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)
- 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
Xu XinyiShi YuTacke FrankWai-Sun Wong VincentLi WenhaoSebastiani GiadaNewsome Philip NRomero-Gomez ManuelPan CalvinCastera LaurentChai JinKim WonValenti LucaYilmaz YusufWin Khin MaungXu XianbinOcama PonsianoGhazinyan HasmikAl Mahtab MamunHamid SaeedLesmana Cosmas Rinaldi ARomeo StefanoCastellanos Fernandez Marlen IvonYu XiaLuukkonen Panu KTakahashi HirokazuCharatcharoenwitthaya PhunchaiBoursier JeromeCua Ian HomerDao Hang VietSpearman C WendyBandara Dassanayake Subhashin UdithaAyurzana MunkhjargalAghayeva GulnaraMuthiah Mark DhineshMendez-Sanchez NahumStedman Catherine AnnAlswat KhalidSharara Ala IDebzi NabilLeite Nathalie CarvalhoAlkhatry Maryam Salemvan Kleef Laurens ABarakat SalmaAl-Busafi Said AAgyei-Nkansah AdwoaFouad YasserGracia-Sancho JordiLupsor-Platon MonicaRyan John DChan Wah-KheongCortez-Pinto HelenaMandorfer MattiasDuseja AjayPapatheodoridis GeorgiosFrancque Sven MByrne Christopher DTargher GiovanniGeorge JacobZheng Ming-Hua - Fatty pancreas is a metabolically active ectopic fat depot, but its cardiometabolic implications have been assessed using heterogeneous thresholds. We investigated the association of fatty pancreas, quantified using MRI-derived proton density fat fraction (PDFF) and categorised according to 2026 international consensus thresholds, with prevalent and incident type 2 diabetes (T2D), chronic kidney disease (CKD) and major adverse cardiovascular events (MACE). - Source: PubMed
Pugliese NicolaJamialahmadi OveisCesaro ArturoFlagiello ValentinaMancina Rosellina MAghemo AlessioRomeo Stefano - Mild hypothermia provides potent neuroprotection in experimental ischemic stroke, however, its implementation in awake stroke patients is hampered by the induction of intense shivering and inconsistent body temperature control. Pharmacological activation of peripheral/peritoneal TRPV1 channels with non-pungent capsinoids offers a means to induce hypothermia while minimizing TRPV1 activation in the injury region. We tested whether capsinoid-mediated mild hypothermia, initiated within the post-stroke period, reduces brain injury and improves functional outcomes in aged mice. - Source: PubMed
Publication date: 2026/06/10
Andersohn Alexander PKim SodamWu TingDoan Andrea NCantrell Charles LJarret Robert LKim Gab SMarrelli Sean P - Esophageal squamous cell carcinoma (ESCC) is characterized by immune evasion and poor clinical outcomes. Autophagy has been implicated in tumor-immune interactions, but the molecular factors linking autophagy-associated processes to immune modulation in ESCC remain incompletely defined. We analyzed PSD3 expression in ESCC tissues and its association with prognosis and MHC-I-related molecules. Protein interactions were assessed by co-immunoprecipitation. Autophagy-associated marker changes, autophagic flux, total MHC-I protein levels, and immune cell infiltration were evaluated following PSD3 knockdown in murine and human ESCC models using Western blotting, tandem fluorescent LC3 reporter assays, immunohistochemistry, and single-cell RNA sequencing. Epistasis analysis was performed by silencing ATG7 following PSD3 knockdown. PSD3 was upregulated in ESCC and associated with unfavorable prognosis. PSD3 knockdown was accompanied by changes in autophagy-associated markers and reduced autophagosome abundance. In KYSE150 cells, tandem fluorescent mCherry-eGFP-LC3B analysis showed that PSD3 silencing impaired autophagic flux. PSD3 co-immunoprecipitated with ATG7, BAG3 and TBK1, supporting its association with autophagy-related protein complexes. PSD3 knockdown increased total MHC-I protein levels and was associated with enhanced immune cell infiltration in syngeneic tumor models. Furthermore, ATG7 silencing following PSD3 knockdown selectively restored HLA-E expression, while HLA-ABC and HLA-F showed no clearly distinguishable change. These findings support a working model in which PSD3 is linked to autophagy-associated immune modulation in ESCC. While additional studies are required to define pathway hierarchy and antigen-presentation function more directly, PSD3 emerges as a candidate molecular node for further mechanistic and translational investigation. - Source: PubMed
Publication date: 2026/05/18
Luo ShujuanNurbahati AididarCai BangwuCui HongPeng TianyuanWang WeiLi HuifangChen JiaoLiu QingLu XiaomeiZheng Shutao