Search results for: GATA4
#39366304 
2024/10/03
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Perfluorooctanoic acid (PFOA) induces cardiotoxicity by activating the Keap1/Nrf2 pathway in zebrafish (Danio rerio) embryos.
Perfluorooctanoic acid (PFOA), a perfluoroalkyl compound, is linked to congenital heart diseases, though its underlying mechanisms remain unclear. We hypothesized that PFOA induces cardiac defects through the inhibition of the Keap1/Nrf2 pathway, leading to oxidative damage in cardiomyocytes. In this study, zebrafish embryos exposed to PFOA showed significant cardiac malformations and dysfunction, characterized by excessive reactive oxygen species (ROS), malondialdehyde (MDA) production, decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. Additionally, we observed dysregulation in the expression of key cardiac development genes (vmhc, gata4, nkx2.5, and sox9b). PFOA also reduced the expression of keap1, nrf2, and ho-1. After overexpression of Nrf2, levels of ROS and MDA decreased, while levels of SOD, CAT, and GSH-Px increased. Additionally, cardiomyocyte apoptosis and cardiac malformations were alleviated. These findings have suggested that PFOA induces oxidative stress through Keap1/Nrf2 pathway inhibition, ultimately leading to cardiac defects.Xing Liu, Ruobing Chen, Yuting Peng, Yueyue Zhou, Mingzhu Xia, Xinyi Wu, Yuchi Wang, Wenjiao Yin, Yuyang Han, Meng Yu
2811 related Products with: Perfluorooctanoic acid (PFOA) induces cardiotoxicity by activating the Keap1/Nrf2 pathway in zebrafish (Danio rerio) embryos.
10 mg2 Pieces/Box100ug Lyophilized 100 G14 inhibitors2 Pieces/Box100 μg2 Pieces/Box 1 G2 Pieces/Box100ug
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#39352623 2024/10/01
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A genome-wide CRISPR/Cas9 knockout screen identifies SEMA3F gene for resistance to cyclin-dependent kinase 4 and 6 inhibitors in breast cancer.
Palbociclib is a cell-cycle targeted small molecule agent used as one of the standards of care in combination with endocrine therapy for patients with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer. Although several gene alterations such as loss of Rb gene and amplification of p16 gene are known to be conventional resistance mechanisms to cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors, the comprehensive landscape of resistance is not yet fully elucidated. The purpose of this study is to identify the novel resistant genes to the CDK4/6 inhibitors in HR-positive HER2-negative breast cancer.Yuko Kawai, Aiko Nagayama, Kazuhiro Miyao, Makoto Takeuchi, Takamichi Yokoe, Tomoe Kameyama, Xinyue Wang, Tomoko Seki, Maiko Takahashi, Tetsu Hayashida, Yuko Kitagawa
2205 related Products with: A genome-wide CRISPR/Cas9 knockout screen identifies SEMA3F gene for resistance to cyclin-dependent kinase 4 and 6 inhibitors in breast cancer.
400Tests
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#39349833 2024/10/01
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FGF4 and ascorbic acid enhance the maturation of induced cardiomyocytes by activating JAK2-STAT3 signaling.
Direct cardiac reprogramming represents a novel therapeutic strategy to convert non-cardiac cells such as fibroblasts into cardiomyocytes (CMs). This process involves essential transcription factors, such as Mef2c, Gata4, Tbx5 (MGT), MESP1, and MYOCD (MGTMM). However, the small molecules responsible for inducing immature induced CMs (iCMs) and the signaling mechanisms driving their maturation remain elusive. Our study explored the effects of various small molecules on iCM induction and discovered that the combination of FGF4 and ascorbic acid (FA) enhances CM markers, exhibits organized sarcomere and T-tubule structures, and improves cardiac function. Transcriptome analysis emphasized the importance of ECM-integrin-focal adhesions and the upregulation of the JAK2-STAT3 and TGFB signaling pathways in FA-treated iCMs. Notably, JAK2-STAT3 knockdown affected TGFB signaling and the ECM and downregulated mature CM markers in FA-treated iCMs. Our findings underscore the critical role of the JAK2-STAT3 signaling pathway in activating TGFB signaling and ECM synthesis in directly reprogrammed CMs. Schematic showing FA enhances direct cardiac reprogramming and JAK-STAT3 signaling pathways underlying cardiomyocyte maturation.Seongmin Jun, Myeong-Hwa Song, Seung-Cheol Choi, Ji-Min Noh, Kyung Seob Kim, Jae Hyoung Park, Da Eun Yoon, Kyoungmi Kim, Minseok Kim, Sun Wook Hwang, Do-Sun Lim
1476 related Products with: FGF4 and ascorbic acid enhance the maturation of induced cardiomyocytes by activating JAK2-STAT3 signaling.
