Cell Death and Differentiation最新文献_第5页

127aa encoded by circSpdyA promotes FA synthesis and NK cell repression in breast cancers 由 circSpdyA 编码的 127aa 可促进乳腺癌中的 FA 合成和 NK 细胞抑制作用

IF 12.4 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-14 DOI: 10.1038/s41418-024-01396-1

Xinya Gao, Zicheng Sun, Xin Liu, Jiayue Luo, Xiaoli Liang, Huijin Wang, Junyi Zhou, Ciqiu Yang, Tiantian Wang, Jie Li

{"title":"127aa encoded by circSpdyA promotes FA synthesis and NK cell repression in breast cancers","authors":"Xinya Gao, Zicheng Sun, Xin Liu, Jiayue Luo, Xiaoli Liang, Huijin Wang, Junyi Zhou, Ciqiu Yang, Tiantian Wang, Jie Li","doi":"10.1038/s41418-024-01396-1","DOIUrl":"https://doi.org/10.1038/s41418-024-01396-1","url":null,"abstract":"Lipid metabolism reprogram plays key roles in breast cancer tumorigenesis and immune escape. The underlying mechanism and potential regulator were barely investigated. We thus established an in vivo tumorigenesis model, mice-bearing breast cancer cells were treated with an ordinary diet and high-fat diet, species were collected and subjected to circRNA sequence to scan the potential circRNAs regulating the lipid metabolism. CircSpdyA was one of the most upregulated circRNAs and had the potential to encode a 127-aa micro peptide (referred to as 127aa). 127 aa promotes tumorigenesis through promoting the fatty acid de novo synthesis by directly binding to FASN. Single-cell sequence indicated 127aa inhibited NK cell infiltration and function. This was achieved by inhibiting the transcription of NK cell activators epigenetically. Moreover, lipid-laden from 127aa positive cancer cells transferred to NK cells inhibited the cytotoxicity. Taken together, circSpdyA encoded 127aa promotes fatty acid de novo synthesis through directly binding with FASN and induced NK cell repression by inhibiting the transcription of NK cell activators.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"229 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142431523","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

SLAMF7 (CD319) on activated CD8+ T cells transduces environmental cues to initiate cytotoxic effector cell responses 活化的 CD8+ T 细胞上的 SLAMF7 (CD319) 通过环境线索启动细胞毒性效应细胞反应

IF 12.4 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-10 DOI: 10.1038/s41418-024-01399-y

Holger Lingel, Laura Fischer, Sven Remstedt, Benno Kuropka, Lars Philipsen, Irina Han, Jan-Erik Sander, Christian Freund, Aditya Arra, Monika C. Brunner-Weinzierl

{"title":"SLAMF7 (CD319) on activated CD8+ T cells transduces environmental cues to initiate cytotoxic effector cell responses","authors":"Holger Lingel, Laura Fischer, Sven Remstedt, Benno Kuropka, Lars Philipsen, Irina Han, Jan-Erik Sander, Christian Freund, Aditya Arra, Monika C. Brunner-Weinzierl","doi":"10.1038/s41418-024-01399-y","DOIUrl":"https://doi.org/10.1038/s41418-024-01399-y","url":null,"abstract":"CD8+ T-cell responses are meticulously orchestrated processes regulated by intercellular receptor:ligand interactions. These interactions critically control the dynamics of CD8+ T-cell populations that is crucial to overcome threats such as viral infections or cancer. Yet, the mechanisms governing these dynamics remain incompletely elucidated. Here, we identified a hitherto unknown T-cell referred function of the self-ligating surface receptor SLAMF7 (CD319) on CD8+ T cells during initiation of cytotoxic T-cell responses. According to its cytotoxicity related expression on T effector cells, we found that CD8+ T cells could utilize SLAMF7 to transduce environmental cues into cellular interactions and information exchange. Indeed, SLAMF7 facilitated a dose-dependent formation of stable homotypic contacts that ultimately resulted in stable cell-contacts, quorum populations and commitment to expansion and differentiation. Using pull-down assays and network analyses, we identified novel SLAMF7-binding intracellular signaling molecules including the CRK, CRKL, and Nck adaptors, which are involved in T-cell contact formation and may mediate SLAMF7 functions in sensing and adhesion. Hence, providing SLAMF7 signals during antigen recognition of CD8+ T cells enhanced their overall magnitude, particularly in responses towards low-affinity antigens, resulting in a significant boost in their proliferation and cytotoxic capacity. Overall, we have identified and characterized a potent initiator of the cytotoxic T lymphocyte response program and revealed advanced mechanisms to improve CD8+ T-cell response decisions against weak viral or tumor-associated antigens, thereby strengthening our defense against such adversaries.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"227 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142397743","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

