Communications Biology最新文献_第4页

Systematic mRNA interactome analysis reconceptualizes translational quiescence in bovine sperm. 系统的mRNA相互作用组分析重新定义了牛精子的翻译静止。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-03 DOI: 10.1038/s42003-025-08919-7

Saurabh Tiwari, Nehal Thakor, Jacob Thundathil

{"title":"Systematic mRNA interactome analysis reconceptualizes translational quiescence in bovine sperm.","authors":"Saurabh Tiwari, Nehal Thakor, Jacob Thundathil","doi":"10.1038/s42003-025-08919-7","DOIUrl":"10.1038/s42003-025-08919-7","url":null,"abstract":"Ejaculated mammalian sperm must undergo a series of biochemical changes called capacitation to gain fertilizing competence. Mounting evidence on protein synthesis during capacitation contradicts the widely accepted dogma of translational quiescence in sperm. However, mechanisms regulating mRNA translation in sperm is ambiguous, necessitating elucidation and understanding its role in enabling fertilizing competence. Here, we perform proteome analysis from bovine sperm and identify proteins involved in translation, encompassing initiation and elongation factors, ribosomal proteins, tRNA synthetase, ligase, and RNA-binding proteins (RBPs) involved in mRNA export, degradation, and binding. We further explore the mRNA-binding activity of RBPs during capacitation, identifying 48 RBPs; 13 and 8 RBPs were exclusive to fresh-uncapacitated and capacitation groups, respectively, with an overlap of 27 RBPs present in both groups. Interestingly, cytoskeletal proteins and metabolic enzymes associate differentially with mRNAs during capacitation. Since phosphorylation is a known regulatory mechanism dynamically modulating RBPs' interactions with mRNAs, we performed sperm phosphoproteome analysis, revealing few RBPs to phosphorylate during capacitation. These observations suggest that RNA-binding functions of these proteins are coupled with capacitation-associated phosphorylation events, enabling concomitant protein synthesis and fertilizing competence in sperm. These findings will assist in elucidating translational regulation of mRNA in sperm and advancing our knowledge in regulation of male fertility.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1419"},"PeriodicalIF":5.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

T3SS effector EseJ in Edwardsiella piscicida inhibits PANoptosis in macrophages. 鱼氏爱德华菌T3SS效应体EseJ抑制巨噬细胞PANoptosis。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-03 DOI: 10.1038/s42003-025-08823-0

Tian Tian He, Pu Yu Tang, Xiu Long Jiang, Shan Shan Sun, Pin Nie, Hai Xia Xie

{"title":"T3SS effector EseJ in Edwardsiella piscicida inhibits PANoptosis in macrophages.","authors":"Tian Tian He, Pu Yu Tang, Xiu Long Jiang, Shan Shan Sun, Pin Nie, Hai Xia Xie","doi":"10.1038/s42003-025-08823-0","DOIUrl":"10.1038/s42003-025-08823-0","url":null,"abstract":"Edwardsiella piscicida T3SS protein EseJ plays a dual role. As a regulator, EseJ suppresses type 1 fimbriae, inhibiting macrophage apoptosis stimulated by FimH. As an effector, it promotes E. piscicida replication in host cells. In this study, the mechanism of EseJ in converting apoptotic cell rounding to pyroptotic cell rupture in murine macrophages was explored. Overexpressing EseJ in the ΔfimH strain suppresses pyroptosis in murine macrophages by deactivating the caspase-8 and NLRP3 inflammasome. This is evidenced by pretreatment with the pharmacological inhibitors z-IETD-fmk (a caspase-8 inhibitor) and MCC950 (an NLRP3 inhibitor), or by knocking down caspase-8 and NLRP3. This finding lends support to the idea that EseJ is involved in the inhibition of pyroptosis. Furthermore, EseJ translocation significantly increased the phosphorylation of TAK1, while reducing necroptosis, which is driven by the activation of receptor-interacting protein kinase 1 (RIPK1) and the phosphorylation of mixed lineage kinase domain-like (p-MLKL). Therefore, EseJ inhibits PANoptosis (pyroptosis, apoptosis and necroptosis) by activating TAK1 and disrupting the formation of the NLRP3-caspase-8-RIPK1 PANoptosome. Interestingly, E. piscicida is attenuated upon EseJ depletion, especially in the early phase after infection. These findings reveal a new way in which E. piscicida circumvents host cell death pathways, thereby increasing its virulence.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1420"},"PeriodicalIF":5.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

How SecB maintains clients in a translocation competent state. SecB如何维持客户处于易位胜任状态。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-03 DOI: 10.1038/s42003-025-08821-2

