BMB Reports最新文献_第4页

Multi-omics analysis sandbox toolkit for swift derivations of clinically relevant genesets and biomarkers. 多组学分析沙盒工具包，用于快速推导临床相关基因组和生物标记物。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Jin-Young Lee, Won Park, Hyunjoong Kim, Hong Seok Lee, Tae-Wook Kang, Dong-Hun Shin, Kyung Su Kim, Yoon Kyeong Lee, Seon-Young Kim, Ji Hwan Park, Young-Joon Kim

{"title":"Multi-omics analysis sandbox toolkit for swift derivations of clinically relevant genesets and biomarkers.","authors":"Jin-Young Lee, Won Park, Hyunjoong Kim, Hong Seok Lee, Tae-Wook Kang, Dong-Hun Shin, Kyung Su Kim, Yoon Kyeong Lee, Seon-Young Kim, Ji Hwan Park, Young-Joon Kim","doi":"","DOIUrl":"","url":null,"abstract":"The utilization of multi-omics research has gained popularity in clinical investigations. However, effectively managing and merging extensive and diverse datasets presents a challenge due to its intricacy. This research introduces a Multi-Omics Analysis Sandbox Toolkit, an online platform designed to facilitate the exploration, integration, and visualization of datasets ranging from single-omics to multi-omics. This platform establishes connections between clinical data and omics information, allowing for versatile analysis and storage of both single and multi-omics data. Additionally, users can repeatedly utilize and exchange their findings within the platform. This toolkit offers diverse alternatives for data selection and gene set analysis. It also presents visualization outputs, potential candidates, and annotations. Furthermore, this platform empowers users to collaborate by sharing their datasets, analyses, and conclusions with others, thus enhancing its utility as a collaborative research tool. This Multi-Omics Analysis Sandbox Toolkit stands as a valuable asset in comprehensively grasping the influence of diverse factors in diseases and pinpointing potential biomarkers. [BMB Reports 2024; 57(12): 521-526].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"521-526"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141449592","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

Transmembrane E3 ligase RNF128 regulates N-glycosylation by promoting ribophorin I ubiquitination and degradation. 跨膜 E3 连接酶 RNF128 通过促进核糖蛋白 I 泛素化和降解来调节 N-糖基化。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Eun-Bee Cho, Van Anh Vu, Sang-Hee Park, Lan Thi Trinh, Jong-Bok Yoon, Sungjoo Kim

{"title":"Transmembrane E3 ligase RNF128 regulates N-glycosylation by promoting ribophorin I ubiquitination and degradation.","authors":"Eun-Bee Cho, Van Anh Vu, Sang-Hee Park, Lan Thi Trinh, Jong-Bok Yoon, Sungjoo Kim","doi":"","DOIUrl":"","url":null,"abstract":"Ring finger protein 128 (RNF128) is a transmembrane E3 ubiquitin ligase mainly localized in the endoplasmic reticulum that is involved in various processes, including T cell anergy and tumor progression. However, the biological function of RNF128 in N-glycosylation remains unexplored. To investigate the functional role of RNF128, we used the proximity-directed biotin labeling method, and identified ribophorin I (RPN1) as a novel RNF128 substrate, demonstrating that RNF128 ubiquitinated RPN1 and promoted its degradation. RPN1 is a subunit of oligosaccharyltransferase complexes that facilitate N-glycosylation by binding substrates, and presenting them to the catalytic core. RPN1 also functions as an N-glycosylation-dependent chaperone that helps export a subset of newly synthesized glycoproteins to the plasma membrane. We found that RNF128 affects the N-glycosylation of model glycoproteins, such as sex hormone- binding globulin and asialoglycoprotein receptor 1. Furthermore, RNF128 inhibits the export of the opioid receptor mu 1 (OPRM1) to the plasma membrane, while expressing ubiquitination-incompetent RPN1 mutant, rescues the defect of OPRM1 export caused by RNF128 overexpression. Additionally, RNF128 influences colorectal cancer cell migration. The RNF128-dependent degradation of RPN1 likely inhibits the cell surface expression of specific glycoproteins, thereby affecting distinct cellular functions. This study contributes to understanding of the biological and functional roles of RNF128- and RPN1-dependent N-glycosylation. [BMB Reports 2024; 57(12): 546-552].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"546-552"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680082","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

DNA regulatory element cooperation and competition in transcription. DNA 调控元件在转录中的合作与竞争。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Haram Lee, Meyer Joseph Friedman, Sang Bum Kim, Soohwan Oh

