PSN2_CHICK PSEN2 ELISA tesk kit
- Known as:
- PSN2_CHICK PSEN2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16372
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- PSN2_CHICK PSEN2 ELISA tesk kit
Related genes to: PSN2_CHICK PSEN2 ELISA tesk kit
- Gene:
- PSEN2 NIH gene
- Name:
- presenilin 2
- Previous symbol:
- AD4
- Synonyms:
- AD3L, STM2, PS2
- Chromosome:
- 1q42.13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-30
- Date modifiied:
- 2019-04-23
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- Neurodegenerative disorders such as Parkinson's disease (PD) arise from interconnected mechanisms including mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein homeostasis, leading to progressive dopaminergic neuron loss and limited benefit from current single target therapies. Parkin (PARK2), an E3 ubiquitin ligase central to mitochondrial quality control and mitophagy, has therefore emerged as an attractive therapeutic node, with its functional stabilization representing a promising strategy to restore mitochondrial homeostasis in PD. In this study, phytocompounds from Althaea officinalis were evaluated using an integrated in silico pipeline combining ADMET prediction, molecular docking, 100 ns molecular dynamics simulations, MM-GBSA binding free energy analysis, and network pharmacology to identify potential PARK2 modulating lead compounds relevant to Parkinson's disease. Forty bioactive constituents were screened, and computational ADMET modeling highlighted flavonoids and coumarin derivatives such as scopolin, astragalin, isoquercitrin, and quercetin derivatives as having acceptable oral absorption, limited predicted toxicity, and low risk of major metabolic or cardiotoxic liabilities. Structure-based docking against PARK2 (PDB ID: 5C23) revealed that several A. officinalis metabolites, notably scopolin, β-D-glucose, quercetin-3-glucoside, and L-arabinose, exhibit favorable binding affinities (docking scores - 7.232 to - 6.648 kcal/mol) and form energetically stable complexes with key catalytic and regulatory residues, in some cases outperforming co-crystal ligand. Subsequent 100 ns molecular dynamics simulations confirmed that the scopolin- and quercetin-3-glucoside-PARK2 complexes remain structurally stable, with low RMSD fluctuations, compact Rg profiles, and persistent hydrogen-bonding, while MM-GBSA calculations yielded consistently favorable ΔGbind values, further supporting their high-affinity interaction with PARK2. Network pharmacology analysis further showed that these phytochemicals converge on core PD-related targets such as AKT1, PIK3R1, MAPT, SNCA, PSEN2, BCL2L1, HK1, RPS6KA3, TLR1, and TLR2 within PI3K-Akt, MAPK, mTOR, HIF-1, autophagy, apoptosis, insulin, Toll-like receptor, and Parkinson disease pathways, indicating a multi-target, multi-pathway mode of action. Overall, the findings suggest that A. officinalis phytocompounds especially scopolin and quercetin glycosides possess drug-like ADMET properties, strong PARK2 binding, MD-validated complex stability with favorable MM-GBSA binding energies, and systems-level engagement with PD-relevant signaling networks, supporting their candidacy as plant-derived leads for PARK2-centered therapeutic strategies in PD. - Source: PubMed
Publication date: 2026/06/15
Heshetha MHaneesh MuthineniKarthick VenkatesanThamarai RajkumarAmalraj Singamoorthy - Alzheimer's Disease (AD) is a prevalent neurodegenerative disorder which involves a complex pathobiology driven by amyloid-beta (Aβ) and tau pathologies, among other factors. Aβ peptides are generated β-secretase (BACE1) and γ-secretase cleavage of amyloid precursor protein (APP). While long isoforms like Aβ42 are neurotoxic and aggregation-prone, shorter isoforms (Aβ38, Aβ37) are non-amyloidogenic. γ-secretase modulators (GSMs) shift production from longer to shorter peptides which is expected to slow down or halt (prevent) amyloid accumulation and its downstream effects. - Source: PubMed
Publication date: 2026/05/28