Activating the NFE2L1-ubiquitin-proteasome system by DDI2 protects from ferroptosis. DDI2激活NFE2L1-泛素-蛋白酶体系统可防止铁变态反应。

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-09 DOI: 10.1038/s41418-024-01398-z

Anahita Ofoghi, Stefan Kotschi, Imke L Lemmer, Daniel T Haas, Nienke Willemsen, Batoul Bayer, Anna S Jung, Sophie Möller, Stefanie Haberecht-Müller, Elke Krüger, Natalie Krahmer, Alexander Bartelt

{"title":"Activating the NFE2L1-ubiquitin-proteasome system by DDI2 protects from ferroptosis.","authors":"Anahita Ofoghi, Stefan Kotschi, Imke L Lemmer, Daniel T Haas, Nienke Willemsen, Batoul Bayer, Anna S Jung, Sophie Möller, Stefanie Haberecht-Müller, Elke Krüger, Natalie Krahmer, Alexander Bartelt","doi":"10.1038/s41418-024-01398-z","DOIUrl":"https://doi.org/10.1038/s41418-024-01398-z","url":null,"abstract":"Ferroptosis is an iron-dependent, non-apoptotic form of cell death initiated by oxidative stress and lipid peroxidation. Recent evidence has linked ferroptosis to the action of the transcription factor Nuclear factor erythroid-2 derived,-like-1 (NFE2L1). NFE2L1 regulates proteasome abundance in an adaptive fashion, maintaining protein quality control to secure cellular homeostasis, but the regulation of NFE2L1 during ferroptosis and the role of the ubiquitin-proteasome system (UPS) herein are still unclear. In the present study, using an unbiased proteomic approach charting the specific ubiquitylation sites, we show that induction of ferroptosis leads to recalibration of the UPS. RSL3-induced ferroptosis inhibits proteasome activity and leads to global hyperubiquitylation, which is linked to NFE2L1 activation. As NFE2L1 resides in the endoplasmic reticulum tethered to the membrane, it undergoes complex posttranslational modification steps to become active and induce the expression of proteasome subunit genes. We show that proteolytic cleavage of NFE2L1 by the aspartyl protease DNA-damage inducible 1 homolog 2 (DDI2) is a critical step for the ferroptosis-induced feed-back loop of proteasome function. Cells lacking DDI2 cannot activate NFE2L1 in response to RSL3 and show global hyperubiquitylation. Genetic or chemical induction of ferroptosis in cells with a disrupted DDI2-NFE2L1 pathway diminishes proteasomal activity and promotes cell death. Also, treating cells with the clinical drug nelfinavir, which inhibits DDI2, sensitized cells to ferroptosis. In conclusion, our results provide new insight into the importance of the UPS in ferroptosis and highlight the role of the DDI2-NFE2L1 as a potential therapeutic target. Manipulating DDI2-NFE2L1 activity through chemical inhibition might help sensitizing cells to ferroptosis, thus enhancing existing cancer therapies.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":13.7,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388356","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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A novel glucose sensor fuelling cancer growth 助长癌症生长的新型葡萄糖传感器

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-08 DOI: 10.1038/s41418-024-01400-8