引用次数: 0

Identification of CD109 in the extracellular vesicles derived from ovarian cancer stem-like cells. 鉴定卵巢癌干样细胞胞外囊泡中的 CD109。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Ye Eun Kim, Jun Se Kim, Min Joo Shin, Seo Yul Lee, Dae Kyoung Kim, Nam-Kyung Lee, Yang Woo Kwon, Kyung-Un Choi, Dong-Soo Suh, Byoung Soo Kim, Sanghwa Jeong, Jae Ho Kim

{"title":"Identification of CD109 in the extracellular vesicles derived from ovarian cancer stem-like cells.","authors":"Ye Eun Kim, Jun Se Kim, Min Joo Shin, Seo Yul Lee, Dae Kyoung Kim, Nam-Kyung Lee, Yang Woo Kwon, Kyung-Un Choi, Dong-Soo Suh, Byoung Soo Kim, Sanghwa Jeong, Jae Ho Kim","doi":"","DOIUrl":"","url":null,"abstract":"Ovarian cancer is the deadliest gynecological cancer because it has few early symptoms and metastasizes to the surrounding organs at advanced stages. Cancer stem cells (CSCs), a subpopulation of cells with acquired drug resistance, contribute to the recurrence and poor prognosis of ovarian cancer. CD109, a cell surface glycoprotein, has been reported to be a marker of CSCs; however, it remains unclear whether CD109 is secreted by CSCs. In this study, we investigated the amount of CD109 in conditioned media (CM) of CSC populations from ovarian cancer cell lines and patients with ovarian cancer. The CM of sphere-forming CSCs isolated from ovarian cancer cell lines (A2780 and SKOV3) had higher levels of CD109 than those isolated from their adherent cultured parental cells. Furthermore, higher levels of CD109 were detected on the cell surface and in the CM of sphere-forming CSC populations isolated from patient-derived primary ovarian cancer cells. To clarify whether CD109 is localized to the exosomal fraction secreted from CSCs, extracellular vesicles were isolated from the CM by ultracentrifugation. In addition to the CM, the exosomal fraction of ovarian CSCs contained greater levels of CD109 than the parental cells. These results suggest that CD109 is secreted in a soluble or exosomal form from CSCs, and that the measurement of secreted CD109 may be used as a diagnostic or prognostic marker for ovarian cancer. [BMB Reports 2024; 57(12): 527-532].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"527-532"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680669","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 regulates the production of hepatic fibroblast growth factor 23 in diabetes. 脑龙调节糖尿病患者肝成纤维细胞生长因子 23 的产生。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Seungwon An, Balachandar Nedumaran, Hangaram Oh, Taehyun Park, Chul-Seung Park, Ali R Djalilian, Sooyong Shin, Taehoon Chung, Yong Deuk Kim

{"title":"Cereblon regulates the production of hepatic fibroblast growth factor 23 in diabetes.","authors":"Seungwon An, Balachandar Nedumaran, Hangaram Oh, Taehyun Park, Chul-Seung Park, Ali R Djalilian, Sooyong Shin, Taehoon Chung, Yong Deuk Kim","doi":"","DOIUrl":"","url":null,"abstract":"Cereblon (CRBN) is an extensively expressed protein involved in crucial physiological processes. This study reveals CRBN's role in governing hepatic fibroblast growth factor 23 (FGF23) expression and production via the cyclic adenosine monophosphate (cAMP) pathway in diabetic conditions. The expressions of hepatic Crbn, Yin Yang 1 (Yy1), and Fgf23 genes were significantly increased in diabetic mice and forskolin (FSK)-treated primary hepatocytes, correlating with elevated FGF23 production. Overexpression of Crbn and Yy1 increased hepatic FGF23 and cytokines by upregulating YY1 gene expression, which was reduced in Crbn- and Yy1-silenced mice and primary hepatocytes. Besides, we also found that CRBN-mediated regulation of hepatic FGF23 involved YY1 recruitment to the Fgf23 gene promoters, evidenced by reporter assays, deletion studies, and mutant analyses. These findings identify CRBN and YY1 as key contributors to gluconeogenic signaling-driven FGF23 production and inflammation in diabetes, highlighting their potential as therapeutic targets for addressing metabolic disorders like diabetes. [BMB Reports 2024; 57(12): 533-538].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"533-538"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387639","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

