Cellular and Molecular Life Sciences最新文献_第7页

The P132H mutation of SARS-CoV-2 NSP5 relieves its inhibition on interferon-β activation via blocking MAVS degradation. SARS-CoV-2 NSP5的P132H突变通过阻断MAVS降解解除了对干扰素-β激活的抑制。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-30 DOI: 10.1007/s00018-025-05822-6

Yuxin Zhang, Tong-Yun Wang, Huihui Yan, Zhoule Guo, Zhonghao Lian, Hailan Yao, Shuofeng Yuan, Xing-Yi Ge, Ye Qiu

{"title":"The P132H mutation of SARS-CoV-2 NSP5 relieves its inhibition on interferon-β activation via blocking MAVS degradation.","authors":"Yuxin Zhang, Tong-Yun Wang, Huihui Yan, Zhoule Guo, Zhonghao Lian, Hailan Yao, Shuofeng Yuan, Xing-Yi Ge, Ye Qiu","doi":"10.1007/s00018-025-05822-6","DOIUrl":"10.1007/s00018-025-05822-6","url":null,"abstract":"The prevalence of the Omicron variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an important transition in the epidemic of coronavirus disease 2019 (COVID-19). Compared with other SARS-CoV-2 variants, Omicron and its subvariants exhibit decreased pathogenicity, thus contributing to the moderation of the epidemic. However, the mechanism underlying such changes is not fully understood. NSP5 is a SARS-CoV-2-encoded protease that counteracts antiviral immunity, and the P132H mutation of NSP5 is present exclusively in Omicron and its subvariants. In this study, we found that this mutation solely relieved cytopathogenicity and reduced the viral replication during SARS-CoV-2 infection. Further studies suggested that P132H blocked the NSP5-mediated degradation of MAVS by impairing the K136-linked ubiquitination of MAVS, thus restoring the IFN-β activation inhibited by NSP5. Structural analysis in silico suggested that P132H disrupted multiple hydrogen bonds between NSP5 and UbcH5b, an E2 ubiquitin-conjugating enzyme required for K136 ubiquitination. In summary, our results provide a potential mechanism explaining the decreased pathogenicity of the Omicron variant of SARS-CoV-2.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"293"},"PeriodicalIF":6.2,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12311081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

REGγ regulates antiviral response by activating TBK1-IFNβ signaling through degradation of PPP2CB. REGγ通过PPP2CB降解激活TBK1-IFNβ信号通路调控抗病毒应答。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-30 DOI: 10.1007/s00018-025-05816-4

Yi Li, Pei Wang, Jiamin Ma, Qing Tu, Yuan Yuan, Ying Chen, Lin Wang, Yuwei Chen, Feng Chen, Suvi Biesinger, Henry J Li, Jinbao Li, Liangfang Yao

{"title":"REGγ regulates antiviral response by activating TBK1-IFNβ signaling through degradation of PPP2CB.","authors":"Yi Li, Pei Wang, Jiamin Ma, Qing Tu, Yuan Yuan, Ying Chen, Lin Wang, Yuwei Chen, Feng Chen, Suvi Biesinger, Henry J Li, Jinbao Li, Liangfang Yao","doi":"10.1007/s00018-025-05816-4","DOIUrl":"10.1007/s00018-025-05816-4","url":null,"abstract":"Although significant progressions in antiviral studies of IFNβ have been demonstrated, the role of the proteasome in modulating cross-talk between TBK1-IFNβ signaling and viral replication during viral infection is not fully elucidated. Here, we discover that deficiency of REGγ, a proteasome activator, significantly reduces IFNβ production and increases viral replications in mice, leading to increased mortality in virus infection models. Our mechanistic study indicates that REGγ interacts with and degrades the protein phosphatase subunit Protein Phosphatase 2 Catalytic Subunit Beta (PPP2CB). This degradation disrupts the dephosphorylation of TBK1 and its interaction with IRF3, resulting in the activation of IFNβ-mediated antiviral signaling. In response to viral infection, up-regulation of REGγ in macrophages accelerates the degradation of PPP2CB, which increases the activation of TBK1-IRF3-IFNβ axis and thereby restricts viral replications and pathology. Interestingly, IFNβ enhances REGγ expression in viral infection, forming a positive feedback regulatory loop. In conclusion, our work demonstrates that REGγ is a positive modulator of IFNβ signaling during antiviral response, highlighting that this procedure is regulated via REGγ degradation of PPP2CB and provides a new insight into the coordination between antiviral response and proteasome activity. Thus, REGγ-proteasome activity and phosphatase PPP2CB may be potential targets in host defense against viruses.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"296"},"PeriodicalIF":6.2,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12311087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

