Frontiers in Molecular Neuroscience最新文献

NFE2L1 as a central regulator of proteostasis in neurodegenerative diseases: interplay with autophagy, ferroptosis, and the proteasome. NFE2L1作为神经退行性疾病中蛋白平衡的中枢调节因子：与自噬、铁凋亡和蛋白酶体的相互作用

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-05-01 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1551571

Hossein Khodadadi, Kamila Łuczyńska, Dawid Winiarczyk, Paweł Leszczyński, Hiroaki Taniguchi

{"title":"NFE2L1 as a central regulator of proteostasis in neurodegenerative diseases: interplay with autophagy, ferroptosis, and the proteasome.","authors":"Hossein Khodadadi, Kamila Łuczyńska, Dawid Winiarczyk, Paweł Leszczyński, Hiroaki Taniguchi","doi":"10.3389/fnmol.2025.1551571","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1551571","url":null,"abstract":"Maintaining proteostasis is critical for neuronal health, with its disruption underpinning the progression of neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's diseases. Nuclear Factor Erythroid 2-Related Factor 1 (NFE2L1) has emerged as a key regulator of proteostasis, integrating proteasome function, autophagy, and ferroptosis to counteract oxidative stress and protein misfolding. This review synthesizes current knowledge on the role of NFE2L1 in maintaining neuronal homeostasis, focusing on its mechanisms for mitigating proteotoxic stress and supporting cellular health, offering protection against neurodegeneration. Furthermore, we discuss the pathological implications of NFE2L1 dysfunction and explore its potential as a therapeutic target. By highlighting gaps in the current understanding and presenting future research directions, this review aims to elucidate NFE2L1's role in advancing treatment strategies for neurodegenerative diseases.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1551571"},"PeriodicalIF":3.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Editorial: Neuro-immune interplay: unraveling the complexities of neurological complications and immunology. 社论：神经免疫的相互作用：揭示神经并发症和免疫学的复杂性。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-30 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1607675

Pankaj Gaur, Kumar Vaibhav, Meenakshi Ahluwalia, Seema Gupta

引用次数: 0

Hyperbaric oxygen promotes both the proliferation and chemosensitization of glioblastoma cells by inhibiting HIF1α/HIF2α-ABCG2. 高压氧通过抑制HIF1α/HIF2α-ABCG2促进胶质母细胞瘤细胞的增殖和化学增敏。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-30 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1584407

Sheng Gong, Pan Wang, Bin Liao, Lu Zhao, Nan Wu

{"title":"Hyperbaric oxygen promotes both the proliferation and chemosensitization of glioblastoma cells by inhibiting HIF1α/HIF2α-ABCG2.","authors":"Sheng Gong, Pan Wang, Bin Liao, Lu Zhao, Nan Wu","doi":"10.3389/fnmol.2025.1584407","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1584407","url":null,"abstract":"Introduction: Hyperbaric oxygen enhances glioma chemosensitivity, but the mechanism remains unclear. Hypoxia is common in gliomas, and as the main effector molecules of hypoxia, HIF1α and HIF2α promote the malignant progression by inhibiting cell apoptosis and maintaining stemness. ABCG2 is a marker protein of tumor stem cells and drug efflux transporter protein. This study aims to reveal the detailed mechanism of hyperbaric oxygen promote both proliferation and chemosensitization.Methods: Under hyperbaric oxygen and hypoxic conditions, we investigated the differences in cell cycle, proliferation, apoptosis, LDH release, and the expression of proteins and mRNA. We also conducted studies on transcriptional regulation and performed in vivo experiments.Results: It revealed that under hypoxic conditions, HIF1α, HIF2α, and ABCG2 are highly expressed, and both HIF1α and HIF2α promote ABCG2 expression. After hyperbaric oxygen treatment, the expression of HIF1α, HIF2α, and ABCG2 decreased, both cell proliferation and chemosensitivity increased. After knocking out HIF1α and HIF2α, cell proliferation and chemosensitivity increased, but the expression of stem cell marker proteins decreased. ChIP-qPCR revealed that HIF1α and HIF2α target the ABCG2 promoter. Gain-and loss-of-function experiments suggested that ABCG2 can promote the expression of stem cell marker proteins, inhibit cell apoptosis, and promote tumor progression.Conclusion: This study confirmed that hyperbaric oxygen can inhibit ABCG2 expression through HIF1α and HIF2α, thereby promoting the proliferation and chemosensitization of gliomas.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1584407"},"PeriodicalIF":3.5,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12075184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Traumatic brain injury and autophagy: a pilot study about the immunohistochemical expression of LC3B, Beclin 1, p62, and LAMP2A in human autoptic samples. 外伤性脑损伤与自噬：LC3B、Beclin 1、p62、LAMP2A在人自噬样本中免疫组化表达的初步研究

