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Quantitative Imaging Analysis of Internal Structural Complexity in Mouse Heart Organoids; Comparison to Mouse Embryonic Hearts 小鼠心脏类器官内部结构复杂性的定量成像分析小鼠胚胎心脏的比较
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-10-19 DOI: 10.1111/gtc.70055
Rin Kaneko, Fumitoshi Ishino, Jiyoung Lee
{"title":"Quantitative Imaging Analysis of Internal Structural Complexity in Mouse Heart Organoids; Comparison to Mouse Embryonic Hearts","authors":"Rin Kaneko,&nbsp;Fumitoshi Ishino,&nbsp;Jiyoung Lee","doi":"10.1111/gtc.70055","DOIUrl":"https://doi.org/10.1111/gtc.70055","url":null,"abstract":"<div>\u0000 \u0000 <p>We have established mouse heart organoids (mHOs) that are characterized by the presence of atrium- and ventricle-like structures that mimic entire embryonic hearts. However, maturation was not uniform, and little is known about their trabeculation status. Given the essential role of the trabeculae in cardiac morphogenesis, a new method that combines imaging analysis with a machine learning model was developed for quantifying the internal complexity in developing mHOs in a timely manner. We applied this method to screen for modified culture conditions and identified optimal treatment with valproic acid as a Notch activator and both bone morphogenetic protein 10 and Neuregulin 1 as downstream factors of Notch (a trabeculation-regulating signal) to promote mHO maturation. The established method using mouse fetal hearts as tests was suitable for comparing the internal complexity of both mHOs and mouse fetal hearts. The modified culture conditions improved the maturation uniformity as well as the internal structure of mHOs. Thus, this method can be applied to cardiac disorders with trabeculation problems and HOs developed by other methods. In addition, mHOs generated under these modified conditions may be an effective tool for studying the molecular mechanisms of heart development, including the signaling pathway of trabeculation related to these factors.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 6","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145317411","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 Upstream RUNX3 Enhancer, eR3 (−18m/−28h), Regulates the Development of Gut-Associated Anti-Tumorigenic CD8+CD103+ Cytotoxic T Lymphocytes in Mouse and Human 上游RUNX3增强子eR3(−18m/−28h)调节小鼠和人肠道相关抗肿瘤CD8+CD103+细胞毒性T淋巴细胞的发育
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-10-19 DOI: 10.1111/gtc.70052
Giselle Sek Suan Nah, Junichi Matsuo, Avinash Govind Bahirvani, Shunichi Kimura, Desmond Wai Loon Chin, King Pan Ng, Cai Ping Koh, Michelle Meng Huang Mok, Chelsia Qiuxia Wang, Vinay Tergaonker, Dominic C. Voon, Kazuyoshi Kohu, Sawako Muroi, Jizhong Shi, Shuizhou Yu, Md. Zakir Hossain, Wei-Siang Liau, Cao Thi Ngoc Phuong, Takaomi Sanda, Judith Marsman, Julia Horsfield, Hilde Cheroutre, Yiong Huak Chan, Brendan Pang, Pei Yi Chong, Richie Soong, Daniel G. Tenen, Yoichi Maekawa, Byrappa Venkatesh, Yoshiaki Ito, Ichiro Taniuchi, Motomi Osato
{"title":"An Upstream RUNX3 Enhancer, eR3 (−18m/−28h), Regulates the Development of Gut-Associated Anti-Tumorigenic CD8+CD103+ Cytotoxic T Lymphocytes in Mouse and Human","authors":"Giselle Sek Suan Nah,&nbsp;Junichi Matsuo,&nbsp;Avinash Govind Bahirvani,&nbsp;Shunichi Kimura,&nbsp;Desmond Wai Loon Chin,&nbsp;King Pan Ng,&nbsp;Cai Ping Koh,&nbsp;Michelle Meng Huang Mok,&nbsp;Chelsia Qiuxia Wang,&nbsp;Vinay Tergaonker,&nbsp;Dominic C. Voon,&nbsp;Kazuyoshi Kohu,&nbsp;Sawako Muroi,&nbsp;Jizhong Shi,&nbsp;Shuizhou Yu,&nbsp;Md. Zakir Hossain,&nbsp;Wei-Siang Liau,&nbsp;Cao Thi Ngoc Phuong,&nbsp;Takaomi Sanda,&nbsp;Judith Marsman,&nbsp;Julia Horsfield,&nbsp;Hilde Cheroutre,&nbsp;Yiong Huak Chan,&nbsp;Brendan Pang,&nbsp;Pei Yi Chong,&nbsp;Richie Soong,&nbsp;Daniel G. Tenen,&nbsp;Yoichi Maekawa,&nbsp;Byrappa Venkatesh,&nbsp;Yoshiaki Ito,&nbsp;Ichiro Taniuchi,&nbsp;Motomi