MEF2C (dn _ R24L)
- Known as:
- MEF2C (dn _ R24L)
- Catalog number:
- 000600A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MEF2C ( _ R24L)
Related genes to: MEF2C (dn _ R24L)
- Gene:
- MEF2C NIH gene
- Name:
- myocyte enhancer factor 2C
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-02-08
- Date modifiied:
- 2015-08-25
Related products to: MEF2C (dn _ R24L)
Anti-Human MEF2C, Rabbit Polyclonalanti-MEF2Canti-MEF2Canti-MEF2Canti-MEF2Canti-MEF2C (Ser396)anti-MEF2C (Ser59)Anti-MEF2C Antibodyanti-MEF2C type: Primary antibodies host: Mouseanti-MEF2C type: Primary antibodies host: RabbitAnti-MEF2C, Rabbit Polyclonal to MEF2C, Isotype , Host RabbitAnti-MEF2C, Rabbit Polyclonal to MEF2C, Isotype , Host RabbitBovine myocyte enhancer factor 2C (MEF2C) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Myocyte-specific enhancer factor 2C (MEF2C) ELISA KitBovine Myocyte-specific enhancer factor 2C (MEF2C) ELISA Kit Related articles to: MEF2C (dn _ R24L)
- The pathogenesis of heart failure involves a highly intricate process regulated by diverse epigenetic factors, transcription factors, noncoding RNAs, and cyclins. Notably, the reexpression of embryonic cardiac transcription factors, including , , and , is considered to exert critical influence in the initiation and advancement of heart failure. Nevertheless, the precise mechanisms through which epigenetic modifications drive this reprogramming of gene expression remain poorly defined. This investigation aims to clarify the role of histone acetylation in regulating the reexpression of embryonic cardiac transcription factors during heart failure. Our research indicates that during heart failure of mice, there are distinct histone acetylation modifications associated with the reexpression of these factors. Notably, and show significant increases, whereas shows a decrease compared to normal groups during heart failure progression. These findings imply that embryonic and may promote the development of heart failure, whereas does not appear to participate in disease progression. Furthermore, treatment with curcumin, a known inhibitor of histone acetylation, reduces acetylation levels at H3K4, H3K9, and H3K27 within the promoter regions of and in a murine model of heart failure, leading to downregulation of these genes and subsequent enhancement of cardiac performance. In summary, our study demonstrates that p300 exerts site-specific regulatory effects on various transcription factors via histone modifications, and low acetylation status at specific sites can inhibit reactivation of and during the myocardial dysfunction period thereby improving cardiac performance of mice. - Source: PubMed
Publication date: 2026/03/27
Gan XinruPan BoLiu LingjuanLi MiSun Huichao - The absence of the protein dystrophin in Duchenne muscular dystrophy (DMD) leads to progressive muscle weakness, failing regeneration and deregulation of nitric oxide (NO) signalling. We focused on L-citrulline, a precursor of L-arginine, required for NO production in muscle, which is reduced in dystrophic mdx muscle. - Source: PubMed
Publication date: 2026/04/22
Tulimiero LisamauraBoccanegra BrigidaMantuano PaolaMele AntoniettaDe Bellis MichelaLenti RobertaSanarica FrancescaCirmi SantaConte ElenaCappellari OrnellaSherrard Amber EGreen ArdawnaSrinivasa MiraFiorotto Marta LDe Luca Annamaria - Unfolded protein response (UPR) is a conserved cellular strategy that enhances the protein folding capacity of cells under stress conditions. In Saccharomyces cerevisiae, the dual kinase RNase IRE1 initiates the UPR by catalyzing the cytosolic splicing of HAC1 mRNA, a process conserved in humans where IRE1 splices XBP1 mRNA. The spliced HAC1/XBP1 mRNA yields a transcription factor that upregulates the expression of protein-folding enzymes and chaperones, thereby boosting the cell's ability to cope with unfolded proteins. Our study demonstrates that the UPR involves two distinct phases. The early phase operates predominantly through the canonical IRE1 signaling pathway, while the later phase involves additional regulation by the MAP kinase Slt2 or its human ortholog ERK1/ERK2/ERK5 and the downstream target the MADS-box transcription factor Rlm1 (an ortholog of human MEF2C). We further show that Slt2 promotes IRE1 expression through Rlm1. Together, these findings reveal a previously unrecognized crosstalk between the MAPK and IRE1-mediated arm of the UPR. - Source: PubMed
Publication date: 2026/04/21
Chakraborty AnishChakrabarty SaswataUppala Jagadeesh KumarMayer Kimberly AnnEvans Anna JGeorge JasmineGhosh ChandrimaDey RitishaOhikhuare FrancaMirza ShamaNguyen An Phu TranGouignard NadègeChaluvally-Raghavan PradeepDey Madhusudan - Myocyte enhancer factor 2C (MEF2C) is a critical transcription factor and plays a pivotal role in muscle development, cardiac reprogramming, cellular differentiation, and disease pathogenesis. In this review, we have systematically described the structural characteristics of the MEF2C protein, particularly its DNA-binding MADS-box and transcriptional regulatory domains, and outlined the multi-level regulation mechanism of its expression and activity. We further have highlighted the functional roles of MEF2C in heart and skeletal muscle development, including its involvement in cardiomyocyte differentiation and reprogramming, and its pathological implications in heart and skeletal muscle diseases. Finally, we have summarized the pathological implications of MEF2C in neurological disorders and tumorigenesis and underlined its role as a regulator in the body's inflammatory response, offering a theoretical foundation for understanding its physiological and pathological implications and for the development of therapeutic strategies targeting MEF2C-related diseases. - Source: PubMed
Publication date: 2026/04/21
Zhang JiaweiXie YueyueJiang ShuoHuang ShuoLv HexuanQin YumingXu JingleiDai ZihanWang HaiqiangDai YuanyuanYang YutianAn YangZhang Guosen - This study aims to investigate the pathogenic hallmarks in various subtypes of idiopathic inflammatory myopathies (IIM) using single-cell transcriptomic approaches. - Source: PubMed
Publication date: 2026/04/20
Wang ZhiqinLi YanmeiLi XiaowenZhang JianlinXu JingHan FengDu JunYang TongChen MingGuo YingWang GaoyaXu YongHou HouSun WenwenZhang NaLi DongZhang HuafengCai ZhigangWei Wei