Human WNT7B ELISA Kit
- Known as:
- Human WNT7B Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- abx153515
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Human WNT7B ELISA Kit
Related genes to: Human WNT7B ELISA Kit
- 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: Human WNT7B ELISA Kit
Related articles to: Human WNT7B ELISA Kit
- Urinary tract infections (UTIs) are among the most common bacterial infections, yet the genetic factors influencing susceptibility remain poorly understood. We performed a genome-wide association study of recurrent UTI involving 1,860,836 individuals (213,869 cases and 1,646,967 controls). We identified 36 independent non-HLA genome-wide significant loci encoding kidney epithelial and immune response genes and demonstrated that some loci have sex-specific effects. Integrative functional annotation, expression and protein quantitative trait locus colocalization, and single-cell multi-omic analyses revealed that UTI risk alleles preferentially modulated gene expression in kidney, ureter, and bladder epithelia. Multi-omic prioritization converged on a number of pathogenic pathways: epithelial barrier and mucosal glycocalyx defense ( , , , ), innate immune regulation ( , , ), infection resolution and regulated cell death ( , , ), epithelial identity maintenance ( , , ), urinary tract development ( , , , , ), and nutritional immunity through iron sequestration ( ). Approximately one-third of loci colocalized with gene expression in kidney tubules, suggesting direct modulation of epithelial host-defense programs. Among all loci, , which encodes a GPI-anchored epithelial surface protein expressed in the kidney papilla and urinary tract epithelia, emerged as the strongest candidate causal gene. We demonstrated that PSCA was secreted into urine, bound uropathogenic , and inhibited bacterial growth , implicating it as a constitutive epithelial defense factor. We also demonstrated that while was protective against urinary infections and duodenal ulcers, it was associated with increased risk of bladder, prostate, and gastric cancers, suggesting antagonistic pleiotropy between mucosal defenses and oncogenesis. Together, our findings define the polygenic architecture of UTI susceptibility, highlighting epithelial surface defense, innate immune regulation, developmental patterning, and nutritional immunity as central components of host defense, providing a new framework for host-directed, non-antibiotic interventions. - Source: PubMed
Publication date: 2026/07/10
Xu KatherineKhan AtlasShang NingZeng WenjieWang ChenBerrouet CeciliaShen Tian HuaiNarayanan PadmaDeng JennyDiPerna ChiaraWilliams CharlotteCuacuas SarahOlsen Timothy RArace JeffreyGhotra AryanMonical WayneBorisov OlegHaug StefanLiu HongboHa EunjiBanlengchit RunLevitman AbrahamPatel DiyaChou ClaireHalibart BartlomiejGuo Tai WeiSimmons ShawnGoswami SanyaNesanir KivancFujita MasashiKullo Iftikhar JJarvik Gail PWei Wei-QiFeng QiPingJiang LanStein C MichaelWeng ChunhuaHripscak GeorgeGharavi Ali GSusztak KatalinDe Jager Philip LKöttgen AnnaBarasch JonathanSims Peter AKiryluk Krzysztof - 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