Ask about this productRelated genes to: TNRC6A Blocking Peptide
- Gene:
- TNRC6A NIH gene
- Name:
- trinucleotide repeat containing adaptor 6A
- Previous symbol:
- TNRC6
- Synonyms:
- CAGH26, KIAA1460, GW182
- Chromosome:
- 16p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-27
- Date modifiied:
- 2019-01-11
Related products to: TNRC6A Blocking Peptide
Related articles to: TNRC6A Blocking Peptide
- : Myocardial infarction (MI) remains a leading cause of death worldwide, primarily resulting from abrupt coronary occlusion that induces severe hypoxia and extensive cardiomyocyte loss. Hypoxia triggers mitochondrial dysfunction, oxidative stress, inflammation, and apoptosis, ultimately compromising cardiac function and promoting adverse cardiac remodeling. MicroRNAs (miRNAs) have emerged as critical regulators of cardiomyocyte survival and stress responses under ischemic conditions; however, the functional roles and molecular mechanisms of many hypoxia-responsive miRNAs remain insufficiently defined. : In this study, we focused on miR-30c-1-3p, which is markedly downregulated during the early phase of MI, and investigated its functional role in hypoxia-induced cardiomyocyte injury. We identified trinucleotide repeat-containing 6A (), a key component of the miRNA-induced silencing complex, as a potential downstream target. Using primary neonatal rat cardiomyocytes, we performed gain- and loss-of-function experiments, luciferase reporter assays, and knockdown analyses to evaluate apoptosis, inflammatory cytokine secretion, and release of myocardial injury-related proteins. : Restoration of miR-30c-1-3p significantly attenuated hypoxia-induced pro-apoptotic signaling, reduced inflammatory cytokine release, and decreased myocardial injury markers. These protective effects were associated with regulation of the miR-30c-1-3p/ axis. : Collectively, our findings identify a previously unappreciated functional role of the miR-30c-1-3p/ axis in hypoxia-induced cardiomyocyte injury and highlight its potential relevance in myocardial stress adaptation. - Source: PubMed
Publication date: 2026/06/17
Choi Jung-WonJeong SeongtaeJung Seung EunLim SoyeonSong Byeong-WookLee SeahyoungHan GyoonheeKim Sang Woo - Hypoxia-treated H9c2 cells were used to create an in vitro cells injury model. RT-qPCR analysis revealed DLEU1, miR-23a-3p, and TNRC6A expressions in serum of AMI patients and H9c2 cells. The viability and apoptosis of cardiomyocytes were assessed via the CCK-8 assay and flow cytometry. ELISA assays were employed to detect MDA, SOD, LDH, and CK-MB levels in cells. The direct targeting interactions among DLEU1, miR-23a-3p, and TNRC6A were verified through dual-luciferase reporter assay. Correlations between DLEU1, miR-23a-3p, and TNRC6A in serum samples from AMI patients were assessed by Pearson correlation analysis. In serum from AMI patients and hypoxia-treated H9c2 cells, the expression of DLEU1 and TNRC6A was upregulated, while the miR-23a-3p was downregulated. Functional experiments demonstrated that downregulating DLEU1 enhanced H9c2 cell viability, inhibited apoptosis, elevated SOD levels, and reduced MDA, LDH, and CK-MB levels under hypoxic conditions. Mechanistic studies confirmed that DLEU1 directly binds to miR-23a-3p, and inhibition of miR-23a-3p reversed the effects of downregulating DLEU1 on cardiomyocytes. Further studies identified that TNRC6A was a direct downstream target gene of miR-23a-3p. This study revealed that DLEU1 promotes myocardial cell apoptosis and exacerbates myocardial injury by adsorbing miR-23a-3p to upregulate TNRC6A during AMI. The results confirmed the role of the DLEU1/miR-23a-3p/TNRC6A axis in AMI pathogenesis, providing a novel potential therapeutic target for this disease. - Source: PubMed