Guillaume Roussel, Jochem H Smit, Dries Smets, Spyridoula Karamanou, Anastassios Economou

{"title":"How SecB maintains clients in a translocation competent state.","authors":"Guillaume Roussel, Jochem H Smit, Dries Smets, Spyridoula Karamanou, Anastassios Economou","doi":"10.1038/s42003-025-08821-2","DOIUrl":"10.1038/s42003-025-08821-2","url":null,"abstract":"Bacterial secretory proteins must remain soluble and non-folded until they reach the SecYEG translocase. Preprotein intrinsic features and chaperones can delay protein folding. The SecB chaperone is known to delay folding of some proteins, however the link between the folding state of a client and its interaction with SecB, until the client-transfer to the translocase remains elusive. This study unravels how a model client, maltose binding protein (MBP), is kept in a non-folded state by SecB. Using single-molecule FRET and hydrogen-deuterium exchange mass spectrometry, we describe in detail the folding pathway of the client and demonstrate that SecB acts first as an unfoldase, reverting partial folding and then as holdase, preventing folding. The presence of an SP delays the folding and stabilizes the client to SecB interaction. Single-point mutations that abolish formation of some foldons drastically increase the lifetime of the SecB-bound state. Towards delivery to the translocase, SecA interacts with the MBP:SecB complex forming a quaternary super-assembly thus, further stabilizing the disordered state of the client. Collectively, our study demonstrates the interplay between secretory chaperones and a model client, with SecB combining unfoldase and holdase activities to retain the client in a translocation-competent state while SecA secures this complex until later translocation.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1421"},"PeriodicalIF":5.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Estradiol and dihydrotestosterone exert sex-specific effects on human fibroblast and endothelial proliferation, bioenergetics, and vasculogenesis. 雌二醇和双氢睾酮对人成纤维细胞和内皮细胞增殖、生物能量学和血管生成具有性别特异性作用。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-03 DOI: 10.1038/s42003-025-08822-1

Ashley T Martier, Yasmin V Maurice, K Michael Conrad, Delia A Carlino, Franck Mauvais-Jarvis, Mark J Mondrinos

{"title":"Estradiol and dihydrotestosterone exert sex-specific effects on human fibroblast and endothelial proliferation, bioenergetics, and vasculogenesis.","authors":"Ashley T Martier, Yasmin V Maurice, K Michael Conrad, Delia A Carlino, Franck Mauvais-Jarvis, Mark J Mondrinos","doi":"10.1038/s42003-025-08822-1","DOIUrl":"10.1038/s42003-025-08822-1","url":null,"abstract":"Sex-specific cell culture methods and microphysiological systems can enhance our understanding of how biological sex influences health and disease. Here, we investigated the effects of estradiol and dihydrotestosterone on primary human lung and ocular fibroblasts as well as in human umbilical vein and retinal microvascular endothelial cells from both female and male donors. Treatment of female cells with estradiol and male cells with dihydrotestosterone in 2D culture significantly enhanced proliferation, mitochondrial membrane potential, and upregulated genes associated with bioenergetics and stress responses. Conversely, treatment of female cells with dihydrotestosterone and of male cells with estradiol decreased bioenergetic potential and inhibited cell proliferation. A microphysiological model of bulk tissue vasculogenesis revealed that estradiol enhances vasculogenesis in female tissues and inhibits vasculogenesis in male tissues. Collectively, these findings demonstrate that the sex hormone composition of culture medium significantly influences bioassay readouts in a sex-specific manner.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1422"},"PeriodicalIF":5.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Metabolomic landscape of fetal organ development during late gestation in mice. 小鼠妊娠后期胎儿器官发育的代谢组学景观。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-03 DOI: 10.1038/s42003-025-08820-3

Chanyi Li, Wuping Liu, Xiaodong Li, Bo Lv, Jiaying Qin, Ning Yi, Bianling Xu, Jing Xu, Zhigang Xue, Hongli Yan, Jinfeng Xue

