Garcia-Perez, Ryan M Baxter, Victor G Lui, Tusharkanti Ghosh, Ahmet Eken, Zander Kostka-Newman, John Rhey Mhar Garcia, Jeremy Rahkola, Rachel L Gessner, Cullen M Dutmer, Jared Klarquist, Eric M Pietras, Debashis Ghosh, Sara A Johnson, Ross M Kedl, Elena W Y Hsieh
{"title":"A hypomorphic Il2rb mutant mouse model recapitulates and reveals mechanisms of human T cell immune dysregulation in IL-2Rβ deficiency.","authors":"Berenice Cabrera-Martinez, Josselyn E Garcia-Perez, Ryan M Baxter, Victor G Lui, Tusharkanti Ghosh, Ahmet Eken, Zander Kostka-Newman, John Rhey Mhar Garcia, Jeremy Rahkola, Rachel L Gessner, Cullen M Dutmer, Jared Klarquist, Eric M Pietras, Debashis Ghosh, Sara A Johnson, Ross M Kedl, Elena W Y Hsieh","doi":"10.1016/j.celrep.2025.115902","DOIUrl":"10.1016/j.celrep.2025.115902","url":null,"abstract":"<p><p>Here, we describe the use of a homologous knockin mouse model to further decipher the mechanism(s) of a novel human homozygous IL2RB hypomorphic mutation. Our model recapitulates the human immune dysregulation phenotype, showing decreased mutant interleukin-2Rβ (IL-2Rβ) cell-surface expression, impaired IL-2/15-dependent STAT5 signaling, elevated serum IL-2/15 levels, expanded effector memory CD8<sup>+</sup> T cells, and severely reduced regulatory T cells (Tregs). Using mixed bone marrow chimeras (BMCs) and wild-type (WT) Treg transfers, we distinguish receptor-intrinsic from receptor-extrinsic immunopathogenesis. Both approaches suppress abnormal serum cytokine levels and autoimmunity without affecting endogenous mutant Tregs. Mutant animals receiving WT Tregs neonatally exhibit almost complete restoration of conventional T cell distribution, IL-2Rβ receptor surface expression, and STAT5 signal transduction, while BMC animals exhibit only partial restoration. Our findings demonstrate that CD8<sup>+</sup> T cells and Tregs have distinct IL-2/15 ligand/receptor ratios and signaling thresholds required for proper development/function, revealing mechanistic insights applicable to immunotherapy for autoimmunity.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115902"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504871","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 : 2025-07-22Epub Date: 2025-06-24DOI: 10.1016/j.celrep.2025.115879
Sara Picó, Alba Vílchez-Acosta, João Agostinho de Sousa, María Del Carmen Maza, Calida Mrabti, Alberto Parras, Gabriela Desdín-Micó, Céline Yacoub Maroun, Clémence Branchina, Ferdinand von Meyenn, Alejandro Ocampo
{"title":"Comparative analysis of mouse strains for in vivo induction of reprogramming factors.","authors":"Sara Picó, Alba Vílchez-Acosta, João Agostinho de Sousa, María Del Carmen Maza, Calida Mrabti, Alberto Parras, Gabriela Desdín-Micó, Céline Yacoub Maroun, Clémence Branchina, Ferdinand von Meyenn, Alejandro Ocampo","doi":"10.1016/j.celrep.2025.115879","DOIUrl":"10.1016/j.celrep.2025.115879","url":null,"abstract":"<p><p>In vivo reprogramming through the forced expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) has demonstrated great potential for reversing age-associated phenotypes. However, continuous in vivo OSKM expression has raised safety concerns due to loss of cell identity, decrease in body weight, and premature death. Although cyclic short-term or targeted expression of the reprogramming factors can mitigate some of these detrimental effects, systemic rejuvenation of wild-type mice has remained elusive. To improve the fundamental understanding of in vivo reprogramming, we conduct a comparative analysis of various reprogrammable mouse strains across multiple tissues and organs. In addition, we develop reprogrammable mouse strains by avoiding OSKM expression in specific organs or implementing expression approaches within specific cells, thereby offering safer strategies to induce in vivo reprogramming. We hope that these tools will become valuable resources for future research in this field of research with potential implications to human health.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115879"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494900","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 : 2025-07-22Epub Date: 2025-06-27DOI: 10.1016/j.celrep.2025.115908