Huang LushuangChai FeiChen NinaZhou Zheng - The microRNA (miRNA) induced silencing complex (miRISC) is the targeting apparatus and arguably the rate-limiting step of the miRNA-mediated regulatory subsystem - a major noise reducing, though metabolically costly, mechanism. Recently, we reported that miRISC channels miRNA-mediated regulatory activity back onto its own mRNAs to form negative self-feedback loops, a noise-reduction technique in engineering and synthetic/systems biology. In this paper, our mathematical modeling predicts that mRNA expression noise exhibits a negative correlation with the degradation rate (K) and is attenuated by self-feedback control of degradation. We also calculated K and expression noise of mRNAs detected in a total-RNA single-cell RNA-seq (scRNA-seq) dataset. As predicted, miRNA-targeted mRNAs exhibited higher K values accompanied by reduced cell-to-cell expression noise, confirming the operational trade-off between noise suppression and the increased metabolic/energetic costs associated with producing these mRNAs subjected to accelerated degradation and translational inhibition. Moreover, consistent with the K self-feedback control model, miRISC mRNAs (AGO1/2/3 and TNRC6A/B/C) exhibited further reduced expression noise. In summary, mathematical-modeling and total-RNA scRNA-seq data-analyses provide evidence that negative self-feedback regulation of mRNA degradation reinforces miRISC, the core machinery of the miRNA-mediated noise-reduction subsystem. To our knowledge, this is the first study to concurrently analyze mRNA degradation dynamics and expression noise, and to demonstrate noise reduction by direct self-feedback regulation of mRNA degradation. - Source: PubMed
Publication date: 2025/12/28
Tian ShuangmeiZhao ZiyuKassie Meharie GZhang FangyuanRen BeibeiWang Degeng - Familial adult myoclonic epilepsy (FAME), an autosomal dominant disorder, is characterized by cortical myoclonus and occasional generalized tonic-clonic seizures. To date, intronic pentanucleotide repeat expansions in at least seven genes, including SAMD12, TNRC6A, YEATS2, MARCHF6, STARD7, RAPGEF2, and RAI1, have been reported as causative. Detecting these repeat expansions using conventional sequencing techniques (Sanger or short-read next-generation sequencing) is not feasible as they cannot reliably span or characterize long repetitive elements. Although genetic testing has been performed in some research laboratories, comprehensive long read-based panel is unavailable for clinical application. To address this gap, we developed a targeted long-read sequencing panel and applied it in a clinical diagnostic context for the first time. - Source: PubMed
Publication date: 2025/11/11
Urabe HarukaNakajima TakashiMitsuhashi SatomiOhta KentaroFujinaka HidehikoGoto KiyoeSato Aki - Cardiomyocyte apoptosis is the underlying pathogenic factor of myocardial ischemia-reperfusion injury (MIRI). Long non-coding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) plays a crucial role in cell apoptosis regulation. In this study, we investigated the mechanism of lncRNA NORAD in promoting MIRI via the miR-144-3p/trinucleotide repeat-containing gene 6a (TNRC6A) axis.H9C2 cells were induced by oxygen-glucose deprivation/reperfusion (OGD/R) in vitro, and then treated with oe-NORAD, si-NORAD, miR-144-3p inhibitor, and oe-TNRC6A. Meanwhile, an MIRI rat model was established and treated with sh-NORAD. The expression of NORAD, miR-144-3p, TNRC6A, apoptosis proteins, and inflammatory factors (tumor necrosis factor-α [TNF-α] and interleukin [IL]-6) was determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot, and enzyme-linked immunosorbent assay. Cell viability and apoptosis were assessed using Cell Counting Kit-8 and flow cytometry. Echocardiography, 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining were used to evaluate cardiac function, pathological changes in myocardial tissues, and myocardial apoptosis. Additionally, the potential binding sites of miR-144-3p with NORAD and TNRC6A were predicted using the StarBase database and then validated by the dual-luciferase reporter gene assay.NORAD expression, cell apoptosis, and TNF-α and IL-6 levels were augmented, whereas miR-144-3p expression and cell viability were diminished in OGD/R-exposed cells. NORAD knockdown impeded OGD/R-induced cardiomyocyte apoptosis and inflammatory responses. Repression of miR-144-3p or TNRC6A overexpression partially offset the inhibitory effect of NORAD knockdown on OGD/R-induced cardiomyocyte apoptosis. In vivo tests confirmed that NORAD knockdown reduced MIRI in rats.Highly expressed NORAD promoted cardiomyocyte apoptosis and inflammatory responses. However, NORAD knockdown suppressed cardiomyocyte apoptosis to reduce MIRI through the miR-144-3p/TNRC6A axis. - Source: PubMed
Wei WeiXie PingWang Xuemei