100tests2.5 mg10 mg1001 g 100 G500 µl 100 assays 1KG100 μl100 assays
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#39341264 2024/09/26
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Mechanistic Insights into Suanzaoren Decoction's Improvement of Cardiac Contractile Function in Anxiety-Induced Cardiac Insufficiency.
According to traditional Chinese medicine, Anxiety-induced cardiac blood insufficiency leads to palpitations and restlessness. Suanzaoren Decoction (SD) is effective in replenishing blood and promoting blood circulation. Clinical practice has shown that it has a better therapeutic effect on cardiac insufficiency. However, its mechanism of action is still unclear.Yinjie Zhang, Yue Jin, Ni Zhao, Ting Wang, Xuanlin Wang, Zhenyu Li, Yan Yan
1591 related Products with: Mechanistic Insights into Suanzaoren Decoction's Improvement of Cardiac Contractile Function in Anxiety-Induced Cardiac Insufficiency.
100ug Lyophilized 1 kit(s) 100ul100ug Lyophilized100ul96 tests100ug Lyophilized200 100ug Lyophilized100ul100ug Lyophilized100 ul
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#39330331 2024/09/04
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Direct Cardiac Reprogramming in the Age of Computational Biology.
Heart disease continues to be one of the most fatal conditions worldwide. This is in part due to the maladaptive remodeling process by which ischemic cardiac tissue is replaced with a fibrotic scar. Direct cardiac reprogramming presents a unique solution for restoring injured cardiac tissue through the direct conversion of fibroblasts into induced cardiomyocytes, bypassing the transition through a pluripotent state. Since its inception in 2010, direct cardiac reprogramming using the transcription factors Gata4, Mef2c, and Tbx5 has revolutionized the field of cardiac regenerative medicine. Just over a decade later, the field has rapidly evolved through the expansion of identified molecular and genetic factors that can be used to optimize reprogramming efficiency. The integration of computational tools into the study of direct cardiac reprogramming has been critical to this progress. Advancements in transcriptomics, epigenetics, proteomics, genome editing, and machine learning have not only enhanced our understanding of the underlying mechanisms driving this cell fate transition, but have also driven innovations that push direct cardiac reprogramming closer to clinical application. This review article explores how these computational advancements have impacted and continue to shape the field of direct cardiac reprogramming.Rachelle Ambroise, Paige Takasugi, Jiandong Liu, Li Qian
2734 related Products with: Direct Cardiac Reprogramming in the Age of Computational Biology.
50 UG148 samples5 mg
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#39287768 2024/09/17
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Sodium Fluoride Exposure Induces Developmental Toxicity and Cardiotoxicity in Zebrafish Embryos.
Fluorosis is a worldwide public health problem, in which the heart is an important target organ. However, studies on its toxicological mechanism in embryonic development are limited. This study assessed the toxicity of sodium fluoride (NaF) toward zebrafish embryos. We determined the mortality, hatching rate, phenotypic malformation, heart function, and morphology of zebrafish embryos after exposure to NaF. Subsequently, the molecular mechanism was revealed using high-throughput RNA sequencing analysis. The expression levels of key genes for heart development were detected using quantitative real-time reverse transcription PCR. The 50% lethal concentration (LC50) value of NaF toward zebrafish embryos at 96 h post-fertilization was 335.75 mg/L. When the concentration of NaF was higher than 200 mg/L, severe deformities, such as pericardial edema, yolk sac edema, spine curvature, shortened body length, reduced head area, and eye area, were observed. The heart rate of the embryos exposed to NaF decreased in a dose-dependent fashion. The distance between the sinus venosus and bulbus arteriosus was significantly increased in the NaF-exposed group compared with that in the control group. The stroke volume and cardiac output decreased significantly in the NaF groups. Compared with the control group, the expression levels of Gata4, Tbx5a, Hand2, Tnnt2c, Nppa, and Myh6 were significantly increased in the NaF-treated group. Through transcriptome sequencing, 1354 differentially expressed genes (DEGs) were detected in the NaF (200 mg/L) treated groups, including 1253 upregulated genes and 101 downregulated genes. Gene ontology functional analysis and Kyoto Encyclopedia of Genes and Genomes pathway analyses of the DEGs showed that cardiac-related pathways, such as actin cytoskeleton regulation, Jak-Stat, PI3k-Akt, and Ras, were activated in the NaF-exposed group. This study revealed the underlying mechanism of fluoride-induced cardiac morphological and functional abnormalities and provides clues for the clinical prevention and treatment of fluorosis.Feiqing Wang, Fa Chen, Wen Song, Yanju Li, Haiyan Wu, Tingting Tian, Mengxian Tian, Dongxin Tang, Yang Liu
1538 related Products with: Sodium Fluoride Exposure Induces Developmental Toxicity and Cardiotoxicity in Zebrafish Embryos.
