Journal of Biological Chemistry最新文献

{"title":"Glyceraldehyde-3-Phosphate Dehydrogenase/1,3-Bisphosphoglycerate-NADH as Key Determinants in Controlling Human Retinal Endothelial Cellular Functions: Insights from Glycolytic Screening.","authors":"Nicole Oska, Ahmed M Awad, Shaimaa Eltanani, Mohamed Shawky, Armaan Naghdi, Thangal Yumnamcha, Lalit Pukhrambam Singh, Ahmed S Ibrahim","doi":"10.1016/j.jbc.2025.108472","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108472","url":null,"abstract":"<p><p>Maintaining barrier integrity, along with cell adhesion to the extracellular matrix and the subsequent process of cell spreading, are essential functions of endothelial cells, including human retinal endothelial cells (HRECs). Disruptions in these processes can lead to vision-threatening conditions like diabetic retinopathy. However, the bioenergetic mechanisms that regulate HREC barrier function and cell spreading remain incompletely understood. This study investigates the role of lower glycolytic components in modulating these critical functions of HRECs. In vitro, Electric Cell-Substrate Impedance Sensing (ECIS) technology was used to measure real-time changes in HREC barrier integrity (electrical resistance) and cell spreading (capacitance). Pharmacological inhibitors targeting lower glycolytic components were tested: heptelidic acid for glyceraldehyde-3-phosphate dehydrogenase (GAPDH), NG-52 for phosphoglycerate kinase (PGK), shikonin for pyruvate kinase M (PKM), galloflavin for lactate dehydrogenase (LDH), AZD3965 for lactate transporter (MCT-1), and MSDC-0160 for the mitochondrial pyruvate carrier (MPC). GAPDH knockdown was performed using siRNA, and cell viability was assessed via lactate dehydrogenase (LDH) release assays. For in vivo studies, wild-type C57BL/6J mice received intravitreal injections of heptelidic acid, while control mice received vehicle (DMSO). Retinal vascular permeability was assessed by fluorescein angiography (FA) and retinal albumin leakage. The most significant decrease in electrical resistance and increase in capacitance of HRECs were observed following the dose-dependent inhibition of GAPDH and the resulting reduction in 1,3-bisphosphoglycerate (1,3-BPG) and NADH by heptelidic acid. LDH level analysis at 24-48 hours post-treatment with heptelidic acid (1 and 10 μM) showed no significant difference compared to controls, indicating that the observed disruption of HREC functionality was not due to cell death. Supporting these findings, inhibition of downstream glycolytic steps that result in the accumulation of 1,3-BPG and NADH, such as treatment with NG-52 for PGK or shikonin for PKM, led to a significant increase in electrical resistance and a decrease in cell capacitance. Furthermore, GAPDH knockdown via siRNA also led to a significant decrease in cellular resistance in HRECs. In vivo, FA imaging demonstrated that intravitreal injection of heptelidic acid led to significant retinal vascular leakage, further supported by increased albumin extravasation in treated eyes. Conversely, pharmacological inhibition of other lower glycolytic components, including LDH, MCT, and MPC, did not significantly alter HREC barrier function or spreading behavior. This study highlights the distinct roles of lower glycolytic components in regulating HREC functionality. GAPDH and its downstream products (1,3-BPG and NADH) are shown to play a pivotal role in maintaining barrier integrity and promoting HREC adhesion and spreading.","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108472"},"PeriodicalIF":4.0,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752851","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":"Maackia amurensis seed lectin (MASL) structure and sequence comparison with other Maackia amurensis lectins.","authors":"Ashok R Nayak, Cayla J Holdcraft, Ariel C Yin, Rachel E Nicoletto, Caifeng Zhao, Haiyan Zheng, Dmitry Temiakov, Gary S Goldberg","doi":"10.1016/j.jbc.2025.108466","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108466","url":null,"abstract":"<p><p>Maackia amurensis lectins, including MASL, MAA, and MAL2, are widely utilized in biochemical and medicinal research. However, the structural and functional differences between these lectins have not been defined. Here, we present a high-resolution cryo-EM structure of MASL revealing that its tetrameric assembly is directed by two intersubunit disulfide bridges. These bridges, formed by C272 residues, are central to the dimer-of-dimers assembly of a MASL tetramer. This cryo-EM structure also identifies residues involved in stabilizing the dimer interface, multiple glycosylation sites, and calcium and manganese atoms in the sugar-binding pockets of MASL. Notably, our analysis reveals that Y250 in the carbohydrate-binding site of MASL adopts a flipped conformation, likely acting as a gatekeeper that obstructs access to non-cognate substrates, a feature that may contribute to MASL's substrate specificity. Sequence analysis suggests that MAA is a truncated version of MASL, while MAL2 represents a homologous isoform. Unlike MASL, neither MAL2 nor MAA contains a cysteine residue required for disulfide bridge formation. Accordingly, analysis of these proteins using reducing and nonreducing SDS-PAGE confirms that the C272 residue in MASL drives intermolecular disulfide bridge formation. These findings provide critical insights into the unique structural features of MASL that distinguish it from other Maackia amurensis lectins, offering a foundation for further exploration of its biological and therapeutic potential.