BMB Reports最新文献_第3页

Multi-scale imaging and recording of in-vivo neural activity. 体内神经活动的多尺度成像和记录。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Min Yong Lee, Hyo Won Kim, Kwang Lee

{"title":"Multi-scale imaging and recording of in-vivo neural activity.","authors":"Min Yong Lee, Hyo Won Kim, Kwang Lee","doi":"","DOIUrl":"","url":null,"abstract":"Most in vivo neural technologies have been developed to enhance the resolution of subcellular neuronal activity or to expand the spatial range for tracking ensembles of neurons in the brains of live animals. While these approaches offer great promise for understanding cellular and circuit functions in behaving mammals, their cross-sectional observations are inherently limited in accounting for causal interactions of neural dynamics across various scales of brain architecture. Consequently, the simultaneous observation of multi-scale neural activity has emerged as a crucial strategy for achieving a more comprehensive understanding of brain function. These advancements facilitate the simultaneous detection of diverse signals, providing unprecedented insights into dynamic neurophysiological mechanisms within three-dimensional brain structures that remain poorly understood. Here, we review state-of-the-art technologies for the parallel observation of multiple neural targets in vivo. We highlight strategies for simultaneously observing brain signals at multiple resolutions, aiming to bridge the spatiotemporal gaps between microscopic and macroscopic domains of neurobiology. We also emphasize the technical integration of neural tools to concurrently acquire electrophysiological activity and optical imaging, leveraging their complementary strengths. Finally, we discuss the future challenges and potential prospects of multimodal neural techniques, paving the way for a deeper understanding of brain functions and disorders. [BMB Reports 2026; 59(2): 124-136].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"124-136"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773345","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}

引用次数: 0

Differential regulation of type 2 immunity by glucocorticoids. 糖皮质激素对2型免疫的差异调节。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Hyeonji Song, Jaechul Lim

{"title":"Differential regulation of type 2 immunity by glucocorticoids.","authors":"Hyeonji Song, Jaechul Lim","doi":"","DOIUrl":"","url":null,"abstract":"Glucocorticoids (GCs) are steroid hormones that are commonly utilized in clinical practice due to their immunosuppressive properties. While GCs are commonly understood to diminish various aspects of the immune response, there is evidence suggesting that they may, under certain conditions, enhance immune responses, particularly within the realm of type 2 immunity. In this mini review, we delineate the current understanding of how GCs differentially affect immune responses related to type 2 immunity, including both in vivo and in vitro-such as Th2 (T helper type 2) cell differentiation, regulatory T cell functions, immunoglobulin E production by B cells, and the roles of myeloid cells like dendritic cells, mast cells, eosinophils, and basophils. Furthermore, we probe the molecular mechanisms by which GCs selectively influence these cell types, and discuss how these insights enhance our basic understanding of GC-driven immune regulation. Unraveling these intricate, context-dependent effects could inform the development of more precise and efficacious GC-based treatments, while reducing adverse outcomes associated with Th1/Th2 imbalance, including heightened infection risks and exacerbation of allergic responses. [BMB Reports 2026; 59(2): 101-111].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"101-111"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144727680","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}

引用次数: 0

CodonMutator: a python-based automated oligonucleotide design framework for deep mutational scanning library construction. CodonMutator：一个基于python的自动寡核苷酸设计框架，用于深度突变扫描库的构建。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Jeongha Lee, Seong Kyoon Park, Byung Joon Hwang, Murim Choi

{"title":"CodonMutator: a python-based automated oligonucleotide design framework for deep mutational scanning library construction.","authors":"Jeongha Lee, Seong Kyoon Park, Byung Joon Hwang, Murim Choi","doi":"","DOIUrl":"","url":null,"abstract":"Deep mutational scanning (DMS) enables systematic evaluation of protein sequence-function relationships, but its utility is often limited by the complexity of library construction. Existing mutagenesis strategies are either biased, labor-intensive, or prone to design errors, restricting their scalability for comprehensive variant generation. Here, we present a systematic cloning framework coupled with an automated Python-based pipeline for oligonucleotide design in DMS library construction. Our strategy employs restriction enzyme-guided tiling to partition coding sequences into manageable fragments, ensuring uniform coverage and compatibility with standard cloning workflows. The pipeline supports both strict and relaxed design modes, minimizes redundancy, and incorporates silent mutations to prevent restriction site conflicts. This platform optimizes library design efficiency, improves accuracy, and provides a flexible framework adaptable to diverse genes and experimental contexts. By integrating molecular cloning constraints with computational automation, our method offers a scalable and accessible solution to accelerate DMS library construction and functional genomics studies. [BMB Reports 2026; 59(2): 137-142].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"137-142"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773315","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}

