Selina Bopp, Lọla Fagbami, Amy Deik, Claudia Taccheri, Akansha Pant, Madeline Luth, Daisy Chen, Mark A. Tye, Imran Ullah, Johannes Kreuzer, Robert Morris, Wilhelm Haas, Elizabeth A. Winzeler, Clary Clish, Amanda K. Lukens, Ralph Mazitschek, Dyann F. Wirth
{"title":"Disruption of P. falciparum amino acid transporter elevates intracellular proline and induces resistance to Prolyl-tRNA synthetase inhibitors","authors":"Selina Bopp, Lọla Fagbami, Amy Deik, Claudia Taccheri, Akansha Pant, Madeline Luth, Daisy Chen, Mark A. Tye, Imran Ullah, Johannes Kreuzer, Robert Morris, Wilhelm Haas, Elizabeth A. Winzeler, Clary Clish, Amanda K. Lukens, Ralph Mazitschek, Dyann F. Wirth","doi":"10.1016/j.chembiol.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.007","url":null,"abstract":"<em>Plasmodium falciparum</em> evades the antimalarial activity of proline-competitive prolyl-tRNA synthetase (PfProRS) inhibitors, such as halofuginone (HFG), by a resistance mechanism termed the adaptive proline response (APR). The APR is characterized by a marked elevation of intracellular proline following drug exposure. Contrary to initial expectations, the APR is not mediated by alterations in canonical proline metabolic pathways involving arginase (<em>P. falciparum</em> arginase [PfARG]) and ornithine aminotransferase (<em>P. falciparum</em> ornithine aminotransferase [PfOAT]). Instead, we identified loss-of-function mutations in the apicomplexan amino acid transporter 2 (<em>P. falciparum</em> apicomplexan amino acid transporter 2 [PfApiAT2]) as the primary genetic driver of this resistance phenotype. Importantly, reversion of these mutations to wild type effectively suppresses the APR, establishing PfApiAT2 as the molecular determinant of this resistance mechanism.The elucidation of the APR significantly advances our understanding of antimalarial drug resistance. By delineating the role of PfApiAT2 in this process, we establish critical insights for the development of strategies to circumvent PfProRS inhibitor resistance for future antimalarial therapies.","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"06 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241395","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}
Louis P. Conway, Michelle A. Estrada, Weichao Li, Stephen Walker, Benjamin Mielich-Süss, Anurupa Shrestha, Matthew Townsend, Jürgen Korffmann, Greg Potts, Janice Lee, Kenneth P. Robinson, Shiyao Wang, Brian Bierie, John R. Koenig, Phil Cox, Paul Richardson, Manisha Jhala, Becca McCloud, Sujatha Gopalakrishnan, Kevin Woller, Christopher G. Parker
{"title":"Discovery of a tau-aggregate clearing compound that covalently targets P4HB","authors":"Louis P. Conway, Michelle A. Estrada, Weichao Li, Stephen Walker, Benjamin Mielich-Süss, Anurupa Shrestha, Matthew Townsend, Jürgen Korffmann, Greg Potts, Janice Lee, Kenneth P. Robinson, Shiyao Wang, Brian Bierie, John R. Koenig, Phil Cox, Paul Richardson, Manisha Jhala, Becca McCloud, Sujatha Gopalakrishnan, Kevin Woller, Christopher G. Parker","doi":"10.1016/j.chembiol.2025.09.006","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.006","url":null,"abstract":"The improper folding and aggregation of tau are linked to several neurodegenerative diseases affecting millions worldwide. However, the pathogenesis of tauopathies remains poorly understood, resulting in limited effective treatments. Here, we employ an integrated chemoproteomic phenotypic strategy to identify druggable targets and corresponding chemical probes for the treatment of tauopathies. We identified and optimized an indole-amine compound that potently and extensively clears tau aggregates in two human tauopathy models. Mechanistic and chemoproteomic studies implicate protein disulfide isomerase 1 (P4HB) as the primary target, forming covalent adducts upon metabolic activation. Knockdown of P4HB reduced tau aggregates in three tauopathy models, including an <em>ex vivo</em> murine neuron preclinical model. Functional characterization revealed the compound induces mild endoplasmic reticulum (ER)-stress responses as assessed by RNA sequencing and whole proteomic profiling. Our findings highlight P4HB as a potential therapeutic target for treatment of tauopathies.","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"12 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145229399","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}
Huiti Li, Ying Xu, Yimin Zheng, Zian Xue, Qingqing Li, Xinglong Jia, Lietao Weng, Lulu Jiang, Xiaoxue Ruan, Rong Zhang, Yue Yin, Liying Zhou, Fuyuan Li, He Huang, Jin Li, Minjia Tan, Jia Fan, Jiabin Cai, Guoqiang Chen, Lu Zhou