Luisa Ricci, Simone Cardaci

引用次数: 0

HKDC1 functions as a glucose sensor and promotes metabolic adaptation and cancer growth via interaction with PHB2 HKDC1 作为葡萄糖传感器发挥作用，通过与 PHB2 相互作用促进新陈代谢适应和癌症生长

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-07 DOI: 10.1038/s41418-024-01392-5

Panpan Liu, Yao Luo, Hongyu Wu, Yi Han, Shoujie Wang, Rui Liu, Shijun Wen, Peng Huang

{"title":"HKDC1 functions as a glucose sensor and promotes metabolic adaptation and cancer growth via interaction with PHB2","authors":"Panpan Liu, Yao Luo, Hongyu Wu, Yi Han, Shoujie Wang, Rui Liu, Shijun Wen, Peng Huang","doi":"10.1038/s41418-024-01392-5","DOIUrl":"10.1038/s41418-024-01392-5","url":null,"abstract":"Glucose sensing and metabolic adaptation to glucose availability in the tumor microenvironment are critical for cancer development. Here we show that HKDC1, a hexokinase highly expressed in cancer associated with poor prognosis, functions as a glucose sensor that alters its stability in response to environmental glucose. The glucose-sensing domain is located between amino acids 751-917, with Ser896 as a key residue that regulates HKDC1 stability by affecting Lys620 ubiquitination. This sensing mechanism enables cellular adaptation to glucose starvation by promoting mitochondrial fatty acid utilization. Furthermore, HKDC1 promotes tumor growth by sequestering prohibitin 2 (PHB2) to disable its suppressive effect on SP1, thus promoting the expression of pro-oncogenic molecules. Abrogation of HKDC1 by genetic knockout or by glucose depletion releases PHB2, leading to suppression of cancer cell proliferation and inhibition of tumor growth. Our study reveals a previously unrecognized role of HKDC1 in glucose sensing and metabolic adaptation, and identifies HKDC1 as a potential therapeutic target.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1595-1610"},"PeriodicalIF":13.7,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383741","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

Fructose: the sweet(er) side of the Warburg effect 果糖：沃伯格效应的甜蜜一面

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-05 DOI: 10.1038/s41418-024-01395-2

Christian Frezza

引用次数: 0

DNA damage-inducible transcript 3 positively regulates RIPK1-mediated necroptosis DNA 损伤诱导转录本 3 对 RIPK1 介导的坏死有正向调节作用

IF 12.4 1区生物学

Cell Death and Differentiation Pub Date : 2024-10-03 DOI: 10.1038/s41418-024-01385-4

Rui Ni, Ting Cao, Xiaoyun Ji, Angel Peng, Zhuxu Zhang, Guo-Chang Fan, Peter Stathopulos, Subrata Chakrabarti, Zhaoliang Su, Tianqing Peng

{"title":"DNA damage-inducible transcript 3 positively regulates RIPK1-mediated necroptosis","authors":"Rui Ni, Ting Cao, Xiaoyun Ji, Angel Peng, Zhuxu Zhang, Guo-Chang Fan, Peter Stathopulos, Subrata Chakrabarti, Zhaoliang Su, Tianqing Peng","doi":"10.1038/s41418-024-01385-4","DOIUrl":"https://doi.org/10.1038/s41418-024-01385-4","url":null,"abstract":"DNA damage-inducible transcript 3 (DDIT3) is a well-known transcription factor that regulates the expression of apoptosis-related genes for promoting apoptosis during endoplasmic reticulum stress. Here, we report an unrecognized role of DDIT3 in facilitating necroptosis. DDIT3 directly binds and competitively prevents the p38 MAPK-MK2 interaction and thereby blocking MK2 activation while stimulating p38 MAPK activation. This blockage of MK2 activation initially prevents RIPK1 phosphorylation at Ser320 (inactivation), subsequently relieving its suppression of RIPK1 activation. Consequently, p38 MAPK facilitates RIPK1 phosphorylation at Ser166 (activation) through DDIT3 phosphorylation-related mechanisms, leading to necroptosis. Mechanistically, a 10-amino acid segment (Glu19-Val28) within DDIT3’s N-terminus is identified to account for its pro-necroptotic function. In vivo studies demonstrate that forced expression of DDIT3 induces necroptosis, whereas deletion of DDIT3 alleviates necroptosis in mouse hearts under stress. These findings shed light on a novel regulatory mechanism by which DDIT3 promotes RIPK1 activation and subsequent necroptosis.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"221 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368830","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

