Life Science Alliance最新文献

Fishing with two lines: a hybrid approach to spatial transcriptomics discovery. 用两条线钓鱼：空间转录组学发现的混合方法。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-07-27 Print Date: 2026-10-01 DOI: 10.26508/lsa.202603690

Arianna L Williams-Katek, Saahithi Mallapragada, Evan D Mee, Brandon K Fischer, Annika Vannan, Laurie C Eldredge, Gail H Deutsch, Jonathan A Kropski, Jennifer Ms Sucre, Nicholas E Banovich

{"title":"Fishing with two lines: a hybrid approach to spatial transcriptomics discovery.","authors":"Arianna L Williams-Katek, Saahithi Mallapragada, Evan D Mee, Brandon K Fischer, Annika Vannan, Laurie C Eldredge, Gail H Deutsch, Jonathan A Kropski, Jennifer Ms Sucre, Nicholas E Banovich","doi":"10.26508/lsa.202603690","DOIUrl":"10.26508/lsa.202603690","url":null,"abstract":"Spatial transcriptomics faces a trade-off between the number of genes assayed and depth of per-gene sensitivity. We developed a \"dual-chemistry\" method that combines the high sensitivity of a 10x Genomics Xenium V1 custom panel (up to 480 genes) with the broad coverage of the Prime 5K panel (5,001 genes) on a single tissue section. This involved co-hybridizing Prime and V1 probes and sequentially running the V1 and Prime decoding chemistries. Applied to a human lung tissue microarray, we observed high concordance between the V1 and Prime chemistries when run independently (on serial sections) and the dual-chemistry runs. Overlapping genes (profiled on both V1 and Prime chemistries) showed similar expression patterns in the dual run demonstrating the fidelity of the assay. By combining information from both the V1 and Prime chemistries within the same cell, we retain more cells, gain valuable additional information, and enable both high-sensitivity profiling and discovery.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 10","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13404378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Vav2 is a master regulator of repair against bacterial pore-forming toxins. Vav2是修复细菌孔隙形成毒素的主要调节剂。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-07-09 Print Date: 2026-09-01 DOI: 10.26508/lsa.202603633

Victor Gbenga Kayejo, Ashlee Hensley, Tejal Katore, Peter A Keyel

{"title":"Vav2 is a master regulator of repair against bacterial pore-forming toxins.","authors":"Victor Gbenga Kayejo, Ashlee Hensley, Tejal Katore, Peter A Keyel","doi":"10.26508/lsa.202603633","DOIUrl":"10.26508/lsa.202603633","url":null,"abstract":"Despite antibiotic therapy, 25-35% of patients with necrotizing soft tissue infections (NSTIs) die. The etiologic agents for NSTIs include Streptococcus pyogenes and Clostridium perfringens, which secrete the cholesterol-dependent cytolysins (CDCs) streptolysin O and perfringolysin O to disrupt cell membranes. Whereas cells resist this damage by activating Ca2+-dependent repair pathways, including mitogen-activated protein kinase kinase (MEK)-dependent microvesicle shedding, dysferlin-mediated patch repair, and annexin-mediated membrane clogging, the upstream regulators of these responses have remained elusive. Here, we demonstrated that the Rac guanine nucleotide exchange factor Vav2 accounts for almost all of Ca2+-dependent repair against CDCs. Inhibiting or knocking down Vav2 sensitized multiple cell types to CDCs, whereas blocking other Rac guanine nucleotide exchange factors did not. Mechanistically, Vav2 triggered the critical mixed lineage kinase 3-MEK-dependent repair pathway. MEK activation rescued repair in Vav2-inhibited cells. Blocking dysferlin or annexins failed to increase damage beyond Vav2 inhibition, suggesting Vav2 coordinates multiple repair pathways. Thus, Vav2 controls multiple Ca2+-activated repair pathways that protect cells from CDCs produced during NSTIs.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 9","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13351264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

TRK-T3 condensate organization drives growth signaling. TRK-T3凝析液组织驱动生长信号。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-06-17 Print Date: 2026-09-01 DOI: 10.26508/lsa.202603653