Spyridon Makris, Yukti Hari-Gupta, Jesús A Cantoral-Rebordinos, Victor G Martinez, Harry L Horsnell, Agnesska C Benjamin, Isabella Cinti, Martina Jovancheva, Daniel Shewring, Nicola Nguyen, Charlotte M de Winde, Alice E Denton, Sophie E Acton
{"title":"Lymph node fibroblast phenotypes and immune crosstalk regulated by podoplanin activity.","authors":"Spyridon Makris, Yukti Hari-Gupta, Jesús A Cantoral-Rebordinos, Victor G Martinez, Harry L Horsnell, Agnesska C Benjamin, Isabella Cinti, Martina Jovancheva, Daniel Shewring, Nicola Nguyen, Charlotte M de Winde, Alice E Denton, Sophie E Acton","doi":"10.1016/j.celrep.2025.115908","DOIUrl":"10.1016/j.celrep.2025.115908","url":null,"abstract":"<p><p>Lymph nodes are uniquely organized niches for immune interactions. Fibroblastic reticular cells (FRCs) facilitate immune cell communication and regulate immune function by producing growth factors, chemokines, and inflammatory cues. Stromal expression of the glycoprotein podoplanin (PDPN) is required for lymph node development, but the requirement for PDPN signaling in FRCs in adult lymph nodes has not been directly tested. Using a conditional in vivo deletion model PDGFRα<sup>mGFPΔPDPN</sup>, single-cell RNA sequencing (scRNA-seq) reveals that PDPN deletion increases inflammatory signaling in lymph nodes and disrupts stromal-immune cell crosstalk in steady state and during adaptive immune responses. We confirm that PDPN/CLEC-2 signaling in FRCs switches transcriptional states and alters the expression of immune-related genes. We conclude that PDPN expression impacts the immunoregulatory properties of fibroblastic stroma in lymph nodes and is a key transcriptional regulator of fibroblast function in lymph nodes.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115908"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526530","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 : 2025-07-22Epub Date: 2025-06-25DOI: 10.1016/j.celrep.2025.115928
Thomas Hollin, Zeinab Chahine, Steven Abel, Charles Banks, Charisse Flerida A Pasaje, Todd Lenz, Jacques Prudhomme, Caitlyn Marie Ybanez, Anahita S Abbaszadeh, Jacquin C Niles, Laurence Florens, Karine G Le Roch
{"title":"RAP proteins regulate apicoplast noncoding RNA processing in Plasmodium falciparum.","authors":"Thomas Hollin, Zeinab Chahine, Steven Abel, Charles Banks, Charisse Flerida A Pasaje, Todd Lenz, Jacques Prudhomme, Caitlyn Marie Ybanez, Anahita S Abbaszadeh, Jacquin C Niles, Laurence Florens, Karine G Le Roch","doi":"10.1016/j.celrep.2025.115928","DOIUrl":"10.1016/j.celrep.2025.115928","url":null,"abstract":"<p><p>The human malaria parasite, Plasmodium falciparum, contains a non-photosynthetic and essential plastid called the apicoplast. This organelle is of major interest for its unique biology and potential as an attractive drug target. In this study, we characterize PfRAP03 and PfRAP08, two members of the RAP (RNA-binding domain abundant in apicomplexans) protein family. We generate inducible knockdown lines in P. falciparum to validate that both RAP proteins are essential for parasite survival and localize to the apicoplast. Transcriptomic analysis demonstrates that PfRAP03 and PfRAP08 depletion significantly affect apicoplast gene expression. Using enhanced crosslinking immunoprecipitation sequencing (eCLIP-seq) method, we show that apicoplast ribosomal RNAs and transfer RNAs are the targets of PfRAP03 and PfRAP08, respectively. Collectively, our results establish the role of these RAP proteins in controlling apicoplast gene expression in P. falciparum, revealing parasite-specific organellar pathways with biomedical significance.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115928"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511615","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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