DNA and cell biology最新文献

{"title":"MERTK and Fibrosis: A New Target for Therapy.","authors":"Ziyan Pan, Mohammed Eslam","doi":"10.1089/dna.2024.0099","DOIUrl":"10.1089/dna.2024.0099","url":null,"abstract":"<p><p>Organ fibrosis is a devastating medical challenge that is collectively responsible for an estimated 45% of all deaths in developed countries and poses a substantial health and economic burden. The process of fibrosis has common characteristics that can occur in various organs, such as the liver, kidney, lung, and skin. Currently, there is a paucity of effective treatments available for fibrosis. Therefore, it is crucial to identify new approaches to find potential therapeutic targets. Genetic studies have shown great promise in advancing the drug development process. Mer tyrosine kinase (MERTK) was recently identified as a crucial regulator of fibrosis that specifically controls the activity of transforming growth factor beta (TGFβ). In this brief review, we provide an overview of the potential role of MERTK as a targeted and valuable approach for treating organ fibrosis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141181470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shen-Qi-Ling-Bi Decoction Inhibits Colorectal Cancer Cell Growth by Inducing Ferroptosis Through Inactivation of PI3K/AKT Signaling Pathway.","authors":"Lin Liu, Guanlong Ye, Wei Huang, Yang He, Donghao Xie","doi":"10.1089/dna.2023.0434","DOIUrl":"10.1089/dna.2023.0434","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a common malignancy with poor prognosis. Shen-Qi-Ling-Bi Decoction (SQLB), a classic traditional Chinese medicine (TCM) formula, was found to exert antitumor effects in CRC. This study aimed to explore the biological functions of SQLB in CRC. Cell Counting Kit 8 (CCK-8), wound healing, and transwell invasion assays <i>in vitro</i> were used to evaluate the antitumor effects of SQLB in CRC cells. In addition, ferroptosis in CRC cells was determined by evaluating Fe²⁺ content and lipid ROS, MDA, and GSH levels. SQLB treatment partially reduced CRC cell proliferation, migration, and invasion; however, a ferroptosis inhibitor, ferrostatin-1 (Fer-1), abolished these effects. In addition, SQLB treatment triggered CRC cell ferroptosis, as evidenced by increased Fe²⁺, lipid ROS, and MDA levels and decreased GSH levels; conversely, these levels were reversed by Fer-1. Furthermore, SQLB notably suppressed tumor growth in nude mice <i>in vivo.</i> Meanwhile, SQLB decreased phosphorylated PI3K and AKT levels, downregulated Nrf2, GPX4, and SLC7A11 levels, and upregulated ACSL4 levels in CRC cells and in tumor tissues; however, these effects were reversed by Fer-1. Collectively, SQLB inhibited CRC cell proliferation, invasion, and migration by triggering ferroptosis through inactivation of the PI3K/AKT signaling pathway. These findings demonstrate a novel mechanism of action for SQLB in the treatment of CRC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141332735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>FOXO1</i> Single-Nucleotide Polymorphisms Are Associated with Bleeding Severity and Sensitivity of Glucocorticoid Treatment of Pediatric Immune Thrombocytopenia.","authors":"Xingjuan Xie, Hao Gu, Jingyao Ma, Lingling Fu, Jie Ma, Jialu Zhang, Runhui Wu, Zhenping Chen","doi":"10.1089/dna.2023.0431","DOIUrl":"10.1089/dna.2023.0431","url":null,"abstract":"<p><p>Immune thrombocytopenia (ITP) is an autoimmune-mediated hemorrhagic disease. Emerging evidence indicates that <i>FOXO1</i> SNPs are related to the immune dysregulation of several autoimmune diseases suggesting that FOXO1 may be involved in inflammation and pathologic activities in patients with ITP. This study aimed to evaluate whether <i>FOXO1</i> gene single-nucleotide polymorphisms (SNPs) are associated with susceptibility to ITP and clinical priorities of concern include bleeding severity and sensitivity of glucocorticoid treatment. This study recruited 327 newly diagnosed ITP and 220 healthy controls. Four SNPs (rs17446593, rs17446614, rs2721068, and rs2721068) of the <i>FOXO1</i> gene were detected using the Sequenom MassArray system. Bleeding severity were classified into the mild and severe groups based on the bleeding scores. ITP patients were classified as sensitive and insensitive to glucocorticoid treatment according to the practice guideline for ITP (2019 version). The frequencies of the four SNPs did not show any significant differences between the ITP and healthy control groups. Patients with AA genotype at rs17446593 (<i>p</i> = 0.009) and GG genotype at rs17446614 (<i>p</i> = 0.009) suffered more severe bleeding than patients without them. Carriers of