Genes to Cells最新文献_第3页

The SQSTM1 L341V Variant Associated With Sporadic ALS Promotes the Accumulation of Enlarged Ubiquitin-Positive SQSTM1 Bodies 与散发性ALS相关的SQSTM1 L341V变异促进泛素阳性SQSTM1体增大的积累。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-01 DOI: 10.1111/gtc.70134

Kento Shimakura, Akira Oka, Haruka Yudahira, Yutaro Hama, Asako Otomo, Shinji Hadano

{"title":"The SQSTM1 L341V Variant Associated With Sporadic ALS Promotes the Accumulation of Enlarged Ubiquitin-Positive SQSTM1 Bodies","authors":"Kento Shimakura, Akira Oka, Haruka Yudahira, Yutaro Hama, Asako Otomo, Shinji Hadano","doi":"10.1111/gtc.70134","DOIUrl":"10.1111/gtc.70134","url":null,"abstract":"<p><i>SQSTM1</i> is one of the causative genes of neurodegenerative disorders, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The SQSTM1 protein regulates the degradation of polyubiquitinated proteins and autophagosome formation through its interaction with microtubule-associated protein light chain 3 (MAP1LC3/LC3). However, the molecular mechanisms by which SQSTM1-LC3 binding regulates the autophagy-endolysosomal system (APELS) remain unclear. To elucidate the spatiotemporal role of SQSTM1, we transiently expressed wild-type SQSTM1 or missense mutants carrying mutations in the LC3-interacting region (LIR), fused with the photoconvertible fluorescent protein Dendra2. Live-cell fluorescence imaging and co-localization analyses with markers of the APELS were then performed. Particle analysis of photoconverted or non-photoconverted SQSTM1-positive structures in live cells revealed that the pathogenic L341V variant formed larger structures than the wild-type. Co-localization analyses further showed that both the L341V and artificial LIR3A mutants accumulated in large ubiquitin-positive structures, likely due to impaired localization to autophagosomes. These results suggest that mutations within the LIR differentially affect autophagosome formation and cargo degradation within APELS-related compartments, highlighting the importance of SQSTM1 structural integrity in ALS/FTD pathogenesis.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70134","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148371778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Partial Depletion of SART1 Selectively Induces Mitotic Defects and Cell Death in Cancer Cells SART1部分缺失选择性诱导癌细胞有丝分裂缺陷和细胞死亡。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-01 DOI: 10.1111/gtc.70132

Hideki Yokoyama, Saito Akatsu, Kotaro Hayakawa

{"title":"Partial Depletion of SART1 Selectively Induces Mitotic Defects and Cell Death in Cancer Cells","authors":"Hideki Yokoyama, Saito Akatsu, Kotaro Hayakawa","doi":"10.1111/gtc.70132","DOIUrl":"10.1111/gtc.70132","url":null,"abstract":"<div>\u0000 \u0000 <p>Cancer cells proliferate uncontrollably, and a major challenge in cancer research is to identify strategies that selectively eliminate cancer cells while sparing normal cells. Squamous cell carcinoma antigen recognized by T cells 1 (SART1) was originally identified as a carcinoma-associated antigen and is frequently overexpressed in cancer cells. Recently, SART1 has been identified as a microtubule-associated protein required for spindle pole formation and cell division. Here, we show that partial depletion of SART1 by RNA interference selectively disrupts mitotic spindle assembly and induces cell death in cancer cells. siRNA-mediated knockdown reduced SART1 protein levels comparably in multiple human cell types, yet spindle defects and apoptotic cell death were observed in HeLa and U2OS cancer cells but not in non-transformed BJ fibroblasts or RPE1 epithelial cells. Consistent with this cancer-selective sensitivity, SART1 depletion markedly suppressed oncogene c-Myc–induced transformation of RPE1 cells without impairing the growth of untransformed cells. These results demonstrate that partial depletion of SART1 preferentially induces spindle defects and cell death in transformed cells. Given that complete loss of SART1 is incompatible with normal development, our findings suggest that transient or partial inhibition of SART1 may provide a basis for selectively eliminating transformed cells while sparing normal cells.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148364786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

