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Nonhuman primate antigenic cartography of SARS-CoV-2. SARS-CoV-2 的非人灵长类抗原图谱。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-03 DOI: 10.1016/j.celrep.2024.115140
Annika Rössler, Antonia Netzl, Ninaad Lasrado, Jayeshbhai Chaudhari, Barbara Mühlemann, Samuel H Wilks, Janine Kimpel, Derek J Smith, Dan H Barouch
{"title":"Nonhuman primate antigenic cartography of SARS-CoV-2.","authors":"Annika Rössler, Antonia Netzl, Ninaad Lasrado, Jayeshbhai Chaudhari, Barbara Mühlemann, Samuel H Wilks, Janine Kimpel, Derek J Smith, Dan H Barouch","doi":"10.1016/j.celrep.2024.115140","DOIUrl":"10.1016/j.celrep.2024.115140","url":null,"abstract":"<p><p>Virus neutralization profiles against primary infection sera and corresponding antigenic cartography are integral part of the COVID-19 and influenza vaccine strain selection processes. Human single variant exposure sera have previously defined the antigenic relationships among SARS-CoV-2 variants but are now largely unavailable due to widespread population immunity. Therefore, antigenic characterization of future SARS-CoV-2 variants will require an animal model, analogous to using ferrets for influenza virus. We evaluated neutralization profiles against 23 SARS-CoV-2 variants in nonhuman primates (NHPs) after single variant exposure and generated an NHP-derived antigenic map. We identified a distant antigenic region occupied by BA.2.86, JN.1, and the descendants KP.2, KP.3, and KZ.1.1.1. We also found that the monovalent XBB.1.5 mRNA vaccine induced broad immunity against the mapped antigenic space. In addition, substantial concordance was observed between our NHP-derived and two human antigenic maps, demonstrating the utility of NHPs as a surrogate for antigenic cartography in humans.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115140"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926825","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}
引用次数: 0
Spike frequency adaptation in primate lateral prefrontal cortex neurons results from interplay between intrinsic properties and circuit dynamics. 灵长类动物外侧前额叶皮层神经元的脉冲频率适应是内在特性和电路动力学相互作用的结果。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-06 DOI: 10.1016/j.celrep.2024.115159
Nils A Koch, Benjamin W Corrigan, Michael Feyerabend, Roberto A Gulli, Michelle S Jimenez-Sosa, Mohamad Abbass, Julia K Sunstrum, Sara Matovic, Megan Roussy, Rogelio Luna, Samuel A Mestern, Borna Mahmoudian, Susheel Vijayraghavan, Hiroyuki Igarashi, Kartik S Pradeepan, William J Assis, J Andrew Pruszynski, Shreejoy Tripathy, Jochen F Staiger, Guillermo Gonzalez-Burgos, Andreas Neef, Stefan Treue, Stefan Everling, Wataru Inoue, Anmar Khadra, Julio C Martinez-Trujillo
{"title":"Spike frequency adaptation in primate lateral prefrontal cortex neurons results from interplay between intrinsic properties and circuit dynamics.","authors":"Nils A Koch, Benjamin W Corrigan, Michael Feyerabend, Roberto A Gulli, Michelle S Jimenez-Sosa, Mohamad Abbass, Julia K Sunstrum, Sara Matovic, Megan Roussy, Rogelio Luna, Samuel A Mestern, Borna Mahmoudian, Susheel Vijayraghavan, Hiroyuki Igarashi, Kartik S Pradeepan, William J Assis, J Andrew Pruszynski, Shreejoy Tripathy, Jochen F Staiger, Guillermo Gonzalez-Burgos, Andreas Neef, Stefan Treue, Stefan Everling, Wataru Inoue, Anmar Khadra, Julio C Martinez-Trujillo","doi":"10.1016/j.celrep.2024.115159","DOIUrl":"10.1016/j.celrep.2024.115159","url":null,"abstract":"<p><p>Cortical neurons in brain slices display intrinsic spike frequency adaptation (I-SFA) to constant current inputs, while extracellular recordings show extrinsic SFA (E-SFA) during sustained visual stimulation. Inferring how I-SFA contributes to E-SFA during behavior is challenging due to the isolated nature of slice recordings. To address this, we recorded macaque lateral prefrontal cortex (LPFC) neurons in vivo during a visually guided saccade task and in vitro in brain slices. Broad-spiking (BS) putative pyramidal cells and narrow-spiking (NS) putative inhibitory interneurons exhibit both E-SFA and I-SFA. Developing a data-driven hybrid circuit model comprising NS model neurons receiving BS input reveals that NS model neurons exhibit longer SFA than observed in vivo; however, adding feedforward inhibition corrects this in a manner dependent on I-SFA. Identification of this circuit motif shaping E-SFA in LPFC highlights the roles of both intrinsic and network mechanisms in neural activity underlying behavior.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115159"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945538","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}
引用次数: 0
Emotional stress increases GluA2 expression and potentiates fear memory via adenylyl cyclase 5. 情绪压力会增加GluA2的表达，并通过腺苷酸环化酶5增强恐惧记忆。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-08 DOI: 10.1016/j.celrep.2024.115180