STAT1 and STAT6 orchestrate Cbs transcription and transsulfur metabolism in microglia and contribute to parkinson's disease-related neuroinflammation. STAT1和STAT6在小胶质细胞中协调Cbs转录和转硫代谢，并参与帕金森病相关的神经炎症。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-30 DOI: 10.1007/s00018-025-05768-9

Yang Liu, Zhen Wang, Ya-Ting Ma, Yu-Xuan Chen, Xin-Yi Qian, Xiao-Ou Hou, Bo Wan, Hai-Gang Ren, Li-Fang Hu

引用次数: 0

Proteome of oocyte spindle identifies Ccdc69 regulates spindle assembly like "band-tightening spell". 卵母细胞纺锤体蛋白质组学鉴定Ccdc69调控纺锤体组装，类似于“紧带咒语”。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-30 DOI: 10.1007/s00018-025-05821-7

Jia-Ni Guo, Liu Zhu, Tie-Gang Meng, Yi-Na Zhang, Si-Min Sun, Xue-Mei Yang, Bing-Wang Zhao, Yi-Ke Lu, Yuan-Hong Xu, Wei Yue, Zhiming Han, Catherine C L Wong, Zhen-Bo Wang

{"title":"Proteome of oocyte spindle identifies Ccdc69 regulates spindle assembly like \"band-tightening spell\".","authors":"Jia-Ni Guo, Liu Zhu, Tie-Gang Meng, Yi-Na Zhang, Si-Min Sun, Xue-Mei Yang, Bing-Wang Zhao, Yi-Ke Lu, Yuan-Hong Xu, Wei Yue, Zhiming Han, Catherine C L Wong, Zhen-Bo Wang","doi":"10.1007/s00018-025-05821-7","DOIUrl":"10.1007/s00018-025-05821-7","url":null,"abstract":"Meiotic spindle is an intricate structure and required for chromosome segregation and the proper meiotic progression during oocyte maturation, and its function is regulated by a complex network of proteins located at spindle and its peripheral region. However, proteome of meiotic spindle remains poorly characterized. Here, we acquired the proteomic profile of spindles isolated from metaphase I (MI) and metaphase II (MII) mouse oocytes. In particular, we identified Ccdc69 as a novel regulator of spindle assembly in mouse oocytes. Although deletion of Ccdc69 did not affect female fertility, the MI spindles were elongated in Ccdc69 knockout oocytes. Overexpression of Ccdc69 induced spindle defects by reducing microtubule formation and disturbing acentriolar microtubule organization centers (aMTOCs) distribution. Furthermore, Ccdc69 overexpression impaired kinetochore-microtubule (K-MT) attachment and delayed meiotic progression by abnormal activation of spindle assembly checkpoint (SAC). Taken together, our study depicts the proteome of spindles during mouse oocyte maturation and demonstrates that Ccdc69 regulates spindle assembly and meiotic progression the way similar to \"The Tightening Spell of Sun Wukong's Golden Headband\" in the famous Chinese Classic Journey to the West.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"292"},"PeriodicalIF":6.2,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12311101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction: Apache is a neuronal player in autophagy required for retrograde axonal transport of autophagosomes. 更正：Apache是自噬体轴突逆行运输所需的自噬的神经元参与者。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-30 DOI: 10.1007/s00018-025-05675-z

Barbara Parisi, Alessandro Esposito, Enrico Castroflorio, Mattia Bramini, Sara Pepe, Antonella Marte, Fabrizia C Guarnieri, Flavia Valtorta, Pietro Baldelli, Fabio Benfenati, Anna Fassio, Silvia Giovedì

引用次数: 0

An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions. 线粒体质量控制在骨代谢中的新作用：从分子机制到靶向治疗干预。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-29 DOI: 10.1007/s00018-025-05802-w

Ziqi Qin, Xiting Zhu, Yifei Shen, Huiling Ling, Ngaifung Ruan, Wushuang Ye, Yang Xu, Xueqi Gan

