Journal of Biological Chemistry最新文献

{"title":"ARV1 is a component of the enzyme initiating glycosylphosphatidylinositol biosynthesis.","authors":"TianTian Lu,Saori Umeshita,Kae Imanishi,Yicheng Wang,Yi-Shi Liu,Masamichi Nagae,Yuya Senoo,Kazutaka Ikeda,Morihisa Fujita,Taroh Kinoshita,Yoshiko Murakami","doi":"10.1016/j.jbc.2025.110236","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110236","url":null,"abstract":"Glycosylphosphatidylinositol (GPI) serves as a membrane anchor of numerous cell surface proteins. It is synthesized in the endoplasmic reticulum from phosphatidylinositol (PI) by stepwise reactions and transferred to the C-terminus of the protein. Defects in genes involved in GPI biosynthesis affect the expression of GPI-anchored proteins (GPI-APs) or their structure, causing the neurological disorder, inherited GPI deficiency (IGD). Individuals with ARV1 deficiency have symptoms resembling IGD, but how ARV1 regulates GPI biosynthesis is poorly understood. Here, we show that ARV1 acts as a component of the enzyme initiating GPI biosynthesis, GPI N-acetylglucosaminyltransferase (GPI-GnT) complex, which forms a ring structure as predicted by AlphaFold3. ARV1 associates with PIGQ, a GPI-GnT component, and ARV1 mutants defective in this association lose their ability to enhance GPI-GnT activity, showing that association with PIGQ is critical for ARV1's function. ARV1-containing GPI-GnT used PI more efficiently than ARV1-less GPI-GnT in an in vitro enzyme assay. Collectively, our results suggest that ARV1 facilitates efficient recruitment of PI to GPI-GnT, thereby playing a critical role in the regulation of GPI-AP expression.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"42 1","pages":"110236"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluorescent labeling of proteins in vitro and in vivo using encoded peptide tags.","authors":"Maya de Luis,Shuwa Xu,Kai Zinn","doi":"10.1016/j.jbc.2025.110229","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110229","url":null,"abstract":"Epitope tags are a simple and versatile way to label proteins as their sequences can easily be inserted into protein coding sequences, so that the expressed proteins will bear the tag(s). These tags can be used to identify and purify proteins in vitro using Western blots, flow cytometry, affinity chromatography, and other techniques. When labeled with a fluorescent probe, tagged proteins can be visualized in live or fixed cells or tissues using fluorescence microscopy, allowing for the study of protein dynamics. The most widely used epitope tags are those that have affinity to an antibody, which can be used in fixed-sample immunohistochemistry studies. While this will allow insight into a protein's localization, it will not provide any information on its dynamics. Other tags were developed with the intended use in live imaging. In this mini review, we discuss epitope tags that have affinity to antibodies, nanobodies, and small molecules and their use in fluorescence microscopy for fixed and live imaging.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"33 1","pages":"110229"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antioxidant capacity of the iron-sulfur cluster assembly protein IscU2 is mediated by aspartate metabolism to promote tumor survival.","authors":"Xunjun Yang,Na Liang,Dandan Liu,Jimei Yan,Xiali Yang,Jinya Lv,Saijun Xiao,Xiujuan Wei,Xuyang Chen,Zhengquan Yang,Shanying Gui,Liqin Jin,Shihui Yu,Jianxin Lyu,Xiaojun Ren","doi":"10.1016/j.jbc.2025.110234","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110234","url":null,"abstract":"Environmental nutrient levels affect cancer cell metabolism, activating adaptive mechanisms in cancer cells to deal with nutrient stress. However, it remains unclear how tumor cells sustain survival under nutrient-stress circumstances through metabolic reprogramming. Our study focused on nutrient deficiency-induced oxidative damage, revealing that increased expression of the iron-sulfur (Fe-S) cluster assembly protein, IscU2, is essential for the survival of pancreatic ductal adenocarcinoma (PDAC) cells in glucose-deficient conditions. Glucose deficiency induces IscU2 expression via the activation of the AMPK pathway, allowing IscU2 to exhibit antioxidant properties that are absent under glucose-sufficient conditions. Upregulated IscU2 stimulates aspartate synthesis by bolstering mitochondrial metabolism, including respiration and the tricarboxylic acid cycle, in a Fe-S cluster-dependent manner. Notably, oxidative stress and apoptosis induced by IscU2 depletion in glucose-deficient PDAC cells can be restored by aspartate-mediated NADPH production. These findings highlight the importance of IscU2 in PDAC cell metabolism and its essential function in supporting cell survival under nutrient-deficient conditions.