BMB Reports最新文献_第5页

Comparative analyses of ChIP-seq, CUT&RUN and CUT&Tag for Polycomb chromatin profiling. Polycomb染色质分析的ChIP-seq， CUT&RUN和CUT&Tag的比较分析。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-04-01

Yoonji Oh, Hanbyeol Kim, Sanghyun Lee, Soon-Jung Park, Yun-Gwi Park, Sung-Hwan Moon, Inkyung Jung, Chul-Hwan Lee

引用次数: 0

New approach methodologies to model liver fibrosis in metabolic dysfunction-associated steatohepatitis. 代谢功能障碍相关脂肪性肝炎肝纤维化模型的新方法。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-04-01

Seung Min Lee, Da Kyung Hwang, Hyun Young Kim

{"title":"New approach methodologies to model liver fibrosis in metabolic dysfunction-associated steatohepatitis.","authors":"Seung Min Lee, Da Kyung Hwang, Hyun Young Kim","doi":"","DOIUrl":"","url":null,"abstract":"Metabolic dysfunction-associated steatohepatitis (MASH) is a significant global health issue and a leading cause of liver fibrosis, with no effective pharmacological treatments available. Conventional 2D cell cultures and animal models do not fully recapitulate the complex cell-cell interactions and multicellular microenvironment that drive disease progression in humans, which limits their ability to predict therapeutic efficacy accurately. The recent introduction of the FDA Modernization Act 2.0 has paved the way for the use of human-relevant New Approach Methodologies (NAMs) in drug discovery and toxicity testing. This review focuses on recent advancements in NAMs that model MASH-associated liver fibrosis, such as human liver spheroids, iPSC-derived liver organoids, precision-cut liver slices, 3D bioprinting, and liver-on-a-chip systems. By mimicking multicellular interactions and the liver microenvironment, NAMs offer a valuable platform for mechanistic studies and drug screening. Assessing their strengths and limitations can lead to deeper mechanistic insights and expedite the development of new therapeutics for MASH-associated liver fibrosis. [BMB Reports 2026; 59(4): 219-226].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"219-226"},"PeriodicalIF":4.1,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13126071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147688075","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

Reverse beta-oxidation for biochemical production: insights into the functional properties of key enzymes. 生化生产的反β -氧化：对关键酶功能特性的见解。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-04-01

Areum Lee, Hyeoncheol Francis Son

引用次数: 0

CaMKIV negatively regulates osteoblast differentiation by modulating c-Fos and NFATc1 signaling: an in vitro and in vivo mechanistic study. CaMKIV通过调节c-Fos和NFATc1信号负向调节成骨细胞分化：一项体外和体内机制研究。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-04-01

Jung Ha Kim, Kabsun Kim, Inyoung Kim, Semun Seong, Wonbong Lim, Jeong-Tae Koh, Nacksung Kim

引用次数: 0

PPP1R3C functions as a tumor suppressor in endometrial cancer through promotion of glycogen synthesis. PPP1R3C通过促进糖原合成在子宫内膜癌中发挥抑癌作用。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-03-05

Hyang Sook Seol, Jaewon Kim, Ju Hee Oh, Eunhye Choi, Sanghyuk Lee, Eun Ji Nam, Jaesang Kim

引用次数: 0

Sestrin2 protects ovarian granulosa cells by regulating oxidative stress and p53-mediated apoptosis. Sestrin2通过调节氧化应激和p53介导的细胞凋亡来保护卵巢颗粒细胞。

