ACTG1
- Known as:
- ACTG1
- Catalog number:
- 001076A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACTG1
Related genes to: ACTG1
- Gene:
- ACTG1 NIH gene
- Name:
- actin gamma 1
- Previous symbol:
- ACTG, DFNA20, DFNA26
- Synonyms:
- -
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-27
- Date modifiied:
- 2016-02-26
Related products to: ACTG1
Related articles to: ACTG1
- Hearing loss is the most common sensory nervous system defect in humans. Approximately half of hearing loss cases have a genetic etiology. At present, more than 300 genes and 1000 mutations have been identified that cause hereditary hearing loss (HHL). However, there are still a large number of unknown genes related to hearing loss. - Source: PubMed
Zhu YajingWang TianyuSun XianglanLin BojianLiu HuanhaiChen LiCheng YinPeng Hu - A coordinated extracellular matrix (ECM) and cytoskeletal remodeling are critical drivers of hepatocellular carcinoma (HCC) progression, yet the upstream post-transcriptional mechanisms regulating these processes in spontaneous canine HCC remain poorly defined. Previously, we reported significantly downregulated miRNAs and enriched pathways from differentially expressed genes (DEGs) in canine HCC tissues. In the present study, we investigated putative post-transcriptional target interactions between the prioritized miRNAs and enriched ECM-cytoskeleton pathway-associated genes ( = 34). Integrative bioinformatic analysis prioritized and as the key putative targets of cfa-miR-10a based on their concordant prediction by four target-prediction algorithms, high transcript abundance, and inverse correlations with cfa-miR-10a-5p. RNAhybrid and miRanda analyses supported favorable predicted interactions between cfa-miR-10a and the 3'UTRs of both transcripts, with RNAhybrid minimum free energy values ≤ -20 kcal/mol and miRanda scores ≥ 140. In the matched canine transcriptomic subset, cfa-miR-10a and its predicted targets showed inverse expression trends. Cross-species analysis using TCGA-LIHC datasets further demonstrated concordant dysregulation of , and hsa-miR-10a-5p in human HCC, despite their weak or non-concordant correlation with hsa-miR-10a-5p. Collectively, these exploratory findings identify a candidate cfa-miR-10a-/ network associated with coordinated ECM and cytoskeletal transcriptomic alterations in canine HCC. While cross-species analysis supports the conservation of target gene dysregulation, the divergent miRNA-mRNA correlation patterns highlight potential species-specific post-transcriptional co-expression landscapes that warrant future functional validation. - Source: PubMed
Publication date: 2026/08/19
Arif MohammadShathi Most Shumi AkhterNozaki NobuhiroMiura Naoki - The pathological mechanisms underlying cardiac fibrosis after isoproterenol (ISO)-induced cardiac injury remain poorly understood. Additionally, the biological function of ACTG1 in cardiovascular diseases has not been fully elucidated. This study aims to explore the role of ACTG1 and its regulatory mechanism in ISO-triggered cardiac injury and fibrosis. We established ISO-induced cardiomyocyte injury models and TGF-β1-stimulated vascular endothelial cell-endothelial-to-mesenchymal transition (EndoMT) models in vitro, and then evaluated the effects of ACTG1 silencing on cardiomyocyte functions and EndoMT progression in vascular endothelial cells. Conditioned medium (CM) and a TGF-β1 neutralizing antibody were applied to explore the paracrine crosstalk between cardiomyocytes and vascular endothelial cells. In vivo, an ISO-induced mouse model of cardiac injury was constructed to verify the regulatory effects of ACTG1 silencing on myocardial injury, fibrosis, inflammation, and EndoMT. The in vitro results demonstrated that ISO treatment upregulated ACTG1 expression at both the mRNA and protein levels in cardiomyocytes. Moreover, ACTG1 silencing attenuated ISO-induced cardiomyocyte injury and partially suppressed TGF-β1-mediated EndoMT in vascular endothelial cells. Further mechanistic experiments revealed that ACTG1 silencing in ISO-induced cardiomyocytes hindered EndoMT progression in vascular endothelial cells. TGF-β1 neutralization assays further confirmed that TGF-β1 acted as a key paracrine mediator linking cardiomyocyte activation to endothelial EndoMT. In addition, the silencing of ACTG1 in vivo attenuated myocardial injury, reduced collagen deposition, improved cardiac function, and downregulated the expression of EndoMT-related proteins in ISO-treated mice. ACTG1 exacerbated ISO-induced cardiomyocyte injury and facilitated EndoMT to promote cardiac injury and fibrosis, supporting ACTG1 as a promising therapeutic target for the treatment of cardiac injury. - Source: PubMed