Osato","doi":"10.1111/gtc.70052","DOIUrl":"https://doi.org/10.1111/gtc.70052","url":null,"abstract":"<div>\u0000 \u0000 <p>The <i>RUNX3</i> gene is frequently involved in a variety of cancers and immunological diseases. Despite such widespread association with human diseases, the transcriptional regulation of <i>RUNX3</i> remains elusive. Here we report the identification of an enhancer for <i>Runx3</i>, <i>eR3(−18m/−28h)</i>, by employing a combination of in silico prediction and in vivo verification using zebrafish and mouse models. <i>eR3</i> is active in CD8<sup>+</sup>CD103 (integrin α<sub>E</sub>)<sup>+</sup> cytotoxic T lymphocytes (CTLs) that reside in the intestinal epithelium via their interaction with the CD103 ligand, E-cadherin, on epithelial cells. Removal of <i>eR3(−18m)</i> specifically in CD8 T cells compromised the suppression of tumorigenesis in murine cancer models. In humans, single nucleotide polymorphisms (SNPs) in <i>eR3(−28h)</i> were overrepresented and were associated with weakened CTL activity in colorectal cancer patients. Together, our results indicate that <i>eR3</i> plays a role in immune surveillance against gut-associated tumors by upregulating <i>RUNX3</i> expression in specific CTLs.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 6","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145317761","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
The TAP/NXF1-Binding Region of HuD Is Required for Translation and Neuronal Differentiation HuD的TAP/ nxf1结合区是翻译和神经元分化所必需的
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-10-19 DOI: 10.1111/gtc.70057
So Toshima, Ryosuke Satoh, Takumi Tomohiro, Yoshinori Funakami, Akira Fukao, Toshinobu Fujiwara
{"title":"The TAP/NXF1-Binding Region of HuD Is Required for Translation and Neuronal Differentiation","authors":"So Toshima,&nbsp;Ryosuke Satoh,&nbsp;Takumi Tomohiro,&nbsp;Yoshinori Funakami,&nbsp;Akira Fukao,&nbsp;Toshinobu Fujiwara","doi":"10.1111/gtc.70057","DOIUrl":"https://doi.org/10.1111/gtc.70057","url":null,"abstract":"<div>\u0000 \u0000 <p>The neuronal ELAV protein HuD is known to promote neuronal differentiation and stimulate cap-dependent translation, but the underlying mechanism remains incompletely understood. Here, we identify a functional domain within the HuD linker that governs interaction with the nuclear export factor TAP/NXF1 and stimulates translation. Using a series of deletion mutants, we show that TAP/NXF1 binding is functionally separable from cytoplasmic localization, and that loss of this interaction correlates with impaired translation and neurite outgrowth. These findings reveal a critical subdomain within HuD that recruits TAP/NXF1 to promote translation and neuronal differentiation, establishing a mechanistic link between RNA export factors and ELAV-mediated translational control.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 6","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145317762","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
Decreased Mitochondrial Translation Suppresses 3,3′-Diindolylmethane-Induced Reactive Oxygen Species Generation in Schizosaccharomyces Pombe 线粒体翻译减少抑制3,3'-二吲哚甲烷诱导的Pombe裂糖菌活性氧生成。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-10-15 DOI: 10.1111/gtc.70056
Kaiyu Wang, Hidenori Osawa, Hideto Nagai, Masaru Ueno
{"title":"Decreased Mitochondrial Translation Suppresses 3,3′-Diindolylmethane-Induced Reactive Oxygen Species Generation in Schizosaccharomyces Pombe","authors":"Kaiyu Wang,&nbsp;Hidenori Osawa,&nbsp;Hideto Nagai,&nbsp;Masaru Ueno","doi":"10.1111/gtc.70056","DOIUrl":"10.1111/gtc.70056","url":null,"abstract":"<div>\u0000 \u0000 <p>Broccoli-derived 3,3′-diindolylmethane (DIM) exhibits anticancer effects. The compound also inhibits the growth of fission yeast cells. Reduction of mitochondrial translation alleviates the growth defects caused by DIM in fission yeast; however, the underlying molecular mechanisms remain