Recombinant ADAMTS1 promotes muscle cell differentiation and alleviates muscle atrophy by repressing NOTCH1. 重组 ADAMTS1 通过抑制 NOTCH1 促进肌肉细胞分化并缓解肌肉萎缩。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Sang Hyup Lee, Sang Yoon Kim, Yun Gu Gwon, Chanwoo Lee, Changhwan Kim, Ick Hyun Cho, Tae-Won Kim, Bong-Keun Choi

{"title":"Recombinant ADAMTS1 promotes muscle cell differentiation and alleviates muscle atrophy by repressing NOTCH1.","authors":"Sang Hyup Lee, Sang Yoon Kim, Yun Gu Gwon, Chanwoo Lee, Changhwan Kim, Ick Hyun Cho, Tae-Won Kim, Bong-Keun Choi","doi":"","DOIUrl":"","url":null,"abstract":"A disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) plays crucial roles in various biological processes, including myogenesis, by modulating the neurogenic locus notch homolog protein 1 (NOTCH1) signaling pathway. However, the mechanisms through which ADAMTS1 regulates myogenesis remain unclear. In this study, we generated recombinant ADAMTS1 mutants and determined their effects on muscle cell differentiation, focusing on the regulation of NOTCH1 signaling. Treatment of C2C12 cells with recombinant ADAMTS1 protein enhanced muscle cell differentiation. Meanwhile, ADAM10 treatment inhibited muscle differentiation through the activation of NOTCH1 cleavage. Recombinant ADAMTS1 reversed ADAM10-induced muscle cell atrophy by suppressing NOTCH1 activation and downregulating its target gene. Recombinant ADAMTS1 also alleviated dexamethasoneinduced muscle atrophy in a mouse model. In summary, our findings suggest that recombinant ADAMTS1 promotes muscle regeneration by suppressing NOTCH1 and highlight the potential of recombinant ADAMTS1 proteins in the treatment of muscle wasting disease. [BMB Reports 2024; 57(12): 539-545].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"539-545"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680671","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

Targeting proprotein convertase subtilisin/kexin type 7 in macrophages as a therapeutic strategy to mitigate myocardial infarction-induced inflammation. 巨噬细胞中靶向蛋白转化酶枯草素/kexin 7作为缓解心肌梗死诱导炎症的治疗策略

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-12-01

Shin Hye Moon, Inyoung Chung, Na Hyeon Yoon, Jing Jin, Hyae Yon Kweon, Won Kee Yoon, Nabil G Seidah, Goo Taeg Oh

{"title":"Targeting proprotein convertase subtilisin/kexin type 7 in macrophages as a therapeutic strategy to mitigate myocardial infarction-induced inflammation.","authors":"Shin Hye Moon, Inyoung Chung, Na Hyeon Yoon, Jing Jin, Hyae Yon Kweon, Won Kee Yoon, Nabil G Seidah, Goo Taeg Oh","doi":"","DOIUrl":"","url":null,"abstract":"Myocardial infarction (MI), a major form of coronary artery disease (CAD), triggers a severe inflammatory response in the heart, resulting in increased cell death and adverse ventricular remodeling. Despite treatment advancements, MI remains a significant risk factor for heart failure, underscoring the necessity for a more in-depth exploration of immune cell mechanisms. Proprotein convertase subtilisin/kexin type 7 (PCSK7), expressed in various tissues and immune cells, has been implicated in cardiovascular disease, yet its specific role in cardiac immune cells remains poorly understood. This study aimed to elucidate the role of PCSK7 in MI-related inflammation. Our findings indicate that PCSK7 deficiency reduces circulating cholesterol levels, potentially mitigating infarct injury and improving cardiac function by modulating immune cells. Additionally, PCSK7 promotes macrophage activation and lipid uptake at the ischemic site, intensifying the pathology. We also observed that PCSK7 activates the TNF-α/JNK signaling pathway in macrophages intracellularly, amplifying the inflammatory response. Therefore, targeting PCSK7 in macrophages could help mitigate post-MI inflammation, alleviate disease severity, and offer novel therapeutic strategies for patients with CAD. [BMB Reports 2024; 57(12): 553-558].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"553-558"},"PeriodicalIF":2.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11693601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765884","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

Antisense-mediated splicing correction as a therapeutic approach for p53 K120R mutation. 反义介导的剪接校正是治疗 p53 K120R 突变的一种方法。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-11-01

