Ask about this productRelated genes to: WNT7B Blocking Peptide
- 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 Blocking Peptide
Related articles to: WNT7B Blocking Peptide
- 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 - Restoring wild-type p53 has long been viewed as a direct route to cancer therapy, yet clinical efforts have delivered only modest benefit. Here, we show that a critical but underappreciated aspect of p53 biology is its ability to form biomolecular condensates that can be manipulated to selectively enhance specific properties. The modest benefit of current p53-dependent therapeutics stems, in part, from the dual nature of p53; alongside canonical tumor-suppressor genes, wild-type p53 also boosts neuron-associated genes that can foster malignancy. Using live-cell super-resolution imaging we find that endogenous p53 nucleates novel ∼50-nm condensates. Coactivators reinforce droplets, whereas antagonists dissolve them, revealing a previously unappreciated regulatory layer. Guided by these mechanisms, we engineered liquid-liquid phase separation (LLPS)-enhanced p53 constructs with greater condensation propensity (LLPSEp53s). These condensates act as a mesoscale hub that biases promoter occupancy and partner selection. Intriguingly, LLPSEp53s tilt the transcriptome, preferentially strengthening tumor-suppressive transcription while dampening neuro-oncogenic outputs. LLPSEp53s suppress proliferation across multiple cancer cell lines, including those refractories to wild-type p53, and curtails melanoma growth in immunocompetent mice without added toxicity. Our findings establish phase separation as an adjustable layer of p53 target selectivity and highlight condensate engineering as a tractable strategy to unleash the full antitumor potential of p53. - Source: PubMed
Publication date: 2026/03/25
Liu YanJia HaoranGuan XueyingGuo JianshengWang JiaweiXiang SiminChen JiayunLiu YiFanLi YongHaoWang GuoZhen - Osteoarthritis (OA) of the ankle is a disabling and understudied disease, most commonly emerging posttraumatically after ankle fractures (PTOA). Despite its prevalence, the molecular mechanisms linking joint trauma to ankle OA are not well defined, limiting opportunities for early intervention. This study characterized synovial transcriptional changes to identify early molecular drivers of disease onset in fracture-induced ankle PTOA. - Source: PubMed
Publication date: 2026/03/23
Matthias JuliaDavid Michael ABuckley Sara EStark Samuel DAustin Nicholas AZona Nathaniel EZuscik Michael JHunt Kenneth J