Integrated stress response plasticity governs normal cell adaptation to chronic stress via the PP2A-TFE3-ATF4 pathway 综合应激反应可塑性通过 PP2A-TFE3-ATF4 通路调控正常细胞对慢性应激的适应性

IF 13.7 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-30 DOI: 10.1038/s41418-024-01378-3

Rita A. Avelar, Riya Gupta, Grace Carvette, Felipe da Veiga Leprevost, Medhasri Jasti, Jose Colina, Jessica Teitel, Alexey I. Nesvizhskii, Caitlin M. O’Connor, Maria Hatzoglou, Shirish Shenolikar, Peter Arvan, Goutham Narla, Analisa DiFeo

{"title":"Integrated stress response plasticity governs normal cell adaptation to chronic stress via the PP2A-TFE3-ATF4 pathway","authors":"Rita A. Avelar, Riya Gupta, Grace Carvette, Felipe da Veiga Leprevost, Medhasri Jasti, Jose Colina, Jessica Teitel, Alexey I. Nesvizhskii, Caitlin M. O’Connor, Maria Hatzoglou, Shirish Shenolikar, Peter Arvan, Goutham Narla, Analisa DiFeo","doi":"10.1038/s41418-024-01378-3","DOIUrl":"10.1038/s41418-024-01378-3","url":null,"abstract":"The integrated stress response (ISR) regulates cell fate during conditions of stress by leveraging the cell’s capacity to endure sustainable and efficient adaptive stress responses. Protein phosphatase 2A (PP2A) activity modulation has been shown to be successful in achieving both therapeutic efficacy and safety across various cancer models. However, the molecular mechanisms driving its selective antitumor effects remain unclear. Here, we show for the first time that ISR plasticity relies on PP2A activation to regulate drug response and dictate cellular survival under conditions of chronic stress. We demonstrate that genetic and chemical modulation of the PP2A leads to chronic proteolytic stress and triggers an ISR to dictate whether the cell lives or dies. More specifically, we uncovered that the PP2A-TFE3-ATF4 pathway governs ISR cell plasticity during endoplasmic reticular and cellular stress independent of the unfolded protein response. We further show that normal cells reprogram their genetic signatures to undergo ISR-mediated adaptation and homeostatic recovery thereby avoiding toxicity following PP2A-mediated stress. Conversely, oncogenic specific cytotoxicity induced by chemical modulation of PP2A is achieved by activating chronic and irreversible ISR in cancer cells. Our findings propose that a differential response to chemical modulation of PP2A is determined by intrinsic ISR plasticity, providing a novel biological vulnerability to selectively induce cancer cell death and improve targeted therapeutic efficacy.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"31 12","pages":"1761-1775"},"PeriodicalIF":13.7,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41418-024-01378-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142330335","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

Neuronal LAMP2A-mediated reduction of adenylyl cyclases induces acute neurodegenerative responses and neuroinflammation after ischemic stroke 神经元 LAMP2A 介导的腺苷酸环化酶减少诱导缺血性中风后的急性神经退行性反应和神经炎症

IF 12.4 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-28 DOI: 10.1038/s41418-024-01389-0

Dingfang Shi, Yunhao Bai, Ruiling Long, Jing Xia, Wenxuan Xu, Dongshen Qin, Xuejun Yang, Ming Ding, Xiao-Yu Hou

