Bovine Alpha-Synuclein,SNCA ELISA Kit
- Known as:
- Bovine Alpha-Synuclein,SNCA Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- YHB0009BO
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- yehua
- Gene target:
- Bovine Alpha-Synuclein SNCA ELISA Kit
Related genes to: Bovine Alpha-Synuclein,SNCA ELISA Kit
- Gene:
- SNCA NIH gene
- Name:
- synuclein alpha
- Previous symbol:
- PARK1, PARK4
- Synonyms:
- NACP, PD1
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-24
- Date modifiied:
- 2018-04-18
Related products to: Bovine Alpha-Synuclein,SNCA ELISA Kit
Related articles to: Bovine Alpha-Synuclein,SNCA ELISA Kit
- Emerging evidence suggests that the genetic architecture of Alzheimer disease (AD) and Parkinson disease (PD) risk varies across ancestries. This study seeks to explore distinct and universal genetic targets across individuals of Latino, African/African-admixed, East Asian, and European populations by implementing population attributable risk (PAR) comparisons using summary statistics from genome-wide association studies (GWASs). - Source: PubMed
Publication date: 2026/07/16
Jones LietselCerquera-Cleves CatalinaSchuh Artur F SMakarious MaryIwaki HirotakaNalls MikeNoyce Alastair JBlauwendraat CornelisSingleton Andrew BMata Ignacio FCookson Mark RBandres-Ciga Sara - Copy Number Variations (CNVs) play pivotal roles in complex disease etiology, often requiring large sample sizes to analyze disease associations. While genotyping arrays offer a cost-effective approach for CNV detection using Log R Ratio (LRR) and B Allele Frequency (BAF) signals, existing independent array-based callers suffer from high false positive rates and noise susceptibility, burdening manual validation. - Source: PubMed
Publication date: 2026/07/22
Kuznetsov NicoleDaida KensukeMakarious Mary BAl-Mubarak BashayerAtterling Brolin KajsaMalik LakshKouam CedricBaker BreeanaReal RaquelStep KathrynLange Lara MWu LesleyOstrozovicova MiriamAndersh Katherine MKung Pin-JuiMecheri YasserTay Yi-WenSoundous Malek BehloulAl Tassan NadaPeriñan Maria TeresaHong SamanthaKoretsky Mathew JSargeant LanaLevine KristinBlauwendraat CornelisBillingsley Kimberley JBandres-Ciga SaraLeonard Hampton LBardien SorayaMorris Huw RSingleton Andrew BNalls Mike AVitale Dan - AD is a neurodegenerative disorder marked by progressive cognitive decline, particularly memory impairment, largely driven by cholinergic dysfunction. This study aimed to investigate the pharmacological basis and modes of action of the identified TT-TeMac™ compounds againsts cholinergic dysfunction associated with memory loss. TT-TeMac™ compounds targets which were identified by LC-MS were extracted from SwissTarget Prediction and PharmMapper, while cholinergic dysfunction-related targets were obtained from DisGeNET and GeneCards. Fifteen common targets were identified, with nine key targets highlighted by STRING, Cytoscape, and Venny analyses and confirmed by molecular docking using MOE. The validation used a rat model with scopolamine-induced cholinergic dysfunction (1 mg/kg bw/day, ip) for 7 days. Subsequently, behavioral (NOR and MWM), biochemical (AchE and BuhE) and histological (H&E and CV) analyses were performed. Seven compounds were identified in TT-TeMac™ (terminolic acid, sericic acid, arjunolic acid, gallic acid, ellagic acid, 3-O-methyl ellagic acid and 3,3'-di-O-methyl ellagic acid). Network pharmacological analysis showed that TT-TeMac™ acted on 15 common targets of which ACHE, IL6, TNF, SNCA, AKT1, SERPINE1, STAT3, ACE, and ALB were the pivotal genes. Also, docking studies confirmed the involvement of the target within the network with meaningful binding energies. Furthermore, TT-TeMac™ prevented cholinergic dysfunction associated with memory loss in rats by significantly reducing cholinesterase activity and protecting against morphological alterations and neuronal loss in the hippocampus. Our study shows that the ingredient TT-TeMac™ has a multi-targeted mode of action on protein targets involved in cholinergic dysfunction and counteracts this dysfunction in scopolamine-treated rats. - Source: PubMed
Publication date: 2026/08/10
Ambamba Bruno Dupon AkambaJonathan Messanga Me Ngo'oMarc Akono Fama YvesSandrine Nyabissick MondjiepReine Njayou Mbouangouore IngridEmmanuel NgarchindiLaurent Nkodo AbegaBlonde Njanjo Ejanmoua Merveille LaAlexandra Ebogo Enyegue FrançoiseElla Fils ArmandMandob Damaris EnyegueNgondi Judith Laure - Aggregated alpha-synuclein (αsyn) phosphorylated at serine 129 (PS129) accumulates in synucleinopathies, with the olfactory bulb (OB) being severely affected. Non-aggregated physiological PS129 is abundant in the mammalian OB, where it likely modulates αsyn-protein interactions. The impact of aggregation on the PS129 interactome in the OB remains unclear. We hypothesized that αsyn aggregation alters the PS129 interactome, shifting canonical synaptic partners (e.g., SNARE proteins) toward the aggregate-associated network. To test this hypothesis , we mapped PS129 interactions in the OB of PFF-injected WT and SNCA (M83) mice using biotinylation by antibody recognition (BAR) and pretreated with calf-intestine alkaline phosphatase (CIAP) to distinguish physiological from aggregate-associated PS129 interactomes. Seeding and spread were assessed by immunohistochemistry and in situ seeding immunodetection assay (isSID). - Source: PubMed
Publication date: 2026/07/27
Choi Solji GBahrami AtousaDuvernay Jayda BTittle TylerMelki RonaldKordower Jeffrey HKillinger Bryan A - Alpha-synuclein (SNCA) overexpression is implicated in Parkinson's disease (PD) pathogenesis, making SNCA downregulation a promising therapeutic strategy. We developed a SNCA-targeted transcriptional repression therapy using an all-in-one lentiviral vector (LV) carrying deactivated CRISPR/(d)Cas9, gRNA targeted at SNCA-intron1, and either the catalytic domain of DNA-methyltransferase3A (DNMT3A), or an engineered repressor molecule, a fusion of MeCP2's transcription repression domain (TRD) and KRAB. Therapeutic efficacy was evaluated following co-administration of the therapeutic and model vectors in a new PD mouse model, generated with an adeno-associated viral vector carrying an engineered minigene comprised of the human (h)A53T-SNCA expressed via the human native regulatory region. Both therapeutic vectors reduced expression of α-synuclein in the substantia nigra (SN), with LV/dSaCas9- KRAB-MeCP2(TRD) demonstrating greater repression. LV/dSaCas9- KRAB-MeCP2(TRD) also significantly reduced pathological α-synuclein aggregation and phosphorylation (Ser 129), and preserved tyrosine hydroxylase expression in the SN and the striatum. Behavioral analysis following LV/dSaCas9-KRAB-MeCP2(TRD) injection, showed significant improvement in motor deficits characteristic of our PD-mouse model. Preliminary safety assessments found normal blood counts, serum chemistry, and weights. Collectively, these findings provide in vivo proof-of-concept for SNCA-targeted transcriptional repression therapy in a PD-mouse model and support its further preclinical development toward investigational new drug enablement. - Source: PubMed
Publication date: 2026/08/18
O'Donovan BernadetteRittiner JosephUpadhya SurajHodgson DellilaKantor BorisChiba-Falek Ornit