unclear. In this study, we show that DIM-induced reactive oxygen species (ROS) colocalized with mitochondria. Deletion of <i>tsf1</i><sup>+</sup>, which leads to reduced mitochondrial translation, suppressed this colocalization. Deletions of stress response genes, such as <i>sty1</i><sup><i>+</i></sup>, <i>pap1</i><sup><i>+</i></sup>, and <i>atf1</i><sup><i>+</i></sup>, increased DIM sensitivity. Growth defects in the wild-type and <i>sty1</i>, <i>pap1</i>, and <i>atf1</i> disruptants in the presence of DIM were suppressed by the ROS scavenger N-acetylcysteine. Moreover, the ROS scavenger Sod1, which is suggested to function in the mitochondrial intermembrane space and cytoplasm, was important for survival in the presence of DIM. Collectively, the study results suggest that DIM increases ROS levels in mitochondria and suppression of ROS increase in mitochondria via inhibition of mitochondrial translation is the mechanism by which DIM-induced growth defects in wild-type cells are suppressed. Overall, the study highlights the potential use of DIM as an anticancer drug to increase ROS generation in mitochondria in cancer cells.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 6","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294804","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
Correction to “Transcriptional Regulation of the Interferon Alpha-Inducible Protein-27 Like 2b by the Peroxisome Proliferator-Activated Receptor γ in Fatty Liver Disease” 对“过氧化物酶体增殖物激活受体γ对脂肪肝中干扰素α诱导蛋白27样2b的转录调节”的更正。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-10-09 DOI: 10.1111/gtc.70053
{"title":"Correction to “Transcriptional Regulation of the Interferon Alpha-Inducible Protein-27 Like 2b by the Peroxisome Proliferator-Activated Receptor γ in Fatty Liver Disease”","authors":"","doi":"10.1111/gtc.70053","DOIUrl":"10.1111/gtc.70053","url":null,"abstract":"<p>Sakaguchi, A., Aibara, D., Matsusue, K. 2025. “Transcriptional Regulation of the Interferon Alpha-Inducible Protein-27 Like 2b by the Peroxisome Proliferator-Activated Receptor γ in Fatty Liver Disease.” <i>Genes to Cells</i> 30, no. 5: e70049. https://doi.org/10.1111/gtc.70049.</p><p>In Figure 3(A), “−314/−326” was incorrect and should read “+314/+326.” The corrected version of Figure 3 is provided here in full.</p><p>We apologize for this error.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 6","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254431","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
m6A RNA Modification Controls HTLV-1 Tax and Host Gene Expression m6A RNA修饰控制HTLV-1税收和宿主基因表达。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-10-07 DOI: 10.1111/gtc.70054
Rei Gibu, Kodai Gibu, Kako Suzuki, Yuetsu Tanaka, Kaoru Uchimaru, Makoto Yamagishi
{"title":"m6A RNA Modification Controls HTLV-1 Tax and Host Gene Expression","authors":"Rei Gibu,&nbsp;Kodai Gibu,&nbsp;Kako Suzuki,&nbsp;Yuetsu Tanaka,&nbsp;Kaoru Uchimaru,&nbsp;Makoto Yamagishi","doi":"10.1111/gtc.70054","DOIUrl":"10.1111/gtc.70054","url":null,"abstract":"<p>Human T-cell Leukemia Virus Type 1 (HTLV-1) is a pathogenic human retrovirus that is responsible for intractable diseases such as adult T-cell leukemia–lymphoma (ATL), a malignancy with a poor patient prognosis. Although recent studies have delineated several genomic, epigenomic, and transcriptomic abnormalities associated with HTLV-1, to date the importance of epitranscriptomic modifications, particularly <i>N</i><sup><i>6</i></sup>-methyladenosine (m<sup>6</sup>A), remains unclear. Here, we showed that the HTLV-1 RNA genome undergoes m<sup>6</sup>A modification, thereby suggesting that these modifications act as bidirectional regulators of both viral and host processes. Moreover, targeted depletion of m<sup>6</sup>A modification within the viral transactivator HTLV-1 Tax resulted in markedly destabilized Tax mRNA, attenuated Tax protein abundance, and suppression of downstream expression of host genes including <i>IL2RA</i> and <i>TXN</i>. Overall, these findings suggest that m<sup>6</sup>A methylation is an essential determinant of the HTLV-1 life cycle, and understanding it may offer mechanistic insight into viral latency and present novel avenues for therapeutic intervention and prophylaxis.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 6","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12504147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246179","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
