The tumor suppressor BRCA1-associated protein 1 (BAP1) encodes a nuclear deubiquitinase that specifically removes H2A monoubiquitination at Lys119 (H2Aub) and plays a crucial role in the epigenetic regulation of gene expression through cooperating with several transcriptional factors and chromatin-modifying enzymes. Our previous studies have confirmed that BAP1 represses SLC7A11-mediated cystine metabolism and promotes ferroptosis-dependent tumor suppression. However, how BAP1 regulates gene expression at the genome level and whether additional mechanisms are involved in the BAP1 regulation of ferroptosis remain unclear. Here, we integrate multi-omics analyses to explore the effects of BAP1-mediated H2Aub deubiquitination on the regulation of chromatin accessibility and gene transcription. Notably, we identified a novel target gene, ACSL4, which is positively regulated by BAP1 and contributes to BAP1-mediated ferroptosis. Importantly, genetic knockout or pharmacological inhibition of ACSL4 prevents the upregulation of lipid biosynthesis and ferroptotic cell death caused by BAP1. In addition, we demonstrated that BAP1-mediated regulation of gene expression and ferroptosis is dependent on ASXL family members instead of other BAP1-associated factors like FOXK1/2, HCFC1, and OGT. Together, our findings uncover a previously unappreciated epigenetic mechanism underlying the regulation of ACSL4 by H2A monoubiquitination, which connects ACSL4-mediated lipid metabolism to ferroptosis driven by BAP1, providing new insights into the understanding of metabolic regulation of BAP1-related diseases such as cancers.
肿瘤抑制因子BRCA1-associated protein 1 （BAP1）编码核去泛素酶，特异性去除Lys119位点的H2A单泛素化（H2Aub），并通过与多种转录因子和染色质修饰酶合作，在基因表达的表观遗传调控中发挥重要作用。我们之前的研究证实BAP1抑制slc7a11介导的胱氨酸代谢，促进铁中毒依赖性肿瘤抑制。然而，BAP1如何在基因组水平调控基因表达，以及BAP1对铁下垂的调控是否涉及其他机制尚不清楚。在这里，我们结合多组学分析来探讨bap1介导的H2Aub去泛素化对染色质可及性和基因转录调控的影响。值得注意的是，我们发现了一个新的靶基因ACSL4，该基因受BAP1的正调控，并参与BAP1介导的铁下垂。重要的是，基因敲除或药理抑制ACSL4可防止BAP1引起的脂质生物合成上调和铁致细胞死亡。此外，我们证明了bap1介导的基因表达和铁凋亡的调节依赖于ASXL家族成员，而不是其他bap1相关因子，如FOXK1/2、HCFC1和OGT。总之，我们的研究结果揭示了H2A单泛素化调控ACSL4的一个以前未被认识到的表观遗传机制，该机制将ACSL4介导的脂质代谢与BAP1驱动的铁死亡联系起来，为理解BAP1相关疾病（如癌症）的代谢调节提供了新的见解。
{"title":"Epigenetic regulation of ACSL4 via H2A monoubiquitylation connects lipid metabolism to BAP1-mediated ferroptosis","authors":"Kexin Fan, Shuting Zhou, Yakun Ren, Jingwen Xiong, Hua Wang, Yaxin Fu, Yuhan Chen, Bobo Wang, Kun Fan, Min Gao, Tingli Guo, Xiaofeng Wei, Lianying Jiao, Jiejun Shi, Chenguang Ding, Yilei Zhang","doi":"10.1038/s41418-025-01624-2","DOIUrl":"https://doi.org/10.1038/s41418-025-01624-2","url":null,"abstract":"The tumor suppressor BRCA1-associated protein 1 (BAP1) encodes a nuclear deubiquitinase that specifically removes H2A monoubiquitination at Lys119 (H2Aub) and plays a crucial role in the epigenetic regulation of gene expression through cooperating with several transcriptional factors and chromatin-modifying enzymes. Our previous studies have confirmed that BAP1 represses SLC7A11-mediated cystine metabolism and promotes ferroptosis-dependent tumor suppression. However, how BAP1 regulates gene expression at the genome level and whether additional mechanisms