{"title":"Metabolomic landscape of fetal organ development during late gestation in mice.","authors":"Chanyi Li, Wuping Liu, Xiaodong Li, Bo Lv, Jiaying Qin, Ning Yi, Bianling Xu, Jing Xu, Zhigang Xue, Hongli Yan, Jinfeng Xue","doi":"10.1038/s42003-025-08820-3","DOIUrl":"10.1038/s42003-025-08820-3","url":null,"abstract":"Metabolism is the critical basis for mammalian physiological functions. The systematic metabolic characteristics of major organ development during late gestation to adapt to postnatal environmental changes are still absent. Here, we detected metabolic patterns of the ICR mouse fetal organs, including the heart, stomach, liver, brain, and placenta, from embryonic days (E)15.5 to 19.5 using liquid chromatography-mass spectrometry combined with RNA sequencing and proteomics data. Our metabolic and multi-omics data showed that organs exhibited their unique metabolic characteristics during late gestation, and significant metabolic pattern transitions, especially the enhancement of digesting the fatty acids and proteins, occurred at the E16.5 to E18.5 stage. Additionally, we found the abundance of carnosine and histidine in the placenta may serve as a way to test their levels in the newborn brain in vitro. Our dataset provides a comprehensive metabolic landscape of mammalian organ development in late gestation.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1423"},"PeriodicalIF":5.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12494810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver. ABCC4通过抑制肝脏中LDLR的表达而损害血浆LDL胆固醇的清除。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-02 DOI: 10.1038/s42003-025-08818-x

Jiaxin Chen, Hui Huang, Chi Chen, Guofang Xia, Hao Huang, Yan Xiong, Peng Luo, Yu Chen, Jinsong Li, Liang Wen, Lu Li, Jing Lin, Guangre Xu, Chenzhang Ji, Wenjie Tian, Jin Zhou, Peng Wei, Chengxing Shen, Xiaoqing Wang

{"title":"ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver.","authors":"Jiaxin Chen, Hui Huang, Chi Chen, Guofang Xia, Hao Huang, Yan Xiong, Peng Luo, Yu Chen, Jinsong Li, Liang Wen, Lu Li, Jing Lin, Guangre Xu, Chenzhang Ji, Wenjie Tian, Jin Zhou, Peng Wei, Chengxing Shen, Xiaoqing Wang","doi":"10.1038/s42003-025-08818-x","DOIUrl":"10.1038/s42003-025-08818-x","url":null,"abstract":"Low expression level of low-density lipoprotein receptor (LDLR) in hepatocytes leads to hypercholesterolemia and eventually contributes to atherosclerotic cardiovascular disease (ASCVD). Here, we report that inhibition of hepatocyte ABCC4, identified as a top hit from large-scale CRISPR/Cas9 screens, significantly increases hepatic LDLR abundance and enhances LDL cholesterol clearance. As a hepatic transporter for cAMP efflux, ABCC4 silencing alters its intracellular distribution and activates the downstream Epac2/Rap1a signaling pathway, which ultimately blocks PCSK9 protein expression, thereby preventing lysosomal degradation of LDLR. Furthermore, in both male mice and cell models, we demonstrate that liver-specific disruption and pharmacological inhibition of ABCC4 elevate hepatic plasma membrane LDLR levels and reduce plasma LDL cholesterol through ABCC4-cAMP-PCSK9 pathway. Collectively, our genome-wide CRISPR screening offers a valuable resource for identifying LDLR modifiers, providing potential insights for therapeutic strategies in hypercholesterolemia and atherosclerosis.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1414"},"PeriodicalIF":5.1,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ODBAE: a high-performance model identifying complex phenotypes in high-dimensional biological datasets. ODBAE：在高维生物数据集中识别复杂表型的高性能模型。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-02 DOI: 10.1038/s42003-025-08817-y

Yafei Shen, Tao Zhang, Zhiwei Liu, Kalliopi Kostelidou, Ying Xu, Ling Yang

{"title":"ODBAE: a high-performance model identifying complex phenotypes in high-dimensional biological datasets.","authors":"Yafei Shen, Tao Zhang, Zhiwei Liu, Kalliopi Kostelidou, Ying Xu, Ling Yang","doi":"10.1038/s42003-025-08817-y","DOIUrl":"10.1038/s42003-025-08817-y","url":null,"abstract":"Identifying complex phenotypes from high-dimensional biological data is challenging due to the intricate interdependencies among different physiological indicators. Traditional approaches often focus on detecting outliers in single variables, overlooking the broader network of interactions that contribute to phenotype emergence. Here, we introduce ODBAE (Outlier Detection using Balanced Autoencoders), a machine learning method designed to uncover both subtle and extreme outliers by capturing latent relationships among multiple physiological parameters. ODBAE's revised loss function enhances its ability to detect two key types of outliers: influential points (IP), which disrupt latent correlations between dimensions, and high leverage points (HLP), which deviate from the norm but go undetected by traditional autoencoder-based methods. Using data from the International Mouse Phenotyping Consortium (IMPC), we show that ODBAE can identify knockout mice with complex, multi-indicator phenotypes-normal in individual traits, but abnormal when considered together. In addition, this method reveals novel metabolism-related genes and uncovers coordinated abnormalities across metabolic indicators. Our results highlight the utility of ODBAE in detecting joint abnormalities and advancing our understanding of homeostatic perturbations in biological systems.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1415"},"PeriodicalIF":5.1,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ComK2 represses competence development for natural transformation in Staphylococcus aureus grown under strong oxygen limitation. ComK2抑制在强氧限制下生长的金黄色葡萄球菌自然转化的能力发展。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-02 DOI: 10.1038/s42003-025-08816-z