{"title":"CBX4 acetoacetylation as an inhibitory mechanism of HIF-1α activity","authors":"Huiti Li, Ying Xu, Yimin Zheng, Zian Xue, Qingqing Li, Xinglong Jia, Lietao Weng, Lulu Jiang, Xiaoxue Ruan, Rong Zhang, Yue Yin, Liying Zhou, Fuyuan Li, He Huang, Jin Li, Minjia Tan, Jia Fan, Jiabin Cai, Guoqiang Chen, Lu Zhou","doi":"10.1016/j.chembiol.2025.09.005","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.005","url":null,"abstract":"HIF-1α transcriptional activity is enhanced through SUMOylation mediated by CBX4. Despite the recognized importance of the CBX4-HIF-1α axis, the molecular mechanisms governing its regulation remain largely unclear. In this study, phenotypic screening of a 101,254-compound library followed by structural optimization led to the identification of <strong>XZA-1</strong>, a small molecule capable of disrupting CBX4-mediated HIF-1α transcriptional activation. Mechanistic investigations revealed that <strong>XZA-1</strong> activates HADH, a key enzyme in fatty acid β-oxidation, resulting in increased intracellular levels of acetoacetyl-CoA. This metabolite promotes acetoacetylation of CBX4 at lysine 106, thereby reducing its SUMO E3 ligase activity. In a CBX4-overexpressing xenograft model, <strong>XZA-1</strong> demonstrated antitumor effects by enhancing CBX4 K106 acetoacetylation. Additionally, elevated levels of CBX4 K106 acetoacetylation were observed in clinical HCC tissues from patients with better overall survival. These findings suggest that acetoacetyl-CoA functions as a potential antitumor metabolite and establish a novel pharmacological approach for modulating HIF-1α transcriptional activity in cancer.","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"6 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145209455","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}
Gregory G. Theophall, Michaele B. Manigrasso, Parastou Nazarian, Aaron Premo, Sergey Reverdatto, Gautham Yepuri, David S. Burz, Sally M. Vanegas, Kaamashri Mangar, Yanan Zhao, Huilin Li, Robert J. DeVita, Ravichandran Ramasamy, Ann Marie Schmidt, Alexander Shekhtman
{"title":"RAGE-mediated activation of the formin DIAPH1 and human macrophage inflammation are inhibited by a small molecule antagonist","authors":"Gregory G. Theophall, Michaele B. Manigrasso, Parastou Nazarian, Aaron Premo, Sergey Reverdatto, Gautham Yepuri, David S. Burz, Sally M. Vanegas, Kaamashri Mangar, Yanan Zhao, Huilin Li, Robert J. DeVita, Ravichandran Ramasamy, Ann Marie Schmidt, Alexander Shekhtman","doi":"10.1016/j.chembiol.2025.09.004","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.004","url":null,"abstract":"RAGE and its intracellular effector molecule, the actin polymerase DIAPH1, mediate inflammation and the complications of diabetes. Using NMR spectroscopy and mass spectrometry, we built a structural model of the RAGE-DIAPH1 complex, revealing how binding of the cytoplasmic tail of RAGE (ctRAGE) to DIAPH1 stimulates its actin polymerization activity, which is inhibited by a small molecule antagonist of RAGE-DIAPH1 interaction, RAGE406R. The solution structure of the RAGE406R - ctRAGE suggests that RAGE406R prevents the formation of the RAGE-DIAPH1. FRET, actin polymerization assays, smooth muscle cell migration, and THP1 cell inflammation experiments, together with the <em>in vivo</em> interrogation of the effects of RAGE406R in mouse models of inflammation and diabetic wound healing, support this mode of RAGE-DIAPH1 antagonism. Finally, the treatment of macrophages differentiated from peripheral blood-derived mononuclear cells from humans with type 1 diabetes with RAGE406R reduces the mRNA expression of the chemokine <em>CCL2,</em> diminishing the expression of a key node in the inflammatory response.","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"102 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145195133","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":"Inter- and intra-tumoral ALDH1 heterogeneity in breast cancer identifies therapeutic opportunities for ALDH1A-specific inhibitors","authors":"Raquel Pequerul, Andrada Constantinescu, Bassam Janji, Akinchan Kumar, Céline Baier, Iris Manosalva, Xavier Parés, Oscar Palacios, Salvatore Spicuglia, Delphine Colignon, Axelle Berrou, Guy Fournet, Paul Berchard, Guillaume Martin, Ismail Ceylan, Rocio Rebollido-Rios, Jaume Farrés, Mileidys Perez-Alea","doi":"10.1016/j.chembiol.2025.09.003","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.003","url":null,"abstract":"Basal-like breast cancer is an aggressive subtype with limited therapeutic options. Here, transcriptomic analysis of public datasets suggested distinct subtype- and cell-specific expression patterns of ALDH1A isoforms in breast tumors, with <em>ALDH1A3</em> predominantly expressed in the epithelial cells of basal-like tumors, whereas <em>ALDH1A2</em> and <em>ALDH1A1</em> were enriched in stromal and immune-associated