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"56 1","pages":"110234"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABHD18 degrades cardiolipin by stepwise hydrolysis of fatty acids.","authors":"Mindong Ren,Shiyu Chen,Miriam L Greenberg,Michael Schlame","doi":"10.1016/j.jbc.2025.110237","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110237","url":null,"abstract":"Cardiolipin (CL), the signature phospholipid of mitochondria, carries four fatty acids that are remodeled after de novo synthesis. In yeast, remodeling is accomplished by the joint action of Cld1, a lipase that removes a fatty acid from CL, and Taz1, a transacylase that transfers a fatty acid from another phospholipid to monolyso-CL. While taz1 homologues have been identified in all eukaryotes, cld1 homologues have remained obscure. Here we demonstrate that ABHD18, a highly conserved protein of plants, animals, and humans, is functionally homologous to Cld1. Knockdown of Abhd18 decreased the concentration of monolyso-CL in murine, Taz-knockout myoblasts. Inactivation of Abhd18 in Drosophila substantially increased the abundance of CL. Abhd18 inactivation also reversed the increase in the rate of CL degradation, as measured with 13C isotopes, and the accumulation of deacylated CLs, such as monolyso-CL and dilyso-CL, in TAZ-deficient flies. CL species with more than 5 double bonds were resistant to ABHD18. Our data demonstrate that ABHD18 is the elusive lipase that hydrolyzes CL in mice and flies and presumably in other organisms. Rather than removing just one fatty acid, we show that ABHD18 deacylates CL further. Thus, ABHD18 catalyzes the breakdown of CL whereas TAZ protects CL from degradation.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"2 1","pages":"110237"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Throwing a spotlight on genomic dark matter: the power and potential of transposon-insertion sequencing.","authors":"Laura M Nolan,Mark A Webber,Alain Filloux","doi":"10.1016/j.jbc.2025.110231","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110231","url":null,"abstract":"Linking genotype to phenotype is a central goal in biology. In the microbiological field, transposon mutagenesis is a technique that has been widely used since the 1970's to facilitate this connection. The development of modern 'omics approaches and next-generation sequencing, have allowed high-throughput association between genes and their putative function. In 2009, four different variations of modern transposon-insertion sequencing (TIS) approaches were published, being referred to as transposon-directed insertion-site sequencing (TraDIS), transposon sequencing (Tn-seq), insertion sequencing (INSeq) and high-throughput insertion tracking by deep sequencing (HITS). These approaches exploit a similar concept to allow estimation of the essentiality or contribution to fitness of each gene in any bacterial genome. The main rationale is to perform a comparative analysis of the abundance of specific transposon mutants under one or more selective conditions. The approaches themselves only vary in the transposon used for mutagenesis, and in the methodology used for sequencing library preparation. In this review, we discuss how TIS approaches have been used to facilitate a major shift in our fundamental understanding of bacterial biology in a range of areas. We focus on several aspects including pathogenesis, biofilm development, polymicrobial interactions in various ecosystems, and antimicrobial resistance. These studies have provided new insight into bacterial physiology and revealed predicted functions for hundreds of genes previously representing genomic 'dark matter'. We also discuss how TIS approaches have been used to understand complex bacterial systems and interactions and how future developments of TIS could continue to accelerate and enrich our understanding of bacterial biology.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"141 1","pages":"110231"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of cyanobacterial Photosystem I protein environment and spectral capacity in response to changes in electron flow pathways and photon flux.","authors":"Sharon L Smolinski,Monika Tokmina-Lukaszewska,Junia M Holland,Zhanjun Guo,Effie Kisgeropoulos,Brian Bothner,Paul W King,Carolyn E Lubner","doi":"10.1016/j.jbc.2025.110233","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110233","url":null,"abstract":"Cyanobacterial Photosystem I (PSI) can undergo modifications that adjust photosynthetic electron transport in response to fluctuations in environmental and cellular conditions. We recently reported that PSI isolated from Synechocystis sp. PCC 6803 (S. 6803) strains lacking a peripheral oxygen reduction reaction (ORR1) pathway demonstrated altered P700 photooxidation capacity, changes in spectral properties, and a higher proportion of monomers. These changes in PSI were augmented when cells were grown under higher photon flux which creates a greater energy imbalance at PSI. We had shown that the modified PSI is functional in photochemical charge separation and ferredoxin reduction reactions. Thus, we hypothesized that monomerization of PSI was caused by changes in the environment of PsaL, which is known to be essential for stabilizing trimers. To test our hypothesis, we isolated PSI monomers and trimers from ORR1 and wild-type (WT) strains. The electron paramagnetic resonance (EPR) spectra of reduced PSI demonstrated the presence of intact FA and FB [4Fe-4S] clusters, consistent with measurements of functional charge separation and electron transport. Limited proteolysis followed by mass spectrometric analysis showed altered accessibility of PsaL in the ORRI PSI monomers compared to WT monomers, and included regions associated with chlorophyll and carotenoid binding, and in functional interactions with adjacent subunits. In addition, ORR1 PSI monomers had spectral changes compared to WT PSI due to differences in carotenoid compositions. Collectively, these findings reveal new insights into how microbes adjust PSI structure and photochemistry to mitigate photodamage in response to changes in electron utilization by downstream chemical reactions.