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108466"},"PeriodicalIF":4.0,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752852","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":"Activating Transcription Factor 3 regulates hepatic Apolipoprotein A4 upon metabolic stress.","authors":"Jasmine Encarnacion, Danielle M Smith, Joseph Choi, Joseph Scafidi, Michael J Wolfgang","doi":"10.1016/j.jbc.2025.108468","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108468","url":null,"abstract":"<p><p>The liver plays essential roles in maintaining systemic glucolipid homeostasis under ever changing metabolic stressors. Metabolic dysregulation can lead to both adaptive and maladaptive changes that impact systemic physiology. Here we examined disparate genetic and environmental metabolic stressors and identified Apolipoprotein A4 (ApoA4) as a circulating protein upregulated in liver-specific knockouts for Carnitine Palmitoyltransferase 2 and Pyruvate Carboxylase. We found this upregulation to be exacerbated by fasting and high fat or ketogenic diets. Unique among these models was a concomitant increase in Activating Transcription Factor 3 (Atf3). Liver-specific overexpression of Atf3 resulted in increased ApoA4 expression in a sex-dependent manner. To understand the requirement of Atf3 to metabolic stress, we generated liver-specific Atf3, Cpt2 double knockout mice. These experiments demonstrated the requirement for Atf3 in the induction of ApoA4 mRNA, ApoA4 protein, and serum triglycerides that were also sex dependent. These experiments reveal the roles of hepatic Atf3 and ApoA4 in response to metabolic stress in vivo.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108468"},"PeriodicalIF":4.0,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752850","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":"PEX1^G843D remains functional in peroxisome biogenesis but is rapidly degraded by the proteasome.","authors":"Connor J Sheedy, Soham P Chowdhury, Bashir A Ali, Julia Miyamoto, Eric Z Pang, Julien Bacal, Katherine U Tavasoli, Chris D Richardson, Brooke M Gardner","doi":"10.1016/j.jbc.2025.108467","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108467","url":null,"abstract":"<p><p>The PEX1/PEX6 AAA-ATPase is required for the biogenesis and maintenance of peroxisomes. Mutations in HsPEX1 and HsPEX6 disrupt peroxisomal matrix protein import and are the leading cause of Peroxisome Biogenesis Disorders (PBDs). The most common disease-causing mutation in PEX1 is the HsPEX1^G843D allele, which results in a reduction of peroxisomal protein import. Here we demonstrate that in vitro the homologous yeast mutant, ScPex1^G700D, reduces the stability of Pex1's active D2 ATPase domain and impairs assembly with Pex6, but can still form an active AAA-ATPase motor. In vivo, ScPex1^G700D exhibits only a slight defect in peroxisome import. We generated model human HsPEX1^G843D cell lines and show that PEX1^G843D is rapidly degraded by the proteasome, but that induced overexpression of PEX1^G843D can restore peroxisome import. Additionally, we found that the G843D mutation reduces PEX1's affinity for PEX6, and that impaired assembly is sufficient to induce degradation of PEX1^WT. Lastly, we found that fusing a deubiquitinase to PEX1^G843D significantly hinders its degradation in mammalian cells. Altogether, our findings suggest a novel regulatory mechanism for PEX1/PEX6 hexamer assembly and highlight the potential of protein stabilization as a therapeutic strategy for PBDs arising from the G843D mutation and other PEX1 hypomorphs.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108467"},"PeriodicalIF":4.0,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752853","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":"Discovery of potent and selective PROTACs for the protein kinase LZK for the treatment of head and neck cancer.","authors":"Meghri Katerji, Knickole L Bergman, Eric Lindberg, Maxine R Rubin, Amy L Funk, Carolyn C Woodroofe, Katherine Nyswaner, Kamila Karpińska, Remigiusz Serwa, Anna Marusiak, Rolf E Swenson, John F Brognard","doi":"10.1016/j.jbc.2025.108452","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108452","url":null,"abstract":"<p><p>Leucine zipper-bearing kinase (LZK) is overexpressed in 20% of head and neck squamous cell carcinoma (HNSCC) cases and has emerged as a promising therapeutic target in this cancer subtype. LZK promotes HNSCC survival and proliferation by stabilizing c-MYC and GOF-p53 in kinase-dependent and -independent manners, respectively. Herein, we developed a new series of LZK degraders utilizing proteolysis-targeting chimera (PROTAC) technology by modulating the linker region or LZK warhead of LZK-targeting PROTAC-21A, previously developed by our lab. Among the 27 PROTACs synthesized and tested, PROTAC 17 was found to be the most potent, degrading LZK at 250 nM and suppressing HNSCC viability at 500 nM. In summary our lead PROTAC effectively targeted LZK for proteasomal degradation and inhibited oncogenic activity in HNSCC cell lines with amplified LZK.