PSD-95, monoclonal antibody, mouse, 100 ul.
- Known as:
- PSD-95, mab (anti-), mouse, 100 ul.
- Catalog number:
- MO50000-100
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- PSD-95 monoclonal antibody mouse 100 .
Related genes to: PSD-95, monoclonal antibody, mouse, 100 ul.
- Gene:
- DLG4 NIH gene
- Name:
- discs large MAGUK scaffold protein 4
- Previous symbol:
- -
- Synonyms:
- PSD-95, PSD95, SAP90, SAP-90
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-07
- Date modifiied:
- 2016-05-24
Related products to: PSD-95, monoclonal antibody, mouse, 100 ul.
Related articles to: PSD-95, monoclonal antibody, mouse, 100 ul.
- As a widely used organic UV filter and emerging environmental pollutant, 4-methylbenzylidene camphor (4-MBC) accumulates in aquatic ecosystems and human tissues, but its developmental neurotoxicity mechanisms remain unclear. This study integrated network toxicology, molecular docking and dynamics simulations, zebrafish experiments, dose-dependent transcriptomics and the adverse outcome pathway (AOP) framework to elucidate the neurotoxic mechanisms of 4-MBC. Network toxicology identified 150 potential targets and 10 core targets (BDNF, DLG4, EGF, etc.), with enrichment analyses highlighting glutamatergic synaptic signaling, MAPK pathway, and DNA replication as candidate key pathways. Molecular docking and dynamics predicted stable binding of 4-MBC to core targets (e.g., DLG4, GRIN2B). Zebrafish exposed to 4-MBC (1, 10, 100 and 1000 μg/L) showed concentration-dependent developmental malformations, lowered hatching rates and suppressed larval locomotion. Transcriptomic analysis identified 311 dose-responsive genes and enriched key pathways, suggesting disrupted glutamatergic transmission, dysregulated MAPK activity and defective DNA replication as potential core drivers. RT-qPCR further verified dose-dependent transcriptional alterations of representative genes at 100 and 1000 μg/L: the synaptic genes bdnf and dlg4 were downregulated, whereas the neurodevelopmental markers ngn1 and shha were upregulated. AOP-based bioinformatic analysis further indicated impaired DNA repair as a potential converged node that may trigger neural progenitor apoptosis and subsequent growth-inhibition phenotypes. Collectively, these findings propose a working model in which 4-MBC disrupts glutamatergic synapses, activates MAPK signaling, and impairs DNA replication to induce developmental neurotoxicity, though direct functional validation of this cascade is warranted, providing insights for environmental and human health risk assessment. - Source: PubMed
Publication date: 2026/09/01
Lu XiaoyangGuan MiaoTang SuqiHu JunxingSun LiWang JingChen JiaoZhang HuijieXu Shixia - Retinoic acid (RA), a biologically active metabolite of vitamin A, regulates gene expression through retinoic acid receptor/retinoid X receptor (RAR/RXR)-dependent transcription and is important for various biological phenomena. To understand the role of forebrain RA signaling in synaptic plasticity and memory, we generated transgenic mice expressing a dominant-negative form of retinoic acid receptor α (dnRARα) in adult forebrain. We previously showed that dnRARα expression in the adult forebrain impairs α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated synaptic transmission and long-term potentiation (LTP) in hippocampal CA1 neurons and hippocampus-dependent memory. To investigate the molecular basis of these impairments, we here examined expressions of synaptic plasticity-related molecules in the hippocampus of dnRARα mice. We found that protein levels of GluA1 and postsynaptic density protein 95 (PSD-95) were significantly reduced in the hippocampus of dnRARα mice in a dnRARα expression-dependent manner. To further examine protein expression changes in dnRARα mice, we performed proteome analysis and found that expression of actin-related protein 3 (ARP3), a molecule implicated in activity-dependent spine enlargement and maturation, was also reduced. Combined with our previous findings, these results suggest that forebrain RAR/RXR signaling is crucial for maintaining synaptic transmission, plasticity, and memory formation by upregulating GluA1, PSD-95, and ARP3. - Source: PubMed
Nomoto MasanoriMitsuda KojiUchida ShusakuKida Satoshi - - Source: PubMed
Publication date: 2026/08/19
Qian HaoGuo SimengTao KeyangDai ShijieZhao HongMao MingjiangYuan Xiaofeng - We report a 34-year-old male with childhood developmental delay, severe intellectual disability in adulthood, episodes of agitation with a previous diagnosis of schizoaffective disorder and adult-onset cognitive regression who developed progressive generalised dystonia due to a de novo DLG4 pathogenic loss-of-function variant. This case expands the phenotypic spectrum of recognised movement disorder manifestations associated with DLG4-related synaptopathy. - Source: PubMed
Publication date: 2026/08/01
Peraferrer-Montesinos LaiaNagaratnam Sai AForwood CaitlinBerry AlexisAshton KatieDong JackZhu YingArpone MartaBecker PalomaDelves MadelineMorales Briceno Hugo - SHINE syndrome is a rare neurodevelopmental disorder caused by mutations in DLG4, which encodes the postsynaptic scaffolding protein PSD-95. Key symptoms include sleep problems, hypotonia, intellectual disability, neurological disorders, and epilepsy, hence the name 'SHINE.' Here, we developed and characterized a mouse model of SHINE syndrome carrying the patient-derived DLG4V692Wfs*12/+ variant associated with a severe form of the disorder. The mutant transcript escapes nonsense-mediated decay but results in reduced PSD-95 protein expression, faithfully reproducing the molecular phenotype observed in the patient. Behavioral analyses revealed that Dlg4V692Wfs*12/+ mice recapitulate several hallmark features of SHINE syndrome, often in a sex-specific manner. Male mutants showed deficits in learning and cognitive flexibility. Dlg4V692Wfs*12/+ mice also demonstrate trends toward altered sensory processing and socialization. Male mutants exhibited an increased proportion of short sleep bouts and compensatory longer average sleep bout length, suggesting sporadic sleep reminiscent of the patient. While spontaneous seizures were not observed, future studies will test susceptibility to provoked seizures. Together, these findings establish Dlg4V692Wfs*12/+ mice as a robust and translationally relevant model that reproduces key molecular and behavioral features of SHINE syndrome. This model provides a valuable resource for elucidating the mechanisms underlying synaptic neurodevelopmental disorders and for identifying potential therapeutic strategies. - Source: PubMed
Tamir SharonPaulose JiffinNguyen AnhGadara DarshakWitt Rochelle MPrasad BhagwatHogenesch John B