BMB Reports最新文献

{"title":"Recent advances in single-cell bioinformatics for inferring higher-order chromatin contact maps.","authors":"Seung Kyun Noh, Minhyeok Lee, Hyobin Jeong","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>DNA, a large molecule located in the nucleus, carries essential genetic information, including gene loci and cis-regulatory elements. Despite its extensive length, DNA is compactly stored within the limited space of the nucleus due to its hierarchical three-dimensional (3D) organization. In this structure, DNA is organized into territories known as topologically associated domains (TADs). Within each TAD, numerous chromatin loops link promoters and enhancers across the genome. These loops and the interactions between promoters and enhancers are dynamically regulated, thereby controlling gene transcription activities. With the rapid advancements in single-cell genomics technologies, TAD boundaries and chromatin loops can now be observed at the level of individual cells, allowing researchers to explore cellular heterogeneity in tissues. This review will summarize the state-of-the-art bioinformatics methods recently developed to analyze single-cell Hi-C and epigenomics datasets, which infer higher-order chromatin interactions within the 3D genome. Additionally, we will discuss the biological applications of these tools and future directions for comprehensively investigating epigenomic heterogeneity across different species, developmental stages, and disease states.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights to B cell tolerance involving the mechanosensitive ion channel Piezo1.","authors":"Youngjae Hong, Chaiwon Kim, Kihyuck Kwak","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>B cell tolerance is critical for preventing autoimmunity, yet the mechanisms by which B cells discriminate self from non-self antigens remain incompletely understood. While early findings emphasize the role of classical antigen-mediated BCR signaling strength by varying antigen formats, emerging evidence highlights the importance of mechanical cues during antigen recognition. This review explores how mechanosensitive ion channels, particularly Piezo1, contribute to B cell activation and tolerance by integrating physical forces at the immune synapse. We discuss how membrane-bound and particulate antigens induce mechanotransduction through Piezo1, promoting enhanced B cell responses by extracellular calcium influx. Additionally, we consider the differential roles of Piezo1 in various physiological contexts, including shear stress, tissue migration, and substrate stiffness. Understanding mechanosensor-mediated signaling in coordination with other pathways such as antigen recognition, T cell help, or cytokine signaling expands our knowledge of B cell biology and introduces a new paradigm for modulating humoral immunity in health and disease.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cdk1-dependent lamin aggregation underlies oxidative stress-induced nuclear shape abnormalities.","authors":"Ju-Hyun Ahn, Min-Guk Cho, Abdul Basit, In-Kang Song, Kong-Joo Lee, Jae-Ho Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Altered nuclear morphology, one of the characteristics of cancer cells, is often indicative of tumor prognosis. While reactive oxygen species (ROS) are known to induce nuclear morphology changes, mechanisms underlying these effects remain elusive, particularly regarding nuclear assembly. We hypothesized that mitotic cells might exhibit increased susceptibility to ROSinduced nuclear deformation due to the dynamic nature of nuclear envelope during mitosis, i.e., disassembly and reassembly. Interestingly, we discovered that exposure of mitotic cells to hydrogen peroxide (H2O2) resulted in persistence of lamin aggregates during early mitosis, which coincided with aberrant nuclear morphology. Further investigation revealed a dampening effect of H2O2 on Cdk1, a pivotal kinase governing mitotic entry. Our in vitro kinase assays demonstrated that H2O2 mediated reduction of Cdk1 activity, resulting in diminished phosphorylation of lamin, a key Cdk1 substrate. Notably, restoration of Cdk1 activity rescued lamin phosphorylation, thereby mitigating lamin aggregation. Furthermore, persistence of lamin aggregation during mitotic entry correlated with premature reassembly of lamin during mitotic exit, affecting nuclear envelope reassembly. These findings collectively suggest that ROS-mediated perturbation of Cdk1 activity during early mitosis can trigger lamin aggregation that affects lamin reassembly, thereby disrupting nuclear morphology. Our study elucidates a novel mechanism by which ROS can disrupt nuclear architecture by modulating Cdk1 activity during mitosis.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reverse beta-oxidation for biochemical production: insights into the functional properties of key enzymes.","authors":"Areum Lee, Hyeoncheol Francis Son","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The reverse β-oxidation (rBOX) pathway is emerging as a promising alternative to fossil fuel-based chemical production, providing a versatile platform for the synthesis of various valueadded biochemicals. Efficient application of rBOX depends on the selection of enzymes with high catalytic activity, suitable substrate specificity, and strong functional compatibility within the pathway. In this review, we focus on the structural and biochemical characteristics of four key enzymes-thiolase, 3-hydroxyacyl-CoA dehydrogenase, enoyl-CoA hydratase, and enoyl-CoA reductase-and explore how their individual features and combinations influence pathway performance. We then summarize previous studies that highlight the importance of enzyme cooperation in achieving optimal production outcomes. These insights provide valuable guidance for the rational design of rBOX-based biosynthetic pathways tailored to specific chemical targets.