MEF2C (phospho-Ser396) Antibody
- Known as:
- MEF2C (phosphorilated-Ser396) Antibody
- Catalog number:
- abx000148
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MEF2C (phospho-Ser396) Antibody
Related genes to: MEF2C (phospho-Ser396) Antibody
- 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 (phospho-Ser396) Antibody
Related articles to: MEF2C (phospho-Ser396) Antibody
- Elevated prenatal androgen levels have been associated with an increased incidence of several neurodevelopmental conditions in offspring. However, the underlying mechanisms remain poorly understood. Here we showed that elevated prenatal androgens, modeled via aromatase inhibition in mice, disrupt cortical development and behavior in male offspring by activating androgen receptors (AR). AR interacts with MeCP2 to upregulate the transcription factor MEF2C, bypassing standard androgen response elements. Knocking down Mecp2 or Mef2c, or blocking AR, reversed these effects. Mecp2 duplication alone also upregulated MEF2C, driving similar neurogenesis and behavioral changes that were reversed by AR blockade. This reveals a MeCP2-mediated, non-canonical pathway by which androgens may contribute to male-biased neurodevelopmental conditions. - Source: PubMed
Publication date: 2026/05/13
Wang Yu-MengJia YanyanWu YuZhao QiaohangGuo YumengZhang LiJin MinZheng Yufang - Cardiac fibroblast activation into α-smooth muscle actin (α-SMA)-expressing myofibroblasts is a central event in the progression of cardiac fibrosis. Therapeutic strategies capable of reversing or inhibiting this phenotypic transition are therefore of critical interest. Here, we explore associative changes in transcriptional and post-transcriptional regulators linked to fibroblast activation following atorvastatin exposure in primary human cardiac fibroblasts (HCFs). Atorvastatin treatment (10 µM) was associated with a reduction in α-SMA expression, consistent with decreased myofibroblast activation. This change co-occurred with reduced expression of the transcription factors GATA4 and MEF2C, which are implicated in cardiac cell identity and plasticity. Concurrently, atorvastatin treatment was associated with selective increase in specific fibrosis-related microRNAs, including miR-24, miR-26a, and miR-133a, whereas the expression of miR-21 and miR-23a remained unchanged. Together, these findings describe a coordinated pattern of transcriptional and post-transcriptional changes associated with atorvastatin exposure in HCFs, consistent with a shift away from the myofibroblast phenotype. These observations provide descriptive, hypothesis-generating insight into potential regulatory patterns associated with atorvastatin treatment, although further functional studies are required to establish causal relationships and translational relevance. - Source: PubMed
Publication date: 2026/05/06
Chomaničová NikolaAdamičková AdrianaCervenak ZdenkoValášková SimonaGažová AndreaKyselovic Jan - Bipolar disorder (BD) exhibits significant sex differences in its frequency, symptom presentation, and treatment response, suggesting distinct underlying neurobiological mechanisms. However, transcriptomic studies investigating these sex-specific pathways have been fragmented and underpowered. - Source: PubMed
Publication date: 2026/05/08
Davarinejad OmranMoradi Mohammad-TaherSafarzadeh ArashJalalvand MasumehKazemisafa Fatemeh - Type 2 diabetes (T2D) disrupts male reproductive function by impairing Leydig and Sertoli cell activity, leading to hormonal imbalances and defective spermatogenesis. This systematic review explores the molecular mechanisms underlying T2D-induced dysfunction in these testicular cells, emphasizing alterations in steroidogenesis, cell signaling, and metabolic regulation. - Source: PubMed
Publication date: 2026/04/28
Oroojan Ali AkbarEtedali HoomanShirani Lapari Homa - Risk alleles for late-onset Alzheimer's disease (AD) are enriched in myeloid cis-regulatory elements, implicating myeloid gene-regulatory networks in disease susceptibility. A conserved lipid-associated transcriptional signature-spanning disease-associated microglia and peripheral lipid-associated macrophages (DLAM)-emerges across neurodegenerative and metabolic diseases characterized by lipid overload, yet the transcriptional regulators of this gene expression program remain incompletely defined. Here, we show that MEF2C-a candidate AD risk gene-is a master DLAM regulator. Using MEF2C knockout and knockdown in human iPSC-derived microglia and macrophages, we found that total or partial MEF2C loss is sufficient to induce DLAM-associated transcriptional, epigenomic, and functional remodeling, including enhanced lysosomal activity and cholesterol efflux. Integration of chromatin accessibility and regulatory epigenetic profiles with functionally informed fine-mapping linked candidate causal variants in AD risk loci to MEF2C-regulated cis-regulatory elements that target candidate AD risk genes at these loci. In a triculture model of AD, microglial MEF2C loss is associated with an increased DLAM population and a reduced Aβ42/40 ratio, supporting context-dependent reprogramming of microglia as a potential biological mechanism to modulate AD-relevant pathology. - Source: PubMed
Publication date: 2026/04/28
Goate AlisonPodlesny-Drabiniok AnnaKim JeanneBezemer LottePatel TulsiCheng HaoxiangSewell MichaelMontecillo MiaChurch NicholasWalley AnthonyGarretti FrancescaMarcora Edoardo