Ask about this productRelated genes to: WNT5B Blocking Peptide
- Gene:
- WNT5B NIH gene
- Name:
- Wnt family member 5B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-18
- Date modifiied:
- 2016-10-05
Related products to: WNT5B Blocking Peptide
Related articles to: WNT5B Blocking Peptide
- Giant cell tumor of bone (GCTB) induces overproduction of bone-resorbing osteoclasts through receptor activator of nuclear factor kappa B ligand (RANKL), leading to bone resorption and destruction. Consequently, denosumab, a neutralizing antibody against RANKL (a cytokine essential for osteoclast induction), is used to treat patients with GCTB. However, the activity of bone formation in GCTB remains poorly understood. Here, we show that GCTB antagonizes bone formation by expressing WNT5B, which inhibits bone formation. - Source: PubMed
Publication date: 2026/03/23
Shimada MasakiTsuyama TomonoriYoshimura NaotoTateyama MakotoMatsunaga HidetoHomma FukaDainobu KasumiTian XiaoTakata ShuTakata KoseiTanimura ShuntaroShibata YutoMaeda KazuyaKawakami JunkiArima TakahiroKarasugi TatsukiTokunaga TakuyaSato HiroMasuda TetsuroHisanaga SatoshiKai YukiKarata SoichiroGoshogawa HikaruTajiri RuiYamada HibikiUehara YusukeNakamura TakayukiYugami MasakiSugimoto KazukiYonemitsu RyujiTanoue HironoriYamagata KazuyaMiyamoto Takeshi - The wnt gene family encodes a group of highly conserved secreted glycoproteins that play essential roles in vertebrate development, including tissue patterning, cell differentiation, and gonadal regulation. However, the genomic organization, evolutionary dynamics, and functional roles of Wnt signaling components in flatfish remain poorly understood. In this study, we performed a comprehensive genome-wide identification, evolutionary characterization, expression profiling, and functional analysis of wnt genes in , a flatfish species exhibiting ZW/ZZ sex determination and temperature-induced sex reversal. A total of 20 wnt genes were identified and classified into 13 subfamilies, displaying conserved structural organization and phylogenetic relationships consistent with other teleosts. Chromosomal mapping revealed lineage-specific WNT clusters, including a unique wnt3-wnt7b-wnt5b-wnt16 block, as well as syntenic associations with reproduction-related genes (e.g., , , , , ), suggesting coordinated genomic regulation. Tissue transcriptome analysis demonstrated strong sex- and tissue-biased expression patterns, with predominantly expressed in ovaries and specifically upregulated in pseudo-male testes. Functional assays revealed that knockdown of or induced testis-specific genes (, ) and suppressed ovarian markers (, ), indicating antagonistic regulatory roles in gonadal fate determination. Promoter analysis identified as a selective repressor of , but not , providing a mechanistic basis for paralog divergence. Furthermore, pull-down combined with LC-MS/MS analysis showed that WNT5b interacts with proteins enriched in ribosome biogenesis and ubiquitin-mediated proteolysis, suggesting a role in translational regulation and protein turnover during spermatogenesis. Together, these findings establish WNT5 signaling-particularly -as a key driver of testicular development in and provide new insights into the molecular mechanisms underlying sex differentiation and sex reversal in flatfish. - Source: PubMed
Publication date: 2026/01/26
Li ZhengjieWang JunhaoLi ChaoZhu Ying - Huntington's disease (HD) is a fatal neurodegenerative disorder characterized by a triad of behavioral symptoms: involuntary movement, emotional change, and cognitive dysfunction. Although alterations in WNT signaling have been reported in HD, its precise role in pathogenesis remains unclear. In this study, we found that astrocytic WNT5B mRNA and protein levels are elevated in the striatum of both HD patients and HD model mice. The noncanonical WNT5B signaling pathway induced sustained expression of matrix metallopeptidase 14 (MMP14), an extracellular matrix (ECM)-degrading enzyme, via activation of the NFATc2 transcription factor in both human and primary mouse