WNT7A antibody
- Known as:
- WNT7A (anti-)
- Catalog number:
- orb101127
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- WNT7A antibody
Related genes to: WNT7A antibody
- Gene:
- WNT7A NIH gene
- Name:
- Wnt family member 7A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2016-10-05
Related products to: WNT7A antibody
Related articles to: WNT7A antibody
- How extracellular matrix organization shapes signaling-associated transcription during skeletal development remains incompletely understood. Using CRISPR-Cas9-edited human urine-derived stem cells, we show that loss of the laminin gene preserves canonical chondrogenic marker induction but impairs three-dimensional spheroid morphogenesis and disrupts pericellular matrix architecture. Bulk RNA sequencing and weighted gene co-expression network analysis identify a -associated transcriptional module enriched for embryonic limb morphogenesis genes, with and as inversely correlated hub genes. Projection onto a human fetal hindlimb atlas localizes / co-expression to the endothelial compartment, while and map to endothelial and chondrocyte populations, respectively, suggesting a spatially organized signaling axis partially conserved in mouse. Pharmacologic β-catenin stabilization partially restores selected module transcripts, and endothelial-conditioned medium selectively rescues and in -KO cultures. Together, these data link -dependent matrix organization to a WNT-associated transcriptional program and identify endothelium as a candidate niche source. - Source: PubMed
Publication date: 2026/07/10
Schulz AlexanderBrockmann Emily MUebe SteffenEkici Arif BThiel Christian T - Head and neck squamous cell carcinoma (HNSCC) has a poor prognosis, and the extracellular matrix (ECM) plays a key role in tumor progression, emerging as a potential biomarker for prognosis and therapy. - Source: PubMed
Publication date: 2026/06/22
Chen WenwenLiu Yehai - : Cardiac allograft fibrosis is an important limiting factor for long-term graft survival. However, the fibrotic process operating in patients with acute cellular rejection (ACR) remains unclear. We aimed to identify altered serum mRNAs related to cardiac fibrosis in patients with ACR and to evaluate their diagnostic accuracy in detecting rejection episodes. : We included 40 serum samples from recipients of transplants undergoing routine endomyocardial biopsies. : Several altered mRNAs associated with fibrosis were detected in patients with ACR. Specifically, the activators of fibroblasts and myofibroblasts (, and ), TGF-β signaling ( and ) and WNT signaling ( and ) pathways were significantly different when we compared grade ≥ 2R ACR and/or grade 1R ACR groups with the nonrejection group. Furthermore, and presented an area under the curve value > 0.90 for identifying patients with moderate and severe grades of cardiac rejection. : In conclusion, we found alterations in the relative abundance of circulating activators of fibroblasts and myofibroblasts, such as or , as well as in major profibrotic pathways, including TGF-β and WNT signaling, especially in clinically relevant cardiac rejection. These findings may contribute to improving the surveillance of patients with cardiac transplant and provide new therapeutic strategies for targeting fibrosis process activation. - Source: PubMed
Publication date: 2026/06/18
Delgado-Arija MartaPérez-Carrillo LorenaGonzález-Torrent IreneGenovés PatriciaGiménez-Escamilla IsaacBenedicto CarlotaMartínez-Dolz LuisPortolés ManuelTarazón EstefaníaRoselló-Lletí Esther - Frizzled4 (FZD4) is a receptor for Norrin and WNT7A/B ligands, is expressed in endothelial cells (ECs), is required for endothelial blood-central nervous system (CNS) barrier function as well as CNS angiogenesis, and transduces β-catenin-dependent signaling. Despite its fundamental importance in neurovascular biology, including as a drug target, the molecular mechanisms governing FZD4 regulation remain poorly understood. Here, we employed proximity biotinylation to identify proteins that regulate FZD4. We identified ATPase plasma membrane Ca transporting 1 (ATP2B1, also known as PMCA1) as a FZD4 proximity interactor. Functional analyses revealed that ATP2B1 depletion increased EC Ca, activated NFAT, and significantly attenuated Norrin/Frizzled4 signaling. Endothelial-specific Atp2b1 deletion caused CNS vascular phenotypes consistent with compromised Norrin/Frizzled4 signaling. This study identifies ATP2B1 as a regulator of Norrin- and WNT7A/B-induced FZD4 signaling and suggests that in pathological contexts with elevated EC Ca-levels, EC function may be modulated by suppression of β-catenin-dependent signaling. - Source: PubMed
Publication date: 2026/06/25
Jo Ha-NeulKiffmeyer ElizabethZhang ChiZhang LinglingOdame EmmanuelDinh Quynh ChauLevey JacklynHowe MirandaRoux Kyle JFischer Klaus-DieterChen ZheJunge Harald J - This study aimed to identify shared genetic signatures and potential molecular mechanisms linking acute ischemic stroke (AIS) and diabetes by analyzing their transcriptomic profiles. We sought to characterize differentially expressed non-coding RNAs (ncRNAs) and mRNAs, elucidate their functional pathways, and construct regulatory networks to uncover cross-talk between these conditions. - Source: PubMed
Xu CongXu YonghongWang Guangming