Life Science AlliancePub Date : 2024-08-07Print Date: 2024-10-01DOI: 10.26508/lsa.202402755
Peng Wang, Zixian Li, Sung-Hoon Kim, Haijin Xu, Hao Huang, Chutong Yang, Abby Snape, Jung-Hyun Choi, Sara Bermudez, Marie-Noelle Boivin, Nicolas Ferry, Jason Karamchandani, Bhushan Nagar, Nahum Sonenberg
{"title":"PPM1G dephosphorylates eIF4E in control of mRNA translation and cell proliferation.","authors":"Peng Wang, Zixian Li, Sung-Hoon Kim, Haijin Xu, Hao Huang, Chutong Yang, Abby Snape, Jung-Hyun Choi, Sara Bermudez, Marie-Noelle Boivin, Nicolas Ferry, Jason Karamchandani, Bhushan Nagar, Nahum Sonenberg","doi":"10.26508/lsa.202402755","DOIUrl":"10.26508/lsa.202402755","url":null,"abstract":"<p><p>The mRNA 5'cap-binding eukaryotic translation initiation factor 4E (eIF4E) plays a critical role in the control of mRNA translation in health and disease. One mechanism of regulation of eIF4E activity is via phosphorylation of eIF4E by MNK kinases, which promotes the translation of a subset of mRNAs encoding pro-tumorigenic proteins. Work on eIF4E phosphatases has been paltry. Here, we show that PPM1G is the phosphatase that dephosphorylates eIF4E. We describe the eIF4E-binding motif in PPM1G that is similar to 4E-binding proteins (4E-BPs). We demonstrate that PPM1G inhibits cell proliferation by targeting phospho-eIF4E-dependent mRNA translation.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11306785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141902133","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}
Life Science AlliancePub Date : 2024-08-06Print Date: 2024-10-01DOI: 10.26508/lsa.202402713
Sishir Subedi, Tomokazu S Sumida, Yongjin P Park
{"title":"A scalable approach to topic modelling in single-cell data by approximate pseudobulk projection.","authors":"Sishir Subedi, Tomokazu S Sumida, Yongjin P Park","doi":"10.26508/lsa.202402713","DOIUrl":"10.26508/lsa.202402713","url":null,"abstract":"<p><p>Probabilistic topic modelling has become essential in many types of single-cell data analysis. Based on probabilistic topic assignments in each cell, we identify the latent representation of cellular states. A dictionary matrix, consisting of topic-specific gene frequency vectors, provides interpretable bases to be compared with known cell type-specific marker genes and other pathway annotations. However, fitting a topic model on a large number of cells would require heavy computational resources-specialized computing units, computing time and memory. Here, we present a scalable approximation method customized for single-cell RNA-seq data analysis, termed ASAP, short for Annotating a Single-cell data matrix by Approximate Pseudobulk estimation. Our approach is more accurate than existing methods but requires orders of magnitude less computing time, leaving much lower memory consumption. We also show that our approach is widely applicable for atlas-scale data analysis; our method seamlessly integrates single-cell and bulk data in joint analysis, not requiring additional preprocessing or feature selection steps.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897728","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}
Life Science AlliancePub Date : 2024-08-06Print Date: 2024-10-01DOI: 10.26508/lsa.202402754
Robert A Chesters, Jiajie Zhu, Bethany M Coull, David Baidoe-Ansah, Lea Baumer, Lydia Palm, Niklas Klinghammer, Seve Chen, Anneke Hahm, Selma Yagoub, Lídia Cantacorps, Daniel Bernardi, Katrin Ritter, Rachel N Lippert
{"title":"Fasting-induced activity changes in MC3R neurons of the paraventricular nucleus of the thalamus.","authors":"Robert A Chesters, Jiajie Zhu, Bethany M Coull, David Baidoe-Ansah, Lea Baumer, Lydia Palm, Niklas Klinghammer, Seve Chen, Anneke Hahm, Selma Yagoub, Lídia Cantacorps, Daniel Bernardi, Katrin Ritter, Rachel N Lippert","doi":"10.26508/lsa.202402754","DOIUrl":"10.26508/lsa.202402754","url":null,"abstract":"<p><p>The brain controls energy homeostasis by regulating food intake through signaling within the melanocortin system. Whilst we understand the role of the hypothalamus within this system, how extra-hypothalamic brain regions are involved in controlling energy balance remains unclear. Here we show that the melanocortin 3 receptor (MC3R) is expressed in the paraventricular nucleus of the thalamus (PVT). We tested whether fasting would change the activity of MC3R neurons in this region by assessing the levels of c-Fos and pCREB as neuronal activity markers. We determined that overnight fasting causes a significant reduction in pCREB levels within PVT-MC3R neurons. We then questioned whether perturbation of MC3R signaling, during fasting, would result in altered refeeding. Using chemogenetic approaches, we show that modulation of MC3R activity, during the fasting period, does not impact body weight regain or total food intake in the refeeding period. However, we did observe significant differences in the pattern of feeding-related behavior. These findings suggest that the PVT is a region where MC3R neurons respond to energy deprivation and modulate refeeding behavior.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11303869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897729","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}