astrocytes. Robust upregulation of MMP14 led to ECM degradation, medium spiny neuron (MSN) damage, and increased mutant huntingtin aggregation in N171-82Q HD transgenic mice. Furthermore, WNT5B gain-of-function exacerbated neuropathology, impaired motor coordination, and shortened the lifespan of N171-82Q mice. We further demonstrated that the overexpression of the estrogen receptor α (ERα) suppresses NFATc2 transcriptional activity in vitro. A targeted therapy for the WNT5B-NFATc2-MMP14 signaling pathway by genistein, a phytoestrogen, reduced MMP14 transcription by antagonizing NFATc2 activity and preventing ECM degradation in N171-82Q mice. Genistein treatment also ameliorated neuropathology and motor deficits and prolonged the lifespan of HD mice. Together, these findings define a molecular pathological mechanism in which astrocytic MMP14 transcription, driven by the noncanonical WNT5B signaling pathway, promotes ECM degradation and MSN damage and accelerates neurodegeneration in HD. Modulation of the noncell-autonomous WNT5B-NFATc2-MMP14 signaling pathway by genistein may serve as a potential therapeutic strategy for mitigating HD pathogenesis. - Source: PubMed
Publication date: 2026/01/19
Nguyen Phuong Thi ThanhYousefian-Jazi AliHyeon Seung JaeLee SoominKim Seung ChanPark UiyeolJeong YeeunKim SojungKim SuhyunKim YeyunRyu Hannah LLee Kyung EunStein Thor DMyers Richard HHwang Eun MiLee JungheeRyu Hoon - This study investigated the role of in bovine preadipocyte proliferation and adipogenic differentiation. overexpression suppressed proliferation, reducing the percentage of EdU-positive cells and overall cell viability ( < 0.05). It also downregulated proliferative factors and ( < 0.05), and reduced lipid accumulation ( < 0.001) along with key adipogenic markers , , and ( < 0.01). Conversely, knockdown promoted these processes. Mechanistically, overexpression downregulated ( < 0.05), while knockdown had the opposite effect. Silencing significantly decreased transcription ( < 0.05), total protein ( < 0.05), and phosphorylation ( < 0.001). In conclusion, our findings identify as a novel negative regulator of bovine preadipocyte proliferation and differentiation, which exerts its function through the / signaling axis. This discovery elucidates previously uncharacterized regulatory mechanisms underlying adipogenesis in livestock species. - Source: PubMed
Publication date: 2025/12/10
Wang YiranRen WanpingShao WeiZhou YuxinLiu YiliCao JunweiWang FengjuBi JingdongYang Liang - Bone metastsis in advanced breast cancer patients are usually osteolytic. A better understanding of the mechanisms in osteolytic metastasis is critical for the development of new therapies. YTH domain-containing family protein 3 (YTHDF3) has been reported to function as an N6-methyladenosine (m6A)-modified mRNA regulator. In this study, we found YTDHF3 expression was associated with clinical characteristics of breast cancer patients. YTHDF3 expression influenced the migration and invasion capacity of breast cancer cells in vitro and in vivo, and low expression of YTHDF3 suppressed cancer cell-induced osteoclast differentiation and osteolytic bone destruction. Moreover, we found YTHDF3 enhanced the translation of zinc finger E-box-binding protein 1 (ZEB1) and SMAD family member 5 (SMAD5) by reading the m6A modification sites in their mRNAs and further promoted the epithelial-mesenchymal transition (EMT) of breast cancer cells. Enhanced expression of ZEB1 promoted the transcription of bone morphogenetic protein inhibitors such as NOG, FST and CCN2, which boosts osteolytic metastasis. Furthermore, we newly found Wnt family member 5B (WNT5B) expression was regulated by ZEB1, also involved in osteolytic process. In conclusion, YTHDF3 plays an important role in osteolytic metastasis and it may serve as a potential prognostic biomarker and therapeutic target for breast cancer bone metastasis. - Source: PubMed
Publication date: 2025/11/17
Xu LunYu QianPeihang XuLi KunWang BingnanShao YangCheng MoHuang WendingYao QianlanFeng XuSong ShaoliWang ShuoerYan Wangjun