FOXO1 Is Required for Growth and Viability of Cancer-Associated Fibroblasts in Human Breast Carcinomas FOXO1是人类乳腺癌中癌症相关成纤维细胞生长和生存所必需的。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-06-29 DOI: 10.1111/gtc.70133

Takumi Koyama, Tetsuo Kobayashi, Yoshihiro Mezawa, Weibo Gao, Kaishi Yamada, Kazunari Yamashita, Zixu Wang, Yu Koyama, Masaaki Abe, Reo Maruyama, Liying Yang, Hiroaki Daitoku, Akiyoshi Fukamizu, Atsushi Takano, Yohei Miyagi, Tomoyuki Yokose, Toshinari Yamashita, Keisuke Sugahara, Hiroyuki Seimiya, Yataro Daigo, Akira Katakura, Akira Orimo

{"title":"FOXO1 Is Required for Growth and Viability of Cancer-Associated Fibroblasts in Human Breast Carcinomas","authors":"Takumi Koyama, Tetsuo Kobayashi, Yoshihiro Mezawa, Weibo Gao, Kaishi Yamada, Kazunari Yamashita, Zixu Wang, Yu Koyama, Masaaki Abe, Reo Maruyama, Liying Yang, Hiroaki Daitoku, Akiyoshi Fukamizu, Atsushi Takano, Yohei Miyagi, Tomoyuki Yokose, Toshinari Yamashita, Keisuke Sugahara, Hiroyuki Seimiya, Yataro Daigo, Akira Katakura, Akira Orimo","doi":"10.1111/gtc.70133","DOIUrl":"10.1111/gtc.70133","url":null,"abstract":"<div>\u0000 \u0000 <p>Carcinoma-associated fibroblasts (CAFs), frequently present in the stroma of human breast carcinomas, influence tumor characteristics. A forkhead box protein O1 (FOXO1) transcription factor is a critical mediator of the cellular responses to oxidative stress in various cell types. However, the roles of FOXO1 in CAFs have been poorly understood. Here, we show more intense FOXO1 staining in stromal fibroblasts in human breast cancers compared to those in non-cancerous regions. Notably, stronger stromal FOXO1 staining is significantly associated with poorer outcomes in 237 breast cancer patients. FOXO1 expression is also more abundant in cultured human breast CAFs compared to the control counterpart human mammary fibroblasts. FOXO1 expression is upregulated in control fibroblasts by malnutrition and hypoxia, suggesting such starvation to mediate increased FOXO1 expression in CAFs. Of note, treatment with AS1842856, a FOXO1 inhibitor, significantly attenuates growth and viability in CAFs relative to control fibroblasts. Suppression of FOXO1 expression by shRNA also substantially inhibits CAFs' growth in culture. When the FOXO1-knockdowned CAFs were implanted with breast cancer cells into recipient mice, the number of these fibroblasts present in developed tumors tends to decrease. Taken together, these findings indicate that FOXO1 expression in human breast CAFs is required for their growth and viability.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148348694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Strain-Dependent Functional Variation of a Sex Specific Sox9 Enhancer 性别特异性Sox9增强子的品系依赖功能变异

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-06-26 DOI: 10.1111/gtc.70131

Iku Tsuchiya, Atsumi Tsuji-Hosokawa, Suzune Furuhashi, Karin Sugiyama, Yuya Ogawa, Aki Oishi, Miho Terao, Shuji Takada