Life Science AlliancePub Date : 2024-08-05Print Date: 2024-10-01DOI: 10.26508/lsa.202402702
Sam Dawes, Nicholas Hurst, Gabriel Grey, Lukasz Wieteska, Nathan V Wright, Iain W Manfield, Mohammed H Hussain, Arnout P Kalverda, Jozef R Lewandowski, Beining Chen, Anastasia Zhuravleva
{"title":"Chaperone BiP controls ER stress sensor Ire1 through interactions with its oligomers.","authors":"Sam Dawes, Nicholas Hurst, Gabriel Grey, Lukasz Wieteska, Nathan V Wright, Iain W Manfield, Mohammed H Hussain, Arnout P Kalverda, Jozef R Lewandowski, Beining Chen, Anastasia Zhuravleva","doi":"10.26508/lsa.202402702","DOIUrl":"10.26508/lsa.202402702","url":null,"abstract":"<p><p>The complex multistep activation cascade of Ire1 involves changes in the Ire1 conformation and oligomeric state. Ire1 activation enhances ER folding capacity, in part by overexpressing the ER Hsp70 molecular chaperone BiP; in turn, BiP provides tight negative control of Ire1 activation. This study demonstrates that BiP regulates Ire1 activation through a direct interaction with Ire1 oligomers. Particularly, we demonstrated that the binding of Ire1 luminal domain (LD) to unfolded protein substrates not only trigger conformational changes in Ire1-LD that favour the formation of Ire1-LD oligomers but also exposes BiP binding motifs, enabling the molecular chaperone BiP to directly bind to Ire1-LD in an ATP-dependent manner. These transient interactions between BiP and two short motifs in the disordered region of Ire1-LD are reminiscent of interactions between clathrin and another Hsp70, cytoplasmic Hsc70. BiP binding to substrate-bound Ire1-LD oligomers enables unfolded protein substrates and BiP to synergistically and dynamically control Ire1-LD oligomerisation, helping to return Ire1 to its deactivated state when an ER stress response is no longer required.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893775","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}
Life Science AlliancePub Date : 2024-08-01Print Date: 2024-10-01DOI: 10.26508/lsa.202402621
Narasaem Lee, Subin Kim, Na Young Lee, Heeji Jo, Pyeonghwa Jeong, Haushabhau S Pagire, Suvarna H Pagire, Jin Hee Ahn, Mi Sun Jin, Chul-Seung Park
{"title":"Activation mechanism and novel binding sites of the BK<sub>Ca</sub> channel activator CTIBD.","authors":"Narasaem Lee, Subin Kim, Na Young Lee, Heeji Jo, Pyeonghwa Jeong, Haushabhau S Pagire, Suvarna H Pagire, Jin Hee Ahn, Mi Sun Jin, Chul-Seung Park","doi":"10.26508/lsa.202402621","DOIUrl":"10.26508/lsa.202402621","url":null,"abstract":"<p><p>The large-conductance calcium-activated potassium (BK<sub>Ca</sub>) channel, which is crucial for urinary bladder smooth muscle relaxation, is a potential target for overactive bladder treatment. Our prior work unveiled CTIBD as a promising BK<sub>Ca</sub> channel activator, altering <i>V</i> <sub><i>1/2</i></sub> and <i>G</i> <sub><i>max</i></sub> This study investigates CTIBD's activation mechanism, revealing its independence from the Ca<sup>2+</sup> and membrane voltage sensing of the BK<sub>Ca</sub> channel. Cryo-electron microscopy disclosed that two CTIBD molecules bind to hydrophobic regions on the extracellular side of the lipid bilayer. Key residues (W22, W203, and F266) are important for CTIBD binding, and their replacement with alanine reduces CTIBD-mediated channel activation. The triple-mutant (W22A/W203A/F266A) channel showed the smallest <i>V</i> <sub><i>1/2</i></sub> shift with a minimal impact on activation and deactivation kinetics by CTIBD. At the single-channel level, CTIBD treatment was much less effective at increasing <i>P</i> <sub><i>o</i></sub> in the triple mutant, mainly because of a drastically increased dissociation rate compared with the WT. These findings highlight CTIBD's mechanism, offering crucial insights for developing small-molecule treatments for BK<sub>Ca</sub>-related pathophysiological conditions.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875271","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}