Qian Yang, Ahmad Abdulla, Muhammad Farooq, Yoshihiro Ishikawa, Siqiong June Liu
{"title":"Emotional stress increases GluA2 expression and potentiates fear memory via adenylyl cyclase 5.","authors":"Qian Yang, Ahmad Abdulla, Muhammad Farooq, Yoshihiro Ishikawa, Siqiong June Liu","doi":"10.1016/j.celrep.2024.115180","DOIUrl":"10.1016/j.celrep.2024.115180","url":null,"abstract":"<p><p>Stress can alter behavior and contributes to psychiatric disorders by regulating the expression of the GluA2 AMPA receptor subunit. We have previously shown in mice that exposure to predator odor stress elevates GluA2 transcription in cerebellar molecular layer interneurons (MLIs), and MLI activity is required for fear memory consolidation. Here, we identified the critical involvement of adenylyl cyclase 5, in both the stress-induced increase in GluA2 in MLIs and the enhancement of fear memory. We found that noradrenaline release during predator odor stress activates AC5 and downstream PKA-CREB signaling. This pathway interacts synergistically with α1-adrenergic receptors to promote synaptic GluA2 expression in MLIs. At a behavioral level, predator odor stress potentiates associative fear memory, and this is abolished in AC5 knockout mice, suggesting that AC5-dependent plasticity is required for enhanced memory formation. Therefore, AC5 is a promising pharmacological target for preventing stress-enhanced fear memory.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115180"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945547","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}
引用次数: 0
G6PD deficiency triggers dopamine loss and the initiation of Parkinson's disease pathogenesis. G6PD缺乏症触发多巴胺丢失，启动帕金森病发病机制。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-07 DOI: 10.1016/j.celrep.2024.115178
Morgan G Stykel, Shehani V Siripala, Eric Soubeyrand, Carla L Coackley, Ping Lu, Suelen Camargo, Sharanya Thevasenan, Gerardo Balderas Figueroa, Raphaella W L So, Erica Stuart, Rachi Panchal, Elissavet-Kalliopi Akrioti, Jeffery T Joseph, Omid Haji-Ghassemi, Era Taoufik, Tariq A Akhtar, Joel C Watts, Scott D Ryan
{"title":"G6PD deficiency triggers dopamine loss and the initiation of Parkinson's disease pathogenesis.","authors":"Morgan G Stykel, Shehani V Siripala, Eric Soubeyrand, Carla L Coackley, Ping Lu, Suelen Camargo, Sharanya Thevasenan, Gerardo Balderas Figueroa, Raphaella W L So, Erica Stuart, Rachi Panchal, Elissavet-Kalliopi Akrioti, Jeffery T Joseph, Omid Haji-Ghassemi, Era Taoufik, Tariq A Akhtar, Joel C Watts, Scott D Ryan","doi":"10.1016/j.celrep.2024.115178","DOIUrl":"10.1016/j.celrep.2024.115178","url":null,"abstract":"<p><p>Loss of dopaminergic neurons in Parkinson's disease (PD) is preceded by loss of synaptic dopamine (DA) and accumulation of proteinaceous aggregates. Linking these deficits is critical to restoring DA signaling in PD. Using murine and human pluripotent stem cell (hPSC) models of PD coupled with human postmortem tissue, we show that accumulation of α-syn micro-aggregates impairs metabolic flux through the pentose phosphate pathway (PPP). This leads to decreased nicotinamide adenine dinucleotide phosphate (NADP/H) and glutathione (GSH) levels, resulting in DA oxidation and decreased total DA levels. We find that α-syn anchors the PPP enzyme G6PD to synaptic vesicles via the α-syn C terminus and that this interaction is lost in PD. Furthermore, G6PD clinical mutations are associated with PD diagnosis, and G6PD deletion phenocopies PD pathology. Finally, we show that restoring NADPH or GSH levels through genetic and pharmacological intervention blocks DA oxidation and rescues steady-state DA levels, identifying G6PD as a pharmacological target against PD.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115178"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945549","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}
引用次数: 0
Conserved patterns of transcriptional dysregulation, heterogeneity, and cell states in clear cell kidney cancer. 透明细胞肾癌中转录失调、异质性和细胞状态的保守模式。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-09 DOI: 10.1016/j.celrep.2024.115169
Olivia Lombardi, Ran Li, Faiz Jabbar, Hannah Evans, Silvia Halim, Joanna D C C Lima, Lisa Browning, Helen M Byrne, Hani Choudhry, Peter J Ratcliffe, David R Mole
