STRA6 (mouse, rat)
- Known as:
- STRA6 (mouse, rat)
- Catalog number:
- Y213755
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- STRA6 (mouse rat)
Related genes to: STRA6 (mouse, rat)
- Gene:
- SRRT NIH gene
- Name:
- serrate, RNA effector molecule
- Previous symbol:
- -
- Synonyms:
- Asr2, serrate, ARS2
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-02
- Date modifiied:
- 2016-10-05
- Gene:
- STRA6 NIH gene
- Name:
- stimulated by retinoic acid 6
- Previous symbol:
- -
- Synonyms:
- FLJ12541
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-12-20
- Date modifiied:
- 2017-09-08
Related products to: STRA6 (mouse, rat)
Related articles to: STRA6 (mouse, rat)
- Endothelial cell (EC) senescence is a fundamental driver of atherosclerosis. This review posits that the primary pathogenic role of Stimulated by Retinoic Acid 6 (STRA6) in the endothelium is not its canonical vitamin A transport but its non-classical function as a signaling receptor for its ligand retinol-binding protein 4 (RBP4). In metabolic diseases such as obesity and type 2 diabetes, elevated RBP4 levels engage endothelial STRA6, initiating a signaling cascade independent of retinol nuclear activity. This process begins with STRA6 activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. The signal is then amplified via crosstalk with the NLRP3 inflammasome, promoting the secretion of pro-senescent cytokines like Interleukin-1β (IL-1β) and establishing a senescence-associated secretory phenotype (SASP). This pro-inflammatory microenvironment subsequently triggers a persistent DNA damage response (DDR), leading to p53/p21-mediated cell cycle arrest and establishing the full senescent phenotype. This perspective reframes STRA6 as a key sensor of metabolic stress that converts systemic signals into a local, pro-atherogenic cellular program. The RBP4-STRA6 signaling axis is thereby identified as a novel therapeutic target. Selectively inhibiting this non-classical pathway may provide a new strategy to uncouple metabolic disease from its destructive vascular consequences. - Source: PubMed
Publication date: 2026/02/17
Yuan YongWang JiaZhang YunfangYu YanShi WeichengChen SulianKuang YeFeng Lei - This study aimed to evaluate FOXC1-mediated regulatory mechanisms on gene and protein expression profiles in primary human limbal epithelial cells (pLECs) using siRNA-mediated FOXC1 knockdown under basal conditions and following lipopolysaccharide (LPS) and interleukin-1β (IL-1β)-induced inflammatory conditions. The gene expression related to inflammation, epithelial differentiation, cell proliferation and remodeling, and retinoic acid metabolism was analyzed using qPCR. Corresponding protein levels were assessed through Western blotting and ELISA. FOXC1 silencing significantly downregulated epithelial differentiation markers KRT12 and KRT13 at the mRNA and protein levels ( ≤ 0.045), whereas KRT3 and KRT19 were unaffected. Inflammatory signaling was markedly altered, with a reduced and mRNA expression ( ≤ 0.029), increased IL-1α expression ( ≤ 0.015), and condition-dependent changes in IL-6 and IL-8 protein secretion. was increased at the mRNA level only ( = 0.007). mRNA was consistently reduced ( ≤ 0.022) without corresponding protein changes, while TGF-β protein was increased under non-inflammatory and LPS conditions ( ≤ 0.011). Genes involved in retinoid metabolism, including , , , , , and , were significantly downregulated ( ≤ 0.037), with reduced CRABP2 and RDH10 protein levels ( ≤ 0.017) and a decreased FABP5/CRABP2 ratio under IL-1β stimulation ( = 0.006). FOXC1 knockdown affected proliferation-related genes, with decreased ( = 0.048) and increased ( = 0.006). FOXC1 silencing disrupts epithelial differentiation, inflammatory signaling, retinoid metabolism, and selected proliferation-related pathways at the transcriptional level, with more selective effects on protein levels. Such changes may potentially predispose the ocular surface to lineage instability, fibrosis, and impaired regenerative capacity. - Source: PubMed
Publication date: 2026/02/15
Kundu SwarnaliAmini MaryamStachon TanjaFries Fabian NorbertSeitz BertholdLi ZhenLi ShuailinLiu ShanheHsu Shao-LunSuiwal ShwetaSzentmáry Nóra - Endothelial cell senescence, once considered a passive manifestation of vascular aging, is now recognized as an active driver of atherosclerosis. Senescent endothelial cells (sECs) exhibit distinct morphological and molecular hallmarks, including irreversible growth arrest, altered chromatin structure, and secretion of a pro-inflammatory senescence-associated secretory phenotype (SASP). Through SASP factors, extracellular vesicles, and paracrine signaling, sECs orchestrate a pathological communication network that recruits immune cells, reprograms vascular smooth muscle cells, and compromises endothelial integrity, collectively promoting plaque growth and instability. Central signaling pathways such as the p53/p21 and p16/Rb axes establish the senescent state, while mTOR, NF-κB, and cGAS-STING pathways sustain SASP production. We propose the retinol-binding protein 4 (RBP4) axis as a compelling theoretical framework linking metabolic dysfunction to endothelial senescence. While the TLR4-mediated inflammatory pathway is established, we posit a convergent STRA6-mediated axis that may integrate systemic metabolic stress with local vascular inflammation. Recognizing sECs as "commanders" of the atherosclerotic microenvironment highlights their potential as therapeutic targets. Strategies including senolytics, senomorphics, and upstream pathway inhibition offer promising avenues for attenuating vascular aging. Crucially, our analysis emphasizes the necessity of sex-specific therapeutic approaches, distinguishing between inflamm-aging driven pathologies in men and mechanisms centered on metabolic resilience in women. - Source: PubMed
Publication date: 2026/02/04
Xie FujiaXi ChengBao GuoqingYang BinZheng XiaoyuFu BowenZheng Zhibin - Dry eye following eye surgery represents a common obstacle to recovery and general life satisfaction. Pranoprofen, an anti-inflammatory drug, frequently co-administered with adjuvants such as sodium hyaluronate and polyvinyl alcohol, represents a common response to dry eye. The relative efficacy of pranoprofen and sodium hyaluronate compared with pranoprofen and polyvinyl alcohol as a treatment for dry eye and as an aid to corneal endothelial function will be ascertained. - Source: PubMed
Bi HuatingXu Fang - [This corrects the article DOI: 10.3389/fonc.2020.579561.]. - Source: PubMed
Publication date: 2025/12/19
Muñiz-Hernández SaéVelázquez-Fernández Jesús BernardinoDíaz-Chávez JoséMondragón-Fonseca OmarMayén-Lobo YeryeOrtega AlbertoLópez-López MarisolArrieta Oscar