Human Gene最新文献

{"title":"Potential Anticancer Effect of Thymoquinone on Glioblastoma Cancer Cells through Alteration in CTSB and CTSD Gene Expression Level","authors":"Omid Hosseini ,&nbsp;Fatemeh Ataellahi ,&nbsp;Raheleh Masoudi","doi":"10.1016/j.humgen.2024.201374","DOIUrl":"10.1016/j.humgen.2024.201374","url":null,"abstract":"<div><h3>Background</h3><div>Glioblastoma is one of the most aggressive and rapidly growing brain tumors. Current therapeutic approaches have proven largely ineffective in treating this malignancy, resulting in a very low survival rate. Accordingly, finding new therapeutic strategies seems inevitable. Recently, some molecular mechanisms that help cancer cells survive, and grow have been elucidated, and targeting critical molecules involved in these processes brings new hopes to cancer treatment. CTSB and CTSD are two important proteins associated with invasion, angiogenesis, and metastasis, which are overexpressed in glioblastoma. A considerable body of evidence demonstrated that Thymoquinone, the main bioactive component of black seeds, has anticancer power against a range of various cancers. The current experiment was designed to determine whether TQ can modulate the mRNA expression level of <em>CTSB</em> and <em>CTSD</em> in glioblastoma cells.</div></div><div><h3>Methods</h3><div>An in vitro study was conducted and relative mRNA level of <em>CTSB</em> and <em>CTSD</em> were assessed using quantitative real-time RT-RCR in U87MG cells treated with 30 or 60 μM concentrations of TQ at two time points; 12 and 24 h post-exposure to capture dynamic changes in gene expression at early and mid-phase intervals.</div></div><div><h3>Results</h3><div>Although there was no reduction in the relative expression of <em>CTSB</em> and <em>CTSD</em> in cells exposed to TQ for 12 h, the mRNA level of both genes significantly decreased at 60 μM of TQ after 24 h exposure.</div></div><div><h3>Conclusion</h3><div>The data presented revealed that at certain concentration and time point, TQ effectively targets two key genes involved in metastasis. Thus, it can be concluded that TQ holds potential as a promising candidate for glioblastoma treatment.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201374"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143810","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":"Comment on doi.org/10.1016/j.humgen.2024.201316 publication entitled “Germline mutations of the putative tumor suppressor gene PTEN/MMAC1 as molecular biomarker in prostate cancer”","authors":"Thomas Pepper ,&nbsp;Madhuri Hegde","doi":"10.1016/j.humgen.2024.201369","DOIUrl":"10.1016/j.humgen.2024.201369","url":null,"abstract":"","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201369"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143144020","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":"Anti-oxidant and anti-inflammatory action of calorie restriction and quercetin in two age groups of rats: Involvement of thioredoxin and heme oxygenase-1","authors":"Nima Mahdei Nasirmahalleh ,&nbsp;Mina Hemmati ,&nbsp;Fereshteh Ghorbani","doi":"10.1016/j.humgen.2024.201363","DOIUrl":"10.1016/j.humgen.2024.201363","url":null,"abstract":"<div><h3>Background</h3><div>Aging associated with an increase in free radicals, inflammatory factors and oxidative stress. This study aimed to investigate potential of calorie restriction (CR) and quercetin (QUER) in alleviating oxidative stress and inflammation in aging.</div></div><div><h3>Methods</h3><div>Two age groups of male Wistar rats (8 and 20 weeks) were included in the study and subdivided to normal diet (ND), ND with QUER (15 mg Kg⁻¹, IP), ND with CR, and ND with QUER and CR groups.</div></div><div><h3>Results</h3><div>We showed higher expression of Tumor Necrosis Factor alpha (TNF-α) in 20-week-old rats compared with 8-week-old rats, and the administration of QUER and CR for 4 weeks restored this value to the normal range. The expression of heme oxygenase-1 (HO-1) and thioredoxin (TXN) are also affected by CR and QUER. CR alone and in combination with QUER significantly raised the expression of the TXN and HO-1 genes. Also, CR alone and in combination with QUER significantly reduced thioredoxin-interacting protein (TXNIP) gene expression.</div></div><div><h3>Conclusions</h3><div>QUER and CR jointly improved the adverse impacts of aging through the regulation of antioxidant signaling pathways, indicating the potential of this blend as a supplementary therapeutic approach for aging and age-related ailments.