Sindy R Chavez, Savannah M Bogus, Samantha N Cheung, Winnie Zhou, Lilja Gudmundsson, Kaho Kato, Andreas M Ernst

{"title":"TRK-T3 condensate organization drives growth signaling.","authors":"Sindy R Chavez, Savannah M Bogus, Samantha N Cheung, Winnie Zhou, Lilja Gudmundsson, Kaho Kato, Andreas M Ernst","doi":"10.26508/lsa.202603653","DOIUrl":"10.26508/lsa.202603653","url":null,"abstract":"Oncogenic fusion proteins involving receptor tyrosine kinases can hijack cell signaling cascades to promote oncogenesis. Here, we show that the TRK-T3 fusion protein, generated by joining the N-terminal region of the condensate-forming protein TFG with the C-terminal region of TrkA, assembles into sheet-like biomolecular condensates after putative prewetting of the ER. These structures are distinct from those formed by either parent protein. We find that ER wetting and the condensate morphology of TRK-T3 are controlled by a hydrophobic transmembrane segment encoded in the TrkA moiety. Removing this segment abolishes the sheet-like morphology of TRK-T3 condensates in cells and in vitro. This loss of morphology diminishes the recruitment of the first-layer signal-transduction protein GRB2 and suppresses activation of the MAPK pathway. A minimal segment that mimics the transmembrane domain efficiently disrupts TRK-T3 condensation. Together, our findings highlight condensate morphology as an encoded property of this oncogenic fusion protein, controlling the alignment and signaling competence of TRK-T3 assemblies. They further suggest that hydrophobic interactions within TRK-T3 condensates represent a potential vulnerability in this oncogenic signaling mechanism.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 9","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13276355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

GPLD1 is a scavenger carrier mediating lysosomal degradation of extracellular aberrant proteins. GPLD1是一种清道夫载体，介导细胞外异常蛋白的溶酶体降解。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-06-05 Print Date: 2026-08-01 DOI: 10.26508/lsa.202603717

Mizuki Tsuchiya, Yoichiro Yagishita, Eisuke Itakura

{"title":"GPLD1 is a scavenger carrier mediating lysosomal degradation of extracellular aberrant proteins.","authors":"Mizuki Tsuchiya, Yoichiro Yagishita, Eisuke Itakura","doi":"10.26508/lsa.202603717","DOIUrl":"10.26508/lsa.202603717","url":null,"abstract":"Loss of proteostasis leads to the accumulation of aberrant proteins, including aggregated proteins and amyloid fibrils, contributing to various diseases. Protein quality control systems are essential for maintaining proteostasis. Although intracellular mechanisms are well characterized, pathways responsible for the degradation of aberrant proteins outside the cell remain poorly understood. We previously identified the chaperone/carrier- and receptor-mediated extracellular protein degradation pathway, in which the extracellular chaperone clusterin binds misfolded proteins and the resulting complex is delivered to lysosomes via endocytosis. However, it remains unclear whether other factors are involved in this pathway. To identify novel regulators, plasma factors binding serum amyloid A1 were investigated. Glycosylphosphatidylinositol-specific phospholipase D1 (GPLD1) was found to directly bind serum amyloid A1 and promote its lysosomal degradation. This activity was independent of GPLD1's cleavage activity for GPI-anchored proteins. Furthermore, GPLD1 mediates lysosomal degradation of misfolded proteins, with cell surface heparan sulfate acting as its receptor. Our data demonstrate that GPLD1 is a novel scavenger carrier with substrate specificity distinct from clusterin, responsible for degrading extracellular aberrant proteins.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13241479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148175833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

A "scan and stop" assay identifies CD40 and CD70 as selective regulators of T-cell arrest on APCs. 一项“扫描和停止”试验确定CD40和CD70是apc上t细胞阻滞的选择性调节因子。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-06-04 Print Date: 2026-08-01 DOI: 10.26508/lsa.202503401