Knockdown of Cav2.2 Calcium Channel in Macrophages Aggravates Colitis Induced by Dextran Sodium Sulfate 葡聚糖硫酸钠诱导巨噬细胞Cav2.2钙通道下调加重结肠炎
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-09-21 DOI: 10.1111/gtc.70051
Hironao Saegusa, Xiaoxu Li, Xinshuang Wang, Tsutomu Tanabe
{"title":"Knockdown of Cav2.2 Calcium Channel in Macrophages Aggravates Colitis Induced by Dextran Sodium Sulfate","authors":"Hironao Saegusa,&nbsp;Xiaoxu Li,&nbsp;Xinshuang Wang,&nbsp;Tsutomu Tanabe","doi":"10.1111/gtc.70051","DOIUrl":"https://doi.org/10.1111/gtc.70051","url":null,"abstract":"<div>\u0000 \u0000 <p>Voltage-dependent calcium channels (VDCCs) have previously been thought to be functional in excitable cells, but recently accumulating evidence suggests that they are also functional in non-excitable cells such as microglia. In the present study, we investigated the role of the N-type VDCC (Cav2.2) in macrophages, a kind of non-excitable cell, in a mouse model of inflammatory bowel disease (IBD). The dextran sodium sulfate (DSS) colitis model, a widely used chemically induced model of IBD, was applied to Cav2.2 knockdown (KD) mice, where Cav2.2 expression in macrophages can be downregulated by the application of tamoxifen. After the 7 days of oral administration of 2.5% DSS, Cav2.2KD mice had a significantly higher disease activity index for colitis compared to wild-type (WT) mice, and histological examination of the colon from DSS-treated mice also suggested more severe intestinal damage in Cav2.2KD mice. Moreover, the densities of Iba1<sup>+</sup> cells (macrophages/dendritic cells) in the colon were also elevated in Cav2.2KD mice. TNFα levels were significantly higher in Cav2.2KD mice as revealed by ELISA experiments. Collectively, these data suggest that the Cav2.2KD mice had more severe colonic inflammation compared to WT mice. Therefore, Cav2.2 in macrophages may play some roles in suppressing inflammation in the intestinal immune system.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 5","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145110929","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
Machine Learning Extracts Radiation Resistant-Specific EdU Fluorescence Pattern in Cancer Cells 机器学习提取肿瘤细胞抗辐射特异性EdU荧光模式。
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-09-16 DOI: 10.1111/gtc.70050
Masae Ikura, Tsuyoshi Ikura, Kanji Furuya
{"title":"Machine Learning Extracts Radiation Resistant-Specific EdU Fluorescence Pattern in Cancer Cells","authors":"Masae Ikura,&nbsp;Tsuyoshi Ikura,&nbsp;Kanji Furuya","doi":"10.1111/gtc.70050","DOIUrl":"10.1111/gtc.70050","url":null,"abstract":"<div>\u0000 \u0000 <p>The thymidine analog EdU (5-ethynyl-2-deoxyuridine) is incorporated into DNA during replication and has traditionally been used as a marker of S-phase cells. In this study, we discovered that EdU fluorescence images display substantial cell-to-cell variability, which could be classified into multiple clusters by unsupervised machine learning. This suggests that seemingly random EdU patterns contain reproducible, computationally recognizable features. Building on our observation that distinct patterns emerged in response to radiation stress, we investigated whether radioresistant cancer cells exhibit specific EdU signatures. Analysis of PLK1-overexpressing cells, which acquire radioresistance through altered DNA replication, revealed