引用次数: 0

Multi-layered gene regulation by long non-coding RNAs: from chromatin to genome architecture. 长链非编码rna的多层基因调控：从染色质到基因组结构。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Jaeryoung Kyung, Minjae Kim, Hye-Rim Shin, Eunsu Kim, Hyun Jung Oh

{"title":"Multi-layered gene regulation by long non-coding RNAs: from chromatin to genome architecture.","authors":"Jaeryoung Kyung, Minjae Kim, Hye-Rim Shin, Eunsu Kim, Hyun Jung Oh","doi":"","DOIUrl":"","url":null,"abstract":"Long non-coding RNAs (lncRNAs) are now recognized as pivotal regulators that enable the fine-tuned control of gene expression. While the functional diversity of lncRNAs challenges comprehensive understanding of their mechanisms, recent advances have revealed how these molecules coordinate epigenomic control, ranging from local chromatin regulation to large-scale nuclear organization. By scaffolding, recruiting, or antagonizing transcription factors and chromatin-modifying complexes, lncRNAs shape chromatin states, including histone modifications and DNA methylation patterns. In parallel, lncRNAs regulate three-dimensional genome architecture by modulating chromatin loops, topologically associating domains, and nuclear compartments. These regulatory mechanisms frequently operate in a coordinated manner, as exemplified by X chromosome inactivation, in which lncRNAs direct chromosome-wide silencing through combined epigenetic reprogramming and architectural remodeling. This review synthesizes current mechanistic insights into how lncRNAs integrate epigenetic modification with architectural regulation to achieve spatiotemporal gene expression, and highlights how lncRNA dysregulation contributes to human disease. We provide an integrative perspective on how lncRNAs link epigenetic programs with genome topology to control normal physiology and pathogenesis. [BMB Reports 2026; 59(2): 112-123].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"112-123"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773327","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}

引用次数: 0

Multi-omics identification of a microbial metabolite driving OXPHOS-mediated epithelial damage in experimental autoimmune encephalomyelitis. 实验性自身免疫性脑脊髓炎中驱动oxphos介导的上皮损伤的微生物代谢物的多组学鉴定

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Eunike Tiffany, Panida Sittipo, Chanyoung Lee, Ju Yeon Lee, Soojin Lee, Yun Kyung Lee

{"title":"Multi-omics identification of a microbial metabolite driving OXPHOS-mediated epithelial damage in experimental autoimmune encephalomyelitis.","authors":"Eunike Tiffany, Panida Sittipo, Chanyoung Lee, Ju Yeon Lee, Soojin Lee, Yun Kyung Lee","doi":"","DOIUrl":"","url":null,"abstract":"Bowel syndrome is a prevalent and debilitating symptom in patients with multiple sclerosis (MS), substantially impairing their quality of life. However, the underlying mechanisms of MS development remain poorly understood. In this study, we demonstrated that intestinal epithelial cells (IECs) and the mucosal barrier were disrupted during experimental autoimmune encephalomyelitis (EAE) induction, driven by the inhibition of mitochondrial oxidative phosphorylation (OXPHOS). Proteomic analysis confirmed alterations in OXPHOS complexes, with a pronounced decrease in the expression of cytochrome c oxidase and ATP synthase subunits in small intestinal epithelial cells (sIECs). We identified a gut microbiota-derived metabolite that induces IEC dysfunction by downregulating OXPHOS protein complexes. Specifically, metabolomic analysis revealed an enrichment of phenyllactic acid (PLA), a phenolic acid typically produced by Lactobacillus murinus, in the cecal contents of EAE mice. Our findings indicate that PLA actively downregulates OXPHOS complexes and restrains maximal mitochondrial respiration. Using a multi-omics approach, this study elucidated a potential mechanism by which gut microbiota dysbiosis observed in EAE mice compromises IEC integrity and disrupts the mucosal barrier. [BMB Reports 2026; 59(2): 151-160].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"151-160"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773316","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}