Vincent Gloe, Richard Schregle, Christoph Ratswohl, Jérémie Rossy

{"title":"A \"scan and stop\" assay identifies CD40 and CD70 as selective regulators of T-cell arrest on APCs.","authors":"Vincent Gloe, Richard Schregle, Christoph Ratswohl, Jérémie Rossy","doi":"10.26508/lsa.202503401","DOIUrl":"10.26508/lsa.202503401","url":null,"abstract":"T-cell activation requires firm arrest on APCs, a process essential for effective clonal expansion and differentiation. Although the role of co-inhibitory signals and integrin-mediated adhesion in modulating T-cell arrest is established, the contribution of co-stimulatory molecules to this process remains poorly understood. Here, we developed a quantitative \"scan and stop\" assay using engineered CHO cells as minimalistic APCs to systematically assess the influence of co-stimulatory proteins on T-cell arrest. These APCs express only selected peptide-MHC complexes and co-stimulatory ligands, allowing controlled investigation of their roles in both naïve and experienced CD4+ and CD8+ T cells. We found that CD40 selectively promotes the arrest of pre-activated CD4+ T cells, whereas CD70 enhances the arrest of CD8+ T cells, correlating with expression patterns of their respective receptors, CD40L and CD27. High-resolution imaging further revealed mechanical deformation of APCs during synapse formation, suggesting force generation by T cells. Altogether, our results identify CD40 and CD70 as subtype-specific regulators of T-cell arrest and reveal a novel dimension in co-stimulatory control of immune synapse formation.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13237129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

A novel SLC2A10 gain-of-function variant links glycolytic macrophage polarization to chronic nonbacterial osteomyelitis. 一种新的SLC2A10功能获得变体将糖酵解巨噬细胞极化与慢性非细菌性骨髓炎联系起来。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-06-03 Print Date: 2026-08-01 DOI: 10.26508/lsa.202603772

Xiang Li, Lihang Shen, KuanKuan Jia, Shuo Chen, Jingang An

{"title":"A novel SLC2A10 gain-of-function variant links glycolytic macrophage polarization to chronic nonbacterial osteomyelitis.","authors":"Xiang Li, Lihang Shen, KuanKuan Jia, Shuo Chen, Jingang An","doi":"10.26508/lsa.202603772","DOIUrl":"10.26508/lsa.202603772","url":null,"abstract":"Chronic nonbacterial osteomyelitis is a rare autoinflammatory bone disorder with unclear etiology. In a Chinese family, whole-exome sequencing identified a heterozygous missense variant in SLC2A10 that cosegregated with disease. Structural modeling suggested that the substitution disrupts hydrogen bond within the transmembrane domain, potentially altering glucose transport activity. In vitro, the expression of the p.Asp292Glu variant in macrophages enhanced glucose uptake, increased glycolytic activity, and promoted pro-inflammatory polarization, accompanied by increased production of inflammatory mediators. The variant also accelerated osteoclast differentiation and suppressed osteoblast-mediated mineralization, indicating a disruption of bone homeostasis. Zebrafish expressing the p.Asp292Glu variant exhibited enhanced inflammatory responses, increased reactive oxygen species accumulation, elevated macrophage infiltration in the mandibular region, and impaired bone mineralization. Transcriptomic analysis confirmed activation of glycolytic and inflammatory signaling pathways, as well as enrichment of osteoclast differentiation networks. These findings demonstrate that the SLC2A10 variant exerts a gain-of-function effect driving glycolysis-dependent macrophage polarization and osteoclastogenesis, leading to chronic inflammatory bone destruction. This study broadens the genetic understanding of chronic nonbacterial osteomyelitis and suggests a potential therapeutic target.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13234206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148157202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The ER anchoring and abundance of the EEF1B complex is affected by tissue-specific alternative EEF1D splicing. EEF1B复合物的内质网锚定和丰度受到组织特异性替代EEF1D剪接的影响。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-06-02 Print Date: 2026-08-01 DOI: 10.26508/lsa.202503513

Muhammad Jamous, Masaki Hosogane, Xiaoxin Huang, Mikiko Suzuki, Atsushi Hatano, Yuichi Shichino, Shintaro Iwasaki, Kazutaka Murayama, Masaki Matsumoto, Keiko Nakayama