Doyeong Kim, Sang-Min Park, Seo-Young Lee, Jinchul Kim, Han-Byul Jung, Young Sook Kim, Sun-Ku Chung

{"title":"Antisense-mediated splicing correction as a therapeutic approach for p53 K120R mutation.","authors":"Doyeong Kim, Sang-Min Park, Seo-Young Lee, Jinchul Kim, Han-Byul Jung, Young Sook Kim, Sun-Ku Chung","doi":"","DOIUrl":"","url":null,"abstract":"The TP53 c.359A＞G mutation significantly disrupts the expression of the major TP53 transcript variant encoding p53 K120R by generating a new splice donor site. An antisense morpholino oligomer (AMO) targeting this mutation successfully restored normal splicing and the expression of the major TP53 variant. Given that p53 exerts its tumor suppressor function by regulating target genes responsible for growth arrest or apoptosis, the p53 K120R protein enhanced by AMO exhibits impaired transcriptional regulation of CDKN1A, a key growth arrest gene, while maintaining normal induction of the pro-apoptotic BBC3 gene. As a result, the mutant p53 K120R protein shows a defective cell growth arrest phenotype but retains apoptotic function, suggesting that it may still possess some tumor suppressor activity. Furthermore, lysine 120, known to provide a critical acetylation site for p53 activation, highlights the relevance of acetylation in tumor suppression through studies of the p53 K120R mutant. However, our findings demonstrate that targeting mutant TP53 mRNA with AMO is essential for restoring p53 function. In conclusion, this study emphasizes the potential of AMO-mediated splice correction as a therapeutic approach for TP53 mutations. [BMB Reports 2024; 57(11): 503-508].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"503-508"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387638","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

Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-κB pathways in PM₁₀-exposed keratinocytes. 通过调节 PM10 暴露角质细胞中的 ROS/p38/ERK/NF-κB 通路，特化的促溶解介质 7S MaR1 可抑制 IL-6 的表达。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-11-01

Jinju Kim, Hyo-Min Park, Chae-Min Lim, Kyeong-Bae Jeon, Seonhwa Kim, Jin Lee, Jin Lee, Jin-Tae Hong, Deok-Kun Oh, Young Yang, Do-Young Yoon

引用次数: 0

Differential roles of N- and C-terminal LIR motifs in the catalytic activity and membrane targeting of RavZ and ATG4B proteins. N 端和 C 端 LIR 基团在 RavZ 和 ATG4B 蛋白的催化活性和膜靶向性中的不同作用。

IF 2.9 3区生物学

BMB Reports Pub Date : 2024-11-01

Sang-Won Park, Ju-Hui Park, Haneul Choi, Pureum Jeon, Seung-Hwan Lee, Won-Dong Shin, Hun-Joo Kim, Jin-A Lee, Deok-Jin Jang

{"title":"Differential roles of N- and C-terminal LIR motifs in the catalytic activity and membrane targeting of RavZ and ATG4B proteins.","authors":"Sang-Won Park, Ju-Hui Park, Haneul Choi, Pureum Jeon, Seung-Hwan Lee, Won-Dong Shin, Hun-Joo Kim, Jin-A Lee, Deok-Jin Jang","doi":"","DOIUrl":"","url":null,"abstract":"Mammalian ATG8 proteins (mATG8s) are essential for selective autophagy because they recruit various proteins with LC3- interacting region (LIR) motifs to autophagic membranes. The RavZ protein, secreted by Legionella pneumophila, and mammalian ATG4B possess functional LIR motifs that participate in lipidated mATG8 deconjugation on autophagic membranes. RavZ comprises three functional LIR motifs at the N- and Cterminal sides of its catalytic domain (CAD). This study demonstrated that LIR motifs at the N-terminal side of the CAD of RavZ are involved in autophagic membrane targeting and substrate recognition, while LIR motif at the C-terminal side facilitate autophagic membrane targeting. Our results also revealed that the C-terminal LIR motif in human ATG4B is pivotal in delipidating LC3B-phosphatidylethanolamine (PE), but it plays a minor role in pro-LC3B priming in the cytosol. Therefore, introducing a functional LIR motif to the N-terminal of ATG4B does not affect LC3B-PE delipidation. This study clearly described the position-dependent roles of LIR motifs in RavZ and ATG4B in cellular contexts. [BMB Reports 2024; 57(11): 497-502].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"497-502"},"PeriodicalIF":2.9,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387640","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