Ask about this productRelated genes to: WNT9B antibody
- Gene:
- WNT9B NIH gene
- Name:
- Wnt family member 9B
- Previous symbol:
- WNT15
- Synonyms:
- WNT14B
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-12
- Date modifiied:
- 2016-03-18
Related products to: WNT9B antibody
Related articles to: WNT9B antibody
- Adult zebrafish regenerate their kidneys after injury by activating quiescent renal stem cells, however the injury signals that activate kidney stem cells are not known. We show here that an innate immune, cytokine response after tubule injury is required and sufficient to induce adult zebrafish kidney regeneration. An injury reporter zebrafish transgenic, revealed that tubule injury occurred specifically in kidney proximal tubules and was associated with a rapid accumulation of neutrophils and macrophages. Injury also activated a reporter transgene specifically in kidney tubules where RNA seq revealed NFkB target gene and cytokine expression. Inhibition of NFkB signaling with JSH-23 blocked reporter activation and also inhibited induction of new nephrons. Systemic injection of the immune activators lipopolysaccharide or zymosan into uninjured fish rapidly induced cytokine expression followed by nephrogenic gene expression and the appearance of new, functional nephrons. Analysis of injury-induced cytokines revealed that several paralogs of were strongly expressed throughout the regeneration response and injection of recombinant Cxcl11 was sufficient to induce FGF-dependent kidney stem cell aggregation, but not Wnt-dependent epithelial differentiation. Kidney injury in zebrafish expressing a neutrophil dominant negative transgene activated Fgf signaling but failed to induce or downstream Wnt target genes. Nephrogenic gene expression and epithelial tubule formation was rescued by treatment with the canonical Wnt agonist CHIR. Our findings demonstrate that an injury-induced, sterile immune response regulates kidney regeneration by establishing a nephrogenic niche of Fgf and Wnt signaling that supports tissue-resident kidney stem cell differentiation into functional nephrons. - Source: PubMed
Publication date: 2026/04/10
Olajuyin OlaleyeSchenk HeikoSampson Will G BAdekeye OmodasolaKamei Caramai NUpadhyay Rohan MKennedy RyanMorrison EmmaCallahan RileyBonnet FredericGraber JoelSeaman RyanFuqua HeathWheeler RobertOxburgh LeifDrummond Iain A - Hsa-miR-99a has been linked to the advancement of several malignancies, including colorectal cancer (CRC). This investigation seeks to elucidate its function and regulatory network in CRC. - Source: PubMed
Publication date: 2026/03/17
Yang XuejingZhang TingtingSun HuFeng HuijingSong Dong - Wingless/Int-1 (Wnts) proteins are canonical Frizzled receptor ligands. Recent evidence indicates that some Wnts, including Wnt9b and Wnt5a, bind to polycystin 1 (PKD1), a transmembrane protein which can couple to polycystin 2 (PKD2) to form a non-selective cation channel. The functional significance of Wnts binding to PKD1 is unclear. Here, we tested the hypothesis that Wnts act through PKD1/PKD2 channels on endothelial cells (ECs) to regulate arterial contractility and blood pressure and investigated the cellular source and secretory regulation of vasoactive Wnt proteins. - Source: PubMed
Publication date: 2026/03/20
Mbiakop Ulrich CMackay Charles EMata-Daboin AlejandroPontes Roberto BrazLeo M DennisJaggar Jonathan H - Puffy Snout Syndrome (PSS) is an emerging, high-mortality condition of captive scombrids characterized by collagenous craniofacial overgrowth and tissue remodeling. Despite its prevalence in aquaculture, the molecular mechanisms underlying PSS remain unknown. Here, we performed mRNA and small RNA sequencing on facial tissues from wild-caught healthy, asymptomatic captive, and symptomatic captive Pacific mackerel (Scomber japonicus) to characterize transcriptional and post-transcriptional changes associated with the syndrome. Principal component analysis revealed strong separation between captive and wild groups, with symptomatic fish exhibiting the most pronounced transcriptional divergence. Across comparisons, 2293 genes were differentially expressed, with symptomatic fish showing enrichment of cancer-associated pathways (e.g., Wnt signaling, extracellular matrix-receptor interactions) and immune processes including leukocyte activation and MAPK signaling. Asymptomatic fish also exhibited cancer-related and proliferative gene signatures, suggesting early molecular changes precede visible pathology. Key Wnt ligands (wnt9b, wnt3a, wnt10a) were overexpressed in captive groups, while immune effectors (ccl20a.4, perforin-1) were downregulated in symptomatic fish, indicating concurrent proliferative activation and immune suppression. MicroRNA profiling identified differential expression of tumor-suppressive gmo-let-7h-2, immune-regulatory ola-miR-223, and stress-responsive tni-miR-212, with predicted targets enriched for extracellular matrix organization, cytokine signaling, and neuronal processes. This study provides the first transcriptomic and miRNA evidence linking neoplastic signaling, immune dysregulation, and extracellular matrix remodeling to PSS. The detection of cancer-like molecular signatures in asymptomatic fish highlights potential for early diagnosis and monitoring. These findings establish a molecular framework for investigating PSS etiology, inform biomarker development, and underscore the need to evaluate environmental and infectious triggers in scombrid aquaculture. - Source: PubMed
Publication date: 2026/02/12
Leidholt Savanah LBistolas KaliaPastey ManojDasenko MarkMiller EmilyNorton AlexanderVan Houtan Kyle SBoustany AndreGalvin TatianaThurber Rebecca Vega - In the adult zebrafish kidney, nephrogenesis occurs as a regenerative response to injury and provides a model to explore cell signaling pathways required for nephron formation and engraftment. Differentiating kidney tubules interconnect with collecting system epithelia to generate a pathway for fluid excretion. We show that canonical Wnt signaling induces a mesenchymal, invasive cell phenotype and is required, along with Src kinase and Rac1, to generate basal cell protrusions on new nephrons. The Wnt ligands wnt9b and wnt4 are both required for new nephron formation after injury. Mutation in wnt4 and wnt9b, or treatment with the canonical Wnt inhibitor IWR1 blocks the formation of basal protrusions in forming nephrons. Mutation in the Wnt receptor frizzled9b reveals a fusion-associated non-canonical Wnt pathway that acts to (1) restrict canonical Wnt gene expression, (2) drive Rho kinase-dependent apical constriction of epithelial cells and (3) position basal protrusions to generate orthogonal tubule lumenal connections. Mutation in wnt9b phenocopies fzd9b mutants, indicating that a single ligand can induce canonical and non-canonical Wnt signaling in the same cells to orient and drive tubule interconnection in the regenerating zebrafish kidney. - Source: PubMed
Publication date: 2026/02/20
Kamei Caramai NSampson William G BAlbertz CarolinAries OliverWolf AmberUpadhyay Rohan MHughes Samuel MSchenk HeikoBonnet FredericDraper Bruce B WMcCracken Kyle WMarciano Denise KOxburgh LeifDrummond Iain A