{"title":"The ER anchoring and abundance of the EEF1B complex is affected by tissue-specific alternative EEF1D splicing.","authors":"Muhammad Jamous, Masaki Hosogane, Xiaoxin Huang, Mikiko Suzuki, Atsushi Hatano, Yuichi Shichino, Shintaro Iwasaki, Kazutaka Murayama, Masaki Matsumoto, Keiko Nakayama","doi":"10.26508/lsa.202503513","DOIUrl":"10.26508/lsa.202503513","url":null,"abstract":"The EEF1B complex plays a central role in translation elongation by reactivating EEF1A for the delivery of aminoacyl-tRNAs to the ribosome. Among its components, EEF1D undergoes alternative splicing to produce one long and several short isoforms, each with distinct N-terminal domains and tissue-specific expression patterns. Although the short isoforms are broadly expressed, their physiological functions remain poorly characterized. In this study, we show that short EEF1D isoforms containing exon 5 interact with the ER-resident scaffold protein KTN1 and RRBP1, thereby anchoring the EEF1B complex to the ER. Mass spectrometry analyses of FLAG-tagged EEF1D identified these interactions, and deletion of exon 5 disrupted ER anchoring, resulting in diffuse cytoplasmic localization of the EEF1B complex. In exon 5 KO mice, this altered localization was accompanied by a reduction in EEF1B subunit abundance in multiple tissues, including the liver, although global protein synthesis rates remained unchanged. Together, these findings uncover an ER-anchoring mechanism controlled by alternative splicing that shapes the spatial organization and abundance of the elongation machinery in vivo.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Loss of U11/U12 spliceosome gene ZCRB1 leads to aberrant ciliogenesis and WNT signaling. U11/U12剪接体基因ZCRB1的缺失导致纤毛发生和WNT信号的异常。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-05-27 Print Date: 2026-08-01 DOI: 10.26508/lsa.202503607

Mujeeb Ur Rehman Pirzada, Geralle Powell-Rodgers, Jahmiera Richee, Antto J Norppa, Courtney F Jungers, Sarah Colijn, Mikko J Frilander, Amber N Stratman, Sergej Djuranovic

{"title":"Loss of U11/U12 spliceosome gene ZCRB1 leads to aberrant ciliogenesis and WNT signaling.","authors":"Mujeeb Ur Rehman Pirzada, Geralle Powell-Rodgers, Jahmiera Richee, Antto J Norppa, Courtney F Jungers, Sarah Colijn, Mikko J Frilander, Amber N Stratman, Sergej Djuranovic","doi":"10.26508/lsa.202503607","DOIUrl":"10.26508/lsa.202503607","url":null,"abstract":"The U12-dependent, or minor, spliceosome processes only 0.5% of human introns, and yet, it is known to profoundly influence gene expression and cellular signaling. The ZCRB1 protein is a core component of the U12 mono-snRNP, but its functional significance to minor splicing, gene regulation, and biological signaling cascades remains poorly understood. Using CRISPR-Cas9 and siRNA-targeted knockout and knockdown strategies, we show that human cell lines with a partial reduction in ZCRB1 expression exhibit significant abnormal splicing events and altered expression of minor intron-containing genes. RNA-sequencing and targeted analyses of minor intron-containing genes indicate direct mis-splicing and expression of genes involved in ciliogenesis, with a coinciding up-regulation of WNT signaling pathway components. CRISPR-Cas12a knockdown of zcrb1 in zebrafish embryos leads to developmental patterning and body axis abnormalities, disrupted ciliogenesis, and up-regulated WNT signaling, complementing our human cell studies. This work highlights a conserved and essential biological role of the minor spliceosome, via ZCRB1, in cellular and developmental processes across species, shedding light on the molecular crosstalk that integrates splicing regulation, ciliogenesis, and WNT signaling.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Annulus fracture underlies radiation-induced sperm dysfunction revealed by multimodal nano-imaging. 多模态纳米成像揭示了环断裂是辐射诱发精子功能障碍的基础。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-05-27 Print Date: 2026-08-01 DOI: 10.26508/lsa.202603693