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-28 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1562954

Tommaso Livieri, Letizia Alfieri, Emiliana Giacomello, Djordje Alempijević, Tijana Petrovic, Yanko Georgiev Kolev, Davide Radaelli, Margherita Neri, Stefano D'Errico

{"title":"Traumatic brain injury and autophagy: a pilot study about the immunohistochemical expression of LC3B, Beclin 1, p62, and LAMP2A in human autoptic samples.","authors":"Tommaso Livieri, Letizia Alfieri, Emiliana Giacomello, Djordje Alempijević, Tijana Petrovic, Yanko Georgiev Kolev, Davide Radaelli, Margherita Neri, Stefano D'Errico","doi":"10.3389/fnmol.2025.1562954","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1562954","url":null,"abstract":"Introduction: Autophagy is a cellular stress response that has been shown in the literature to be active in cerebral cells after a traumatic brain injury (TBI). The aim of this study is to investigate the potential use of four proteins involved in autophagy (LC3B, Beclin 1, p62, and LAMP2A), as a forensic diagnostic marker for TBI.Methods: We analyzed histological samples obtained from the frontal lobe of 10 subjects who died within 1 h of a TBI (Group A), 13 who died between 1 h and 32 days post-TBI (Group B), and a control group of 10 subjects who died without head trauma (Group C). Immunohistochemical (IHC) staining using anti-LC3B, anti-Beclin 1, anti-p62 and anti-LAMP2A antibodies was performed.Results and discussion: The results show that LC3B staining was the only one that show a statistically significant difference between groups. In particular, the percentage of neurons displaying an autophagic pattern was calculated from six random acquisitions per subject, and the results were compared across groups using one way ANOVA. Significant differences were observed between Groups A and B, and between Groups B and C, with p-values of 0.0055 and 0.0035, respectively. While the difference between Groups A and C was not statistically significant (p-value of 0.9845). These findings suggest that LC3B may serve as a useful diagnostic marker for TBI in cases where death is not immediate and open the door for further research.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1562954"},"PeriodicalIF":3.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12066584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143997195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptomic analysis of the TRP gene family in human brain physiopathology. TRP基因家族在人脑生理病理中的转录组学分析。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-24 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1576941

Barbara Olejniczak, Arpita Balakrishnan, Justyna Augustyniak, Elżbieta Salińska, Agnieszka Bronisz, Jakub Godlewski

{"title":"Transcriptomic analysis of the TRP gene family in human brain physiopathology.","authors":"Barbara Olejniczak, Arpita Balakrishnan, Justyna Augustyniak, Elżbieta Salińska, Agnieszka Bronisz, Jakub Godlewski","doi":"10.3389/fnmol.2025.1576941","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1576941","url":null,"abstract":"The transient receptor potential (TRP) gene family is vital to cellular physiology, mediating ion flow across membranes and facilitating sensory signal transduction. This article examines the transcriptomic landscape of TRP genes, emphasizing their varying expression across organs, tissues, and cells, with a particular focus on the brain. Analysis reveals a distinct spatial distribution of TRP gene expression, notably enriched in the hippocampus during brain development, highlighting their essential role in neuronal function. Utilizing datasets from the Human Protein Atlas, Allen Human Brain Atlas, and studies on aging and dementia, associations are identified between TRP gene expression and the development or pathophysiology of neural tissue, highlighting the therapeutic potential of TRP channels in addressing, e.g., sensory impairments and cognitive decline. These insights into the regulatory dynamics of TRP channels lay a foundation for developing targeted interventions for neurodegenerative disorders.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1576941"},"PeriodicalIF":3.5,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12058757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of SUR1 isoforms in the brain and heart after ischemia/reperfusion. 缺血/再灌注后脑和心脏SUR1亚型的表达。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-17 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1536409

Iván Alquisiras-Burgos, Irlanda Peralta-Arrieta, Mónica Espinoza-Rojo, Alejandro Salazar-Salgado, Iván Antonino-Olguín, Alicia Sánchez-Mendoza, María Sánchez-Aguilar, Martha-Eugenia Ruiz-Tachiquín, Hilda-Alicia Valdez-Salazar, Alma Ortiz-Plata, Javier Franco-Pérez, Arturo Hernández-Cruz, Penélope Aguilera