are involved in the BAP1 regulation of ferroptosis remain unclear. Here, we integrate multi-omics analyses to explore the effects of BAP1-mediated H2Aub deubiquitination on the regulation of chromatin accessibility and gene transcription. Notably, we identified a novel target gene, ACSL4, which is positively regulated by BAP1 and contributes to BAP1-mediated ferroptosis. Importantly, genetic knockout or pharmacological inhibition of ACSL4 prevents the upregulation of lipid biosynthesis and ferroptotic cell death caused by BAP1. In addition, we demonstrated that BAP1-mediated regulation of gene expression and ferroptosis is dependent on ASXL family members instead of other BAP1-associated factors like FOXK1/2, HCFC1, and OGT. Together, our findings uncover a previously unappreciated epigenetic mechanism underlying the regulation of ACSL4 by H2A monoubiquitination, which connects ACSL4-mediated lipid metabolism to ferroptosis driven by BAP1, providing new insights into the understanding of metabolic regulation of BAP1-related diseases such as cancers.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"20 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145609205","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}
Pub Date : 2025-11-26DOI: 10.1038/s41418-025-01623-3
Ine Koeken, Magali Walravens, Roberto Fernández-Acosta, Ruben Van Hoyweghen, Iuliana Vintea, Yingyi Kong, Bianka Golba, Jonas Dehairs, Ali Talebi, Johannes V. Swinnen, Kaat Durinck, Adriana Mañas, Shinya Toyokuni, Gerben Menschaert, Maria Fedorova, Bruno G. De Geest, Behrouz Hassannia, Tom Vanden Berghe
Ferroptosis—an iron-dependent form of cell death triggered by phospholipid peroxidation—has emerged as a promising therapeutic avenue in cancer treatment. Although neuroblastoma (NB) has been identified as a ferroptosis susceptible cancer, our studies reveal striking heterogeneity in ferroptosis sensitivity across high-risk NB models. Through a targeted metabolic compound screen, we identified stearoyl-CoA desaturase 1 (SCD1)—a key enzyme in monounsaturated fatty acid (MUFA) synthesis—as a robust ferroptosis-sensitizing target. Genetic and pharmacological inhibition of SCD1 restored ferroptosis sensitivity in resistant NB cells. Notably, high SCD1 expression correlates with poor patient prognosis. Co-treatment with arachidonic acid (AA), a polyunsaturated fatty acid (PUFA), further enhanced ferroptotic cell death via increased PUFA/MUFA ratio. Nevertheless, neither baseline lipidomic profiles nor transcriptomes of key ferroptosis regulators reliably predicted ferroptosis sensitivity. To overcome AA’s poor solubility, we engineered AA-loaded lipid nanoparticles (AA-LNPs), which selectively accumulated in high-risk NB tumors and synergized with SCD1 inhibition. This dual-sensitization strategy, termed LipidSens, significantly suppressed tumor growth and induced ferroptosis in cell-derived xenograft mouse models without systemic toxicity. Together, these findings establish MUFA synthesis blockade and PUFA enrichment as a tumor-targeted, ferroptosis-enhancing strategy, and offer a nanomedicine-based therapeutic platform for high-risk NB.