haplotype G_rs17446593A_rs17446614C_rs2721068T_rs2755213 were protective to severe bleeding (<i>p</i> = 0.002). The AA genotype at rs17446593 was significantly higher in ITP patients sensitive to glucocorticoid treatment than in those insensitive to glucocorticoid treatment (<i>p</i> = 0.03). Haplotype G_rs17446593G_rs17446614T_rs2721068T_rs2755213 increases the risk of glucocorticoid resistance (<i>p</i> = 0.007). Although <i>FOXO1</i> gene polymorphisms were not associated with susceptibility to ITP, the AA genotype at rs17446593 and GG genotype at rs17446614 were associated with bleeding severity. Haplotype GACT have a protective effect against severe bleeding. Patients with AA genotype at rs17446593 may tend to have good responds to glucocorticoid treatment. However, the <i>FOXO1</i> gene haplotype GGTT increases the risk of glucocorticoid-resistant. Trial registration: ChiCTR1900022419.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140857618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reg3A Overexpression Facilitates Hepatic Metastasis by Altering Cell Adhesion in LoVo Colon Cancer Cells.","authors":"Ke-Yi Xu, Mao Li, Wei-Hong Yu, Xin Li, Yuan Zeng, Fei-Lu Xie, Yi-Han Zhou, Pin-Shen Xu, Chun-Cheng Pu, Bing-Bing Xie, Lu-Ting Yu, Chen Luo","doi":"10.1089/dna.2024.0029","DOIUrl":"10.1089/dna.2024.0029","url":null,"abstract":"","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141072431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>microRNA-141-3p</i> Suppressed the Progression of the Clear Cell Renal Cell Carcinoma by Targeting <i>Transforming Growth Factor Beta 2</i> Gene Expression.","authors":"Xinming Hu, Desheng Li, Jiangtao Zhan, Changmin Yang, Pengfei Wang, Xusong Meng, Sheng Xu, Xianping Che, Lei Xu","doi":"10.1089/dna.2023.0405","DOIUrl":"10.1089/dna.2023.0405","url":null,"abstract":"<p><p>Clear cell renal cell carcinoma (ccRCC) is a malignant tumor of kidney epithelial cells, one of the most common tumors in the world. Transforming growth factor beta (TGFβ)1 is a crucial factor that induces epithelial-mesenchymal transition (EMT) in cancer cells. <i>microRNA-141-3p (miR-141-3p)</i> is a microRNA that is considered a tumor suppressor. However, the role and mechanism of <i>miR-141-3p</i> in TGFβ1-induced ccRCC cells are not fully understood. This study investigated the roles of <i>miR-141-3p</i> and its target gene in regulating EMT in ccRCC development. 786-0 and Caki-1cells were treated with TGFβ1 to induce EMT. The levels of <i>miR-141-3p</i> and TGFβ2 were determined by quantitative real-time polymerase chain reaction and Western blotting. The progression of EMT was evaluated by E-cadherin detection by immunofluorescence, and E-cadherin, N-cadherin, and vimentin detection by Western blotting. Furthermore, migration and invasion capacities were assessed using a Transwell system. The direct binding of <i>miR-141-3p</i> with the target gene <i>TGFβ2</i> was confirmed by dual luciferase reporter gene assay. Results indicated that TGFβ1 treatment decreased the protein abundance of E-cadherin while increasing the protein expression of N-cadherin and vimentin, indicating TGFβ1-induced EMT was constructed successfully. Moreover, TGFβ1 treatment repressed the expression of <i>miR-141-3p</i>. <i>miR-141-3p</i> mimics reversed the effect of TGFβ1 on the migration, invasion, and expression of E-cadherin, N-cadherin, and vimentin. The <i>miR-141-3p</i> directly binds with the 3' untranslated region of <i>TGFβ2</i> mRNA and suppresses its expression. Furthermore, TGFβ2 overexpression abrogated the above changes regulated by <i>miR-141-3p</i> mimics. Taken together, <i>miR-141-3p</i> inhibited TGFβ1-induced EMT by suppressing the migration and invasion of ccRCC cells via directly targeting <i>TGFβ2</i> gene expression.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140137547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EIF4A3-Bound hsa_circ_0006847 Exerts a Tumor-Suppressive Role in Gastric Cancer.","authors":"Chunli Cao, Xinxin Wu, Zhe Li, Yaoyao Xie, Shiyi Xu, Junming Guo, Weiliang Sun","doi":"10.1089/dna.2023.0397","DOIUrl":"10.1089/dna.2023.0397","url":null,"abstract":"<p><p>Numerous studies have shown that circular RNAs are associated with the occurrence and development of various cancers, but the biological functions and mechanisms of hsa_circ_0006847 (circASPHD1) in gastric cancer (GC) remain unclear. The expression of hsa_circ_0006847 in GC cell lines, tissue, and plasma from GC patients was assayed by quantitative real-time reverse transcription-polymerase chain reaction. Hsa_circ_0006847 expression in cells was downregulated or upregulated by transfected small interfering RNA (siRNA) or