{"title":"An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.","authors":"Ziqi Qin, Xiting Zhu, Yifei Shen, Huiling Ling, Ngaifung Ruan, Wushuang Ye, Yang Xu, Xueqi Gan","doi":"10.1007/s00018-025-05802-w","DOIUrl":"10.1007/s00018-025-05802-w","url":null,"abstract":"The mitochondrial quality control system is the principal regulatory framework governing mitochondrial quantity, morphology, distribution, and functional integrity. This surveillance and regulatory machinery is essential for preserving cellular homeostasis and determining cellular differentiation. Mitochondria play a central role in maintaining the dynamic equilibrium between osteogenic differentiation and osteoclastic differentiation. Dysregulation of mitochondrial quality control can lead to disrupted mitochondrial homeostasis and functional impairments, disrupting the physiological processes of bone formation and bone resorption. However, comprehensive reviews elucidating the relationship between mitochondrial quality control and bone homeostasis are conspicuously lacking. This review systematically deconstructs the molecular architecture of mitochondrial quality control, elucidating the regulatory mechanism of each part (mitochondrial dynamics, mitophagy, mitochondrial biogenesis, mitochondrial redox) in bone-related cells. In addition, the mitochondrial quality control system in orchestrating cellular physiological activities is summarized to establish its indispensable in governing cellular homeostatic networks. Furthermore, the regulatory roles of the mitochondrial quality control system in bone-related cells and the balance between bone formation and resorption are reviewed. Finally, this review delineates the dysregulation of mitochondrial quality control in bone metabolic diseases and further advances mitochondrial quality control-targeted approaches for restoring mitochondria homeostasis, offering transformative strategies to treat bone metabolic diseases.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"291"},"PeriodicalIF":6.2,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144728348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

ISG-15, beyond its functions in the cell: a mini review. ISG-15，在细胞内的功能之外：一个小回顾。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-28 DOI: 10.1007/s00018-025-05705-w

Mudassir S Ali, Yun Sang Tang, Horace Hok Yeung Lee, Susan C Baker, Chris Ka Pun Mok

{"title":"ISG-15, beyond its functions in the cell: a mini review.","authors":"Mudassir S Ali, Yun Sang Tang, Horace Hok Yeung Lee, Susan C Baker, Chris Ka Pun Mok","doi":"10.1007/s00018-025-05705-w","DOIUrl":"10.1007/s00018-025-05705-w","url":null,"abstract":"Interferon-stimulated gene 15 (ISG15) is an interferon-stimulated gene and a ubiquitin-like protein, traditionally known for its role in ISGylation. In addition to its intracellular functions, recent studies have revealed a novel role for extracellular ISG15, particularly in the context of viral infections. Beyond type I interferons, various stimuli, including viral and bacterial infections, have been found to trigger its secretion. Notably, the integrin receptor LFA-1 has been identified as a receptor for extracellular ISG15. Despite these advancements, the precise mechanisms by which extracellular ISG15 functions-such as the pathways regulating its secretion and receptor interactions-remain unclear. Viral proteins and de-ISGylating enzymes are known to influence ISG15 secretion levels, thereby impacting its immunomodulatory potential. This mini-review summarizes the existing studies aimed at understanding the mechanisms behind the secretion and functions of extracellular ISG15, with a particular focus on its immunomodulatory effects during infection. We also explore the contrasting roles of extracellular ISG15 in mice and humans, highlighting the need for more species-specific research. Further investigation into the role of extracellular ISG15 may uncover novel therapeutic strategies for infectious diseases, cancer, and inflammatory conditions.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"289"},"PeriodicalIF":6.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144728349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Quantifying the mRNA epitranscriptome reveals epitranscriptome signatures and roles in cancer. 量化mRNA外转录组揭示了外转录组特征及其在癌症中的作用。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-28 DOI: 10.1007/s00018-025-05805-7

Ying Feng, Xiaoli He, Mingxin Guo, Ying Tang, Guantong Qi, Qian Huang, Wenran Ma, Hong Chen, Yifan Qin, Ruiqi Li, Jin Wang, Yu Liu

{"title":"Quantifying the mRNA epitranscriptome reveals epitranscriptome signatures and roles in cancer.","authors":"Ying Feng, Xiaoli He, Mingxin Guo, Ying Tang, Guantong Qi, Qian Huang, Wenran Ma, Hong Chen, Yifan Qin, Ruiqi Li, Jin Wang, Yu Liu","doi":"10.1007/s00018-025-05805-7","DOIUrl":"10.1007/s00018-025-05805-7","url":null,"abstract":"Post-transcriptional modifications on mRNA are crucial for mRNA fate and function. The current lack of a comprehensive method for high-coverage and sensitive quantitative analysis of mRNA modifications significantly limits the discovery of new mRNA modifications and understanding mRNA modifications' occurrence, dynamics and function. Here, a highly sensitive, high-throughput and robust LC-MS/MS-based technique, mRQuant, was developed to simultaneously detect and quantify 84 modified ribonucleosides in cellular mRNA. Using mRQuant, we quantified 32-34 modified ribonucleosides across several human cancer and non-cancer cell lines and uncovered cancer- and cancer type-specific signatures. Analyses of cisplatin- and paclitaxel-treated HeLa cells and drug-resistant variants revealed several drug resistance-associated modifications. Among them, m1A exhibited significant differences across multiple cell types and between cancerous and non-cancerous cells. Knocking down mRNA m1A writer or eraser protein resulted in altered cell viability, cell cycle and apoptosis in HeLa cells, suggesting a role of mRNA m1A in cancer. Transcriptomic and proteomic analyses further revealed the molecular mechanisms underlying the phenotypic variation.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"290"},"PeriodicalIF":6.2,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144728350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The oily nucleus- role of phospholipids in genome biology: membrane-directed roles and signaling in the nucleoplasm. 磷脂在基因组生物学中的作用：核质中的膜导向作用和信号传导。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-25 DOI: 10.1007/s00018-025-05825-3