subpopulations. High expression of <em>ALDH1A3</em> and <em>ALDH1A2</em>, but not <em>ALDH1A1</em>, is associated with poor prognosis in high-grade, lymph-node-positive tumors. To evaluate therapeutic targeting, we developed ABD0171, an irreversible, selective ALDH1A3 inhibitor with additional ALDH1A1 activity. ABD0171 disrupted key oncogenic pathways, including IL6/JAK/STAT3, tPA, and Src/FAK, resulting in robust antitumor and antimetastatic effects <em>in vitro</em> and <em>in vivo</em>, with a favorable safety profile. These findings establish ALDH1A3 as a therapeutic target in breast cancers with epithelial-basal traits and validate ABD0171 as a promising clinical candidate to address current treatment challenges.","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"23 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145189340","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}
Mohamed A. Anany, Daniela Siegmund, Olena Zaitseva, Isabell Lang, Bayan Mouhandes, Mervat Salah, Daniela Weisenberger, Svetlana Stepanzow, Juan Gamboa Vargas, Julia Dahlhoff, Theresa Schneider, Giel Tanghe, Frederik Stevenaert, Tugsan Tezil, Tom Van Belle, Bipasa Kar, Thomas Dandekar, Heike Margarete Hermanns, Luc van Rompaey, Andreas Beilhack, Harald Wajant
{"title":"Valence and avidity determine the agonistic activity of anti-TNFR2 nanobody fusion proteins","authors":"Mohamed A. Anany, Daniela Siegmund, Olena Zaitseva, Isabell Lang, Bayan Mouhandes, Mervat Salah, Daniela Weisenberger, Svetlana Stepanzow, Juan Gamboa Vargas, Julia Dahlhoff, Theresa Schneider, Giel Tanghe, Frederik Stevenaert, Tugsan Tezil, Tom Van Belle, Bipasa Kar, Thomas Dandekar, Heike Margarete Hermanns, Luc van Rompaey, Andreas Beilhack, Harald Wajant","doi":"10.1016/j.chembiol.2025.09.002","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.002","url":null,"abstract":"We identified several TNFR2-specific nanobodies (Nbs). When formatted as dimeric Fc fusion proteins, these nanobodies exhibited no agonistic activity. To improve activity, we genetically fused one, two, or three copies of the TNFR2-specific Nb:188 to the constant regions of an IgG1 antibody, an Fab fragment, an Fc domain or the trimerization domain of tenascin-C resulting in constructs with 2–12 Nb:188 domains. Constructs with 2 or 3 Nb:188 domains displayed no or minimal activity, while those with 4 and 5 Nb:188 domains demonstrated moderate activity. However, constructs with 6 or more Nb:188 domains exhibited potent agonism, reaching half-maximal TNFR2 activation at concentrations in the low picomolar range. Similarly, hexameric constructs generated with other TNFR2-specific Nb domains demonstrated robust agonism, too. Benchmarking against various other ligand- and antibody-based TNFR2 agonists revealed that the hexameric 3xNb:188-Fc format displays superior specific activity and efficiently expands regulatory T cells (Tregs).","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"30 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183027","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":"Sensing within: Mitochondrial inside-out signal transduction","authors":"Alva G. Sainz, Furkan E. Oflaz, Xinnan Wang","doi":"10.1016/j.chembiol.2025.09.001","DOIUrl":"https://doi.org/10.1016/j.chembiol.2025.09.001","url":null,"abstract":"The prevailing theory on the origins of mitochondria proposes that they were once independent organisms. Though symbiotically integrated into eukaryotic cells, they have retained a striking degree of autonomy. This self-governance manifests as the capacity to sense internal metabolic, ionic, and redox states and transduce these into signals that modulate cellular function—a process we refer to as <em>mitochondrial inside-out signaling.</em> These mitochondria-initiated signaling mechanisms are crucial for bioenergetic homeostasis of all cells, including neurons. Unlike conventional outside-in signaling, these mitochondria-initiated signals stem from within the organelle and propagate outward, tuning cytosolic signaling pathways, nuclear transcriptional programs, and neuronal behavior. In this review, we provide mechanistic insights into this distinct and underappreciated signaling modality, discussing how internal mitochondrial conditions are sensed and transmitted to the cytosol and how these signaling events influence mitochondrial and cellular health with a focus on their implications for neuronal physiology and disease vulnerability.","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"17 1","pages":""},"PeriodicalIF":8.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145134469","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}
Raffaella De Pace , Saikat Ghosh , Chad D. Williamson , Juan S. Bonifacino