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201363"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143785","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":"LDLR variants and structure-function predictions of protein models related to familial hypercholesterolemia in Vietnam","authors":"Ngoc-Thanh Kim ,&nbsp;Doan-Loi Do ,&nbsp;Mai-Ngoc Thi Nguyen ,&nbsp;Hong-An Le ,&nbsp;Thanh-Tung Le ,&nbsp;Thanh-Huong Truong","doi":"10.1016/j.humgen.2025.201381","DOIUrl":"10.1016/j.humgen.2025.201381","url":null,"abstract":"<div><div>Here, we explore familial hypercholesterolemia (FH) in the Vietnamese population which is an understudied FH ethnicity, addressing genetic and clinical variability to improve personalized healthcare. Utilizing next-generation sequencing (NGS), Multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing, 103 FH cases from the Vietnam Familial Hypercholesterolemia (VINAFH) Program were analyzed, identifying 21 low-density lipoprotein receptor (LDLR) variants in 39.8 % of the patients, including 3 novel variants. Advanced computational modeling was used to obtain insights into the biological impact of these mutations. Most variants (81 %) were located in ligand-binding and Epidermal growth factor (EGF) homology domains, critical for LDLR-LDL binding and subsequent clearance. Disruptive mutations in these domains (<em>e.g.</em>, Gln660Ter, Cys104Tyr, Cys318Arg), impaired LDLR function by destabilizing protein structure, reducing solvent-accessible surface area, and increasing root-mean-square deviation (RMSD) values, which weakened receptor-ligand interactions, leading to elevated plasma LDL-C levels. Notably, Asp227Glu enhanced stability without functional impairment, indicating mutation-specific effects. Mutations in transmembrane and cytoplasmic domains, such as Val797Met and Gly844Ser, disrupted intracellular signaling and receptor recycling, further compromising LDL clearance. Molecular dynamics simulations revealed dynamic instabilities in mutants carrying Ser586Pro and His583Tyr, linking structural flexibility and misfolding to impaired LDLR-LDL binding and trafficking (critical processes in cholesterol homeostasis). We established genotype-phenotype relationships, with homozygous FH (HoFH) and compound heterozygous FH (cHeFH) patients exhibiting more severe symptoms, including significantly higher LDL-C levels and premature atherosclerotic cardiovascular disease (ASCVD), compared to heterozygous FH (HeFH) patients. HoFH patients showed average LDL-Cholesterol (LDL-C) levels (14.83 mmol/L), consistent with severe receptor dysfunction. Variability in plasma LDL-C levels among mutation carriers and non-carriers highlights population-specific clinical diversity and suggests influence of genetic and non-genetic factors.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201381"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143144836","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":"Elucidation of potential miRNAs as prognostic biomarkers for coronary artery disease","authors":"Summan Thahiem ,&nbsp;Malik Faisal Iftekhar ,&nbsp;Muhammad Faheem ,&nbsp;Ayesha Ishtiaq ,&nbsp;Muhammad Ishtiaq Jan ,&nbsp;Riaz Anwar Khan ,&nbsp;Iram Murtaza","doi":"10.1016/j.humgen.2025.201385","DOIUrl":"10.1016/j.humgen.2025.201385","url":null,"abstract":"<div><div>Coronary Artery Disease (CAD) is a cardiovascular disorder characterized by narrowing of arteries due to metabolic dysregulations, which severely impedes blood flow through cardiac tissues. Genetic factors significantly contribute to the susceptibility of CAD and miRNAs play a crucial role in gene expression and regulation. In this study, we aim to identify highly specific miRNA-mRNA interactions and gene targets by employing machine learning approaches such as association rules mining (ARM) and singular value decomposition (SVD), followed by differential expression analysis of microarray datasets. For this, genes associated to CAD and its lethal sequelae (valvular heart disease, fibrosis, atherosclerosis, hyperlipidemia, oxidative stress and inflammation) were obtained from databases i-e., <em>National Center for Biotechnology Information</em>, Genetic Testing Registry (GTR). Highly conserved miRNAs were selected using bioinformatics repositories TargetScan, miRBase, and miRanda. Furthermore, ARM and SVD were utilized to discover significant association patterns and frequently occurring miRNAs. For the validation of hub miRNAs, differential expression analysis was carried out on two independent cohorts of miRNA expression datasets of cardiac patients. This integrated approach identified 3 hub miRNAs (miR-200a-3p, miR-32-5p and miR-92-3p). Functional enrichment analysis revealed their involvement in diabetes, cholesterol metabolism, inflammation, and atherosclerosis. Moreover, disease enrichment analysis showed their association with heart diseases, vascular diseases, and endothelial dysfunction. Conclusively, this is the first study that employed ARM and SVD approaches to identify hub miRNAs and novel gene targets involved in CAD. The identification of these miRNAs as putative biomarkers may lead to a more accurate prognostic score for early detection of CAD.