IF 3.3 3区生物学

BMB Reports Pub Date : 2026-03-05

Jeongyun Bae, Joon H Lee, Jong-Seok Kim, Hwan-Woo Park, Jongdae Shin

{"title":"Sestrin2 protects ovarian granulosa cells by regulating oxidative stress and p53-mediated apoptosis.","authors":"Jeongyun Bae, Joon H Lee, Jong-Seok Kim, Hwan-Woo Park, Jongdae Shin","doi":"","DOIUrl":"","url":null,"abstract":"Reactive Oxygen Species (ROS) accumulation disrupts cellular homeostasis, leading to lipid peroxidation, mitochondrial dysfunction, DNA damage, and apoptosis. Sestrin2 (Sesn2) is a critical antioxidant protein that regulates intracellular oxidative stress and protects cells from oxidative damage and apoptosis. However, the role of Sesn2 in ovarian reproductive function remains unclear. In this study, we examined Sesn2 expression in response to oxidative stress using granulosa-like KGN cells derived from human ovarian granulosa cell tumors, mouse granulosa cells, and an oxidative stress mouse model. Additionally, we investigated the protective Sesn2 functions and its mechanisms of action in promoting granulosa cell survival. The results showed that Sesn2 expression markedly increased in granulosa cells exposed to hydrogen peroxide (H2O2) and in oxidative stress models induced by 3-nitropropionic acid (3-NP). Oxidative stress in ovarian granulosa cells increases ROS levels, decreases cell viability, and triggers apoptosis. Sesn2 silencing further aggravates granulosa cell damage, whereas targeting Sesn2 under oxidative stress conditions reduces ROS levels and modulates apoptosis through the p53/Caspase-3 signaling pathway. These findings highlight the pivotal role of Sesn2 in protecting cells against ROS-induced damage, preserving follicular health, and supporting ovarian function and reproductive capacity.","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353747","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}

引用次数: 0

Improved efficiency of protein aggregate removal using ubiquitin with a signal peptide. 利用泛素和信号肽提高蛋白质集合体去除效率。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-03-01

Taek-Yeong Kim, Kwon-Yul Ryu

{"title":"Improved efficiency of protein aggregate removal using ubiquitin with a signal peptide.","authors":"Taek-Yeong Kim, Kwon-Yul Ryu","doi":"","DOIUrl":"","url":null,"abstract":"Lipocalin-2 (LCN2) is a protein secreted by activated astrocytes, and its signal peptide (SP) is essential for secretion and recruitment to the autophagic pathway. SP is a short sequence present at the N-terminus of secreted proteins, such as LCN2, which facilitates transport to the endoplasmic reticulum (ER). Although SP is cleaved during the initial stages of translation in the ER, it influences the subsequent pathways of mature proteins produced in the ER lumen. ER-generated proteins are secreted or recruited to the autophagic pathway. To explore this further, we sought to determine the functional role of SP from a novel perspective. In this study, we fused LCN2 SP to the N-terminus of ubiquitin (Ub), an intracellular protein used for the proteasomal degradation of misfolded proteins and autophagic degradation of protein aggregates. We demonstrated that SP enabled the secretion of free Ub and facilitated the targeting of Ub conjugates to the autophagic pathway. We also found that SP affected intracellular Ub conjugate levels by regulating their degradation via the autophagic pathway. Furthermore, the ER-generated Ub (UbE) showed increased participation in polyubiquitinating protein aggregates generated under proteotoxic stress conditions, promoting the formation of perinuclear aggresome-like structures, and recruitment to the autophagosome. It is highly likely that UbE shares a common route with protein aggregates before being recruited to autophagosomes. Thus, this study suggests that UbE confers an altered trafficking pathway compared with endogenous Ub, thereby facilitating protein aggregate clearance without altering Ub's intrinsic biochemical activity. [BMB Reports 2026; 59(3): 187-192].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"187-192"},"PeriodicalIF":4.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407892","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

Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles. 线粒体数量质量不平衡在细胞衰老：实际读数和最小的分析束。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-03-01

