Ask about this productRelated genes to: WNT7B antibody
- Gene:
- WNT7B NIH gene
- Name:
- Wnt family member 7B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2016-10-05
Related products to: WNT7B antibody
Related articles to: WNT7B antibody
- statistics fine-mapping methods offer advantages over classical methods, including avoiding data-sharing constraints and improved modelling of correlated variables and sparse effects. However, its performance has not been comprehensively evaluated in breast cancer using real-world data. Previous multinomial stepwise regression (MNR) fine-mapping analyses for breast cancer identified 196 credible sets. Here, we apply summary statistics fine-mapping, compare methods, and assess parameters influencing performance. Using summary statistics from the Breast Cancer Association Consortium, we compared , and to published MNR results across 129 regions. Performance was assessed by recall using in-sample and out-of-sample LD. Discordant credible sets were examined for technical factors, and target genes were defined using the INQUISIT pipeline. showed the closest agreement with MNR. Results varied across regions depending on the assumed number of causal variants ( ), with higher values reducing recall and no single maximising performance. At optimal per region, identified 8,192 CCVs in 244 credible sets, with recall of 88%, 86%, and 72% for overall, ER-positive, and ER-negative breast cancer. Thirty MNR sets were missed. Discordance was partially explained by allele flips, imputation quality, and array heterogeneity. Fifty-two MNR-identified genes, including and were not recovered, while additional candidate genes were identified. Using out-of-sample LD reduced recall by 3% but identified novel variants. Fine-mapping results vary across methods, and no single approach is sufficient. The choice of strongly influences results, and combining analytical approaches with functional validation can improve causal variant identification. - Source: PubMed
Publication date: 2026/04/22
O'Mahony Denise GBeasley JonathanZanti MariaDennis JoeDutta DiptavoKraft PeterKristensen VesselaChenevix-Trench GeorgiaEaston Douglas FMichailidou Kyriaki - Transition from the transient hyaloid vasculature to the mature retinal vascular network is a critical step in mammalian eye development. While WNT7B signaling in endothelial cells regulates programmed hyaloid vessel regression, the specific receptors and downstream mechanisms remain poorly defined. Here, we identify GPR124, a ligand-specific co-receptor for WNT7A/B, as a key regulator of this process. Using an endothelial-specific, tamoxifen-inducible Gpr124 knockout mouse model, we show that loss of GPR124 in hyaloid endothelium markedly impairs postnatal hyaloid vessel clearance. Notably, GPR124 function in the developing eye was highly compartment-specific: although crucial for hyaloid vessel regression, it was dispensable for retinal angiogenesis, despite being expressed in both vascular beds. Gpr124 deletion led to downregulation of several established WNT target genes in hyaloid endothelial cells, consistent with a role for GPR124 in mediating WNT/β-catenin signaling, as previously shown in brain endothelium. While GPR124 was not required for induction of isolated apoptotic events in hyaloid vessels, it promoted segmental vessel regression, characterized by linear clusters of apoptotic endothelial cells. Single-cell RNA sequencing of hyaloid endothelial cells, combined with immunostaining, revealed transcriptional changes consistent with partial endothelial-mesenchymal transition (EndMT). Our findings identify GPR124 as a key mediator of hyaloid vessel regression and suggest that GPR124-dependent WNT/β-catenin signaling and EndMT may contribute to vascular remodeling during ocular development. - Source: PubMed
Publication date: 2026/04/29
Hannig LauraHeiden RobinErgün SüleymanBraunger Barbara MVallon Mario - Regulatory T cells (Tregs) are essential for maintaining immune homeostasis by suppressing excessive activation of effector T cells. Although several mechanisms of Treg-mediated suppression have been described, the molecular signals that contribute to this regulation remain incompletely understood. WNT signaling, best known for its roles in development and tissue homeostasis, has recently emerged as an important regulator of immune function, but its contribution to Treg-mediated immune suppression is largely unknown. Here, we show that Tregs preferentially express multiple canonical WNT ligands, including WNT2B, WNT3, WNT7B, and WNT10B, compared with conventional CD4 T cells. These WNT proteins were detected intracellularly in Tregs, and WNT2B and WNT3 were actively secreted into culture supernatants. Conventional CD4 T cells expressed Frizzled receptors capable of sensing these ligands. Pharmacological inhibition of canonical WNT signaling using the antagonist mDKK-1 enhanced CD4 T cell activation and proliferation and increased pro-inflammatory cytokine expression, while anti-inflammatory IL-10 remained unchanged. Together, these findings identify Tregs as a source of canonical WNT ligands and suggest that Treg-derived WNT signaling contributes to the suppression of effector CD4 T cell responses. This work reveals a previously underappreciated pathway through which Tregs regulate immune activity and identifies WNT signaling as a potential target for modulating inflammatory immune responses. - Source: PubMed
Publication date: 2026/04/14
Singh Parihar KashishNiemeier Margaret RIfergan Igal - Inflammation critically determines dental pulp regenerative outcomes, with dental pulp stem cells (DPSCs) orchestrating tissue homeostasis through differentiation, self-renewal and immunomodulation processes dynamically regulated by Wnt/β-catenin and NF-κB signaling crosstalk. Given the rising therapeutic potential of Wnt-targeted interventions in dental tissue engineering, elucidating these molecular interactions under pathological conditions is essential for developing regenerative therapeutics capable of simultaneously promoting reparative dentinogenesis while resolving inflammatory insults. - Source: PubMed
Publication date: 2026/04/24
Rajasekar VHuang MAbdalla M MNeelakantan PYiu C K Y - Cochlear hair cells are crucial for sound transduction and are precisely oriented by planar cell polarity (PCP). Wnt proteins direct PCP in vertebrates, but their roles in regulating cochlear PCP remain unclear. Here, we inhibited Wnt secretion by ablating Wntless in the cochlear epithelium and found shortened cochlea, mild hair cell misorientation and mislocalization of PCP proteins, Fzd6 and Dvl2, representing defects less severe than classic PCP mutants. Computational cell-communication analysis predicted that candidate Wnts from the cochlear epithelium (Wnt5a, Wnt7a, Wnt7b) and surrounding periotic mesenchyme (Wnt5a) act on developing hair cells. Deletion of Wnt5a, Wnt7a, and Wnt7b additively shortened the cochlea without causing hair cell misorientation or mislocalization of PCP proteins. Moreover, deletion of Wnt5a alone in the periotic mesenchyme failed to cause PCP defects. However, ablating both epithelial and mesenchymal Wnts caused a severely shortened cochlea with apically malrotated hair cells devoid of polarized core PCP proteins. Thus, Wnts serve as global instructive cues directing cochlear outgrowth and hair cell polarization, with remarkable redundancy of distinct Wnts across epithelial and mesenchymal compartments to ensure a fail-safe developmental program. - Source: PubMed
Publication date: 2026/03/27
Kishimoto IppeiDavid Abel PRose Kevin PNarasimhan BalasubramanianEfron BradleyBillings Sara ESu Erin LDong WuxingJan Taha AHertzano RonnaCheng Alan G