WNT7B antigen
- Known as:
- WNT7B antigenic
- Catalog number:
- 'H00007477-P01-25
- Product Quantity:
- 25
- Category:
- -
- Supplier:
- ACR
- Gene target:
- WNT7B antigen
Related genes to: WNT7B antigen
- 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 antigen
'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Anti_Tg)Thyroglobulin Antigen(Des-Asp187)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187)-ME20M_ME20S (185-193) (human, bovine, mouse), (Des-Asp187)-Melanocyte Lineage-Specific Antigen GP100 (185-193) (hu(Des-Asp187,Met186)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187,Met186)-Melanoma-Associated ME20 Antigen (185-193) (human, bovine, mouse), (Des-Asp187,Met186)-95 kDa Melano(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Draxin) C1ORf187, Antigen blocking peptide(Val438)-Tyrosinase (432-444) (human)
(Val438)-LB24-AB (432-444) (human), (Val438)-Monophenol Monooxygenase (432-444) (human), (Val438)-SK29-AB (432-444) (human), (Val438)-Tumor Rejection Antigen AB (0x19 Antigen0x2 Antigen1,25-dihydroxyvitamin D3 Competitive ELISA, Coated with Antigen105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P Related articles to: WNT7B antigen
- Endocrine therapy (ET) selection in estrogen receptor-positive breast cancer (ER + BC) is guided by menopausal status and tolerability rather than tumor biology, despite substantial heterogeneity in recurrence. We hypothesized that baseline gene expression differentially associates with recurrence depending on initial ET class. In a retrospective cohort of 74 ER+/HER2- patients treated with adjuvant ET, we profiled baseline tumor RNA and fitted adjusted Cox models for gene and ET interactions on time-to-recurrence and time-to-switch. Among selective estrogen receptor modulators-initiated patients, higher expression of , , , , and was associated with markedly increased recurrence, while no comparable association was observed among aromatase inhibitors-initiated patients. Forty-one percent of patients switched ET at least once, predominantly due to intolerance (joint pain, unspecified side effects); switching was not consistently associated with tumor biology. These hypothesis-generating findings identify candidate gene and ET interactions and motivate validation in larger, independent cohorts. - Source: PubMed
Publication date: 2026/06/30
Jones VeronicaWang YongzheQuinones ChristineAljaber DanaNelson EvaNath AritroKang IreneRugo HopeYee LisaSeewaldt VictoriaMortimer Joanne - To identify baseline gene expression programs associated with recurrence timing in estrogen receptorpositive (ER+) breast cancer (BC) using a multi-state modeling framework. - Source: PubMed
Publication date: 2026/06/30
Wang YongzheQuinones ChristineKang IreneRugo HopeMartinez ErnestSeewaldt VictoriaMortimer JoanneNath AritroJones Veronica - Our previous research has shown that lipopolysaccharide (LPS) derived from Gram-negative bacteria in the intestine promoted rheumatoid arthritis (RA) after entering peripheral blood, but the specific molecular mechanism was unclear. - Source: PubMed
Publication date: 2026/07/03
Wang BingSong YingqiuXu WenboChen JiaqingHuang YurongZhou XinyueCai YikangXia AixinLi YanpingJiang LiweiLiao FaxueHuang JianMiao Chenggui - 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