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201385"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143264831","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":"Inflammatory memory in interleukin-1β promoter methylation of bone marrow-derived stromal cells from healthy humans","authors":"D.V. Karpenko","doi":"10.1016/j.humgen.2024.201367","DOIUrl":"10.1016/j.humgen.2024.201367","url":null,"abstract":"<div><div>The role of bone marrow mesenchymal cells is demonstrated both in normal conditions and in various pathologies of the hematopoietic system. The regulatory functions of mesenchymal cells are so significant that they themselves and their secretome or extracellular vesicles are used for the treatment and prevention of immune complications during transplantation and in other aspects of regenerative medicine. As shown earlier, interleukin-1β is an important factor regulating the activity of the bone marrow stroma. Methylation profile of <em>IL1B</em> promoter and <em>IL1B</em> expression were measured in cultured mesenchymal cells obtained from the bone marrow of healthy humans in the presenting study. <em>IL1B</em> expression was also measured upon different inflammatory stimuli including tumor necrosis factor-α (TNF). In cultured bone marrow-derived stromal cells from healthy donors, variations were observed in <em>IL1B</em> promoter methylation profile at the position of one CpG at −299 bp from transcription start site, which is a part of or in immediate proximity to binding sites of NF-kB transcription factors. The study establishes a link among TNF exposure, the CpG methylation, and <em>IL1B</em> expression during and after exposure. Since TNF is a pro-inflammatory factor that is associated with damage and aging, it is concluded that for healthy donor, the observed differences in <em>IL1B</em> promoter methylation profile may be a long-term imprint of inflammatory processes previously sustained by a person, as well as a marker of physiological differences in the human bone marrow stroma.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201367"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143786","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":"Identification of key protein-coding genes, lncRNAs and their regulatory network associated with the progression of lung adenocarcinoma in humans","authors":"Aparna Chaturvedi ,&nbsp;Arindam Ghosh ,&nbsp;Anup Som","doi":"10.1016/j.humgen.2024.201368","DOIUrl":"10.1016/j.humgen.2024.201368","url":null,"abstract":"<div><div>Lung adenocarcinoma (LUAD) is an aggressive subtype of non-small cell lung cancer (NSCLC) known for its high propensity for early metastasis and rapid progression, often leading to late-stage diagnosis and poor prognosis. This cancer type frequently spreads to distant organs, including the brain, liver, and bones, contributing to its high mortality rate among lung cancer subtypes. Therefore, effective strategies need to be developed for early detection and prognosis of LUAD. Transcriptomic advancements have helped in better prognosis by analyzing the complex interplay among protein-coding and non-coding genes across various cancers. However, the regulatory mechanisms and the interactions between the coding and non-coding elements involved in LUAD progression is poorly understood. In this quest, we used weighted gene co-expression network analysis (WGCNA) approach on RNA-Seq data and identified a set of protein-coding genes (PCGs) and lncRNAs that are crucial for the development of LUAD. Further, we derived the networks of PCGs with lncRNAs at the mRNA (i.e., transcriptional) and protein (i.e., post-transcriptional) levels. Our analysis revealed 405 PCGs as the candidate biomarkers among which ADAMTS8, PECAM1, RGCC, and TCF21 were detected as key PCGs. Gene ontology and pathway analysis suggested angiogenesis as the crucial pathway regulated by the candidate biomarkers. BANCR was the only lncRNA among those analyzed that showed both differential expression in tumor tissues and a significant association with better survival, making it a promising candidate for further investigation as a prognostic biomarker in LUAD. Further, we identified MALAT1-TCF21-NORAD-SELP-BANCR-KLF2, as the key regulatory mechanism through which BANCR might be regulating the LUAD progression.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201368"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143787","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":"Potential modifier genes for cystic fibrosis disease","authors":"Hajra Aqeel ,&nbsp;Muhammad Usman Ghani ,&nbsp;Zartashay Naeem ,&nbsp;Farheena Iqbal Awan ,&nbsp;Muhammad Umer Khan ,&nbsp;Shazia Tanveer ,&nbsp;Nauman Chaudary ,&nbsp;Rehan Sadiq Shaikh","doi":"10.1016/j.humgen.2025.201377","DOIUrl":"10.1016/j.humgen.2025.201377","url":null,"abstract":"<div><h3>Background</h3><div>Cystic Fibrosis (CF) is a genetic disease caused primarily by mutations in the <em>CFTR</em> gene. However, CF patients with the same mutations in the CFTR gene can manifest the disease with varying severity, likely due to the role of modifier genes.</div></div><div><h3>Methodology</h3><div>To uncover the underlying non-<em>CFTR</em> genetic factors, we compiled a list of CF modifier genes through an extensive literature review and conducted pathway enrichment analysis using ENRICHR and DAVID tools to understand their biological significance and functional roles in CF disease. We also used the STRING tool to explore the protein-protein interaction of genes identified by pathway enrichment analysis with the CFTR gene.