PSD3 (aa 395_409)
- Known as:
- PSD3 (aa 395_409)
- Catalog number:
- Y213851
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PSD3 ( 395_409)
Related genes to: PSD3 (aa 395_409)
- Gene:
- PSD3 NIH gene
- Name:
- pleckstrin and Sec7 domain containing 3
- Previous symbol:
- -
- Synonyms:
- KIAA0942, HCA67, EFA6R, DKFZp761K1423, EFA6D
- Chromosome:
- 8p22
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-06
- Date modifiied:
- 2016-10-05
Related products to: PSD3 (aa 395_409)
Related articles to: PSD3 (aa 395_409)
- Parkinsons disease, characterized by the aggregation of alpha-synuclein is a complex neurodegenerative disorder with the fastest global prevalence growth. The identification of shared genes expressed in both blood and brain of Parkinson's disease patients improves the knowledge on peripheral pathophysiology of the disease and facilitates identification of minimally invasive potential biomarkers from these shared genes. Our study intends to identify a shared transcriptomic signature between the blood and brain critical for developing minimally invasive biomarkers and understanding systemic disease progression. This study implemented an integrative bioinformatic approach towards the public microarray dataset comprising of both human Parkinson's disease blood and post-mortem brain cohorts. After routine data preparation and differential gene expression analysis across tissues, functional annotation, protein-protein interaction networks, and topological hub analysis were utilized to delineate underlying systemic pathways. A robust nine-gene signature-ANK1, CMAS, GUCY1B1, PRKAR2B, PSD3, RAB27B, SLC18A2, SNCA, and UCHL1-was downregulated in both blood and brain tissue, as demonstrated by the comparative gene expression analysis. Functional enrichment revealed a fundamental impairment in vesicle processing and synaptic maintenance, implying a failure in the cellular mechanisms necessary for neurotransmitter transport and the removal of protein aggregates-both of which play a crucial role in the neurodegenerative advancement of Parkinson's Disease. Non-compensated cellular homeostatic collapse indicated by concurrent decreases in RAB27B (vesicular clearance), UCHL1 (protein recycling), and SLC18A2 (synaptic transmission). NANOG, SNCA, UCHL1, SLC18A2, and ANK1 were found to be important regulatory hubs by topological analysis. This coordinated downregulation offers molecular evidence of an uncompensated systemic homeostatic failure in Parkinson's disease. - Source: PubMed
Publication date: 2026/10/02
Mohammad HafsaSingh AkankshaBansal Dipika - Fibrosis development in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) is a key indicator of disease progression and clinical outcome. Bulk and single-cell transcriptomics on human tissue have advanced understanding of fibrosis progression, but interstudy heterogeneity and limited sample size hinder the identification of consistent and targetable fibrogenic mechanisms. - Source: PubMed
Publication date: 2026/09/16
Maiers Jessica LLiang TiebingGuo TingboCao ShaRamachandran PrakashRaba Teresa JRomeo StefanoJamialahmadi OveisShahrisa Etu ArmanChalasani Naga - MASLD is a disorder linked to lipid metabolism and obesity, increasingly prevalent among sedentary people and leading to hepatic fibrosis. Cyclodipeptides (CDPs) have promising anti-obesogenic and liver-protective potential. CDP treatment was evaluated in a chronic MASLD model using female Wistar rats fed an obesogenic diet, with assessments of insulin resistance, glucose tolerance, liver damage, oxidative stress, and the expression of genes related to metabolic function. MASLD CDP-treated rats showed low visceral adipose tissue (VAT) content, improved insulin responsiveness and glucose tolerance, reduced steatosis, and reversed oxidant stress and the , , and expression. Furthermore, MASLD-related dysregulation of genes involved in lipid metabolism was restored, including vLDL transport (, , and ), β-oxidation (, , and ), lipogenesis ( and ), and fatty acid transport ( and ). In accordance, genes of key signaling pathways were also restored, including , , and , along with fibrosis and inflammation , , , and . In VAT of MASLD animals, crown-like structures and adiposity density were diminished by CDP treatment, with increased expression of genes associated with beige-like adipose tissue remodeling, including , , , , , , , and . Consistently, the UCP1 and PGC-1α protein expression was increased in the VAT of MASLD animals treated with CDPs. The anti-MASLD effects of CDPs were associated with reversal of key pathogenic markers in the liver and VAT, suggesting remodeling of white adipose tissue (WAT) toward a beige-like adipose tissue phenotype. The findings suggest that CDPs may modulate adipose tissue structure and adipogenesis, underscoring their therapeutic relevance for MASLD. - Source: PubMed
Publication date: 2026/07/15
Figueroa-Guzmán CitlaliCampos-Morales Marlene EstefaníaMartínez-Alcantar LorenaHernández-Padilla LauraSánchez-Duarte ElizabethSánchez-Briones Luis AlbertoLópez-Bucio Jesús SalvadorCampos-García Jesús - Hepatology is experiencing major shifts in disease etiologies and is raising demand for multidisciplinary care. However, a globally harmonized framework defining core training content remains lacking. We aimed to develop a globally informed expert consensus framework for the content of core hepatology training, to provide a structured foundation for curriculum development. - Source: PubMed
Publication date: 2026/07/08
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Pugliese NicolaJamialahmadi OveisCesaro ArturoFlagiello ValentinaMancina Rosellina MAghemo AlessioRomeo Stefano