Life Science AlliancePub Date : 2024-08-01Print Date: 2024-10-01DOI: 10.26508/lsa.202402653
Luisa P Mori, Michael J Corley, Andrew T McAuley, Alina Pang, Thomas Venables, Lishomwa C Ndhlovu, Matthew E Pipkin, Susana T Valente
{"title":"Transcriptional and methylation outcomes of didehydro-cortistatin A use in HIV-1-infected CD4<sup>+</sup> T cells.","authors":"Luisa P Mori, Michael J Corley, Andrew T McAuley, Alina Pang, Thomas Venables, Lishomwa C Ndhlovu, Matthew E Pipkin, Susana T Valente","doi":"10.26508/lsa.202402653","DOIUrl":"10.26508/lsa.202402653","url":null,"abstract":"<p><p>Ongoing viral transcription from the reservoir of HIV-1 infected long-lived memory CD4<sup>+</sup> T cells presents a barrier to cure and associates with poorer health outcomes for people living with HIV, including chronic immune activation and inflammation. We previously reported that didehydro-cortistatin A (dCA), an HIV-1 Tat inhibitor, blocks HIV-1 transcription. Here, we examine the impact of dCA on host immune CD4<sup>+</sup> T-cell transcriptional and epigenetic states. We performed a comprehensive analysis of genome-wide transcriptomic and DNA methylation profiles upon long-term dCA treatment of primary human memory CD4<sup>+</sup> T cells. dCA prompted specific transcriptional and DNA methylation changes in cell cycle, histone, interferon-response, and T-cell lineage transcription factor genes, through inhibition of both HIV-1 and Mediator kinases. These alterations establish a tolerogenic Treg/Th2 phenotype, reducing viral gene expression and mitigating inflammation in primary CD4<sup>+</sup> T cells during HIV-1 infection. In addition, dCA suppresses the expression of lineage-defining transcription factors for Th17 and Th1 cells, critical HIV-1 targets, and reservoirs. dCA's benefits thus extend beyond viral transcription inhibition, modulating the immune cell landscape to limit HIV-1 acquisition and inflammatory environment linked to HIV infection.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875272","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}
Life Science AlliancePub Date : 2024-07-31Print Date: 2024-10-01DOI: 10.26508/lsa.202402651
Youhei Egami, Katsuhisa Kawai, Nobukazu Araki
{"title":"Rit1-TBC1D10B signaling modulates FcγR-mediated phagosome formation in RAW264 macrophages.","authors":"Youhei Egami, Katsuhisa Kawai, Nobukazu Araki","doi":"10.26508/lsa.202402651","DOIUrl":"10.26508/lsa.202402651","url":null,"abstract":"<p><p>Phagocytosis is an important immune response that protects the host from pathogen invasion. Rit1 GTPase is known to be involved in diverse cellular processes. However, its role in FcγR-mediated phagocytosis remains unclear. Our live-cell imaging analysis revealed that Rit1 was localized to the membranes of F-actin-rich phagocytic cups in RAW264 macrophages. Rit1 knockout and expression of the GDP-locked Rit1 mutant suppressed phagosome formation. We also found that TBC1D10B, a GAP for the Rab family GTPases, colocalizes with Rit1 in the membranes of phagocytic cups. Expression and knockout studies have shown that TBC1D10B decreases phagosome formation in both Rab-GAP activity-dependent and -independent manners. Notably, the expression of the GDP-locked Rit1 mutant or Rit1 knockout inhibited the dissociation of TBC1D10B from phagocytic cups. In addition, the expression of the GTP-locked Rit1 mutant promoted the dissociation of TBC1D10B in phagocytic cups and restored the rate of phagosome formation in TBC1D10B-expressing cells. These data suggest that Rit1-TBC1D10B signaling regulates FcγR-mediated phagosome formation in macrophages.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11291910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860198","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}
{"title":"Differential roles of lysosomal cholesterol transporters in the development of <i>C. elegans</i> NMJs.","authors":"Amin Guo, Qi Wu, Xin Yan, Kanghua Chen, Yuxiang Liu, Dingfa Liang, Yuxiao Yang, Qunfeng Luo, Mingtao Xiong, Yong Yu, Erkang Fei, Fei Chen","doi":"10.26508/lsa.202402584","DOIUrl":"10.26508/lsa.202402584","url":null,"abstract":"<p><p>Cholesterol homeostasis in neurons is critical for synapse formation and maintenance. Neurons with impaired cholesterol uptake undergo progressive synapse loss and eventual degeneration. To investigate the molecular mechanisms of neuronal cholesterol homeostasis and its role during synapse development, we studied motor neurons of <i>Caenorhabditis elegans</i> because these neurons rely on dietary cholesterol. Combining lipidomic analysis, we discovered that