overexpression plasmid. The role of hsa_circ_0006847 in GC was investigated with Cell Counting Kit-8, EdU, Transwell, flow cytometry assays, and in a subcutaneous xenograft tumor model. In addition, the interaction of eukaryotic translation initiation factor 4A3 (EIF4A3) and hsa_circ_0006847 was determined with western blot, biotin-labeled RNA pull-down, and RNA immunoprecipitation assays. Co-immunoprecipitation and mass spectrometry were used to validate the combination of EIF4A3 and synaptopodin-2 (SYNPO2). The expression of hsa_circ_0006847 was decreased in GC tissues and cells and indicated poor survival and prognosis. Overexpression of hsa_circ_0006847 inhibited cell proliferation, migration, and invasion. Flow cytometry showed that upregulation of hsa_circ_0006847 resulted in promotion of apoptosis of GC cells and inhibited their progression through the G0/G1 phase. Downregulation of hsa_circ_0006847 expression had the opposite effects. Overexpression of hsa_circ_0006847 in subcutaneous tumor xenografts inhibited tumor growth. Mechanically, hsa_circ_0006847 promoted the binding of EIF4A3 to SYNPO2 by recruiting EIF4A3, which inhibited the growth of GC. The tumor suppressor activity of hsa_circ_0006847, inhibition of the occurrence and development of GC, was mediated by promotion of EIF4A3 and the binding of EIF4A3 to SYNPO2. The results support the study of hsa_circ_0006847 as a novel therapeutic target for the treatment of GC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ-EIF3I Promotes Hepatocellular Carcinoma Progression Through Modulating miR-361-3p/DUSP2 Axis.","authors":"Lingna Ni, Qianqian Gao, Qiu Zhao, Kejun Dai, Mingming Jin, Cong Fu, Min Xiao, Wenyu Zhu, Yanzhi Bi","doi":"10.1089/dna.2023.0400","DOIUrl":"10.1089/dna.2023.0400","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most common malignant cancers globally. Circular RNAs (circRNAs) have been implicated in the development of HCC. Previous studies have confirmed that circ-EIF3I plays an important role in the progress of lung cancer. Nevertheless, the biological functions of circ-EIF3I and the underlying mechanisms by which they regulate HCC progression remain unclear. In this study, the regulatory mechanism and targets were studied with bioinformatics analysis, luciferase reporting analysis, transwell migration, Cell Counting Kit-8, and 5-Ethynyl-2'-deoxyuridine analysis. In addition, <i>in vivo</i> tumorigenesis and metastasis assays were employed to evaluate the roles of circ-EIF3I in HCC. The result shows that the circ-EIF3I expression was increased in HCC cell line, which means that circ-EIF3I plays a role in the progression of HCC. Downregulation of circ-EIF3I suppressed HCC cells' proliferation and migration in both <i>in vivo</i> and <i>in vitro</i> experiments. Bioinformatics and luciferase report analysis confirmed that both miR-361-3p and Dual-specificity phosphatase 2 (DUSP2) were the downstream target of circ-EIF3I. The overexpression of DUSP2 or inhibition of miR-361-3p restored HCC cells' proliferation and migration ability after silence circ-EIF3I. Taken together, our study found that downregulation of circ-EIF3I suppressed the progression of HCC through miR-361-3p/DUSP2 Axis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone Remodeling and Bone Structural Genes in Legg-Calvé-Perthes Disease: The OPG rs2073618 and IL-6 rs1800795 Are Associated with High Risk in Mexican Patients.","authors":"Blanca Lucía Cruz-Ortíz, Edgar Hernández-Zamora, Elba Reyes-Maldonado, A. O. Rodríguez-Olivas, J. Rubio-Lightbourn, Celeste O. Martínez-Ramírez, C. Castro-Hernández, Ruth Lezama-Palacios, L. Casas-Avila","doi":"10.1089/dna.2023.0411","DOIUrl":"https://doi.org/10.1089/dna.2023.0411","url":null,"abstract":"Legg-Calve-Perthes disease (LCPD) is an idiopathic avascular necrosis of the pediatric femoral head. Bone remodeling and bone structural genes have the potential to contribute to the progression of LCPD when there is disequilibrium between bone resorption and bone formation. A case-control study was performed to search for associations of several common polymorphisms in the genes Receptor Activator for Nuclear Factor κappa B (RANK), Receptor Activator for Nuclear Factor κappa B Ligand (RANKL), osteoprotegerin (OPG), interleukin (IL)-6, and type 1 collagen (COL1A1) with LCPD susceptibility in Mexican children. A total of 23 children with LCPD and 46 healthy controls were genotyped for seven polymorphisms (rs3018362, rs12585014, rs2073618, rs1800795, rs1800796, rs1800012, and rs2586498) in the RANK, RANKL, OPG, IL-6, and COL1A1 genes by real-time polymerase chain reaction with TaqMan probes. The variant allele (C) of IL-6 rs1800795 was