Myeongwoo Jung, Seongho Cha, Eun Kyung Lee

{"title":"Mitochondrial quantity-quality imbalance in cellular senescence: practical readouts and minimal assay bundles.","authors":"Myeongwoo Jung, Seongho Cha, Eun Kyung Lee","doi":"","DOIUrl":"","url":null,"abstract":"Cellular senescence is an irreversible program of cell-cycle arrest that accumulates with age, contributing to chronic inflammation and various age-related diseases. A key feature of senescence paradigms is mitochondrial dysfunction, which involves not just a single defect but a series of coordinated changes in bioenergetics, redox homeostasis, mitochondrial quality control, and organelle interaction. Senescent cells often display a \"quantity-quality imbalance\" in their mitochondria: while the mitochondrial mass may increase, their efficiency in oxidative phosphorylation decreases, leading to a destabilized membrane potential (ΔΨm) and elevated levels of mitochondrial reactive oxygen species (mtROS). These interrelated changes can exacerbate senescence through persistent stress signaling, impaired turnover of damaged mitochondrial components, and alterations in organelle contacts, such as those between endoplasmic reticulum (ER) and mitochondria, and between mitochondria and lysosomes. Given that these phenotypes differ depending on cell type, triggering factors, and timing, no single assay can adequately define senescenceassociated mitochondrial dysfunction. In this review, we present practical, complementary strategies that include extracellular flux-based respiration profiling, ATP output measurement, ΔΨm and ROS assessments, flux-based mitophagy reporters, quantitative network imaging, and contact-site assays. We propose minimal assay bundles that allow for a thorough multidimensional analysis. By establishing standardized, orthogonal measures of mitochondrial quantity and quality, we aim to enhance mechanistic understanding and facilitate the rational evaluation of mitochondria-targeted senolytic and senomorphic therapies. [BMB Reports 2026; 59(3): 177-186].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"177-186"},"PeriodicalIF":4.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147376162","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

HERV-R (ERV3-1) Env gene knockout reduces invasion, migration, and tumor growth in DLD1 colon cancer cells. HERV-R (ERV3-1) Env基因敲除可减少DLD1结肠癌细胞的侵袭、迁移和肿瘤生长。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-03-01

Min-Hye Kim, Eun-Ji Ko, Hyojin An, Seongsoo Choi, Heui-Soo Kim, Sun-Hee Leem, Hee-Jae Cha

{"title":"HERV-R (ERV3-1) Env gene knockout reduces invasion, migration, and tumor growth in DLD1 colon cancer cells.","authors":"Min-Hye Kim, Eun-Ji Ko, Hyojin An, Seongsoo Choi, Heui-Soo Kim, Sun-Hee Leem, Hee-Jae Cha","doi":"","DOIUrl":"","url":null,"abstract":"The human genome contains sequences derived from endogenous retroviruses (HERVs), which constitute approximately 8% of chromosomal DNA. Most HERVs are currently inactive and noninfectious due to recombination, deletion, and mutation after integration into the host genome. However, recent studies have implicated HERVs as mutagens of intracellular genes, contributing to autoimmune diseases and tumors. Several studies have shown a significant association between HERVs and certain cancers. We focused on knocking out the HERV-R (ERV3-1) env gene in the DLD1 colon cancer cell line. A 208-bp deletion was confirmed by genomic PCR and DNA sequencing. As a result, HERV-R env gene expression was significantly lower in DLD1 HERV-R knockout (HERV-R KO) cells compared to control cells at both RNA and protein levels. Additionally, the invasion and migration abilities of HERV-R KO cells were significantly reduced. In vivo experiments on mice injected with HERV-R KO cells showed smaller tumor sizes compared to mice injected with control cells, suggesting that HERV-R env plays an important role in tumor growth. Further mRNA-seq analysis identified genes associated with cell invasion and migration. The STRING tool, which analyzes gene correlations, confirmed that HERV-R is linked to genes involved in cancer proliferation, migration, and invasion in colon cancer. This study suggests that the expression of the HERV-R env gene influences the tumorigenic properties of colon cancer, providing valuable evidence for potential clinical studies in colon cancer patients. [BMB Reports 2026; 59(3): 201-207].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"201-207"},"PeriodicalIF":4.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145556259","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

Cereblon upregulation overcomes thalidomide resistance in multiple myeloma through mitochondrial functional reprogramming. 小脑上调通过线粒体功能重编程克服多发性骨髓瘤的沙利度胺耐药性。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-03-01

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

{"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":"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. [BMB Reports 2026; 59(3): 193-200].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"193-200"},"PeriodicalIF":4.1,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036566/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0