WNT7B
- Known as:
- WNT7B
- Catalog number:
- ARP41291_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- WNT7B
Related genes to: WNT7B
- 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
anti-WNT7Banti-WNT7Banti-WNT7Banti-WNT7Banti-WNT7B type: Primary antibodies host: MouseChicken Protein Wnt-7b(WNT7B) ELISA kitChicken Protein Wnt-7b(WNT7B) ELISA kit SpeciesChickenChicken wingless-type MMTV integration site family, member 7B (WNT7B) ELISA kit, Species Chicken, Sample Type serum, plasmaChicken,Gallus gallus,Protein Wnt-7b,WNT7BCLIA Kit for Wingless Type MMTV Integration Site Family, Member 7B (WNT7B) Organism: Homo sapiens (Human)ELISA Kit FOR Protein Wnt-7b; organism: Human; gene name: WNT7BELISA Kit FOR Protein Wnt-7b; organism: Mouse; gene name: Wnt7bELISA Kit for Wingless Type MMTV Integration Site Family, Member 7B (WNT7B)ELISA Kit for Wingless Type MMTV Integration Site Family, Member 7B (WNT7B)ELISA Kit for Wingless Type MMTV Integration Site Family, Member 7B (WNT7B) Homo sapiens (Human) Related articles to: WNT7B
- Voltage-gated calcium channels (VGCCs) are crucial membrane proteins that mediate calcium influx. The CACNA gene family, which encodes the alpha subunits of VGCC complexes, is essential for forming functional calcium channels and plays significant roles in various cancers. This review focuses on the CACNA1E gene, which encodes the Cav2.3 channel α1E subunit, and systematically elaborates its role in cancer. Studies have identified CACNA1E as a key prognostic stemness-related gene in bladder cancer. Its somatic mutations are associated with the development of air pollution-related lung cancer and non-small cell lung cancer. In breast cancer, genetic variations and DNA methylation differences in CACNA1E have also been reported. Functionally, CACNA1E drives tumor progression by regulating calcium signaling. For example, in osteosarcoma, METTL3-mediated m⁶A modification stabilizes CACNA1E mRNA, activating the WNT7B/Ca²⁺ signaling pathway and thereby promoting tumor progression and chemoresistance. The expression of CACNA1E is closely linked to patient prognosis, with its amplification and overexpression correlating with relapse in favorable histology Wilms' tumor. Additionally, CACNA1E is involved in therapy resistance, as evidenced by its downregulation being associated with temozolomide resistance in glioblastoma. Collectively, this evidence suggests that CACNA1E, along with other VGCC members, may serve as a potential prognostic biomarker and therapeutic target in cancer. Future research should further explore their molecular mechanisms, interactions with the tumor microenvironment, and clinical translation potential. - Source: PubMed
Publication date: 2026/06/04
Hou Wei - Prostate cancer (PCa) commonly metastasizes to bone, leading predominantly to osteoblastic lesions driven by intricate cellular interactions within the bone microenvironment. While osteoclasts (OCLs) initiate bone remodeling through resorption, their contribution to PCa progression appears limited, as pharmacological inhibition with bisphosphonates and RANKL antagonists yields only modest clinical benefit. In contrast, osteoblasts (OBs) exert dual roles, either promoting or restraining tumor growth through context-dependent signaling pathways, including Wnt5a-mediated dormancy and transforming growth factor-beta (TGF-β)-induced epithelial-mesenchymal transition (EMT). Bone-derived growth factors such as insulin-like growth factor I/II (IGF-I/II), fibroblast growth factor 23 (FGF-23), and platelet-derived growth factor (PDGF) further enhance tumor colonization. Osteocytes (OCYs), the most abundant and long-lived bone cells, directly interact with PCa cells and, in response to altered mechanotransduction, release pro-metastatic mediators including CCL5 and matrix metalloproteinases (MMPs). Moreover, PCa cells actively reprogram the bone niche by secreting exosomes and paracrine factors such as parathyroid hormone-related peptide (PTHrP) and Wnt7b, driving OBs and OCYs toward tumor-supportive phenotypes. Together, these reciprocal interactions establish a self-reinforcing cycle of bone remodeling and tumor progression. This review underscores the central role of bone remodeling in PCa bone metastasis and highlights promising therapeutic targets within the PCa-bone axis. - Source: PubMed
Publication date: 2026/06/09