{"title":"BLOC-1 and BORC: Complex regulators of endolysosomal dynamics","authors":"Raffaella De Pace , Saikat Ghosh , Chad D. Williamson , Juan S. Bonifacino","doi":"10.1016/j.chembiol.2025.08.001","DOIUrl":"10.1016/j.chembiol.2025.08.001","url":null,"abstract":"<div><div>Endolysosomes are dynamic organelles that undergo movement along the cytoskeleton, fusion, fission, and tubulation during their lifetime. These processes are regulated by complex molecular machineries, including the structurally related hetero-octameric complexes BLOC-1 and BORC. BLOC-1 associates with early endosomes to mediate the biogenesis of lysosome-related organelles (LROs), such as melanosomes and platelet dense bodies. Accordingly, mutations in BLOC-1 subunits cause Hermansky-Pudlak syndrome (HPS), a disorder characterized by pigmentation defects and bleeding abnormalities. In contrast, BORC associates with lysosomes, late endosomes, and synaptic vesicle precursors, promoting their transport along microtubules. BORC also regulates endolysosome fusion with other endolysosomes, as well as with phagosomes and autophagosomes. Mutations in BORC subunits cause a severe neurodevelopmental disorder in humans. In this article, we review recent progress in the elucidation of the structure, evolution, physiological roles, and regulation of BLOC-1 and BORC, highlighting their critical contributions to maintaining endolysosomal organization and function.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"32 9","pages":"Pages 1106-1124"},"PeriodicalIF":7.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144901103","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}
Ariana S. Bratt , Susan Kilgas , Maria I. Tarazona Guzman , Robert S. Magin , Isabella Jaen Maisonet , Cara A. Starnbach , Wei Pin Teh , Anthony C. Varca , Bin Hu , Esteban Tarazona Guzman , Hyuk-Soo Seo , Sirano Dhe-Paganon , Nicholas M. Girardi , Guillaume Adelmant , Jarrod A. Marto , Dipanjan Chowdhury , Sara J. Buhrlage
{"title":"Pharmacologic interrogation of USP28 cellular function in p53 signaling","authors":"Ariana S. Bratt , Susan Kilgas , Maria I. Tarazona Guzman , Robert S. Magin , Isabella Jaen Maisonet , Cara A. Starnbach , Wei Pin Teh , Anthony C. Varca , Bin Hu , Esteban Tarazona Guzman , Hyuk-Soo Seo , Sirano Dhe-Paganon , Nicholas M. Girardi , Guillaume Adelmant , Jarrod A. Marto , Dipanjan Chowdhury , Sara J. Buhrlage","doi":"10.1016/j.chembiol.2025.08.002","DOIUrl":"10.1016/j.chembiol.2025.08.002","url":null,"abstract":"<div><div>Deubiquitinating enzymes (DUBs) are crucial regulators of ubiquitin signaling and protein degradation that remain incompletely understood in part due to the lack of high-quality chemical probes. To address this challenge, we developed <strong>CAS-010</strong>, a low nanomolar, ubiquitin-competitive inhibitor of USP28 that demonstrates preferential activity against USP28 over other DUBs, while also exhibiting some activity against the closely related USP25. We rationalized our SAR trends and observed selectivity using a crystal structure of USP28 in complex with an inhibitor. We validated on-target effects of <strong>CAS-010</strong> on the negative regulation of p53 transactivation in the wild-type setting. We demonstrated that <strong>CAS-010</strong> disrupts the 53BP1-USP28 interaction, and more broadly showed that USP28 catalytic activity contributes to this key interaction. Taken together, <strong>CAS-010</strong> and the accompanying negative control compound <strong>WPT-086</strong> and inhibitor-resistant mutant provide well-validated tools for further characterizing the role of USP28 in p53-mediated effect on cell cycle control and cell fate.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"32 9","pages":"Pages 1166-1182.e27"},"PeriodicalIF":7.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928376","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":"Meet the authors: Canyong Guo and Kurt Wüthrich","authors":"Canyong Guo, Kurt Wüthrich","doi":"10.1016/j.chembiol.2025.08.009","DOIUrl":"10.1016/j.chembiol.2025.08.009","url":null,"abstract":"<div><div>In an interview with Dr. Mishtu Dey, Editor-in-Chief of <em>Cell Chemical Biology</em>, the authors of the article entitled “Structural basis of Adenosine 2A Receptor balanced signaling activation relies on allosterically mediated structural dynamics” share their thoughts on technological advances in structural biology and how applications of genetic labeling techniques made it possible to probe into the core of a GPCR.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"32 9","pages":"Pages 1089-1090"},"PeriodicalIF":7.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145078422","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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