Lindemann LotharLambotte JulieRothe JudithMesser JürgDiener CatherinePichereau SolenCantrill CarinaMueggler ThomasHoner MichaelBeck JenniferSteinbrecher ThomasTortelli RosannaGerlach IreneRatni HasaneRodriguez Sarmiento Rosa MariaBaumann Karlheinz - Familial Alzheimer's disease (FAD) is a rare form of Alzheimer's. FAD is mainly caused by one or multiple mutations in the genes encoding for amyloid precursor protein (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2), with the majority occurring in PSEN1. Despite extensive research in animal models and numerous promising treatment trials, there is still no curative treatment for FAD. Recently, ZL006 (Med Chem Express cat. Number HY-100456) was shown to reduce over-produced nitric oxide and oxidative stress in ischemic stroke and could protect neurons against Aβ-induced neurotoxicity (in vitro study). With this in mind, we tested ZL006 at different doses (10 μM, 25 μM, 50 μM and 100 μM) in zebrafish embryo injected with ctrl-MO and -MO, investigating the effects on pathological phenotype in vivo. We showed that ZL006 exposure suppresses inflammation, oxidative stress and accumulation of Aβ in -MO. In conclusion, our study showed that ZL006 was able to ameliorate the pathological phenotype of -morphant zebrafish embryos, supporting its potential as a candidate for further investigations in the context of FAD treatment. - Source: PubMed
Publication date: 2026/05/30
Ricci SerenaBenuzzi MariaFazzina MartinaCacialli Pietro - Endolysosomal dysfunction has been increasingly implicated in the pathogenesis of neurodegenerative diseases. The charged multivesicular body protein 2B (CHMP2B) gene encodes a component of the endosomal sorting complexes required for transport (ESCRT-III), which regulates endosomal trafficking, multivesicular body formation, and autophagosome-lysosome fusion. Mutations in CHMP2B are classically associated with autosomal dominant frontotemporal dementia. Here, we report a 59-year-old woman with biomarker-confirmed Alzheimer disease (AD) (A+T+N+) carrying a heterozygous CHMP2B c.90C>T (p.Ala30Ser) variant identified by targeted exome sequencing after negative testing for APP, APOE, PSEN1, and PSEN2. The patient presented with progressive episodic memory impairment and spatial disorientation over 3 years. Brain MRI showed prominent posterior cortical atrophy, and cerebrospinal fluid biomarkers demonstrated decreased Aβ42 and elevated phosphorylated and total tau levels consistent with AD pathology. Dysfunction of CHMP2B-mediated endolysosomal pathways may impair intracellular protein degradation and influence tau clearance mechanisms. This observation suggests that rare variants in endolysosomal pathway genes may contribute to AD pathophysiology. - Source: PubMed
Publication date: 2026/06/04
Totuk Ozlem - Most genetic variants associated with complex diseases lie in non-coding regions, complicating efforts to identify effector genes and relevant cell types. Here we map cis-expression quantitative trait loci (eQTLs) across 2.2 million single cells using intestinal biopsies and blood from 421 individuals, including 125 with inflammatory bowel disease (IBD). Cell-type-level eQTLs were more distal to transcription start sites, enriched in enhancers, less likely to regulate the nearest gene, and more than 3.5-fold more likely to colocalize with IBD loci detected in genome-wide association studies (GWASs) than eQTLs detected at tissue-level resolution. We nominate effector genes at more than half of known IBD loci, including MAML2, PSEN2 and ZMIZ1 in myeloid cells, implicating reduced Notch signalling in intestinal immune dysfunction. We also identify Wnt-regulated genes, including MYC, in epithelial stem and progenitor cells, suggesting that impaired renewal contributes to barrier breakdown. Our results provide a mechanistic map that links genetic risk to specific genes and cell types in IBD, and a generalized framework for interpretation of GWAS loci using single-cell eQTL mapping of disease-relevant tissues in complex diseases. - Source: PubMed
Publication date: 2026/06/03
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