{"title":"Dual lipid modulation overcomes ferroptosis resistance in high-risk neuroblastoma","authors":"Ine Koeken, Magali Walravens, Roberto Fernández-Acosta, Ruben Van Hoyweghen, Iuliana Vintea, Yingyi Kong, Bianka Golba, Jonas Dehairs, Ali Talebi, Johannes V. Swinnen, Kaat Durinck, Adriana Mañas, Shinya Toyokuni, Gerben Menschaert, Maria Fedorova, Bruno G. De Geest, Behrouz Hassannia, Tom Vanden Berghe","doi":"10.1038/s41418-025-01623-3","DOIUrl":"https://doi.org/10.1038/s41418-025-01623-3","url":null,"abstract":"Ferroptosis—an iron-dependent form of cell death triggered by phospholipid peroxidation—has emerged as a promising therapeutic avenue in cancer treatment. Although neuroblastoma (NB) has been identified as a ferroptosis susceptible cancer, our studies reveal striking heterogeneity in ferroptosis sensitivity across high-risk NB models. Through a targeted metabolic compound screen, we identified stearoyl-CoA desaturase 1 (SCD1)—a key enzyme in monounsaturated fatty acid (MUFA) synthesis—as a robust ferroptosis-sensitizing target. Genetic and pharmacological inhibition of SCD1 restored ferroptosis sensitivity in resistant NB cells. Notably, high SCD1 expression correlates with poor patient prognosis. Co-treatment with arachidonic acid (AA), a polyunsaturated fatty acid (PUFA), further enhanced ferroptotic cell death via increased PUFA/MUFA ratio. Nevertheless, neither baseline lipidomic profiles nor transcriptomes of key ferroptosis regulators reliably predicted ferroptosis sensitivity. To overcome AA’s poor solubility, we engineered AA-loaded lipid nanoparticles (AA-LNPs), which selectively accumulated in high-risk NB tumors and synergized with SCD1 inhibition. This dual-sensitization strategy, termed LipidSens, significantly suppressed tumor growth and induced ferroptosis in cell-derived xenograft mouse models without systemic toxicity. Together, these findings establish MUFA synthesis blockade and PUFA enrichment as a tumor-targeted, ferroptosis-enhancing strategy, and offer a nanomedicine-based therapeutic platform for high-risk NB.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"16 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145609460","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}
Pub Date : 2025-11-25DOI: 10.1038/s41418-025-01618-0
Ismael Sánchez-Vera, Ana M. Cosialls, Nekane Maritorena-Hualde, Max-Hinderk Schuler, Rodolfo Lavilla, Gabriel Pons, Lucas T. Jae, Daniel Iglesias-Serret, Joan Gil
{"title":"Targeting prohibitins activates the ISR through DELE1-HRI by impairing protein import into the mitochondrial matrix","authors":"Ismael Sánchez-Vera, Ana M. Cosialls, Nekane Maritorena-Hualde, Max-Hinderk Schuler, Rodolfo Lavilla, Gabriel Pons, Lucas T. Jae, Daniel Iglesias-Serret, Joan Gil","doi":"10.1038/s41418-025-01618-0","DOIUrl":"https://doi.org/10.1038/s41418-025-01618-0","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"120 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145599436","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}
Pub Date : 2025-11-24DOI: 10.1038/s41418-025-01622-4
Yonghwan Shin, Sungmin Kim, Suhn K. Rhie, Woojin An
{"title":"HDAC1 has intrinsic protease activity and regulates transcription through clipping histone H3 N-terminal tail","authors":"Yonghwan Shin, Sungmin Kim, Suhn K. Rhie, Woojin An","doi":"10.1038/s41418-025-01622-4","DOIUrl":"https://doi.org/10.1038/s41418-025-01622-4","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"187 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145583229","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}
Pub Date : 2025-11-21DOI: 10.1038/s41418-025-01625-1
Runa Wang, Guizhi Guo, Renshuai Zhang, Lin Li, Yingxin Gong, Long Yin, Shuhua Li, Changfeng Wei, Jun Zhou, Min Liu, Jie Ran
{"title":"UFL1-mediated UFMylation antagonizes IFT88 ubiquitination and degradation to maintain ciliary homeostasis","authors":"Runa Wang, Guizhi Guo, Renshuai Zhang, Lin Li, Yingxin Gong, Long Yin, Shuhua Li, Changfeng Wei, Jun Zhou, Min Liu, Jie Ran","doi":"10.1038/s41418-025-01625-1","DOIUrl":"https://doi.org/10.1038/s41418-025-01625-1","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"186 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145559931","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}