{"title":"Conserved patterns of transcriptional dysregulation, heterogeneity, and cell states in clear cell kidney cancer.","authors":"Olivia Lombardi, Ran Li, Faiz Jabbar, Hannah Evans, Silvia Halim, Joanna D C C Lima, Lisa Browning, Helen M Byrne, Hani Choudhry, Peter J Ratcliffe, David R Mole","doi":"10.1016/j.celrep.2024.115169","DOIUrl":"10.1016/j.celrep.2024.115169","url":null,"abstract":"<p><p>Clear cell kidney cancers are characterized both by conserved oncogenic driver events and by marked intratumor genetic and phenotypic heterogeneity, which help drive tumor progression, metastasis, and resistance to therapy. How these are reflected in transcriptional programs within the cancer and stromal cell components remains an important question with the potential to drive novel therapeutic approaches to treating cancer. To better understand these programs, we perform single-cell transcriptomics on 75 multi-regional biopsies from kidney tumors and normal kidney. We identify conserved patterns of transcriptional dysregulation and their upstream regulators within the tumor and associated vasculature. We describe recurrent subclonal transcriptional consequences of Chr14q loss linked to metastatic potential. We identify prognostically significant conserved patterns of intratumor transcriptional heterogeneity. These reflect co-existing cell states found in both cancer cells and normal kidney cells, indicating that rather than arising from genetic heterogeneity they are a consequence of lineage plasticity.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115169"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142961975","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}
引用次数: 0
Transketolase attenuates the chemotherapy sensitivity of glioma cells by modulating R-loop formation. 转酮醇酶通过调节r环的形成来减弱胶质瘤细胞的化疗敏感性。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-09 DOI: 10.1016/j.celrep.2024.115142
Minjie Fu, Mengli Zhang, Licheng Zhang, Yuan Feng, Chao Gao, Hao Xu, Jinsen Zhang, Huaichao Zhang, Tianping Peng, Youjun Chu, Yonghe Wu, Pu Wang, Dan Ye, Ying Mao, Wei Hua
{"title":"Transketolase attenuates the chemotherapy sensitivity of glioma cells by modulating R-loop formation.","authors":"Minjie Fu, Mengli Zhang, Licheng Zhang, Yuan Feng, Chao Gao, Hao Xu, Jinsen Zhang, Huaichao Zhang, Tianping Peng, Youjun Chu, Yonghe Wu, Pu Wang, Dan Ye, Ying Mao, Wei Hua","doi":"10.1016/j.celrep.2024.115142","DOIUrl":"10.1016/j.celrep.2024.115142","url":null,"abstract":"<p><p>Glioblastoma (GBM) is a highly lethal malignant brain tumor with poor survival rates, and chemoresistance poses a significant challenge to the treatment of patients with GBM. Here, we show that transketolase (TKT), a metabolic enzyme in the pentose phosphate pathway (PPP), attenuates the chemotherapy sensitivity of glioma cells in a manner independent of catalytic activity. Mechanistically, chemotherapeutic drugs can facilitate the translocation of TKT protein from the cytosol into the nucleus, where TKT physically interacts with XRN2 to regulate the resolution and removal of R-loops. Depletion of TKT leads to increased R-loop accumulation and genome instability, increasing the susceptibility of glioma cells to chemotherapy. In conclusion, our study reveals a non-metabolic function of TKT in regulating R-loop dynamics, genome instability, and chemotherapy sensitivity in gliomas.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115142"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962039","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}
引用次数: 0
Dietary selective effects manifest in the human gut microbiota from species composition to strain genetic makeup. 饮食选择效应体现在人类肠道微生物群从物种组成到菌株基因组成。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-17 DOI: 10.1016/j.celrep.2025.115252
Kun D Huang, Mattea Müller, Pavaret Sivapornnukul, Agata Anna Bielecka, Lena Amend, Caroline Tawk, Anja Bruns, Till-Robin Lesker, Andreas Hahn, Till Strowig
{"title":"Dietary selective effects manifest in the human gut microbiota from species composition to strain genetic makeup.","authors":"Kun D Huang, Mattea Müller, Pavaret Sivapornnukul, Agata Anna Bielecka, Lena Amend, Caroline Tawk, Anja Bruns, Till-Robin Lesker, Andreas Hahn, Till Strowig","doi":"10.1016/j.celrep.2025.115252","DOIUrl":"10.1016/j.celrep.2025.115252","url":null,"abstract":"","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115252"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000732","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}
引用次数: 0
MetA is a ''thermal fuse'' that inhibits growth and protects Escherichia coli at elevated temperatures. MetA是一种“热保险丝”，在高温下抑制生长并保护大肠杆菌。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-18 DOI: 10.1016/j.celrep.2025.115257
Severin J Schink, Zara Gough, Elena Biselli, Mariel Garcia Huiman, Yu-Fang Chang, Markus Basan, Ulrich Gerland
{"title":"MetA is a ''thermal fuse'' that inhibits growth and protects Escherichia coli at elevated temperatures.","authors":"Severin J Schink, Zara Gough, Elena Biselli, Mariel Garcia Huiman, Yu-Fang Chang, Markus Basan, Ulrich Gerland","doi":"10.1016/j.celrep.2025.115257","DOIUrl":"10.1016/j.celrep.2025.115257","url":null,"abstract":"","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115257"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000782","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}
引用次数: 0
CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells.