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cereblon upregulation overcomes thalidomide resistance in multiple myeloma through mitochondrial functional reprogramming.","authors":"Jubert Marquez, Nammi Park, Jae Hyeog Choi, Maria Victoria Faith Garcia, Jessa Flores, Bayalagmaa Nyamaa, Jung Eun Seol, Hyoung Kyu Kim, Myung Geun Shin, Sae Gwang Park, Jin Han","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Patients with multiple myeloma develop resistance to thalidomide during therapy, and the mechanisms to counteract thalidomide resistance remain elusive. Here, we explored the interaction between cereblon and mitochondrial function to mitigate thalidomide resistance in multiple myeloma. Measurements of cell viability, ATP production, mitochondrial membrane potential, mitochondrial ROS, and protein expression via western blotting were conducted in vitro using KSM20 and KMS26 cells to assess the impact of thalidomide on multiple myeloma. An in vivo analysis using xenografted multiple myeloma cells in BALB/c nude mice revealed that KMS20 cells were resistant to thalidomide, whereas KMS26 cells were sensitive. Overexpression of CRBN in a KMS20 xenograft model reversed its resistance to thalidomide, reduced tumor growth, and significantly extended the survival rate of the mice. Overexpression of CRBN in thalidomide-resistant KMS20 cells during thalidomide treatment led to effective cell death through the modulation of mitochondrial function and protein expression, mediated by AMPKα1 signaling. Conversely, both genetic and pharmacological knockdowns of CRBN rendered KMS26 cells resistant to thalidomide, indicating that CRBN level modulation directly influences mitochondrial functions. These findings propose that targeting cereblon offers a promising strategy in overcoming thalidomide resistance in multiple myeloma through mitochondrial reprogramming.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of RNA modifications in aging and age-related diseases.","authors":"Eunseok Kang, Rosa Haque, Hanseul Lee, Seung-Jae V Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>RNA modifications are key epigenetic alterations that play regulatory functions in RNA biology, including RNA stability and translation. Emerging evidence indicates that RNA modification is crucial for various physiological and pathological processes, including aging. This review describes functions of key RNA modifications, including N⁶-methyladenosine (m⁶A), 5-methylcytosine (m⁵C), N⁷-methylguanosine (m⁷G), 2'-O-methylation (Nm), N¹-methyladenosine (m¹A), adenosine-to-inosine (A-to-I) RNA editing, pseudouridylation (ψ), and N4-acetylcytidine (ac4C), highlighting their roles in aging and age-associated diseases. We also discuss dynamics of RNA modifications and associated protein factors during aging. This review provides important information on molecular mechanisms underlying aging regulation, focusing on effects of RNA modifications, which can help us understand healthy longevity in humans. [BMB Reports 2025; 58(9): 389-396].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"389-396"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ubiquitination and ubiquitin-like modifications in metabolic dysfunction-associated steatotic liver disease: mechanisms and implications.","authors":"Hyunjin Rho, Uijin Kim, Jaewhan Song","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a complex metabolic disorder that encompasses a spectrum of conditions, from simple hepatic steatosis to metabolicassociated steatohepatitis (MASH). MASH is characterized by inflammation and accelerated fibrosis progression, which can ultimately lead to cirrhosis and hepatocellular carcinoma. Given its steadily increasing prevalence, MASLD has emerged as a global health epidemic. Significantly, MASLD represents a stage where liver function can still be partially restored through dietary interventions and physical exercise. However, the longterm sustainability of these lifestyle changes poses a significant challenge. Furthermore, the complex and heterogeneous nature of MASH complicates the development of pharmacotherapeutic strategies and the identification of reliable biomarkers for effective treatment. Therefore, it is essential to gain a comprehensive understanding of the molecular mechanisms driving MASLD and to develop targeted therapeutic interventions. Recent studies have underscored the critical role of posttranslational modifications (PTMs) of proteins in regulating MASLD. PTMs, such as ubiquitination, SUMOylation, Neddylation, and UFMylation, are known to modulate protein function and diverse cellular processes. Among these, ubiquitination is particularly noteworthy for its dual role in mediating protein degradation through the ubiquitin-proteasome system and in regulating cellular signaling pathways in a non-proteolytic manner, depending on the specific linkages formed at the seven distinct lysine residues (K6, K11, K27, K29, K33, K48, and K63) and the Met1-linked (M1) linear ubiquitin chain. Despite significant progress in this area, studies focusing on linkage-specific ubiquitination events that regulate MASLD remain relatively limited. Thus, this review aims to provide a comprehensive summary of the role of linkage-specific ubiquitination in regulating MASLD, as well as exploring other ubiquitinlike modifications that may contribute to its pathophysiology. [BMB Reports 2025; 58(9): 371-388].