NCR-1, a lysosomal cholesterol transporter, promotes cholesterol absorption and synapse development. Loss of <i>ncr-1</i> causes smaller synapses, and low cholesterol exacerbates the deficits. Moreover, NCR-1 deficiency hinders the increase in synapses under high cholesterol. Unexpectedly, NCR-2, the NCR-1 homolog, increases the use of cholesterol and sphingomyelins and impedes synapse formation. NCR-2 deficiency causes an increase in synapses regardless of cholesterol concentration. Inhibiting the degradation or synthesis of sphingomyelins can induce or suppress the synaptic phenotypes in <i>ncr-2</i> mutants. Our findings indicate that neuronal cholesterol homeostasis is differentially controlled by two lysosomal cholesterol transporters and highlight the importance of neuronal cholesterol homeostasis in synapse development.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11291935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860197","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}
{"title":"Golgi pH homeostasis stabilizes the lysosomal membrane through <i>N</i>-glycosylation of membrane proteins.","authors":"Yu-Shin Sou, Junji Yamaguchi, Keisuke Masuda, Yasuo Uchiyama, Yusuke Maeda, Masato Koike","doi":"10.26508/lsa.202402677","DOIUrl":"10.26508/lsa.202402677","url":null,"abstract":"<p><p>Protein glycosylation plays a vital role in various cellular functions, many of which occur within the Golgi apparatus. The Golgi pH regulator (GPHR) is essential for the proper functioning of the Golgi apparatus. The lysosomal membrane contains highly glycosylated membrane proteins in abundance. This study investigated the role of the Golgi luminal pH in <i>N</i>-glycosylation of lysosomal membrane proteins and the effect of this protein modification on membrane stability using <i>Gphr</i>-deficient MEFs. We showed that <i>Gphr</i> deficiency causes an imbalance in the Golgi luminal pH, resulting in abnormal protein <i>N</i>-glycosylation, indicated by a reduction in sialylated glycans and markedly reduced molecular weight of glycoproteins. Further experiments using FRAP and PLA revealed that <i>Gphr</i> deficiency prevented the trafficking dynamics and proximity condition of glycosyltransferases in the Golgi apparatus. In addition, incomplete <i>N</i>-glycosylation of lysosomal membrane proteins affected lysosomal membrane stability, as demonstrated by the increased susceptibility to lysosomal damage. Thus, this study highlights the critical role of Golgi pH regulation in controlling protein glycosylation and the impact of Golgi dysfunction on lysosomal membrane stability.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855907","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}
{"title":"pyRBDome: a comprehensive computational platform for enhancing RNA-binding proteome data.","authors":"Liang-Cui Chu, Niki Christopoulou, Hugh McCaughan, Sophie Winterbourne, Davide Cazzola, Shichao Wang, Ulad Litvin, Salomé Brunon, Patrick Jb Harker, Iain McNae, Sander Granneman","doi":"10.26508/lsa.202402787","DOIUrl":"10.26508/lsa.202402787","url":null,"abstract":"<p><p>High-throughput proteomics approaches have revolutionised the identification of RNA-binding proteins (RBPome) and RNA-binding sequences (RBDome) across organisms. Yet, the extent of noise, including false positives, associated with these methodologies, is difficult to quantify as experimental approaches for validating the results are generally low throughput. To address this, we introduce pyRBDome, a pipeline for enhancing RNA-binding proteome data in silico. It aligns the experimental results with RNA-binding site (RBS) predictions from distinct machine-learning tools and integrates high-resolution structural data when available. Its statistical evaluation of RBDome data enables quick identification of likely genuine RNA-binders in experimental datasets. Furthermore, by leveraging the pyRBDome results, we have enhanced the sensitivity and specificity of RBS detection through training new ensemble machine-learning models. pyRBDome analysis of a human RBDome dataset, compared with known structural data, revealed that although UV-cross-linked amino acids were more likely to contain predicted RBSs, they infrequently bind RNA in high-resolution structures. This discrepancy underscores the limitations of structural data as benchmarks, positioning pyRBDome as a valuable alternative for increasing confidence in RBDome datasets.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"7 10","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855908","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}