{"title":"Expression of SUR1 isoforms in the brain and heart after ischemia/reperfusion.","authors":"Iván Alquisiras-Burgos, Irlanda Peralta-Arrieta, Mónica Espinoza-Rojo, Alejandro Salazar-Salgado, Iván Antonino-Olguín, Alicia Sánchez-Mendoza, María Sánchez-Aguilar, Martha-Eugenia Ruiz-Tachiquín, Hilda-Alicia Valdez-Salazar, Alma Ortiz-Plata, Javier Franco-Pérez, Arturo Hernández-Cruz, Penélope Aguilera","doi":"10.3389/fnmol.2025.1536409","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1536409","url":null,"abstract":"The sulfonylurea receptor 1 (SUR1) has been classified as a member of the adenosine triphosphate (ATP)-binding cassette (ABC) transporter superfamily. SUR1, unlike the classic ABC transporters, assembles with Kir6.2, forming KATP channels to regulate the flux of potassium ions. In the central nervous system, SUR1 is weakly expressed in some brain regions but is induced by pathological conditions in the different cell types of the neurovascular unit. Therefore, we first analyzed the expression of SUR1 in various rat tissues and brain regions to identify SUR1 isoforms and their mRNA exon composition under physiological conditions. Later, we focused on the SUR1 expression in the brain and heart after ischemia/reperfusion. We observed two SUR1 isoforms (170 and 60-75 kDa) abundantly expressed in most rat tissues, except for the testis and brain, where basal expression of these isoforms was relatively low and exhibit a band of 100 kDa. Every exons coding for the functional domains of SUR1 mRNA were amplified from the tissues and brain regions analyzed. Results from in vitro and in vivo experiments indicated that SUR1 isoforms previously identified (170 and 60-75 kDa) were dramatically overexpressed in the brain after middle cerebral artery occlusion followed by reperfusion. In contrast, myocardial infarction followed by reperfusion significantly reduced SUR1 isoform expression in the heart. This study demonstrates the expression of at least two SUR1 isoforms in various tissues and suggests that ischemic processes may differentially regulate SUR1 expression depending on the tissue injured.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1536409"},"PeriodicalIF":3.5,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12043708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Redox homeostasis and inflammation in fibroblasts of patients with Friedreich Ataxia: a possible cross talk. 弗里德赖希共济失调患者成纤维细胞的氧化还原稳态和炎症：可能的串扰。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-16 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1571402

Andrea Quatrana, Sara Petrillo, Caterina Torda, Eleonora De Santis, Enrico Bertini, Fiorella Piemonte

{"title":"Redox homeostasis and inflammation in fibroblasts of patients with Friedreich Ataxia: a possible cross talk.","authors":"Andrea Quatrana, Sara Petrillo, Caterina Torda, Eleonora De Santis, Enrico Bertini, Fiorella Piemonte","doi":"10.3389/fnmol.2025.1571402","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1571402","url":null,"abstract":"Redox homeostasis is impaired in Friedreich's Ataxia (FRDA), a neurodegenerative disease caused by the decreased expression of the mitochondrial protein frataxin. Nrf2, the master regulator of tissue redox balance, is defective in the disease, driving cells to ferroptosis. Neuro-inflammation is recently emerging as an additional pathological mechanism in FRDA and has to be understood in order to go deeper into the pathogenesis of the disease. As a functional cross talk between Nrf2 and NF-kB pathways has been previously reported, we wonder if inflammation may be activated in FRDA as a consequence of Nrf2 deficiency. Thus, we analyzed the expression of proteins involved in the antioxidant and inflammatory responses in fibroblasts of patients with FRDA. We found a significant activation of the TLR4/NF-kB/IL-1β axis in patients, associated to a consistent increase of the redox enzymes thioredoxin 1 (TRX1) and glutaredoxin 1 (GLRX1), which are essential to activate NF-kB under oxidative stress conditions. Furthermore, we investigated the role of 4-HNE, a by-product of lipid peroxidation, as a potential mediator between ferroptosis and inflammation in FRDA.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1571402"},"PeriodicalIF":3.5,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Brain microvascular endothelial cells differentiated from a Friedreich's Ataxia patient iPSC are deficient in tight junction protein expression and paracellularly permeable. 从弗里德里希共济失调患者iPSC分化的脑微血管内皮细胞缺乏紧密连接蛋白表达和细胞旁通透性。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-15 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1511388