Tang HaoChen JunWu HonghanLv YuanhaoWa QingdeHe Sisi - WNT proteins have been recognized as key regulators of skeletal health. However, developing WNT-associated bone anabolic agents is clinically challenging and expensive. Here we identify the reconstructed thumb and index domains of WNT7B (WNT7B) as a WNT-derived bone anabolic peptide via Alphafold-empowered sequence prediction and in silico docking screening. In aged mice and pigs models of osteoporosis, WNT7B peptides demonstrate therapeutic potential by improving the osteogenic potential of mesenchymal stromal/stem cells (MSCs) and enhancing bone regeneration. Using single-cell sequencing, transgenic lineage tracking and biochemical approaches, we show that WNT7B harnesses the function and osteogenic lineage generation of intrinsic tissue-residual MSCs without needing MSC transplantation to repair a critical-sized defect effectively. Mechanistically, WNT7B activates non-canonical Ca-NFAT signalling through RECK/GPR124 to drive its bone anabolic effects, independent of canonical Wnt/β-catenin signalling known for its oncogenic effects. Our results suggest that WNT7B could work as bone anabolic agent for alleviating bone loss in aging and for fracture repair by promoting MSC function via Ca-NFAT signalling. - Source: PubMed
Publication date: 2026/06/12
Yu FanyuanLi FeifeiYu PengZhou BinWang Cun-YuYe Ling - Paraquat, a highly toxic herbicide, frequently causes acute poisoning, predominantly inducing pulmonary injury and fibrosis with high mortality, and no specific antidote is available. This study aimed to explore its pathogenesis using a paraquat-induced mouse model. Results showed that paraquat caused dose-dependent body weight changes, pulmonary edema, and pathological damage (alveolar structure destruction, inflammatory cell infiltration), with elevated levels of inflammatory factors (IL-6, TNF-α, IL-1β) in BALF and lung tissues. It also induced pulmonary early pro-fibrotic responses, evidenced by increased collagen deposition and upregulated mesenchymal markers (α-SMA, Vimentin, Collagen I). RNA sequencing revealed KLF4 was significantly downregulated, and differentially expressed genes (DEGs) were enriched in inflammatory pathways. KLF4 negatively correlated with core genes (GSK3B, MLH1, PRKACA, VDAC1, WNT7B) in pathways like Wnt signaling pathway. These findings indicated that paraquat-induced pulmonary injury and early pro-fibrotic responses are associated with KLF4 downregulation and inflammatory pathway activation, identifying KLF4 as a potential therapeutic target for clinical intervention. - Source: PubMed
Publication date: 2026/05/24
Zhang WeiYe SisiChen JiabaoCao JingjingXie DongyangJin XiaoXie ZhefanFu Chunlai - Titanium dioxide nanoparticles (nano-TiO₂) and carbamazepine (CBZ) are both emerging contaminants of concern in coastal environments. Current monitoring data indicate that nano-TiO₂ occur in nearshore seawater affected by land-based inputs, and CBZ is persistently detected in estuarine and nearshore waters; therefore, these contaminants may co-occur at a regional scale. In this study, the thick-shelled mussel (Mytilus coruscus) was used as a model organism. Nominal concentrations of nano-TiO₂ (100 μg/L) and CBZ (10 μg/L) were applied in single and combined exposure experiments over 14 days. Particle characterization, gonadal morphology, sex steroid hormone levels, and key gene expression analyses were integrated to evaluate reproductive hormone-disrupting effects. The results showed that nano-TiO₂ readily aggregated in seawater, and distinct nano-TiO₂ aggregates were observed on the surface of CBZ crystals in dried mixed samples. Phenotypically, exposure to either pollutant alone reduced the gonadal area and gonadosomatic index, showing significant sex-specific differences in the CBZ group. In contrast, combined exposure caused more pronounced reproductive tissue damage. Hormonally, exposure disrupted sex steroid homeostasis, decreasing progesterone, estrone, and estradiol (E2), accompanied by increased testosterone (T). These hormonal changes exhibited sex-dependent patterns across treatments, with a decrease in E2 and an increase in T being more pronounced in the combined-exposure group. Molecularly, exposures significantly downregulated SF-1 and Wnt signaling genes (β-catenin, Wnt4), while upregulating Wnt7b. Overall, single exposure to nominal concentrations of nano-TiO₂ or CBZ was sufficient to induce sex-specific reproductive damage in M. coruscus, whereas combined exposure caused more pronounced changes at the morphological, hormonal, and transcriptional levels. - Source: PubMed
Publication date: 2026/05/14
Hu ChunLi ZiyinWu GuanglinLee Jae-SeongMiao JingjingDong YunweiMaszczyk PiotrSharifinia MoslemSingh NishaShang YueyongWang Youji