{"title":"Strain-Dependent Functional Variation of a Sex Specific Sox9 Enhancer","authors":"Iku Tsuchiya, Atsumi Tsuji-Hosokawa, Suzune Furuhashi, Karin Sugiyama, Yuya Ogawa, Aki Oishi, Miho Terao, Shuji Takada","doi":"10.1111/gtc.70131","DOIUrl":"https://doi.org/10.1111/gtc.70131","url":null,"abstract":"<div>\u0000 \u0000 <p>In mammalian sex differentiation, <i>Sox9</i> expression in undifferentiated gonads determines male development. <i>Sox9</i> is regulated by multiple enhancers, of which Enh13/mXYSRa is the most critical. Disruption of the GATA4 binding site in Enh13/mXYSRa causes XY sex reversal in the C57BL/6J (B6J) strain, but not in the mixed genetic background of B6J × DBA/2. To clarify the cause of these differences, mice with the same mutation were generated in DBA/2. Homozygous mutants developed as XY males. We hypothesized that the phenotypic differences between strains were due to functional differences of another enhancer. Mice lacking TESCO and carrying a mutation in the GATA4 binding site were generated and analyzed. The mutants developed according to their chromosomal sex despite reduced <i>Sox9</i> expression. These findings imply that the DBA/2 genetic background contains factors preventing <i>Sox9</i> expression from falling below the threshold required for male development. Bulk RNA-seq analysis of fetal gonads during sex determination identified strain-dependent differences in intermediate mesoderm development and protease inhibition pathways; the study also revealed that the expression of <i>Sox8</i> has a redundant role in Sertoli cell differentiation to that of <i>Sox9</i> in male embryonic gonads. These differences may contribute to the phenotypic variation observed between strains.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148324907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development 心脏发育过程中Sema3c位点的流出道心肌特异性增强子。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-06-21 DOI: 10.1111/gtc.70130

Yunce Wang, Yukihiro Harada, Tomoe Ueyama, Daiki Seya, Osamu Nakagawa, Teruhisa Kawamura

{"title":"An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development","authors":"Yunce Wang, Yukihiro Harada, Tomoe Ueyama, Daiki Seya, Osamu Nakagawa, Teruhisa Kawamura","doi":"10.1111/gtc.70130","DOIUrl":"10.1111/gtc.70130","url":null,"abstract":"<p><i>Sema3c</i> is specifically expressed in the cardiac outflow tract (OFT) of the developing mouse heart and has been implicated in OFT polarization and great artery formation. However, the regulatory basis underlying its spatially restricted expression remains unclear. To investigate the mechanisms underlying OFT-specific <i>Sema3c</i> expression, we utilized chromatin accessibility data from distinct segments of the developing heart and identified a differentially accessible region as an OFT-specific <i>Sema3c</i> enhancer candidate. Unlike previously characterized <i>Sema3c</i> enhancers, this region is located distal to the transcription start site. Reporter analysis using transgenic mouse embryos demonstrated that this region exhibits transcriptional activity from E8.5 onward and remains specifically active in the OFT myocardium throughout heart development. We further defined a minimal 603 bp enhancer whose activity depends on GATA binding sites. This enhancer provides insight into the mechanisms underlying spatially restricted <i>Sema3c</i> expression involved in OFT development.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148298760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 Persistent Homology Approach Enables Single-Cell Detection of Chromatin Spatial Organization Changes During Pathological Senescence Transition 一种持久的同源性方法使单细胞检测在病理性衰老过渡期间染色质空间组织的变化。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-06-16 DOI: 10.1111/gtc.70127

Kanji Furuya, Yoshitaka Umeno, Masae Ikura, Yasuka Ikura, Seiya Nishikawa, Tsuyoshi Ikura