引用次数: 0

MT1B overexpression enhances malignancy of non-small cell lung cancer cells. MT1B过表达增强A549非小细胞肺癌细胞的恶性。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Yoon Hee Park, Hong Lee, Haewon Kim, Hayan Park, Su A Park, Jin Young Choi, Chaewon Park, Yoon Jeong Nam, Hyejin Lee, Yu-Seon Lee, Jaeyoung Kim, Byoungcheun Lee, Hye-Jin Kim, Ju-Han Lee, Sang Hoon Jeong

{"title":"MT1B overexpression enhances malignancy of non-small cell lung cancer cells.","authors":"Yoon Hee Park, Hong Lee, Haewon Kim, Hayan Park, Su A Park, Jin Young Choi, Chaewon Park, Yoon Jeong Nam, Hyejin Lee, Yu-Seon Lee, Jaeyoung Kim, Byoungcheun Lee, Hye-Jin Kim, Ju-Han Lee, Sang Hoon Jeong","doi":"","DOIUrl":"","url":null,"abstract":"Metallothioneins (MTs) are metal-binding proteins that are involved in heavy metal homeostasis and protection against oxidative stress. The MT1 family comprises several isoforms that are implicated in various diseases, including cancer. Although the dysregulated expression of MT1 isoforms has been observed in lung cancer, the specific role of MT isoform MT1B remains unclear. To investigate the role of MT1B in lung cancer progression, A549 lung cancer cells were transfected with an MT1B expression vector. In vitro assays were performed to assess cell viability, migration, invasion, and colony formation. Western blot analysis revealed increased expression of epithelial-mesenchymal transition (EMT) markers Snail, Vimentin, and N-cadherin, and decreased levels of E-cadherin, indicating EMT induction. In the xenograft model, the MT1Btransfected group formed tumors more rapidly and exhibited significantly increased tumor growth compared to the controls. In addition, RNA sequencing was performed to identify MT1Bdependent gene alterations, and Ingenuity Pathway Analysis (IPA) was applied to characterize the canonical pathways and predicted biological functions associated with these MT1Bspecific genes. These findings suggest that cellular MT1B overexpression has the potential to promote lung cancer growth. [BMB Reports 2026; 59(2): 161-168].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"161-168"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951205","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}

引用次数: 0

Cell-penetrating H3 tail peptides suppress osteoclast differentiation via inhibition of MMP-9-mediated histone H3 clipping. 细胞穿透H3尾肽通过抑制mmp -9介导的组蛋白H3剪切来抑制破骨细胞分化。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Seokchan Lee, Jisu Lee, Sun-Ju Yi, Kyunghwan Kim

{"title":"Cell-penetrating H3 tail peptides suppress osteoclast differentiation via inhibition of MMP-9-mediated histone H3 clipping.","authors":"Seokchan Lee, Jisu Lee, Sun-Ju Yi, Kyunghwan Kim","doi":"","DOIUrl":"","url":null,"abstract":"Osteoclast-mediated bone resorption is closely linked to bone formation, and any disruption in this process can lead to diseases such as osteoporosis. Matrix metalloproteinase-9 (MMP-9) is a nuclear histone protease that specifically cleaves the N-terminal tail (NT) of histone H3 at osteoclastogenic gene loci, thereby facilitating transcription and osteoclast differentiation. In this study, we developed tandem H3 tail peptides (residues 1-40) fused to a cell-penetrating peptide (CPP) to serve as competitive inhibitors of MMP-9. Both wild-type (WT) and P16G mutant peptides effectively localized to the nucleus, inhibited RANKLinduced osteoclast differentiation, and downregulated MMP-9 target genes (Xpr1, Nfatc1) as well as osteoclast-specific genes (Ctsk, Mmp9, Trap, Oscar) without impacting precursor proliferation. Mechanistically, both peptides inhibited MMP-9- mediated H3 NT clipping and decreased H3K18 acetylation by competitively binding to p300, thus disrupting a crucial epigenetic step necessary for histone clipping. While WT and P16G peptides exhibited similar binding affinities to MMP-9, the P16G mutant was resistant to proteolytic cleavage, allowing it to remain associated with MMP-9 for a longer period, which resulted in more effective inhibition of H3 NT clipping and osteoclastogenesis. Collectively, these findings indicate that histone H3 tail-derived peptides inhibit osteoclast differentiation by simultaneously targeting p300-dependent histone acetylation and MMP-9-mediated histone proteolysis. Our study provides valuable mechanistic insights into the epigenetic regulation of osteoclastogenesis and emphasizes engineered histone-derived peptides as a promising class of selective therapeutic inhibitors for osteoclast-driven bone diseases. [BMB Reports 2026; 59(2): 169-175].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"169-175"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146141297","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}