Shi Yuan Feng, Yannis Arab, Yolande Hauck, Pierre Poirette, Magali Noiray, Sophie Quevillon-Cheruel, Stéphanie Marsin, Jessica Andreani, Nicolas Mirouze

{"title":"ComK2 represses competence development for natural transformation in Staphylococcus aureus grown under strong oxygen limitation.","authors":"Shi Yuan Feng, Yannis Arab, Yolande Hauck, Pierre Poirette, Magali Noiray, Sophie Quevillon-Cheruel, Stéphanie Marsin, Jessica Andreani, Nicolas Mirouze","doi":"10.1038/s42003-025-08816-z","DOIUrl":"10.1038/s42003-025-08816-z","url":null,"abstract":"The facultative anaerobe and major human pathogen Staphylococcus aureus is able to sustain growth under a wide range of oxygen concentrations. Importantly, we have already demonstrated that under microaerobic conditions, sensed by the two-component system SrrAB, S. aureus efficiently induces the development of competence for natural transformation, one of the three main horizontal gene transfer mechanisms present in bacteria. Here, we show that when the oxygen concentration decreases even further (reaching almost anaerobic conditions) the development of competence for natural transformation is still allowed but with much less efficiency than under microaerobic conditions. This inhibition is controlled by a central competence regulator, named ComK2, that was not found involved under intermediate oxygen concentrations. This ComK2-dependent inhibitory pathway also involves the SA2107 protein, of unknown function, through a direct protein-protein interaction. Finally, we demonstrate that this inhibition of competence is controlled by this strong oxygen limitation, sensed by another two-component system named NreBC, probably involved in the same pathway as ComK2 and SA2107. All in all, our results show that the oxygen concentration, which varies drastically depending on the site in the human body but also during bacterial infections, is a key environmental factor that tightly modulates S. aureus genomic plasticity.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1416"},"PeriodicalIF":5.1,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A genomic view of the bacterial family Endozoicomonadaceae in marine symbioses. 海洋共生细菌家族内生单胞菌科的基因组观。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-02 DOI: 10.1038/s42003-025-08828-9

Daniela M G da Silva, Rodrigo Costa, Tina Keller-Costa

引用次数: 0

BCL11A deficiency protects epidermis from UVB-induced damage through promotion of autophagy. BCL11A缺乏通过促进自噬来保护表皮免受uvb诱导的损伤。

IF 5.1 1区生物学

Communications Biology Pub Date : 2025-10-02 DOI: 10.1038/s42003-025-08814-1

Xuyi Deng, Hui Liu, Xiaoxu Wang, Xinfeng Dong, Zhengzheng Fu, Xinli Niu, Zhi Guo, Peiqi Lian, Yinyun Deng, Zhenhua Ding, Yinghui Wang, Meijuan Zhou

{"title":"BCL11A deficiency protects epidermis from UVB-induced damage through promotion of autophagy.","authors":"Xuyi Deng, Hui Liu, Xiaoxu Wang, Xinfeng Dong, Zhengzheng Fu, Xinli Niu, Zhi Guo, Peiqi Lian, Yinyun Deng, Zhenhua Ding, Yinghui Wang, Meijuan Zhou","doi":"10.1038/s42003-025-08814-1","DOIUrl":"10.1038/s42003-025-08814-1","url":null,"abstract":"As a major environmental pathogenic factor for various skin diseases, UVB radiation leads to oxidative stress and biomacromolecule damage. Autophagy is a highly conserved catabolic process and serves as one of the main mechanisms to maintain cellular homeostasis. Here, by CRISPR/Cas9-mediated gene deletion, we demonstrate that the essential transcriptional repressor BCL11A is involved in autophagy regulation and participates in the UVB-induced stress response. BCL11A deficiency increases autophagosome formation and enhances the intensity of autophagy flux with or without UVB stress. Mechanistically, ACSS3, rather than autophagy-related genes, is identified as the direct target gene and transcriptionally repressed by BCL11A. Further, BCL11A deficiency reduces DNA damage and ROS to promote survival and inhibit apoptosis under UVB irradiation, which is blocked by pharmacological inhibition of autophagy or BCL11A overexpression. Collectively, BCL11A deficiency promotes autophagy activation to clear ROS and DNA damage, thereby protecting epidermal cells from UVB-induced death.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"1417"},"PeriodicalIF":5.1,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12491459/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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