{"title":"A Persistent Homology Approach Enables Single-Cell Detection of Chromatin Spatial Organization Changes During Pathological Senescence Transition","authors":"Kanji Furuya, Yoshitaka Umeno, Masae Ikura, Yasuka Ikura, Seiya Nishikawa, Tsuyoshi Ikura","doi":"10.1111/gtc.70127","DOIUrl":"10.1111/gtc.70127","url":null,"abstract":"<div>\u0000 \u0000 <p>Chromatin organization changes during aging, accompanied by alterations in higher-order chromosome architecture, contributing to the acquisition of senescent cell–specific functions. Recent studies have revealed that chromatin states and their regulatory mechanisms vary between individual cells. However, analyses of higher-order chromosome structure have been performed mostly at the population level. Therefore, approaches capable of directly quantifying such alterations at the single-cell level are required. Here, we applied persistent homology (PH), a topological data analysis framework, to quantify spatial features of γH2AX foci and DAPI-stained chromatin in single-cell fluorescence images. Using a model of pathological senescence induced by impaired acetylation-dependent histone H2AX exchange, we extracted topological features followed by machine learning analysis. Unsupervised analysis revealed spatial patterns associated with pathological senescence in both γH2AX and DAPI signals. Notably, classifications derived from γH2AX foci showed correspondence with those from DAPI-based chromatin organization, suggesting that local DNA damage patterns reflect global chromatin structure. Supervised models further distinguished normal and pathological senescent cells, with DAPI-derived features highlighting the contribution of nuclear intensity gradients. These findings demonstrate that PH enables quantitative characterization of nuclear architecture at the single-cell level and provides a framework for dissecting chromatin reorganization during cell state transitions.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148261199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Stepwise Evaluation of Plasmid- and Adeno-Associated Virus-Based Knock-In Using A Triple-Reporter Platform 使用三重报告平台逐步评估质粒和腺相关病毒的敲入。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-06-14 DOI: 10.1111/gtc.70129

Hiromasa Hara, Hideki Uosaki, Fumio Nakahara, Makoto Inoue, Yutaka Hanazono

{"title":"Stepwise Evaluation of Plasmid- and Adeno-Associated Virus-Based Knock-In Using A Triple-Reporter Platform","authors":"Hiromasa Hara, Hideki Uosaki, Fumio Nakahara, Makoto Inoue, Yutaka Hanazono","doi":"10.1111/gtc.70129","DOIUrl":"10.1111/gtc.70129","url":null,"abstract":"<div>\u0000 \u0000 <p>Homology-directed repair (HDR)-mediated knock-in efficiency is a composite of double-strand break (DSB) induction and repair pathway selection during targeted insertion. Thus, optimization of HDR-mediated knock-in presents significant challenges. To address this, we employed a mouse embryonic stem cell-based triple-reporter platform to examine how donor design and experimental parameters are associated with DSB induction and the balance between HDR-mediated knock-in and end-joining-mediated targeted insertion (EJ-TI). Our analysis reveals that donor design directly impacts DSB induction: co-electroporation of donor plasmids with Cas9/gRNA reduced cleavage efficiency, and Homology-Independent Targeted Integration (HITI) sequences further reduced this efficiency, thereby biasing overall knock-in efficiency. When normalized to DSB levels, HITI increased total targeted insertion yield (knock-in + EJ-TI) with shorter arms and favored HDR-mediated knock-in over EJ-TI with longer arms. Conversely, under adeno-associated virus (AAV) donor conditions, HITI showed donor-format dependency. It increased knock-in and decreased EJ-TI only with a self-complementary AAV donor, but had little effect with a single-stranded AAV donor. These results highlight the importance of separately evaluating DSB induction, total targeted insertion yield, and the balance between HDR-mediated knock-in and EJ-TI using a triple-reporter platform when optimizing knock-in strategies.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148255466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Interaction Between Rec8 and Mis4 Is Required for Axis-Loop Chromatin Formation and Homologous Chromosome Recombination During Meiosis 在减数分裂过程中，轴环染色质形成和同源染色体重组需要Rec8和Mis4相互作用。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2026-06-10 DOI: 10.1111/gtc.70128