</div></div><div><h3>Results</h3><div>The literature review identified 36 CF modifier genes: <em>GSTM1, IL10, SLC26A9, IL1B, MUC6, CLC-2, CXCL8/IL8, EDNRA, DCTN4, SLC9A3, ADRB2, AGER, EZR, HLAII, HFE, CFTR, IFRD1, CAV1, PRKAR2B, PPP2R4, MBL2, EHF, SCNN1A, SERPINA1, AHSAI, SNAP23, SCNN1B, SCNN1G, PRSS8, SLC9A3R1/NHERF1, KRT19, Nedd4L, TGFB1, CALR, SLC6A14, MMP9 and MIF.</em> Pathway enrichment analysis predicted three key pathways linked to CF and enriched with 13 modifier genes. Furthermore, the STRING tool predicted that six out of the thirteen modifier genes (SLC9A3R1, EZR, ADRB2, SERPINA1, IL1B, and IFRD1<em>)</em> interact with <em>CFTR</em>, indicating a complex network of functional relationships supported by various evidence.</div></div><div><h3>Conclusion</h3><div>This research identified 36 modifier genes associated with cystic fibrosis, alongwith three key pathways enriched with 13 of these genes. Six of these genes were found to have a complex network of interactions with CFTR genes, highlighting their probable role as CF modifier genes.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201377"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143789","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":"Downregulation of miR-1269a pronounces breast cancer bone metastasis","authors":"Smit Patel ,&nbsp;Ishita Agarwal ,&nbsp;Nishita Adnani ,&nbsp;Deepshikha Rathore ,&nbsp;Nandani Dharwal ,&nbsp;Nirali Shukla ,&nbsp;Heena V. Dave","doi":"10.1016/j.humgen.2025.201380","DOIUrl":"10.1016/j.humgen.2025.201380","url":null,"abstract":"<div><div>Breast cancer (BC) is the most prevalent cancer among women globally. Metastasis poses a significant challenge for BC patients and its complete mechanism is yet to be discovered. Bone is one of the most common sites for metastasis in BC patients, making early diagnosis of bone metastasis necessary. To identify potential biomarkers for early diagnosis, we analyzed transcriptomic data from The Cancer Genome Atlas (TCGA) database, focusing on differentially expressed microRNAs. Among the screened miRNAs, miR-1269a was significantly downregulated based on log2 FC ±2 and adjusted <em>p</em>-value ≤0.05. Receiver operating curve (ROC) analysis revealed that miR-1269a could effectively distinguish between bone-metastatic and primary breast cancer patients. Additionally, we found a significant downregulation of miR-1269a in metastatic breast cancer cells (MDA-MB-231) compared to non-metastatic breast cancer cells (MCF-7). TargetScan and miRDB were used to identify targets of miR-1269a, leading to a focus on cyclin D1 (CCND1), a cell cycle regulator gene, significantly overexpressed in primary breast cancer patients. Overall, this study uncovers the unique role of hsa-miR-1269a as a biomarker associated with the biological and transcriptional processes in bone metastasis in breast cancer. The study also identifies a novel miRNA-mRNA axis, miR-1269a-CCND1, which possesses a potential biomarker role in BC patients with Bone metastasis.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201380"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143144019","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":"A higher proportion of craniosynostosis genes are cancer driver genes","authors":"Suchir Misra ,&nbsp;Andrew Shih ,&nbsp;Xiao-Jie Yan ,&nbsp;Wentian Li","doi":"10.1016/j.humgen.2025.201378","DOIUrl":"10.1016/j.humgen.2025.201378","url":null,"abstract":"<div><div>Craniosynostosis (CS) is a congenital abnormality deformity with a heterogeneous genetic contribution. There were previously two attempts to collect genes that are genetically associated with craniosynostosis and some related syndromes with 57 (<span><span>Twigg and Wilkie, 2015</span></span>), 39 (<span><span>Goos and Mathijssen, 2019</span></span>) genes identified, respectively. We expanded this list of craniosynostosis genes by adding another 17 genes with an updated literature search, plus 7 more from a recent update (<span><span>Tooze et al., 2023</span></span>), leading to a combined of 120 genes. These genes are shown to be more likely to be intolerant to functional mutations. Of these 120 craniosynostosis genes, 32 (26.7 % vs. 3.5 % baseline frequency) are cancer driver genes, a 7.6-fold enrichment. The cancer-craniosynostosis connection is further validated by an over-representation analysis of craniosynostosis genes in KEGG cancer pathway and several cancer related gene-sets. Many cancer-craniosynostosis overlapping genes participate in intracellular signaling pathways, which play a role in both development and cancer. This connection can be viewed from the “oncogenesis recapitulates ontogenesis” framework. Twenty-five craniosynostosis genes are transcription factor genes (20.8 % vs. 10.3 % baseline), and craniosynostosis genes are also enriched in targets of certain transcription factors or micro RNAs.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"43 ","pages":"Article 201378"},"PeriodicalIF":0.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143144835","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}