associated with increased risk of LCPD (odds ratio [OR]: 3.8, 95% confidence interval [CI]: [1.08-13.54], p = 0.033), adjusting data by body mass index (BMI) and coagulation factor V (FV), the association with increased risk remained (OR: 4.9, 95% CI: [1.14-21.04], p = 0.025). The OPG polymorphism rs2073618, specifically GC-GG carriers, was associated with a more than fourfold increased risk of developing LCPD (OR: 4.34, 95% CI: [1.04-18.12], p = 0.033) when data were adjusted by BMI-FV. There was no significant association between RANK rs3018362, RANKL rs12585014, IL-6 rs1800796, COL1A1 rs1800012, and rs2586498 polymorphisms and LCPD in a sample of Mexican children. The rs1800975 and rs2037618 polymorphisms in the IL-6 and OPG genes, respectively, are informative markers of increased risk of LCPD in Mexican children.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140676198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A RNA Methylation and Implications for Hepatic Lipid Metabolism.","authors":"Xinyue Ming, Shirui Chen, Huijuan Li, Yun Wang, Le Zhou, Yuncheng Lv","doi":"10.1089/dna.2023.0410","DOIUrl":"https://doi.org/10.1089/dna.2023.0410","url":null,"abstract":"This review presents a summary of recent progress in research on the N6-methyladenosine (m6A) modification and regulatory roles in hepatic lipid metabolism. As the most abundant internal modification of eukaryotic RNA, the m6A modification is a dynamic and reversible process of the m6A enzyme system, which includes writers, erasers, and readers. m6A methylation depressed lipid synthesis and facilitated lipolysis in liver. The depletion of m6A methyltransferase Mettl14/Mettl3 raised fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD1), acetyl-CoA carboxylase (ACC), and elongase of very long chain fatty acids 6 (ELOVL6) in rodent liver, causing increases in liver weight, triglyceride (TG) production, and content in hepatocytes. FTO catalyzed m6A demethylation and the suppression m6A reader YTHDC2 promoted hepatocellular TG generation and hepatic steatosis in C57BL/6 mice through sterol regulatory element-binding protein 1c (SREBP-1c) signaling pathway, which upregulated the lipogenic genes FAS, SCD1, ACC, recombinant acetyl coenzyme a carboxylase alpha, and cell death-inducing DNA fragmentation factor-like effector C (CIDEC). Furthermore, FTO overexpression did not only enhance mitochondrial fusion to impair mitochondrial function and lipid oxidation but also promoted lipid peroxidation, accompanied by excessive TG in hepatocytes and rodent liver. Elevated m6A modification potently suppressed hepatic lipid accumulation, while the shrinkage of m6A modification arose hepatic lipid deposition. These findings have highlighted the beneficial role of m6A RNA methylation in hepatic lipid metabolism, potentially protecting liver from lipid metabolic disorders.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140687036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PANoptosis Features, a Humanized NSG Murine Model of Sjogren's Syndrome.","authors":"Yiying Yang, Huali Zhang, Xiaoyu Xiao, Muyao Guo","doi":"10.1089/dna.2023.0374","DOIUrl":"https://doi.org/10.1089/dna.2023.0374","url":null,"abstract":"Sjogren's syndrome (SS) is a complex systemic autoimmune disease. This study aims to elucidate a humanized NOD-PrkdcscidIl2rgem1/Smoc (NSG) murine model to better clarify the pathogenesis of SS. NSG female mice were adoptively transferred with 10 million peripheral blood mononuclear cells (PBMCs) through the tail vein from healthy controls (HCs), primary Sjogren's syndrome (pSS), and systemic lupus erythematosus (SLE) patients on D0. The mice were subcutaneously injected with C57/B6j submandibular gland (SG) protein or phosphate-buffered saline on D3, D17 and D31, respectively. NSG mice were successfully transplanted with human PBMCs. Compared with NSG-HC group, NSG-pSS and NSG-SLE mice exhibited a large number of lymphocytes infiltration in the SG, decreased salivary flow rate, lung involvement, decreased expression of genes related to salivary secretion, and the production of autoantibodies. Type I interferon-related genes were increased in the SG of NSG-pSS and NSG-SLE mice. The ratio of BAX/BCL2, BAX, cleaved caspase3, and TUNEL staining were increased in the SG of NSG-pSS and NSG-SLE mice. The expressions of p-MLKL and p-RIPK3 were increased in the SG of NSG-pSS and NSG-SLE mice. Increased expression of type I interferon-related genes, PANoptosis (apoptosis and necroptosis) were identified in the SG of this typical humanized NSG murine model of SS.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140689898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}