radiation-induced EdU patterns distinct from control cells. Prompted by the observation that these cells displayed markedly enlarged and intensified γ-H2AX foci, a marker of DNA damage, we employed a supervised machine learning model based on γ-H2AX patterns to isolate the radioresistant cell subpopulation. We then extracted the EdU signals from these isolated cells and, through further unsupervised machine learning, successfully identified a characteristic pattern specific to radioresistance. This establishes a machine learning framework capable of extracting universal rules from the dynamic networks that vary among individual cells, which provides a novel platform for a screening system to identify molecules involved in radioresistance, focusing on cancer heterogeneity.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 5","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145077166","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
Correction to “The Meeting Report on the Fifth International Conference of the Chromosomal SMC Complexes” 更正“第五届国际染色体SMC复合体会议报告”
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-09-08 DOI: 10.1111/gtc.70048
{"title":"Correction to “The Meeting Report on the Fifth International Conference of the Chromosomal SMC Complexes”","authors":"","doi":"10.1111/gtc.70048","DOIUrl":"https://doi.org/10.1111/gtc.70048","url":null,"abstract":"<p> <span>Niki, H.</span>, and <span>Y. Murayama</span>. <span>2025</span>. “ <span>The Meeting Report on the Fifth International Conference of the Chromosomal SMC Complexes</span>.” <i>Genes to Cells</i> <span>30</span>, no. <span>5</span>: e70039. https://doi.org/10.1111/gtc.70039.</p><p>The legend for Figure 2 “Poster session at SMC2024.” was incorrect. This should have read: “Barbara Meyer and Tatsuya Hirano talked about their seminal papers on the discovery of condensin.”</p><p>We apologize for this error.</p>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 5","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145012224","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
Transcriptional Regulation of the Interferon Alpha-Inducible Protein-27 Like 2b by the Peroxisome Proliferator-Activated Receptor γ in Fatty Liver Disease 过氧化物酶体增殖物激活受体γ对脂肪肝中干扰素α诱导蛋白27样2b的转录调节
IF 1.3 4区 生物学
Genes to Cells Pub Date : 2025-09-07 DOI: 10.1111/gtc.70049
Ai Sakaguchi, Daisuke Aibara, Kimihiko Matsusue
{"title":"Transcriptional Regulation of the Interferon Alpha-Inducible Protein-27 Like 2b by the Peroxisome Proliferator-Activated Receptor γ in Fatty Liver Disease","authors":"Ai Sakaguchi,&nbsp;Daisuke Aibara,&nbsp;Kimihiko Matsusue","doi":"10.1111/gtc.70049","DOIUrl":"https://doi.org/10.1111/gtc.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor abundantly expressed in the fatty liver of type 2 diabetic <i>ob/ob</i> mice. Herein, we investigated how PPARγ regulates the expression of the interferon alpha-inducible protein 27-like 2b (<i>lfi27l2b</i>) gene in the mouse liver. High expression of <i>lfi27l2b</i> was observed in the fatty liver of <i>ob/ob</i> mice, and the expression was further upregulated by PPARγ ligands; however, liver-specific <i>Pparg</i> knockout ameliorated this increase. Moreover, high <i>lfi27l2b</i> expression was observed in the fatty liver of alcohol-fed mice. Reporter assays indicated that the PPARγ-responsive element (PPRE) is necessary for PPARγ-dependent induction of <i>Ifi27l2b</i> promoter activities. Furthermore, electrophoretic mobility shift assays showed that PPARγ is capable of directly binding the PPRE. Overall, our results indicate that <i>lfi27l2b</i> is a novel PPARγ target in the fatty liver.</p>\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"30 5","pages":""},"PeriodicalIF":1.3,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145012423","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
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