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2025-01-22 DOI: 10.1016/j.celrep.2024.115211
Kiel T Tietz, Braedan M McCluskey, Conor R Miller, Yingming Li, Sarah A Munro, Scott M Dehm
{"title":"CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells.","authors":"Kiel T Tietz, Braedan M McCluskey, Conor R Miller, Yingming Li, Sarah A Munro, Scott M Dehm","doi":"10.1016/j.celrep.2024.115211","DOIUrl":"10.1016/j.celrep.2024.115211","url":null,"abstract":"<p><p>Localized prostate cancer can be cured by radiation or surgery, but advanced prostate cancer continues to be a clinical challenge. Altered alternative polyadenylation occurs in numerous cancers and can downregulate tumor-suppressor genes and upregulate oncogenes. We found that the cleavage and polyadenylation specificity factor (CPSF) complex factor CPSF1 is upregulated in patients with advanced prostate cancer, with high CPSF1 expression correlating with worse progression-free survival. Knockdown of CPSF1 selectively inhibited the growth of prostate cancer cells and reduced glycolytic output. Evaluating the changes in global poly(A) site usage in prostate cancer cells following CPSF1 knockdown revealed widespread usage of intergenic poly(A) sites distal to annotated 3' UTRs, which lengthened 3' UTRs and decreased levels of thousands of mRNAs, including key glycolysis genes. These findings uncover a role for CPSF1 in the suppression of intergenic poly(A) sites in prostate cancer and nominate CPSF1 as a therapeutic target in advanced prostate cancer.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 1","pages":"115211"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028046","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}
引用次数: 0
A nonsecretory antimicrobial peptide mediates inflammatory organ damage in Drosophila renal tubules. 一种非分泌性抗菌肽介导果蝇肾小管的炎症性器官损伤。
IF 7.5 1区 生物学
Cell reports Pub Date : 2025-01-28 Epub Date: 2024-12-23 DOI: 10.1016/j.celrep.2024.115082
Ayano Oi, Natsuki Shinoda, Shun Nagashima, Masayuki Miura, Fumiaki Obata
{"title":"A nonsecretory antimicrobial peptide mediates inflammatory organ damage in Drosophila renal tubules.","authors":"Ayano Oi, Natsuki Shinoda, Shun Nagashima, Masayuki Miura, Fumiaki Obata","doi":"10.1016/j.celrep.2024.115082","DOIUrl":"10.1016/j.celrep.2024.115082","url":null,"abstract":"<p><p>An excessive immune response damages organs, yet its molecular mechanism is incompletely understood. Here, we screened a factor mediating organ damage upon genetic activation of the innate immune pathway using Drosophila renal tubules. We found that an antimicrobial peptide, Attacin-D (AttD), causes organ damage upon immune deficiency (Imd) pathway activation in the Malpighian tubules. Loss of AttD function suppresses most of the pathological phenotypes induced by Imd activation, such as cell death, bloating of the whole animal, and mortality, without compromising the immune activation. AttD is required for the immune-induced damage specifically in the Malpighian tubules and not the midgut. Unlike other antimicrobial peptides, AttD lacks a signal peptide and stays inside tubular cells, potentially damaging the tubular cells via aggregation and oligomerization. Suppression of AttD almost completely attenuates the pathology caused by a gut-tumor-induced immune activation. Our study elucidates the mechanistic effector of immune-induced organ damage.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":" ","pages":"115082"},"PeriodicalIF":7.5,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142884977","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}
引用次数: 0
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