Zobia Umair, Zahid Nawaz, Sumaiya Hasnain, Wolfgang Fischle

{"title":"The oily nucleus- role of phospholipids in genome biology: membrane-directed roles and signaling in the nucleoplasm.","authors":"Zobia Umair, Zahid Nawaz, Sumaiya Hasnain, Wolfgang Fischle","doi":"10.1007/s00018-025-05825-3","DOIUrl":"10.1007/s00018-025-05825-3","url":null,"abstract":"Phospholipids, widely known for their structural role in cellular membranes, are now also recognized to play pivotal roles in signal transduction, metabolism, and cellular homeostasis. However, the nucleus is often overlooked in the context of phospholipid biology. The dynamic abundance and precise management of the turnover of nuclear phospholipids by dedicated kinases, phosphatases, and phospholipases implies specialized functions. Like the cytoplasm, many of these biological roles occur or are initiated within the nuclear membrane. However, several aspects of nuclear phospholipid biology appear to be based in the nucleoplasm and are mediated by dynamic and soluble lipoprotein complexes. In many cases, the exact working spaces and molecular mechanisms of action of nuclear phospholipids are not yet clearly defined, and their physiology is likely underestimated due to technical challenges. Nonetheless, in recent years, the impact of nuclear phospholipids on the structure and function of the genome has been found to be more multifaceted and complex. In this review, we summarize recent insights into the interactions and biological roles of phospholipids with respect to chromatin, gene regulation, and nuclear physiology, and discuss these roles in the context of two broad functional domains - the nuclear membrane and the nucleoplasm. We argue that a more detailed understanding of the molecular working modes of nuclear phospholipids is crucial to enable their full scientific comprehension, especially when the exploration of the biology of nuclear phospholipids and their dysregulation may offer promising avenues for diagnosis and therapeutic interventions for various genome-linked diseases.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"286"},"PeriodicalIF":6.2,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

MyD88 polymerization and association to cellular membranes in a yeast heterologous model. 酵母异源模型中MyD88的聚合和与细胞膜的结合。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-07-25 DOI: 10.1007/s00018-025-05827-1

Elba Del Val, Alejandro Fernández-Vega, María Molina, Víctor J Cid

{"title":"MyD88 polymerization and association to cellular membranes in a yeast heterologous model.","authors":"Elba Del Val, Alejandro Fernández-Vega, María Molina, Víctor J Cid","doi":"10.1007/s00018-025-05827-1","DOIUrl":"10.1007/s00018-025-05827-1","url":null,"abstract":"MyD88 is a key mediator of Toll-like receptor (TLR) signaling, orchestrating the innate immune response upon stimulation by pathogen-associated molecular patterns (PAMPs). Structurally, MyD88 consists of a Death domain (DD), a 20-amino acid N-terminal extension, and an intermediate (INT) region that connects it to a Toll/Interleukin-1 receptor (TIR) domain. At the core of the signaling complex known as myddosome, MyD88 undergoes homopolymeric interactions to propagate the signal. In this study, we use Saccharomyces cerevisiae as a heterologous model to assess the contribution of individual MyD88 domains to self-interaction and subcellular localization. In yeast, MyD88 localizes to endoplasmic reticulum-mitochondria encounter sites (ERMES). Here, we show that its DD is sufficient for attachment to the ERMES. Deletion of its 20 N-terminal residues increased MyD88 stability, shifting its aggregation pattern from patches to filaments. In contrast, a chimeric MyD88 variant bearing the plasma membrane-binding N-terminal extension of TIRAP, another TLR4-associated myddosome component, exhibited diffuse mitochondrial distribution. Moreover, we found that the ERMES-associated dynamin-like protein Dnm1, involved in mitochondrial fission, played a crucial role in MyD88 expression in yeast. On the other hand, the MyD88 TIR domain alone accumulated at lipid droplets in yeast, and its overexpression led to growth impairment and mitochondrial condensation. These findings suggest that MyD88 association with cellular membranes promotes self-assembly, a process essential for functional TLR signaling. Additionally, we adapted a tripartite GFP system to titrate MyD88 homopolymerization in yeast. Using this system, we observed that the oncogenic L252P mutation significantly reduced MyD88 ability to self-interact.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"288"},"PeriodicalIF":6.2,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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