Nuo Chen, Hongyu Chen, Jingcheng Xiao, Bo He, Difei Zhang, Xinye Yuan, Pingping Wen, Huaidong Jiang

{"title":"Annulus fracture underlies radiation-induced sperm dysfunction revealed by multimodal nano-imaging.","authors":"Nuo Chen, Hongyu Chen, Jingcheng Xiao, Bo He, Difei Zhang, Xinye Yuan, Pingping Wen, Huaidong Jiang","doi":"10.26508/lsa.202603693","DOIUrl":"10.26508/lsa.202603693","url":null,"abstract":"Ionizing radiation impairs male fertility, but the ultrastructural lesions linking radiation to sperm dysfunction remain unclear. The sperm annulus, a ring structure essential for flagellar integrity, is a potential but unresolved target. Here, we integrate synchrotron X-ray ptychography, cryogenic soft X-ray tomography, electron microscopy, and confocal imaging for cross-scale visualization of radiation-induced injury. Ptychography enables quantitative imaging of the annulus at ∼40-nm resolution, bridging light and electron microscopy. In irradiated mice, we find annulus fracture, loss of cytomembrane coverage, and disruption at the midpiece-principal piece junction. These defects worsen during maturation, correlating with reduced motility and increased abnormalities. Protein analyses show down-regulation of SEPT12 and AKAP4, indicating compromised annulus and fibrous sheath. Cryogenic tomography confirms ultrastructural deterioration in the axoneme, fibrous sheath, and mitochondria. These findings identify the sperm annulus and fibrous sheath as primary radiation targets, defining a structural basis for radiation-induced male infertility. This multimodal approach offers a generalizable strategy for nanoscale 3D cellular architecture analysis.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Development of K-CORE: a web-based platform for integrated clinico-genomic analysis. 开发K-CORE：一个基于网络的综合临床基因组分析平台。

IF 3.1 2区生物学

Life Science Alliance Pub Date : 2026-05-22 Print Date: 2026-08-01 DOI: 10.26508/lsa.202603659

Juyeon Hwang, Jae Woo Ahn, Jae Wook Lee, So-Youn Jung, Eun-Gyeong Lee, Heejung Chae, Harim Koo, Hyosoung Cha, Junetae Kim, Kwangmin Kim, Dongwoo Lee, Junhyung Park, Sun-Young Kong, Kui Son Choi, Hyun-Jin Kim

{"title":"Development of K-CORE: a web-based platform for integrated clinico-genomic analysis.","authors":"Juyeon Hwang, Jae Woo Ahn, Jae Wook Lee, So-Youn Jung, Eun-Gyeong Lee, Heejung Chae, Harim Koo, Hyosoung Cha, Junetae Kim, Kwangmin Kim, Dongwoo Lee, Junhyung Park, Sun-Young Kong, Kui Son Choi, Hyun-Jin Kim","doi":"10.26508/lsa.202603659","DOIUrl":"10.26508/lsa.202603659","url":null,"abstract":"One of the key challenges in cancer treatment and precision oncology is the use of multi-omics data and their integration into matched clinical information. Although several analytical portals have been developed, most platforms do not support user-uploaded data or the integrated analysis of clinical and multi-omics datasets. To address these limitations, we developed the Korea Cancer Omics Research (K-CORE) portal, a user-friendly analytical platform designed to integrate and analyze multi-omics and clinical data. K-CORE supports various omics levels and a wide range of analytical tools. To validate the utility and reproducibility of the K-CORE, we designed synthetic datasets that reflected real-world omics data distributions. The analytical results from K-CORE were compared side by side with those from widely used R packages such as maftools and edgeR. In conclusion, K-CORE offers a practical and intuitive platform for the multidomain integration of clinical and omics data, supporting the advancement of precision oncology. Nevertheless, as analytical technologies and precision oncology continue to evolve, continuous maintenance and user feedback will become essential for future platform improvements.","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 8","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13197607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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