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"371-388"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metal-stabilized G-quadruplexes: biological insights and sensing applications.","authors":"Seongmin Kim, Dahoon Kim, Yoori Kim","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Repeat sequences account for approximately 45% of the human genome, and can produce noncanonical DNA secondary structures that include G-quadruplexes (G4s). Among these, G4s are unique, in that their formation and stability are largely influenced by metal cations, such as Na^＋, K^＋, Ca^2＋, and Mg^2＋. These cations stabilize G4 structures, while also influencing their folding and biological activities. Interactions between G4s and metal ions affect key cellular processes that include transcription, replication, and genome stability. This review highlights the structural diversity and functional roles of G4s, and further explores how their ion-dependent properties have been harnessed for applications in biosensing and therapeutic development. Future research directions to advance G4-targeted technologies for both diagnostic and clinical use are also discussed. [BMB Reports 2025; 58(9): 397-405].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"397-405"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to: Decoding tau acetylation in Alzheimer's disease and tauopathies: from site-specific mechanisms to therapeutic horizons.","authors":"Yoonah R Oh, Min-Kyoo Shin","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[Erratum to: BMB Reports 2025; 58(8): 325-339, PMID: 40635200, PMCID: PMC12402691] BMB Reports recently published the article \"Decoding tau acetylation in Alzheimer's disease and tauopathies: from site-specific mechanisms to therapeutic horizons\" (BMB Rep. 2025; Vol. 58, No.8, pp.325-339) by Yoonah R. Oh et al. The original publication inadvertently omitted the ACKNOWLEDGEMENTS section. This section has now been added to the online version. ACKNOWLEDGEMENTS This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (RS-2023-00209597). All figures were created using BioRender. The authors and editorial office apologize for any inconvenience or confusion this omission may have caused to the authors and readers.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":"58 9","pages":"424"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The antioxidant effects of decursin inhibit EndMT progression through PI3K/AKT/NF-κB and Smad signaling pathways.","authors":"Ran Kim, Sejin Kim, Hojin Kim, Seongtae Jeong, Hanbyeol Moon, Jongmin Kim, Byeong-Wook Song, Woochul Chang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Endothelial cells (ECs) undergo endothelial-to-mesenchymal transition (EndMT) during the pathophysiology of cardiovascular diseases, a complex cellular transdifferentiation process closely associated with increased oxidative stress under adverse conditions such as myocardial infarction (MI). Decursin, a major constituent of Angelica gigas Nakai, displays diverse pharmacological properties. This study aimed to examine the antioxidant impact of decursin on EndMT regulation in both in vitro and in vivo models as a potential therapeutic strategy for MI. In vitro the inhibitory effects of decursin treatment were analyzed by measuring the expression of EndMT-associated genes, assessing endothelial function, intracellular ROS levels, and mitochondrial membrane potential. Furthermore, the study elucidated antioxidation-related signaling mechanisms within EndMT-induced ECs. In vivo, the therapeutic potential of decursin was investigated using a mouse model of MI. Decursin administration attenuated the EndMT process by upregulating CD31 and VE-Cadherin while decreasing fibronectin and α-SMA expression in EndMT-induced ECs. It also lowered ROS levels, preserved mitochondrial membrane potential, and modulated functional properties, resulting in enhanced LDL uptake and diminished endothelial permeability. Endothelial integrity was sustained via regulation of the PI3K/AKT/NF-κB and Smad-dependent signaling pathways, both responsive to oxidative stress during EndMT. In the MI mouse model, decursin reversed EndMT, lessened myocardial fibrosis and apoptosis, and promoted recovery of infarcted regions. The treated hearts demonstrated improved cardiovascular performance. Decursin represents a novel therapeutic strategy targeting intracellular oxidative stress induced by EndMT. By exerting antioxidant activity through the PI3K/AKT/NF-κB and Smaddependent pathways, decursin maintains endothelial function, suppresses myocardial fibrosis, and supports cardiac recovery following MI therapy. [BMB Reports 2025; 58(9): 406-414].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"406-414"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}