Frances M Smith, Daniel J Kosman

{"title":"Brain microvascular endothelial cells differentiated from a Friedreich's Ataxia patient iPSC are deficient in tight junction protein expression and paracellularly permeable.","authors":"Frances M Smith, Daniel J Kosman","doi":"10.3389/fnmol.2025.1511388","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1511388","url":null,"abstract":"Friedreich's Ataxia (FA) is a rare, inherited ataxia resulting from GAA triplet expansions in the first intron of the Frataxin (FXN) gene, which encodes a mitochondrial protein involved in the incorporation of iron into iron-sulfur clusters. We previously identified decreased levels of F-actin and tight junction (TJ) proteins, which coincided with paracellular permeability in an FXN shRNA-mediated knockdown immortalized human brain microvascular endothelial cell (BMVEC) model. This premise is underexplored in the FA literature, prompting us to confirm these findings using a patient-derived iPSC model. One line each of FA patient iPSCs and age- and sex-matched apparently healthy iPSCs were differentiated into BMVEC-like cells. We quantified actin glutathionylation, F-actin abundance, TJ expression and organization, and barrier integrity. In the absence of dysregulated F-actin organization, FA iBMVEC exhibited a loss of 50% ZO-1, 63% Occludin, and 19% Claudin-5 protein expression, along with a disruption in the bi-cellular organization of the latter two proteins. Functionally, this correlated with barrier hyperpermeability, delayed barrier maturation, and increased flux of the fluorescent tracer Lucifer Yellow. These data indicate that decreased barrier integrity is a pathophysiological phenotype of FA brain microvascular endothelial cells. Clinically, this may represent a targetable pathway to reduce brain iron accumulation, neuroinflammation, and neurodegeneration profiles in FA. Additionally, an investigation into other barrier systems, such as the blood-nerve barrier, blood-CSF barrier, or cardiac vasculature, may provide insights into the extra-neural symptoms experienced by FA patients.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1511388"},"PeriodicalIF":3.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Profiling the expression and functional roles of mRNAs and lncRNAs associated with post-stroke aphasia. 分析与脑卒中后失语相关的mrna和lncrna的表达和功能作用。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-09 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1513218

Yanling Xi, Hui Chang, Mei Qu

{"title":"Profiling the expression and functional roles of mRNAs and lncRNAs associated with post-stroke aphasia.","authors":"Yanling Xi, Hui Chang, Mei Qu","doi":"10.3389/fnmol.2025.1513218","DOIUrl":"https://doi.org/10.3389/fnmol.2025.1513218","url":null,"abstract":"Objective: Post-stroke aphasia (PSA) is one of the primary causes of post-stroke impairment, although its underlying mechanism is unknown; therefore, this study aimed to identify the long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) linked to PSA and to understand the potential processes by which they may operate.Methods: RNA sequencing was used to determine the lncRNA and mRNA expression profiles for PSA patients and healthy control peripheral blood mononuclear cells. This allowed for the discovery of lncRNAs and differentially expressed genes (DElncRNAs and DEGs). Gene Ontology (GO) and KEGG enrichment analyses were performed on these DElncRNAs and DEGs, and qPCR was used to confirm their expression. Furthermore, any correlations between these characteristics with differential expression and the language routines of PSA patients were evaluated.Results: In total, comparisons of the groups yielded 577 DElncRNAs and 892 DEGs. Functional enrichment analyses of these targets demonstrated the strong enrichment of co-expressed DElncRNAs and DEGs in immune system processes and the inflammatory response. The expression levels of the lncRNAs CTD-2545M3.2 and RP11-24N18.1 and the mRNAs RPS10 and LAIR2 were similarly highly connected with verbal conduct in PSA patients upon admission.Conclusion: The results highlight the lncRNA and mRNA profiles linked to PSA, demonstrating the various methods via which these DElncRNAs and DEGs may influence this clinical setting.","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"18 ","pages":"1513218"},"PeriodicalIF":3.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12014634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

How the ghrelin receptor recognizes the acyl-modified orexigenic hormone. 生长素受体如何识别酰基修饰的促氧激素。

IF 3.5 3区医学

Frontiers in Molecular Neuroscience Pub Date : 2025-04-07 eCollection Date: 2025-01-01 DOI: 10.3389/fnmol.2025.1549366

Yuki Shiimura, Masayasu Kojima, Takahiro Sato

引用次数: 0