LIX CXCL5 (93a.a.), Mouse
- Known as:
- LIX CXCL5 (93a.a.), Mouse
- Catalog number:
- Z02851-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- LIX CXCL5 (93a..) Mouse
Related genes to: LIX CXCL5 (93a.a.), Mouse
- Gene:
- CXCL5 NIH gene
- Name:
- C-X-C motif chemokine ligand 5
- Previous symbol:
- SCYB5
- Synonyms:
- ENA-78
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-03
- Date modifiied:
- 2016-10-24
- Gene:
- MIR193A NIH gene
- Name:
- microRNA 193a
- Previous symbol:
- MIRN193, MIRN193A
- Synonyms:
- hsa-mir-193, hsa-mir-193a
- Chromosome:
- 17q11.2
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-30
Related products to: LIX CXCL5 (93a.a.), Mouse
Related articles to: LIX CXCL5 (93a.a.), Mouse
- This study focused on investigating the causal relationship between inflammatory factors and Type 2 Diabetes Mellitus (T2DM) and identifying metabolites associated with inflammatory factors as potential mediators. - Source: PubMed
Publication date: 2026/07/01
Li JiaxinLi XingLi YuanZhou NingYi HuijuanFan QiWang BoTian YushiNi Xiuqin - Pulmonary arterial hypertension (PAH) is a progressive cardiopulmonary disorder marked by pulmonary vascular remodelling and vessel loss, paradoxically occurring despite high VEGF signaling. While VEGF/VEGFR pathways are implicated in disease pathogenesis, their role in endothelial and immune cell crosstalk remains poorly understood. Placental growth factor (PlGF), a VEGF family member that selectively binds VEGFR-1, exerts pro-inflammatory effects in other pathological contexts, but its contribution to PAH pathophysiology is unclear. This study explored the contribution of PlGF to endothelial activation and immune-mediated vascular remodelling in PAH. - Source: PubMed
Publication date: 2026/07/01
Ha My NgocThuillet RaphaëlOttaviani MinaNormand CorinneRobert FabienSurbier MaximeSitbon OlivierHumbert MarcBoucly AthénaïsSavale LaurentGorth Deborah JPetit VanessaTu LyGuignabert Christophe - Inflammaging, a term describing the chronic, low-grade inflammatory state associated with aging, is implicated in various age-related diseases. Inflammatory proteins are central to inflammaging and bone-muscle communication. This study sought to investigate the role of inflammatory proteins as potential myokines and osteokines in the context of sarcopenia-osteoporosis crosstalk using a convenient and efficient method, Mendelian Randomization (MR). - Source: PubMed
Publication date: 2026/06/29
Liu MingchongWang JiamingFu XiaoYang ChensongZhao JingleiSun Guixin - Background Metabolic disorders associated with elevated saturated fatty acids are linked to chronic inflammatory diseases, including periodontitis, yet the mechanisms connecting lipotoxic stress to gingival inflammation remain unclear. This study investigated how palmitate-induced metabolic stress affects purinergic signaling, mitochondrial function, and endoplasmic reticulum (ER) stress in murine gingival fibroblasts (mGF), and whether adenosine modulates these effects. Methods mGF were treated with BSA control, palmitate, IL-1β, or palmitate plus IL-1β, followed by bulk RNA sequencing, Seahorse metabolic analysis, biochemical assays, and transmission electron microscopy. Results Palmitate suppressed expression of key adenosine-generating ectoenzymes and purinergic signaling genes, including Cd73 (Nt5e), Cd39 (Entpd1), Adk, Ada, and adenosine receptors. Concurrently, palmitate amplified IL-1β-induced inflammatory mediators such as Cxcl1, Cxcl2, Cxcl5, Ccl2, and Il6. Gene ontology analysis demonstrated enrichment of pathways related to innate immune activation, oxidative stress, mitochondrial dysfunction, ER stress, and purine metabolism. Palmitate also induced intracellular lipid accumulation and mitochondrial dysfunction, evidenced by reduced NAD+/NADH ratio, increased mitochondrial reactive oxygen species (ROS), elevated protein oxidation, and increased proton leak despite enhanced electron transport chain protein expression. Ultrastructural analyses revealed swollen mitochondria, ER expansion, and increased ER-mitochondrial associations. Mechanistically, palmitate activated the Perk-eIF2α-Atf4 ER stress pathway, increasing phosphorylation of Perk and eIF2α and elevating Atf4 expression. Extracellular adenosine attenuated mitochondrial ROS accumulation, reversed Perk and Atf4 activation, improved mitochondrial respiration, and preserved ER and mitochondrial ultrastructure. Conclusions Palmitate disrupts the Cd73-adenosine axis while promoting mitochondrial dysfunction, oxidative stress, and Perk-mediated ER stress in gingival fibroblasts. Adenosine signaling protects against lipotoxic-induced ER stress, highlighting the Cd73-adenosine pathway as a potential therapeutic target in metabolically driven periodontal inflammation. - Source: PubMed
Publication date: 2026/06/15
Dawson ShantieceBatan SoniaAdams NinaBombin SergeiRamos-Junior Erivan SMorandini Ana Carolina - In this exploratory study with a limited sample size, we aimed to investigate inflammation-related proteins in the aqueous humor of high myopia (HM) patients, analyze their correlations with ocular parameters, and screen for potential biomarkers. - Source: PubMed
Publication date: 2026/06/23
Yang MingWu WeizhenDong NingLi Min