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"141 1","pages":"110233"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular basis for differential PIP2-mediated association between Vinculin and its splice isoform Metavinculin.","authors":"Mohammad Ashhar I Khan,Venkat R Chirasani,Muzaddid Sarker,Laura McCormick,Sharon L Campbell","doi":"10.1016/j.jbc.2025.110232","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110232","url":null,"abstract":"Vinculin (Vcn) and its splice variant metavinculin (MVcn) are cell adhesion proteins that regulate cell morphology, adhesion and motility. They function as scaffold proteins that anchor membrane receptors to filamentous actin (F-actin) at focal adhesions (FA) and cell-cell junctions. MVcn bears an extra 68 amino acid insert in the tail domain and is selectively expressed in cardiac and smooth muscle cells at sub-stoichiometric levels relative to Vcn. Mutations in the MVcn tail domain (MVt) promote cardiomyopathy, yet how these mutations alter ligand interactions to promote defects in force transduction and reduced blood flow is unclear. One difference between Vcn and MVcn lies in the ability to reorganize F-actin, with MVcn negatively regulating Vcn-mediated F-actin bundling. Vcn associates with phosphatidylinositol 4,5-bisphosphate (PIP2) through its tail domain (Vt) to drive recruitment, activation and FA turnover. However, it remains unclear whether MVcn specifically associates with PIP2-containing membranes and how such interactions might influence its functional interplay with Vcn in tissues where both isoforms coexist. To evaluate the interaction of MVt and MVt cardiomyopathy mutants with PIP2-membranes in comparison with Vt, we conducted mutagenesis, phospholipid-association assays and computational modeling. We found that MVt shows reduced association for PIP2-containing liposomes relative to Vt due to sequence differences within the insert region. Moreover, mutations in MVt that promote cardiomyopathies do not affect PIP2-dependent lipid association. These findings suggest that MVcn differs from Vcn in driving PIP2-mediated membrane association and sheds light on the coordinate role of Vcn and MVcn in membrane association as well as MVcn cardiomyopathy defects.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"1 1","pages":"110232"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NDRG1 and its Family Members: More than Just Metastasis Suppressor Proteins and Targets of Thiosemicarbazones.","authors":"Mahan Gholam Azad,Tiffany Russell,Xuanling Gu,Xiao Zhao,Vera Richardson,Tharushi P Wijesinghe,Golap Babu,Xinnong Guo,Busra Kaya,Mahendiran Dharmasivam,Zhao Deng,Des R Richardson","doi":"10.1016/j.jbc.2025.110230","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110230","url":null,"abstract":"N-Myc downstream regulated gene-1 (NDRG1) and the other three members of this family (NDRG2, 3, and 4) play various functional roles in the cellular stress response, differentiation, migration, and development. These proteins are involved in regulating key signaling proteins and pathways that are often dysregulated in cancer, such as EGFR, PI3K/AKT, c-Met, and the Wnt pathway. NDRG1 is the primary, well-examined member of the NDRG family, and is generally characterized as a metastasis suppressor that inhibits the first step in metastasis, the epithelial-mesenchymal transition. While NDRG1 is well-studied, emerging evidence suggests NDRG2, NDRG3, and NDRG4 also play significant roles in modulating oncogenic signaling and cellular homeostasis. NDRG family members are regulated by multiple mechanisms, including transcriptional control by hypoxia-inducible factors, p53, and Myc, as well as post-translational modifications such as phosphorylation, ubiquitination, and acetylation. Pharmacological targeting of the NDRG family is a therapeutic strategy against cancer. For instance, di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT) and di-2-pyridylketone-4-cyclohexyl-4-methyl-3-thiosemicarbazone (DpC) have been extensively shown to up-regulate NDRG1 expression, leading to metastasis suppression and inhibition of tumor growth in multiple cancer models. Similarly, targeting NDRG2 demonstrates its pro-apoptotic and anti-proliferative effects, particularly in glioblastoma and colorectal cancer. This review provides a comprehensive analysis of the structural features, regulatory mechanisms, and biological functions of the NDRG family and their roles in cancer and neurodegenerative diseases. Additionally, NDRG1-4 are explored as therapeutic targets in oncology, focusing on recent advances in anti-cancer agents that induce the expression of these proteins. Implications for future research and clinical applications are also discussed.