100 μg1 g1 g100 μg100 μg2.5 mg100 μg100 μg100 μg100 μg 1KGSize: 1 mL 100 mM x 2
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#39286212 2024/08/29
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Discovery of a novel mutation F184S (c.551T>C) in GATA4 gene causing congenital heart disease in a consanguineous Saudi family.
Congenital heart disease (CHD) is the most common cause of non-infectious deaths in infants worldwide. However, the molecular mechanisms underlying CHD remain unclear. Approximately 30 % of the causes are believed to be genetic mutations and chromosomal abnormalities. In this study, we aimed to identify the genetic causes of CHD in consanguineous families.Mahmood Rasool, Peter Natesan Pushparaj, Absarul Haque, Ayat Mohammed Shorbaji, Loubna Siraj Mira, Sherin Bakhashab, Mohamed Nabil Alama, Muhammad Farooq, Sajjad Karim, Lars Allan Larsen
2948 related Products with: Discovery of a novel mutation F184S (c.551T>C) in GATA4 gene causing congenital heart disease in a consanguineous Saudi family.
500 tests500 tests1-99 mg/ml/ea price x 296 tests300 units
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#39285472 2024/09/16
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Application and insights of targeted next-generation sequencing in a large cohort of 46,XY disorders of sex development in Chinese.
46,XY disorders of sex development (46,XY DSD) are characterized by incomplete masculinization of genitalia with reduced androgenization. Accurate clinical management remains challenging, especially based solely on physical examination. Targeted next-generation sequencing (NGS) with known pathogenic genes provides a powerful tool for diagnosis efficiency. This study aims to identify the prevalent genetic variants by targeted NGS technology and investigate the diagnostic rate in a large cohort of 46,XY DSD patients, with most of them presenting atypical phenotypes.Hongyu Chen, Guangjie Chen, Fengxia Li, Yong Huang, Linfeng Zhu, Yijun Zhao, Ziyi Jiang, Xiang Yan, Lan Yu
1691 related Products with: Application and insights of targeted next-generation sequencing in a large cohort of 46,XY disorders of sex development in Chinese.
0.1ml (1mg/ml)50ul300 units1mg0.1ml100ug Lyophilized100ug Lyophilized0.1ml (1mg/ml) 100ul1mg0.1ml
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#39269625 2024/09/13
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Nomilin Reversed Cardiotoxicity Caused by Co-exposure to Zearalenone and Deoxynivalenol via the Keap1/Nrf2 Signaling Pathway in Zebrafish.
The contamination of food and feed by mycotoxins, particularly zearalenone (ZEA) and deoxynivalenol (DON), is a global issue. Prenatal exposure to ZEA and DON can result in congenital cardiac malformations in fetuses. Addressing the prevention and mitigation of embryonic cardiotoxicity caused by these toxins is crucial. Citrus limonoid nomilin (NOM) is an extract known for its pathological properties in various diseases. This study investigated the potential mechanism of NOM in mitigating cardiotoxicity caused by ZEA and DON co-exposure in a zebrafish model. The findings indicated that NOM pretreatment alleviated cardiac developmental toxicity induced by ZEA and DON and normalized the expression of key genes involved in heart development, including gata4, vmhc, nkx2.5, and sox9b. Co-exposure to NOM, ZEA, and DON enhanced SOD and catalase activity, increased glutathione levels, and reduced ROS and malondialdehyde production. Furthermore, NOM reduced cardiac oxidative damage by activating the Keap1/Nrf2 signaling pathway. In summary, this study offers new insights for preventive interventions against congenital heart disease caused by mycotoxin exposure.Xing Liu, Yuting Peng, Ruobing Chen, Yueyue Zhou, Mingzhu Xia, Xinyi Wu, Meng Yu
1219 related Products with: Nomilin Reversed Cardiotoxicity Caused by Co-exposure to Zearalenone and Deoxynivalenol via the Keap1/Nrf2 Signaling Pathway in Zebrafish.
2 Pieces/Box7 inhibitors2 Pieces/Box2 Pieces/Box11 inhibitors2 Pieces/Box2 Pieces/BoxInhibitors2 Pieces/Box
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#39242200 //
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DNA hypermethylation of tumor suppressor genes TWIST1, GATA4, MUS81 and NTRK1 in endometrial hyperplasia.
To investigate DNA methylation of specific tumor suppressor genes in endometrial hyperplasia compared to normal endometrial tissue. File and methodology: To search for epigenetic events, methylation-specific multiplex ligation-dependent probe amplification was employed to compare the methylation status of 40 tissue samples with atypical endometrial hyperplasia, 40 tissue samples with endometrial hyperplasia without atypia, and 40 control tissue samples with a normal endometrium.Ondřej Dvořák, Marcela Slavíčková, Jan Laco, Martin Štěpán, Eva Čermáková, Jiří Špaček