Ask about this productRelated genes to: WNT10B antibody
- Gene:
- WNT10B NIH gene
- Name:
- Wnt family member 10B
- Previous symbol:
- -
- Synonyms:
- WNT-12, SHFM6
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2016-10-05
Related products to: WNT10B antibody
Related articles to: WNT10B antibody
- - Source: PubMed
Publication date: 2026/05/01
Allison Susan J - 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 - Alkylating agents, particularly cyclophosphamide (CY), are known for their high toxicity, which can lead to iatrogenic premature ovarian insufficiency (POI) and infertility in young cancer survivors. Currently, effective prevention and treatment strategies remain limited. Given that chemotherapy induces cellular senescence, we investigated the therapeutic potential of dasatinib (D) and quercetin (Q), a senolytic combination known to eliminate senescent cells. Using a CY-induced murine model of ovarian injury, we found that CY treatment increased the accumulation of senescent cells in the ovaries. The resulting senescence-associated secretory phenotype (SASP) led to a deterioration of the ovarian microenvironment, characterized by increased follicular atresia and a decline in follicle quantity, ultimately culminating in POI. Our findings demonstrate that DQ therapy effectively mitigated CY-induced damage by clearing senescent cells and reducing SASP secretion. Clinically, DQ administration restored sex hormone levels and regularity of the estrous cycle, resulting in an overall increase in follicle numbers across all developmental stages. Furthermore, DQ treatment significantly normalized estrous cyclicity, restoring regular cycles in 60% of the CY+DQ mice compared to only ~15% in the CY-alone group (p<0.0001). RNA sequencing analysis revealed that DQ treatment upregulated Pagr1a, a gene associated with extraembryonic development, while downregulating genes involved in senescence induction (Itgb3, Wnt10b, Vegfa) and immune function (A2m, Ccl21d). These results suggest that senescent cells drive CY-induced ovarian damage and that DQ represents a promising therapeutic strategy for preserving the ovarian reserve and endocrine function in female cancer patients. - Source: PubMed
Publication date: 2026/04/21
Su HuinaMa RuiqiongSu DehuiTan ChengZhu YeYang Xin - Abnormal cell fate transition determines cell instability, which can contribute to disease development. In chronic kidney disease, many renal tubular cells exhibit senescent phenotypes. The fundamental mechanisms of this fate transition remain undetermined. Here we discover that WNT10B, a ligand of the Wnt family, accelerates CKD progression through tubular senescence and proinflammatory microenvironments. Mechanistically, WNT10B mediates metabolic reprogramming from fatty acid oxidation to glycolysis, thus promoting cell senescence and cytokine secretion. Genetic ablation of Wnt10b in male CKD mouse model effectively inhibits cell senescence, inflammation, and fibrogenesis by maintaining metabolic homeostasis. Conversely, Wnt10b transgene in tubular cells aggravates metabolic imbalance, and promotes tubular senescence and fibrogenesis. Forkhead box O6 (FOXO6), a DNA-binding transcription factor, mediates the signal transduction cascade of WNT10B. ChIP-, bulk RNA-, and single-nucleus RNA- sequencing and biological assays verify that FOXO6 transcriptionally modulates PPARA and PKM to control metabolic reprogramming and regulate senescence fate transition in tubular cells. Therefore, the study reveals that WNT10B/FOXO6 signaling controls tubular cell senescence fate, and sheds a light on potential intervention targets to protect against CKD. - Source: PubMed
Publication date: 2026/04/10
Miao JinhuaLi JiemeiMeng PingLi XiaolongHuang JiewuLiang YeLing XianWang XiaoxuShen WeiweiZhou ShanPeng HongquanZhang YunfangLiu YouhuaHou Fan FanZhou Lili - Cancer-related transcriptional dysregulation involves complex, incompletely understood epigenetic mechanisms. Chromatin states (CSs), defined by recurrent co-occurrence patterns of epigenetic marks, provide a comprehensive view for epigenomic landscape. However, current CS analyses often produce excessive subtly distinct states, making functional interpretation difficult. Building on single-cell clustering principles, we developed chromIDEAS to overcome this challenge. Recognizing that epigenetic function is context-dependent, chromIDEAS groups CSs into functionally coherent clusters by jointly analyzing their epigenetic composition and genomic distribution. When applying to THP1 leukemia and CD34+ cells, chromIDEAS consistently identified five CS clusters (CSCs) preserved across both cell types, exhibiting distinct functional coherence. These CSCs captured core transcriptional states (active and repressive) and key genomic compartments (promoters, gene bodies, and TES). Notably, differential CSC analysis revealed that Wnt signaling activation in THP1 cells, a hallmark of leukemogenesis, is mediated by KDM4A-dependent removal of repressive states. Mechanistically, KDM4A depletion restored repressive states on Wnt signaling and impaired proliferation, while WNT10B overexpression effectively rescued this phenotype. Our work establishes chromIDEAS as a pioneering tool for functional CS annotation and uncovers KDM4A-mediated epigenetic derepression in leukemia pathogenesis. These findings highlight critical role of CSs in mechanistic studies and introduce a novel paradigm for epigenetic exploration. - Source: PubMed
Yang LiuLiu ShanLu TingMo ShaokangQi BinYen Kuangyu