Pub Date : 2025-11-21DOI: 10.1038/s41418-025-01613-5
Sabrina Zema, Francesca Di Fazio, Maria Pelullo, Sara Di Savino, Bruna Cerbelli, Martina Leopizzi, Laura Di Magno, Carmine Nicoletti, Giovanna Peruzzi, Daniel D’Andrea, Maria V. Giuli, Samantha Cialfi, Biagio Palmisano, Alice Turdo, Rocco Palermo, Giulia d’Amati, Gianluca Canettieri, Antongiulio Faggiano, Lucia Di Marcotullio, Matilde Todaro, Isabella Screpanti, Claudio Talora, Saula Checquolo, Diana Bellavia
Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous breast cancer subtype with poor patient outcomes. TNBC heterogeneity arises from multiple dysregulated pathways, including Notch and Hedgehog, which contribute to tumor initiation, progression, and drug resistance. Identifying common molecular regulators of TNBC aggressiveness is crucial for developing effective therapeutic strategies. Here, we demonstrate that the transcriptional coactivator MAML1 drives TNBC aggressiveness by regulating Notch1 and Gli1 stability through the E3 ubiquitin ligase Itch, functioning as an Itch-negative regulator. Mechanistically, MAML1 interacts with Itch via its PPQY motif and promotes K63-linked self-ubiquitylation of Itch, deregulating its expression/activity. Using a Maml1-deficient mouse model, we reveal an inverse correlation between MAML1 and Itch levels, where the loss of MAML1 stabilizes Itch and suppresses Notch1 and Gli1 activity. Conversely, MAML1 upregulation enhances Notch1 and Gli1 expression, driving accelerated TNBC tumor growth and faster multiorgan metastasis in vivo. Accordingly, we show that MAML1 is overexpressed in a cohort of TNBC patients, and the combined overexpression of MAML1/Notch1 and MAML1/Gli1 correlates with poor clinical outcomes by in silico analysis. Our findings establish a dual role for MAML1 as a transcriptional coactivator and a post-translational regulator of Itch, thereby amplifying Notch and Hedgehog oncogenic signaling. This study uncovers MAML1 as a key driver of TNBC progression and a potential therapeutic target for fighting TNBC aggressiveness and heterogeneity.
{"title":"MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancer","authors":"Sabrina Zema, Francesca Di Fazio, Maria Pelullo, Sara Di Savino, Bruna Cerbelli, Martina Leopizzi, Laura Di Magno, Carmine Nicoletti, Giovanna Peruzzi, Daniel D’Andrea, Maria V. Giuli, Samantha Cialfi, Biagio Palmisano, Alice Turdo, Rocco Palermo, Giulia d’Amati, Gianluca Canettieri, Antongiulio Faggiano, Lucia Di Marcotullio, Matilde Todaro, Isabella Screpanti, Claudio Talora, Saula Checquolo, Diana Bellavia","doi":"10.1038/s41418-025-01613-5","DOIUrl":"https://doi.org/10.1038/s41418-025-01613-5","url":null,"abstract":"Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous breast cancer subtype with poor patient outcomes. TNBC heterogeneity arises from multiple dysregulated pathways, including Notch and Hedgehog, which contribute to tumor initiation, progression, and drug resistance. Identifying common molecular regulators of TNBC aggressiveness is crucial for developing effective therapeutic strategies. Here, we demonstrate that the transcriptional coactivator MAML1 drives TNBC aggressiveness by regulating Notch1 and Gli1 stability through the E3 ubiquitin ligase Itch, functioning as an Itch-negative regulator. Mechanistically, MAML1 interacts with Itch <jats:italic>via</jats:italic> its PPQY motif and promotes K63-linked self-ubiquitylation of Itch, deregulating its expression/activity. Using a Maml1-deficient mouse model, we reveal an inverse correlation between MAML1 and Itch levels, where the loss of MAML1 stabilizes Itch and suppresses Notch1 and Gli1 activity. Conversely, MAML1 upregulation enhances Notch1 and Gli1 expression, driving accelerated TNBC tumor growth and faster multiorgan metastasis in vivo. Accordingly, we show that MAML1 is overexpressed in a cohort of TNBC patients, and the combined overexpression of MAML1/Notch1 and MAML1/Gli1 correlates with poor clinical outcomes by in silico analysis. Our findings establish a dual role for MAML1 as a transcriptional coactivator and a post-translational regulator of Itch, thereby amplifying Notch and Hedgehog oncogenic signaling. This study uncovers MAML1 as a key driver of TNBC progression and a potential therapeutic target for fighting TNBC aggressiveness and heterogeneity.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"188 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145567395","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}