引用次数: 0

Corin inhibits microglial inflammatory activation by suppressing mitochondrial dysfunction in intracerebral hemorrhage. Corin通过抑制脑出血线粒体功能障碍抑制小胶质细胞炎症激活。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Rui Yin, Caixia Qiu, Qikai Shen, Zhong Wang

{"title":"Corin inhibits microglial inflammatory activation by suppressing mitochondrial dysfunction in intracerebral hemorrhage.","authors":"Rui Yin, Caixia Qiu, Qikai Shen, Zhong Wang","doi":"","DOIUrl":"","url":null,"abstract":"Microglial activation driving neuroinflammation is a key factor in secondary brain injury after intracerebral hemorrhage (ICH); however, the regulatory mechanisms remain unknown. This study investigates how corin influences microglial inflammatory activation and its underlying mechanisms. Corin expression in rat ICH brain tissue was assessed at multiple time points. To assess corin's effect on neurological function and microglial inflammation, ICH rats and oxygen-glucose deprivation plus hemin (OGD/H)-stimulated HAPI microglia were treated with corin-encoding lentivirus. Neurobehavioral performance was evaluated using the Morris water maze (MWM). Microglial activation was assessed via Iba-1, iNOS, and Arg-1 expression, cytokine secretion, and migration assays. To determine whether AMPK mediates corin's effects, cells were co-treated with Compound C (an AMPK inhibitor) and corin lentivirus. Corin expression decreased in ICH rat brain tissue, reaching its lowest level on day 3 post-ICH. Corin overexpression protected against ICH-induced neuronal apoptosis and improved neurological deficits as confirmed by MWM. Moreover, corin overexpression reduced microglial activation and inflammation in both ICH rats and OGD/H-stimulated microglial cells, ameliorated mitochondrial dysfunction, and increased the p-AMPK/AMPK ratio. The protective effects of corin on cell migration, inflammation, and mitochondrial function were reversed by Compound C, indicating AMPK is a downstream mediator of corin. Targeting corin offers a promising therapeutic strategy for ICH by reducing neuroinflammation and mitochondrial damage through AMPK activation and modulation of microglial inflammatory phenotype polarization. [BMB Reports 2026; 59(2): 143-150].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"143-150"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773329","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}

引用次数: 0

Stress granules as a central hub linking organelle stress, aging, and neurodegeneration. 应激颗粒是连接细胞器应激、衰老和神经退行性变的中心枢纽。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-02-01

Hyun-Ji Ham, Jin-A Lee

{"title":"Stress granules as a central hub linking organelle stress, aging, and neurodegeneration.","authors":"Hyun-Ji Ham, Jin-A Lee","doi":"","DOIUrl":"","url":null,"abstract":"Stress granules (SGs) are dynamic cytoplasmic assemblies composed of RNAs and proteins that form in response to cellular stress, serving to halt translation and protect cellular integrity. In neurons, SGs mediate adaptive, pro-survival responses to acute stress; however, their dysregulation has been increasingly associated with both aging and neurodegenerative diseases. Aging neurons frequently exhibit changes in SG dynamics-with an increased propensity to form SGs while displaying reduced efficiency in their clearance-resulting in persistent granules that can facilitate the accumulation of pathological protein aggregates (e.g., TDP-43 or tau). Aberrant SG formation and defective clearance mechanisms are implicated in the pathogenesis of key neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Alzheimer's disease (AD), and Parkinson's disease (PD). Recent findings have shown that SGs interface with organelles such as lysosomes, mitochondria, and the endoplasmic reticulum, utilizing autophagic and other protein quality-control mechanisms for clearance. As these clearance pathways progressively decline with age, SGs can transition from promoting cellular adaptation to contributing to cellular dysfunction. In this mini-review, we examine how aging influences SG biology, detail the role of SGs in neurodegenerative diseases, and discuss emerging mechanistic insights and therapeutic strategies aimed at modulating SG dynamics in the context of brain aging. [BMB Reports 2026; 59(2): 85-100].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"85-100"},"PeriodicalIF":3.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951289","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}

引用次数: 0

Deep learning application for genomic data analysis. 基因组数据分析的深度学习应用。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-01-01

Chang Beom Jeong, Hyein Cho, Daechan Park

引用次数: 0