Ask about this productRelated genes to: Wnt1 antibody
- Gene:
- WNT1 NIH gene
- Name:
- Wnt family member 1
- Previous symbol:
- INT1
- Synonyms:
- -
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-18
Related products to: Wnt1 antibody
Related articles to: Wnt1 antibody
- Angiogenesis is a pivotal process for tumor progression and metastasis in non-small cell lung cancer (NSCLC). However, the molecular mechanisms by which WNT1-inducible signaling pathway protein 3 (WISP-3) contributes to NSCLC angiogenesis remain poorly defined. This study investigated the role of WISP-3 in regulating pro-angiogenic signaling in lung adenocarcinoma (LUAD) cells. Conditioned medium from H1299 and A549 cells treated with recombinant WISP-3 (0-100 ng/mL) significantly and dose-dependently enhanced the tube formation of human umbilical vein endothelial cells (HUVECs). WISP-3 selectively upregulated platelet-derived growth factor A (PDGF-A) expression at both mRNA and protein levels in NSCLC cell lines, while other angiogenic factors remained unaffected. Notably, knockdown of PDGF-A using siRNA markedly abolished WISP-3-induced HUVEC tube formation, confirming PDGF-A as a critical mediator in this process. Mechanistically, WISP-3 rapidly triggered the phosphorylation of p38 and JNK signaling pathways. These activations led to the phosphorylation of the transcription factor c-Jun, which in turn promoted PDGF-A gene expression. Pharmacological inhibition of p38 (Adezmapimod), JNK (SP600125), or c-Jun (T-5224) effectively suppressed WISP-3-induced c-Jun activation, PDGF-A expression, and subsequent angiogenesis. Collectively, our findings identify a novel WISP-3/p38-JNK/c-Jun/PDGF-A signaling axis that drives vascular remodeling in NSCLC. Targeting WISP-3 or its downstream effectors may represent a promising therapeutic strategy for anti-angiogenic treatment in lung cancer. - Source: PubMed
Publication date: 2026/03/25
Chang En-MingLin Syuan-LingCheng Ching-YuanTang Chih-HsinChen Yu-ChenLee Chiang-WenLin Chih-Yang - Electroacupuncture (EA) combined with neural stem cell transplantation (NSCT) represents a promising therapeutic strategy for neurological recovery after ischemic stroke. This study investigated the enhanced effects of EA at 'Quchi' (LI11) and 'Zusanli' (ST36) acupoints combined with NSCT on motor function and neurogenesis in a rat middle cerebral artery occlusion (MCAO) model, and explored the underlying tsRNA-associated molecular changes. - Source: PubMed
Publication date: 2026/04/24
Wang SinuoShi DanQiu YuxiWang WenjuCao YajunWu BaoLiu WeilinTao JingYang Minguang - - Source: PubMed
Publication date: 2026/04/17
Sahar AtiyaMajid HayaDahalia MansiIslam Sajad UlNidhi - Glucagon-like peptide-1 (GLP-1) medicines improve metabolic liver disease through weight-loss-dependent and -independent actions. Here, we interrogated semaglutide's action in mice with metabolic dysfunction-associated steatohepatitis (MASH). In Glp1r mice resistant to GLP-1RA-induced weight loss, semaglutide improved steatosis, fibrosis, and immune remodeling. GEM-X Flex-seq localized Glp1r expression to pericentral liver sinusoidal endothelial cells (ECs) (LSECs) and CD8 T cells. EC Glp1r deletion in Glp1r mice or AAV8-Cre-mediated hepatic EC Glp1r knockdown substantially abrogated semaglutide's hepatic benefits despite preserved weight loss. Transcriptomic profiling revealed that Glp1r LSECs adopt a stress-responsive phenotype in MASH that is reversed by semaglutide. Glp1r LSECs function as dominant contributors to semaglutide-regulated circuits linked to injury and repair involving VWF, SELE, CEACAM, and BMP. Molecular profiling revealed semaglutide-coordinated transcriptional and protein-level reversal of disease signatures. Together, the data using mouse models of MASH reveal an EC-specific, weight-loss-independent, semaglutide-regulated, GLP-1R-dependent intrahepatic network for improving liver health. - Source: PubMed
Publication date: 2026/04/14
Gonzalez-Rellan Maria JRiobello CristinaFang SusannaMartins da Silva EloisaKoehler Jacqueline AShang RuiHammoud RolaCao XieminVarela-Rey MartaDrucker Daniel J - In the sea urchin embryo, as many as ten Wnts are expressed by cells that undergo gastrulation movements. Here, Wnt1, 5, 6, 7, 8 and 16 are examined to learn details of expression and function over time using results from a temporal scRNA-seq analysis coupled with hybridization chain reaction in situ analysis in which multiple wnt genes are localized simultaneously in the same embryo. The data reveal that many cells express two or three wnt genes at the same time. A single sharp boundary of expression is seen just lateral to the blastopore. Other boundaries of expression are graded and change over developmental time. Functionally, experiments show that Wnts control expression and/or patterning of other wnt genes, and they control expression of marker genes during and following invagination of the archenteron. Stomodeum formation also requires Wnt signaling, indicating that the entire gut uses Wnt signaling for diversification of endodermal fates. - Source: PubMed
Publication date: 2026/04/13
Miranda EstherSlota-Burtt LeslieBerrio AlejandroBardhan AnirbanDeiters AlexanderWray Gregory ACroce Jenifer CMcClay David R