Pub Date : 2025-11-19DOI: 10.1038/s41418-025-01598-1
Sonia S. Shah, Jantina A. Manning, Yoon Lim, Diva Sinha, Ambika Mosale Venkatesh Murthy, Raja Ganesan, Nirmal Robinson, Emad S. Alnemri, Seth L. Masters, James E. Vince, Sharad Kumar
The membrane pore-forming gasdermin (GSDM) proteins are essential executors of pyroptosis. The GSDM family members GSDMD and GSDME can also target mitochondrial membranes, driving apoptosis. Here, we identify the ubiquitin ligase NEDD4L as a key regulator of GSDMD and GSDME, two GSDMs involved in cell death. NEDD4L ubiquitinates both these proteins to control their stability and intracellular expression levels. Knockout of mouse Nedd4l (also called Nedd4-2 ) results in lung and kidney damage with perinatal lethality within three weeks of birth. These mice demonstrated elevated GSDMD in alveolar epithelia and increased GSDME in kidney tubular epithelia, suggesting tissue-specific regulation by NEDD4L. Renal tubule-specific Nedd4l knockout mice showed GSDM activation, tubular cell death and reduced kidney function after high sodium diet. NEDD4L-deficient cells showed increased GSDM activation, IL-1β release and were significantly more susceptible to cell death induced by NLRP3 agonists, cytotoxic agents, and bacterial infection. These results demonstrate that NEDD4L regulates GSDMD and GSDME functions by preventing their accumulation and reveals an unexplored link between GSDM stability and cell death.
{"title":"NEDD4L-mediated Gasdermin D and E ubiquitination regulates cell death and tissue injury","authors":"Sonia S. Shah, Jantina A. Manning, Yoon Lim, Diva Sinha, Ambika Mosale Venkatesh Murthy, Raja Ganesan, Nirmal Robinson, Emad S. Alnemri, Seth L. Masters, James E. Vince, Sharad Kumar","doi":"10.1038/s41418-025-01598-1","DOIUrl":"https://doi.org/10.1038/s41418-025-01598-1","url":null,"abstract":"The membrane pore-forming gasdermin (GSDM) proteins are essential executors of pyroptosis. The GSDM family members GSDMD and GSDME can also target mitochondrial membranes, driving apoptosis. Here, we identify the ubiquitin ligase NEDD4L as a key regulator of GSDMD and GSDME, two GSDMs involved in cell death. NEDD4L ubiquitinates both these proteins to control their stability and intracellular expression levels. Knockout of mouse <jats:italic>Nedd4l</jats:italic> (also called <jats:italic>Nedd4-2</jats:italic> ) results in lung and kidney damage with perinatal lethality within three weeks of birth. These mice demonstrated elevated GSDMD in alveolar epithelia and increased GSDME in kidney tubular epithelia, suggesting tissue-specific regulation by NEDD4L. Renal tubule-specific <jats:italic>Nedd4l</jats:italic> knockout mice showed GSDM activation, tubular cell death and reduced kidney function after high sodium diet. NEDD4L-deficient cells showed increased GSDM activation, IL-1β release and were significantly more susceptible to cell death induced by NLRP3 agonists, cytotoxic agents, and bacterial infection. These results demonstrate that NEDD4L regulates GSDMD and GSDME functions by preventing their accumulation and reveals an unexplored link between GSDM stability and cell death.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"158 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145554414","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":"HERP constrains white adipose expansion and inflammation by STEAP4 stabilization","authors":"Yingchun Chen, Yanyan Wu, Haorui Qin, Zhiqiang Han, Yao Tang, Qiuyan Wang, Fei Xiao","doi":"10.1038/s41418-025-01608-2","DOIUrl":"https://doi.org/10.1038/s41418-025-01608-2","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"11 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145536151","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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