{"title":"Neuronal LAMP2A-mediated reduction of adenylyl cyclases induces acute neurodegenerative responses and neuroinflammation after ischemic stroke","authors":"Dingfang Shi, Yunhao Bai, Ruiling Long, Jing Xia, Wenxuan Xu, Dongshen Qin, Xuejun Yang, Ming Ding, Xiao-Yu Hou","doi":"10.1038/s41418-024-01389-0","DOIUrl":"https://doi.org/10.1038/s41418-024-01389-0","url":null,"abstract":"Lysosomes regulate cellular metabolism to maintain cell survival, but the mechanisms whereby they determine neuronal cell fate after acute metabolic stress are unknown. Neuron-enriched lysosomal membrane protein LAMP2A is involved in selective chaperone-mediated autophagy and exosome loading. This study demonstrates that abnormalities in the neuronal LAMP2A-lysosomal pathway cause neurological deficits following ischemic stroke and that this is an early inducer of the PANoptosis-like molecular pathway and neuroinflammation, simultaneously inducing upregulation of FADD, RIPK3, and MLKL after ischemia. Quantitative proteomic and pharmacological analysis showed that after acute metabolic stress, the neuronal LAMP2A pathway induced acute synaptic degeneration and PANoptosis-like responses involving downregulation of protein kinase A (PKA) signaling. LAMP2A directed post-stroke lysosomal degradation of adenylyl cyclases (ADCY), including ADCY1 and ADCY3 in cortical neurons. Post-stroke treatment with cAMP mimetic or ADCY activator salvaged cortical neurons from PANoptosis-like responses and neuroinflammation, suggesting that the neuronal ADCY–cAMP–PKA axis is an upstream arrester of the pathophysiological process following an ischemic stroke. This study demonstrates that the neuronal LAMP2A-lysosmal pathway drives intricate acute neurodegenerative and neuroinflammatory responses after brain metabolic stress by downregulating the ADCY–PKA signaling cascade, and highlights the therapeutic potential of PKA signal inducers for improving stroke outcomes.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"42 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328631","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

NF-κB regulated expression of A20 controls IKK dependent repression of RIPK1 induced cell death in activated T cells 受 NF-κB 调控的 A20 表达可控制 IKK 依赖性抑制活化 T 细胞中 RIPK1 诱导的细胞死亡

IF 12.4 1区生物学

Cell Death and Differentiation Pub Date : 2024-09-26 DOI: 10.1038/s41418-024-01383-6

By Scott Layzell, Alessandro Barbarulo, Geert van Loo, Rudi Beyaert, Benedict Seddon

{"title":"NF-κB regulated expression of A20 controls IKK dependent repression of RIPK1 induced cell death in activated T cells","authors":"By Scott Layzell, Alessandro Barbarulo, Geert van Loo, Rudi Beyaert, Benedict Seddon","doi":"10.1038/s41418-024-01383-6","DOIUrl":"https://doi.org/10.1038/s41418-024-01383-6","url":null,"abstract":"IKK signalling is essential for survival of thymocytes by repressing RIPK1 induced cell death rather than its canonical function of activating NF-κB. The role of IKK signalling in activated T cells is unclear. To investigate this, we analysed activation of IKK2 deficient T cells. While TCR triggering was normal, proliferation and expansion was profoundly impaired. This was not due to defective cell cycle progression, rather dividing T cells became sensitised to TNF induced cell death, since inhibition of RIPK1 kinase activity rescued cell survival. Gene expression analysis of activated IKK2 deficient T cells revealed defective expression of Tnfaip3, that encodes A20, a negative regulator of NF-κB. To test whether A20 expression was required to protect IKK2 deficient T cells from cell death, we generated mice with T cells lacking both A20 and IKK2. Doing this resulted in near complete loss of peripheral T cells, in contrast to mice lacking one or other gene. Strikingly, this phenotype was completely reversed by inactivation of RIPK1 kinase activity in vivo. Together, our data show that IKK signalling in activated T cells protects against RIPK1 dependent death, both by direct phosphorylation of RIPK1 and through NF-κB mediated induction of A20, that we identify for the first time as a key modulator of RIPK1 activity in T cells.","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"42 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142325111","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