Publication date: 2026/08/20
Zeng XianghuiWang DianYang HaoLi CanqunXiong TingLu TingDai LuChen FengLiu ZhenfangLi Xing - The actin cytoskeleton of the cardiomyocyte is organized into two structurally and functionally distinct filament networks. The sarcomeric thin filaments, built primarily from cardiac α-actin (αCA), generate contractile force, whereas a separate subsarcolemmal cytoplasmic network, built from β-actin ( gene) and γ-actin ( gene), lies beneath the sarcolemma and is comparatively understudied in the mature heart. We hypothesized that this cytoplasmic actin network is required for sarcolemmal membrane integrity, signal transduction, and mechanosensing in the adult cardiomyocyte, and we generated cardiomyocyte-specific and double-gene deleted mice, using loxP (fl)-targeted and alleles combined with an αMHC (Myh6) promoter-driven Cre-recombinase transgene, to test this directly. Deletion of cytoplasmic β-actin and γ-actin from cardiomyocytes ( mice) drove compensatory upregulation of a γ-interferon like stress response with compensatory upregulation of skeletal α-actin (αSKA) and smooth muscle α-actin (αSMA) protein in adult cardiomyocytes, without altering baseline cardiac structure or function. To test if lost β-actin and γ-actin in the mouse heart impacts sarcolemmal stability, we crossed mice onto the dystrophin-deficient background, which is characterized by a fragile sarcolemma. Unexpectedly, hearts from ; mice showed greater membrane stability than hearts alone with intact / . We also observed that mice subjected to chronic pressure overload by transverse aortic constriction (TAC) were protected and developed less cardiac hypertrophy, had better preserved systolic function, and improved survival. Together, these data indicate induction of the cytoplasmic β-actin/γ-actin network in the heart during disease stimulation is maladaptive and weakens the sarcolemma, and 2 downstream mechanisms are considered that could mediate this effect. - Source: PubMed
Publication date: 2026/07/27
Kuwabara YasuhideKeezer CaitlinAbay EamanLin Suh-Chin JMolkentin Jeffery D - Chondrosarcomas are malignant cartilage-forming bone tumors with heterogeneous behavior, making prognostication and clinical management challenging. Histological grading is the primary tool for predicting clinical outcomes in conventional chondrosarcoma. However, its high interobserver variability limits reliable distinction between low- and high-risk patients, potentially leading to suboptimal clinical management. Given the increasing use of DNA methylation profiling as a valuable tool in surgical pathology for tumor classification, we investigated its prognostic value in central conventional chondrosarcoma. We generated methylation data from 69 primary central conventional chondrosarcomas profiled with Illumina's Human MethylationEPIC Array (850 k sites), and identified methylation sites individually linked to patient outcome. A LASSO Cox regression model was applied to these methylation sites to identify an optimal set of eight informative sites. With the regression coefficients of these methylation sites, we constructed a risk score that predicts central conventional Chondrosarcoma Risk Outcome from Methylation (CHROME). CHROME stratifies patients into High or Low risk groups for disease recurrence, onset of metastasis and disease-specific mortality. Survival analysis in an independent validation cohort (n = 68) demonstrated strong discriminatory performance of CHROME, with complete separation of outcomes and no adverse events observed in the Low risk group. Overview of the clinico-pathological information showed that a low grade (ACT/G1) case with an event was correctly assigned to the High risk group, while nine high grade cases without events were classified as Low risk. CHROME provides accurate risk stratification in central conventional chondrosarcoma and may represent a valuable tool for improving its prognostication and clinical management. - Source: PubMed
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