Takeshi Sakuno, Yasuto Murayama, Tokuko Haraguchi, Yasushi Hiraoka

{"title":"Interaction Between Rec8 and Mis4 Is Required for Axis-Loop Chromatin Formation and Homologous Chromosome Recombination During Meiosis","authors":"Takeshi Sakuno, Yasuto Murayama, Tokuko Haraguchi, Yasushi Hiraoka","doi":"10.1111/gtc.70128","DOIUrl":"10.1111/gtc.70128","url":null,"abstract":"<p>The Rec8 cohesin complex is required for the pairing and recombination of homologous chromosomes during meiosis, as well as for the cohesion of sister chromatids. In the fission yeast <i>Schizosaccharomyces pombe</i>, we previously identified a <i>rec8-F204S</i> mutant that lost the ability to assemble the axis-loop chromatin structure without losing sister chromatid cohesion. This mutant showed reduced meiotic recombination, indicating that pairing and recombination of homologous chromosomes require the formation of the axis-loop chromatin structure mediated by the Rec8 cohesin complex. Loading of the Rec8 cohesin complex onto chromatin is mediated by Mis4 (NIPBL in humans; Scc2 in yeast). In this study, to elucidate the functions of Mis4, we identified a <i>mis4-LR</i> mutant (L1150S and R1159G) that reproduced the phenotypes of the <i>rec8-F204S</i> mutant, which is defective in chromatin axis formation and homologous recombination while retaining sister chromatid cohesion. These mutation sites (Mis4-L1150, Mis4-R1159, and Rec8-F204) are all localized at the interaction surface between Mis4 and Rec8. Biochemical analysis revealed that the Mis4-LR mutant protein exhibited reduced Rec8-binding activity. Considering that the <i>mis4-LR</i> mutant phenocopied the <i>rec8-F204S</i> mutant, our results demonstrate that the Mis4-Rec8 interaction is required for proper formation of Rec8-dependent meiotic chromosome axis.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.3,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148221554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Microarray-Based Identification of Time-Sensitive miRNAs as Serum Quality Indicators in Liquid Biopsy 时间敏感mirna作为液体活检血清质量指标的微阵列鉴定。

IF 1.3 4区生物学

Genes to Cells Pub Date : 2026-06-05 DOI: 10.1111/gtc.70122

Satoko Takizawa, Atsuko Mizoguchi, Hiroko Sudo, Yasuhito Nakadera, Hideo Akiyama, Satoshi Kondou

{"title":"Microarray-Based Identification of Time-Sensitive miRNAs as Serum Quality Indicators in Liquid Biopsy","authors":"Satoko Takizawa, Atsuko Mizoguchi, Hiroko Sudo, Yasuhito Nakadera, Hideo Akiyama, Satoshi Kondou","doi":"10.1111/gtc.70122","DOIUrl":"10.1111/gtc.70122","url":null,"abstract":"<div>\u0000 \u0000 <p>Circulating microRNAs (miRNAs) are promising biomarkers and many studies have been reported. However, there are discrepancies between studies due to differences in the inclusion criteria, experimental procedures, and serum/plasma processing conditions. In this study, we aimed to develop a comprehensive set of miRNA markers to assess the serum quality, which fluctuates depending on the storage duration after blood collection. This study was designed to identify circulating miRNAs that were unstable when stored at room temperature (23°C–27°C) for more than 0.5–1 h after centrifugation to separate the serum. The results showed that 17 miRNAs were more than 5% variable in their signals after storage at room temperature for more than 0.5 h. Of these, seven miRNAs were identified whose signals changed significantly by more than 1 in signal level after 1 h of storage at room temperature, showing time-dependent fluctuations in detection levels. These miRNAs were further evaluated between the two clinical sample groups with different preprocessing times. miR-4429 and miR-6511b-5p showed a significant decrease in signals in the sample group with longer processing times. These miRNAs can be used as markers to assess sample quality and reflect the time-dependent storage conditions of clinical samples.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.3,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148166832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

IF 1.3 4区生物学

Genes to Cells Pub Date : 2026-05-21

引用次数: 0