MeCP2 Blocking Peptide target: MeCP2
- Known as:
- MeCP2 Blocking Peptide target: MeCP2
- Catalog number:
- 3199BP-50
- Product Quantity:
- 50 μg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- MeCP2 Blocking Peptide target:
Related genes to: MeCP2 Blocking Peptide target: MeCP2
- Gene:
- MECP2 NIH gene
- Name:
- methyl-CpG binding protein 2
- Previous symbol:
- RTT, MRX16, MRX79
- Synonyms:
- -
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-03
- Date modifiied:
- 2019-04-23
Related products to: MeCP2 Blocking Peptide target: MeCP2
Related articles to: MeCP2 Blocking Peptide target: MeCP2
- Rett syndrome is a severe neurodevelopmental disorder most commonly associated with pathogenic variants of the gene and frequently accompanied by epilepsy. Seizures occur in a substantial proportion of patients and may be resistant to conventional antiepileptic therapy. Emerging evidence suggests that neuroinflammatory processes may contribute to seizure propagation and represent a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/12
Djumaeva Naylya - Rett syndrome (RTT) is an X-linked neurological disorder caused by mutations, creating distinct cellular environments in females (mosaic) versus males (nonmosaic). Despite female patients representing most cases, how mosaicism contributes molecularly to RTT pathogenesis, particularly in presymptomatic stages, remains poorly understood. To address this question, we profiled hippocampal transcriptomes of young female and male RTT mice using bulk and single-nucleus RNA sequencing. We identified a core disease signature of consistently dysregulated genes only in MeCP2 cells across RTT models. Moreover, we uncovered non-cell autonomous effects exclusively in female MeCP2 excitatory neurons, suggesting that these circuits are more vulnerable early in the mosaic RTT environment. The single-nuclei data also revealed an underappreciated MeCP2 interneuron subtype that had the most transcriptional dysregulation in both male and female RTT hippocampi. Together, these data highlight the different effects of MeCP2 loss on excitatory and inhibitory circuits between the mosaic and nonmosaic environments in early RTT pathogenesis. - Source: PubMed
Publication date: 2026/06/10
Li YanAnderson Ashley GQi GuantongWu Sih-RongRevelli Jean-PierreChen HuLiu ZhandongZoghbi Huda Y - Methyl-CpG-binding protein 2 (MeCP2) is a chromatin-associated factor whose dysfunction causes Rett syndrome. Although MeCP2 preferentially binds methylated DNA, its affinity for methylated substrates is only ∼threefold higher than for unmethylated DNA, raising the question of how MeCP2 selectively recognizes its targets. Here, we quantify binding of full-length wild-type MeCP2 and Rett-associated variants (R106W, T158M, R270X, and R306C) to nucleic acid substrates that vary in length, secondary structure, methylation pattern, CpG symmetry, and strand composition. Wild-type and mutant MeCP2 preferentially bind double-stranded DNA but also interact with single- and double-stranded DNA and RNA with nanomolar affinity. Binding to single-stranded targets is largely driven by the formation of local duplex structures, whereas 5-methylcytosine provides stabilizing contacts and enhances MeCP2 affinity when canonical duplex geometry is absent. Rett-associated mutations segregate into mechanistic classes: mutations within the methyl-binding domain (R106W and T158M) weaken methylation-dependent recognition and reduce binding affinity, whereas C-terminal mutations (R270X and R306C) preserve high-affinity binding but diminish cooperative interactions consistent with impaired higher-order bridging. These findings identify MeCP2 as a methyl-sensitive nucleic acid binder whose interactions are shaped by local nucleic acid topology and modulated by cytosine methylation, providing a mechanistic framework for understanding how Rett-associated mutations disrupt chromatin regulation. - Source: PubMed
Publication date: 2026/06/04
Melikishvili MananaRea MatthewCapan ColtLee HyoungjooChandler Darrell PFondufe-Mittendorf Yvonne - Loss-of-function variants of cause Rett syndrome; however, their impact on cerebellar computations for learning remains poorly understood. Here, we show that deletion specifically in Purkinje cells does not broadly disrupt cerebellar-dependent behaviors but selectively compromises those that require precise timing, coordination, and associative updating in the cerebellar cortex. loss altered the emergence of learning-related Purkinje cell activity and disrupted their intrinsic and synaptic properties that support adaptive cerebellar output. These findings identify MeCP2 as a critical player in Purkinje cell function to regulate cerebellar learning signals and suggest that Rett syndrome-related motor dysfunction reflects impaired adaptive computation rather than a generalized loss of motor capacity. - Source: PubMed
Publication date: 2026/05/25
Shen JennyShen PeterGonçalez Julia LopesJackson MikaylaPolepalli LikhithaDheeravath KruthikaLi TimothyHamki AbdullaHamki MariamHicks ChristianLi ChangPozzo-Miller LucasLi Wei - Pubertal onset is driven by the reactivation of the hypothalamic-pituitary-gonadal (HPG) axis, a process orchestrated by a complex interplay of stimulatory and inhibitory factors and influenced strongly by genetic regulation. In this study, we assessed the expression patterns of 3 genes associated with central precocious puberty (CPP) in humans-, , and -across pubertal maturation in male and female mice. Hypothalamic regions were collected for mRNA quantification by reverse transcription and real time quantitative polymerase chain reaction and protein measurement by Western blot for all 3 genes; in addition, serum samples were used for Dlk1 quantification by enzyme-linked immunosorbent assay. Hypothalamic levels of mRNA and protein, a well-established inhibitor of pubertal onset, were high in early postnatal life and declined prior to puberty onset, consistent with its role in suppressing HPG axis activation. In contrast, mRNA and protein levels were higher in adults than younger mice-an unexpected finding since loss of DLK1 expression advances puberty onset. Conversely, serum Dlk1 decreased progressively with age, suggesting a role for peripheral Dlk1 in pubertal regulation. , a key epigenetic regulator implicated recently in puberty regulation, had lower hypothalamic mRNA levels after PND10, whereas protein levels remained unchanged, possibly reflecting splice variant-specific expression or post-transcriptional regulation. These distinct age-dependent expression patterns suggest that and likely contribute primarily to central HPG axis regulation, whereas Dlk1 originating peripherally may act as a central regulator of puberty. Defining these trajectories offers insights into the molecular control of pubertal timing and potential therapeutic targets for pubertal disorders. - Source: PubMed
Publication date: 2026/04/06
Tinano Flavia RMeireles Cinthia GMacedo Delanie BBoris NataliaPereira SidneyMagnuson MelissaAbreu Ana PaulaCarroll Rona SLatronico Ana ClaudiaKaiser Ursula B