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)
- Exposure to natural environments is thought to benefit mental and physical health, but current evidence is mixed, and underlying mechanisms remain unclear. Considering the joint biodiversity, climate, and health crises, a better understanding of the interplay between individuals and their environment is imperative. This study aimed to (1) identify Body Mass Index (BMI) trajectories in the Scania Public Health Cohort (SPHC), (2) characterise trajectories in terms of sociodemographics, lifestyle, health and living environments, (3) study the associations between natural dimensions of residential environment and BMI trajectories. The SPHC was established in southern Sweden in 2000. Participants ( = 13 581 at baseline, 18–80 years old) responded to four surveys (2000–2016), including sociodemographic, lifestyle and health questions. Residential coordinates were linked to the Scania outdoor Environment Database, which comprised perceived sensory dimensions of residential areas, eight dimensions of the outdoor environment that have previously been identified as important to support people’s health. An adapted version of the Perceived Sensory Dimension Score (PSD3-score) was computed by summing up three dimensions related to the natural environment. Sex-specific BMI trajectories, identified using group-based trajectory modelling, were compared using adjusted multinomial regression. Five BMI trajectories were identified with similar shapes in men and women. Two trajectories started in the normal/overweight categories and were relatively stable over time, while the other three were close to or above the commonly used threshold for obesity. Overall, more favourable socioeconomic and lifestyle factors were observed within non-obese trajectories. The PSD3-score varied geographically across Scania, but for the selected environmental characteristics, little differences were observed in relation to BMI trajectories. For this population, our findings suggest that lifestyle and socioeconomic factors are more important than outdoor environment features for the long-term bodyweight and obesity development. - Source: PubMed
Publication date: 2026/04/17
Rebouillat PaulineMattisson KristofferGefenaite GiedreÖstergren Per-OlofNilsson Peter MBjörk Jonas - BACKGROUNDMetabolic dysfunction-associated steatotic liver disease (MASLD) has a substantial inherited component. Rare variants in apolipoprotein B gene (APOB) have been implicated in susceptibility to liver steatosis, but their role in disease progression and outcomes is unclear.METHODSWe investigated APOB rare variants in a case-control cohort of people with advanced MASLD versus healthy controls (n = 510 and 261, respectively), a family-based study (n = 43 and literature meta-analysis), the Million Veteran Program (MVP) cohort (n = 94,885), and the UK Biobank (UKBB) (n = 417,657).RESULTSIn the clinical cohort, APOB variants were enriched in people with advanced MASLD (OR 13.8, 95% CI: 2.7-70.7, P = 0.002) and associated with lower circulating lipids, but higher MASLD activity and fibrosis (P < 0.05). In the family study, APOB variants segregated with hepatic steatosis and fibrosis (P < 0.05). Cross-ancestry meta-analysis of the study cohorts yielded pooled ORs for cirrhosis and hepatocellular carcinoma (HCC) of 1.82, 95% CI: 1.33-2.49 and 3.53, 95% CI: 2.09-5.98, respectively. Variants affecting specifically ApoB100 had a 3-fold greater effect on hepatic lipid metabolism compared with those impairing also ApoB48 and were specifically protective against coronary artery disease (P < 0.05). The variants affected cirrhosis risk similarly, but ApoB48/100 had a larger effect on HCC (P < 0.05).CONCLUSIONSRare APOB variants predispose individuals to advanced MASLD and HCC, with distinct contributions from disrupted VLDL and chylomicrons secretion. These findings highlight the interplay between hepatic and intestinal lipid handling, suggesting that APOB genotyping may enhance MASLD risk stratification and patient identification.FUNDINGEuropean Union, Italian Ministry of Health, Swedish Research Council, Veterans Health Administration, NIH. - Source: PubMed
Publication date: 2026/02/10
Mureddu MatteoPelusi SerenaJamialahmadi OveisVujkovic MarijanaMiano LorenzoEidgah Torghabehei HadiRonzoni LuisaMalvestiti FrancescoSaracino MarcoPeriti GiuliaMoretti VittoriaTeerlink Craig CLynch Julie ATsao Philip SJohnson Josephine PLa Mura VincenzoDilena RobertinoAlqahtani Saleh ACherubini Alessandro Russo Francesco PaoloD'Ambrosio RobertaFraquelli MirellaPetta SalvatoreMiele LucaVespasiani-Gentilucci UmbertoBugianesi ElisabettaMancina Rosellina MParini PaoloPrati DanieleChang Kyong-MiSchneider Carolin VRomeo StefanoValenti Luca Vc - - Source: PubMed
Publication date: 2025/11/15
Romeo Stefano - - Source: PubMed
Publication date: 2025/10/07
Zhang DongdongZhang PeiJing RanChen ZiweiCai Ming - Metabolic-dysfunction-associated steatotic liver disease (MASLD, previously known as non-alcoholic fatty liver disease or NAFLD) is a prevalent and heterogeneous condition affecting nearly 30% of the global population. MASLD is defined as excessive hepatic lipid accumulation with at least one feature of insulin resistance, with potential progression to metabolic dysfunction-associated steatohepatitis, cirrhosis and hepatocellular carcinoma. The disease often coexists with insulin resistance and cardiovascular and chronic kidney diseases. Human genetics has shed light on MASLD predisposition and its causal association with type 2 diabetes and insulin resistance, enabling the field to progress towards precision-medicine therapeutics. Convergent selection of somatic mutations in genes involved in glucose and lipid metabolism in cirrhotic livers suggests adaptive responses to gluco-lipotoxicity that influence end-stage liver disease. Recently, two distinct types of MASLD, with specific clinical trajectories, were identified on the basis of partitioned polygenic risk scores. Future studies are needed to integrate this knowledge, enabling earlier detection, risk stratification and targeted therapies. - Source: PubMed
Publication date: 2025/10/17
Mancina Rosellina MValenti LucaRomeo Stefano