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108452"},"PeriodicalIF":4.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742863","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":"Role of noncanonical histone H2A variant, H2A.Z, to maintain proper centromeric transcription and chromosome segregation.","authors":"Mahmuda Akter, Xiaoai Lyu, Jack Lu, Xiao Wang, Tyson Phonesavanh, Hao Wang, Hongtao Yu, Jungseog Kang","doi":"10.1016/j.jbc.2025.108464","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108464","url":null,"abstract":"<p><p>The genome stability of eukaryotic cells is ensured by proper regulation of histones and their variants. H2A.Z, a conserved and essential histone H2A variant, plays a crucial role in this process by regulating various chromatin-related processes such as gene expression, heterochromatin formation, DNA damage repair, and chromosome segregation. It has two isoforms, H2A.Z1 and H2A.Z2, also known as H2AFZ and H2AFV respectively, which perform both redundant and non-redundant roles in maintaining genome stability. In this study, we investigated the isoform-specific mitotic functions of H2A.Z in Hela cells. Our studies revealed that the depletion of H2AFV or H2AFZ did not alter the overall cell cycle profile. However, H2AFV depletion significantly increased the formation of micronuclei, indicating defects in chromosome segregation. Additionally, H2AFV depletion led to the accumulation of DNA damage at various nuclear loci including centromeres. Interestingly, we discovered that H2AFV depletion significantly increased centromeric transcription, which may interfere with proper centromere function. Furthermore, we discovered that a mitotic kinase, Aurora B, binds to both H2AFV and H2AFZ, but preferentially to H2AFV. Inhibition of Aurora B activity by hesperadin disrupted proper centromeric transcription but not significantly centromeric localization of H2A.Z. Collectively, these data demonstrated that the H2A.Z isoforms play distinctive regulatory roles in maintaining proper centromeric transcription and DNA repair, ensuring accurate chromosome segregation.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108464"},"PeriodicalIF":4.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742914","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":"Circular RNA circ_0004470 accelerates the occurrence of lung cancer by promoting DNA damage and cell cycle arrest.","authors":"Xueqi Li, Yufei Liu, Qiaoxin Zheng, Weizhou Liu, Huanxuan Li, Shan Rao, Ziwei Xue, Qiuhan Hua, Meizhen Li, Yueting Shao, Xun Li, Yun Zhou, Yiguo Jiang","doi":"10.1016/j.jbc.2025.108456","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108456","url":null,"abstract":"<p><p>Defects in the DNA damage response (DDR) are associated with tumorigenesis, and circular RNAs (circRNAs) can also affect the occurrence and progression of cancer by regulating gene expression. However, the relationship between DNA damage in lung cancer and circRNAs remains unexplored. In this study, circ_0004470 was significantly upregulated in various lung cancer cells (H446, A549, H1299) as well as in carcinogenic animal models and clinical lung cancer samples. Circ_0004470 promoted DNA damage and cell cycle S phase arrest in human pulmonary bronchial epithelial cells, inhibited DNA repair, and accelerated malignant transformation in response to continuous DNA damage-inducing stimulation. Circ_0004470 inhibited DNA repair and cell cycle progression by binding specifically to the nucleotide excision repair complex XPC and damage-specific DNA binding protein 1 (DDB1), thus interacting with the DNA damage response process and accelerating the accumulation of DNA damage. These findings suggest that circRNAs are involved in regulating genetic damage-associated lung cancer and provide insight into the mechanism by which circ_0004470 affects the DDR during carcinogenesis.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108456"},"PeriodicalIF":4.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742855","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 Cardioprotective Role of the G Protein-Coupled Receptor FFAR4 in Atherosclerosis is Independent of Macrophage Foam Cell Regulation.","authors":"Gage M Stuttgen, Caroline J Ring, Vishnu S Guda, Guadalupe K Valdivia Esparza, Daisy Sahoo","doi":"10.1016/j.jbc.2025.108463","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108463","url":null,"abstract":"<p><p>Free fatty acid receptor 4 (FFAR4), also known as G-protein coupled receptor 120 (GPR120), is a long-chain unsaturated fatty acid receptor expressed in multiple tissue types including macrophages. Activation of FFAR4 maintains metabolic homeostasis by regulating adipogenesis, insulin sensitivity, and inflammation. While FFAR4 is best known for its protective role in obesity and diabetes, recent studies have demonstrated that FFAR4 may also prevent the development of atherosclerosis and cardiovascular disease (CVD). Given FFAR4's importance in anti-inflammatory signaling in macrophages, we used peritoneal macrophages from wild-type (WT) and FFAR4 knock-out (Ffar4^-/-) mice to test the hypothesis that FFAR4 prevents the development of macrophage foam cell formation. Our data suggest that neither activation of FFAR4 nor deficiency of FFAR4 has any influence on foam cell outcome in oxidized low-density lipoprotein (oxLDL)-treated macrophages. These data suggest that FFAR4's cardioprotective roles in atherosclerosis are independent of the regulation of macrophage foam cell formation.