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"48 1","pages":"110230"},"PeriodicalIF":4.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Guard cell and whole plant expression of AtTOR improves performance under drought and enhances water use efficiency.","authors":"Li Liu,Peng Gao,Huajin Sheng,Achala Bakshi,David Schneider,Daoquan Xiang,Vivijan Babic,Maozhi Ren,Connor Burbridge,Hanh Nguyen,Sheng Wang,Alma Armenta-Medina,Javier Mora-Macias,Andrew Sharpe,Curtis Pozniak,Jurandir Magalhaes,Raju Datla,Leon Kochian","doi":"10.1016/j.jbc.2025.110220","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110220","url":null,"abstract":"Water use efficiency is an important target for breeding of improved drought resistance. Minimizing leaf transpirational water loss plays a key role in drought resistance. But this reduces CO2 levels in leaves, which often reduces photosynthetic efficiency and yield. Signaling pathways play important roles in stress responses, and identifying the molecular, biochemical, and physiological determinants underlying drought signaling may offer new drought mitigating strategies. To explore these possibilities, and because of the importance of stomata in drought response and photosynthesis, we employed guard cell (GC) targeted and constitutive overexpression of the Target of Rapamycin (TOR) kinase, a master regulator of signaling networks, in transgenic Arabidopsis. To investigate the impact of these AtTOR transgenes in drought, we conducted physiological and molecular investigations into drought responses, including leaf water loss, photosynthetic CO2 assimilation, stomatal H2O/CO2 conductance, , leaf chlorophyll content, and global gene expression in response to drought in wild type and AtTOR expressing Arabidopsis. Links between both guard cell-localized and whole plant AtTOR overexpression were identified, revealing TOR is involved in conservation of water and sustained photosynthetic performance, along with identification of genes associated with drought response in WT vs. AtTOR-expressing transgenic lines. These findings suggest that targeted guard cell AtTOR expression should help achieve a balance between plant water conservation during drought, and maintaining plant performance, by minimizing reductions in photosynthesis. Manipulation of guard cell AtTOR expression could be an effective avenue for developing crops with enhanced drought resistance and increased yield under drought stress, resulting in enhanced water use efficiency.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"89 1","pages":"110220"},"PeriodicalIF":4.8,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The LDL receptor related protein 1 (LRP1) facilitates ACE2-mediated endocytosis of SARS-CoV2 spike protein-containing pseudovirions.","authors":"Mashhood M Wani,Joanna M Cooper,Mary Migliorini,Dudley K Strickland","doi":"10.1016/j.jbc.2025.110227","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.110227","url":null,"abstract":"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, employs the viral spike (S) protein to associate with host cells. While angiotensin-converting enzyme 2 (ACE2) is a major receptor for the SARS-CoV-2 spike protein, evidence reveals that other cellular receptors may also contribute to viral entry. We interrogated the role of the low-density lipoprotein receptor-related protein 1 (LRP1) in the involvement of SARS-CoV-2 viral entry. Employing surface plasmon resonance studies, we demonstrated high affinity binding of the trimeric SARS-CoV-2 spike protein to purified LRP1. Further, we observed high affinity interaction of the SARS-CoV-2 spike protein with other low-density lipoprotein receptor (LDLR) family members as well, including LRP2 and the very low-density lipoprotein receptor (VLDLR). Binding of the SARS-CoV-2 spike protein to LRP1 was mediated by its receptor binding domain (RBD). Several LRP1 ligands require surface exposed lysine residues for their interaction with LRP1, and chemical modification of lysine residues on the RBD with sulfo-NHS-acetate ablated binding to LRP1. Using cellular model systems, we demonstrated that cells expressing LRP1, but not those lacking LRP1, rapidly internalized purified 125I-labeled S1 subunit of the SARS-CoV-2 spike protein. LRP1-mediated internalization of the 125I-labeled S1 subunit was enhanced in cells expressing ACE2. By employing pseudovirion particles containing a murine leukemia virus core and luciferase reporter that express the SARS-CoV-2 spike protein on their surface, we confirmed that LRP1 facilitates ACE2-mediated psuedovirion endocytosis. Together, these data implicate LRP1, and perhaps other LDLR family members as host factors for SARS-CoV-2 infection.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":"1 1","pages":"110227"},"PeriodicalIF":4.8,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143932854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}