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108463"},"PeriodicalIF":4.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742976","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":"Transcription blocking properties and transcription-coupled repair of N²-alkylguanine adducts as a model for aldehyde-induced DNA damage.","authors":"Leen Sarmini, Nataliya Kitsera, Mohammed Meabed, Andriy Khobta","doi":"10.1016/j.jbc.2025.108459","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108459","url":null,"abstract":"<p><p>The N² position of guanine is a preferential reaction site in DNA for numerous dietary and environmental carcinogens or their electrophilic metabolites, aldehydes arising from lipid peroxidation as well as reactive by-products of normal metabolism. However, DNA repair mechanisms of the resulting covalent adducts in mammalian cells are not well understood, with nucleotide excision repair (NER), base excision repair (BER), as well as a dioxygenase-mediated damage reversal being discussed as likely pathways. Considering fundamentally different damage recognition principles between the global genome (GG)-NER and the transcription-coupled (TC)-NER, we here assessed transcription blocking capacities of four synthetic deoxyguanosine (dGuo) adducts of variable size and geometry, using a transfection-based reporter assay. Notably, adducts as different as the aliphatic N²-ethylguanine (EtG), the exocyclic 1,N²-ethenoguanine (εG), and the bulky polycyclic 3-(deoxyguanosin-N²-yl)-2-acetylaminofluorene (AAFG), displayed robust DNA strand-specific transcription-blocking properties. The specific TC-NER components CSA and CSB were consistently required for the removal of all transcription-blocking N²-dGuo adducts, whereas the absence of XPC or DDB2/XPE (both specific to GG-NER) did not compromise the repair capacities in the isogenic human cell models. In contrast, no inhibition of the gene expression was detected for reporter constructs carrying N²-methylguanine (MeG) even in the NER-deficient XP-A cell line, suggesting that this adduct is either bypassed with very high efficiency during transcription or repaired by a mechanism different from NER. Collectively, the results identify N²-dGuo adducts bigger than MeG as a structural subclass of transcription-blocking DNA lesions whose repair heavily relies on the TC-NER pathway.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108459"},"PeriodicalIF":4.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742924","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 Green ESCRTs: Newly Defined Roles for ESCRT Proteins in Plants.","authors":"Ethan Weiner, Elizabeth Berryman, Ariadna González Solís, Yuchen Shi, Marisa S Otegui","doi":"10.1016/j.jbc.2025.108465","DOIUrl":"https://doi.org/10.1016/j.jbc.2025.108465","url":null,"abstract":"<p><p>Endocytosis and endosomal trafficking of plasma membrane proteins for degradation regulate cellular homeostasis and development. As part of these processes, ubiquitinated plasma membrane proteins (cargo) are recognized, clustered, and sorted into intralumenal vesicles of multivesicular endosomes by ESCRT (Endosomal Sorting Complexes Required for Transport) proteins. At endosomes, ESCRT proteins recognize ubiquitinated cargo and mediate the deformation of the endosomal membrane in a negative geometry, away from the cytosol. ESCRTs are organized in five major complexes that are sequentially recruited to the endosomal membrane where they mediate its vesiculation and cargo sequestration. ESCRTs also participate in other membrane remodeling events and are widely conserved across organisms, both eukaryotes and prokaryotes. Plants contain both conserved and unique ESCRT components and show a general trend toward gene family expansion. Plant endosomes show a wide range of membrane budding patterns with potential implications in cargo sequestration efficiency, plant development, and hormone signaling. Understanding the diversification and specialization of plant ESCRT proteins can provide valuable insights in the mechanisms of ESCRT-mediated membrane bending. In this review, we discuss the endosomal function of ESCRT proteins, their unique features in plants, and the potential connections to the modes of plant endosomal vesiculation.</p>","PeriodicalId":15140,"journal":{"name":"Journal of Biological Chemistry","volume":" ","pages":"108465"},"PeriodicalIF":4.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742996","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}