Ask about this productRelated genes to: NKD1 antibody
- Gene:
- NKD1 NIH gene
- Name:
- NKD inhibitor of WNT signaling pathway 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-19
- Date modifiied:
- 2019-01-25
Related products to: NKD1 antibody
Related articles to: NKD1 antibody
- Prostate cancer (PCa) is a biologically heterogeneous disease that frequently progresses to castration-resistant prostate cancer (CRPC), a challenging clinical stage. The underlying mechanisms driving CRPC progression and resistance to androgen receptor (AR) signaling inhibition (ARSI) remain incompletely understood. Emerging evidence implicates the canonical Wnt pathway as a key contributor to CRPC progression. This study elucidates the role of Wnt pathway activation in mediating resistance to ARSI and identifies a robust molecular signature for predicting treatment outcomes. By integrating genomic and transcriptomic data from PCa patients, patient-derived xenografts (PDXs), and experimental models harboring or not Wnt-activating mutations, we performed differential expression analysis, unsupervised clustering, survival, and viability analysis to assess Wnt/β-catenin pathway activation and its interaction with AR signaling. A specific Wnt transcriptional signature (AXIN2, RNF43, ZNRF3, NKD1) was found to reliably reflect pathway activation in advanced PCa. AR was found to suppress mutation-driven Wnt signaling, which was upregulated upon AR inhibition, contributing to treatment resistance. Targeting β-catenin interactions with co-activators p300/CBP using selective inhibitors (IQ-1 and ICG-001) effectively mitigated Wnt-driven ARSI resistance, restoring sensitivity to therapy in preclinical models. Thus, canonical Wnt pathway activation emerges as a critical mediator of resistance to ARSI in CRPC. The identified Wnt signature holds potential as a biomarker for predicting and monitoring therapeutic outcomes. Concurrent targeting of AR and Wnt signaling represents a promising strategy to overcome treatment resistance, particularly in patients with Wnt-activating mutations. - Source: PubMed
Publication date: 2026/04/14
Anselmino NicolasSanchis PabloBizzotto JuanLabanca EstefaniaDong JiabinShepherd Peter D AYang JunVazquez Elba SMateo JoaquinGueron GeraldineLogothetis Christopher J - As the main nutrient reservoir in cereal grains, the endosperm largely determines grain yield, performance and nutrition. However, knowledge of genes that coordinate endosperm filling and nutrient deposition, which could offer potential for genetic improvement of grain traits, remain limited. Here we identified ZmMYB127, a filling-endosperm-specific MYB transcription factor. Its knockout disrupted filling-stage aleurone layer morphology and nutrient accumulation, leading to reduced kernel weight, quality and nutrition. ZmMYB127 exerts dual transcriptional control over core endosperm-filling genes, including naked endosperm-1/2 (NKD1/2), crinkly4 (CR4) and opaque2 (O2). ZmMYB127 forms an activation complex with O2 to synergistically induce NKD1/2 expression by binding to two distinct cis-regulatory elements (CREs). Conversely, the co-repressor ZmLUG3 bridges ZmMYB127 and ZmABI4, a B3-domain transcription factor, to form a repressive complex that suppresses O2 and CR4 via another CRE pair. Filling-endosperm-specific overexpression of ZmMYB127 enhanced kernel weight, quality and nutrition. Introducing this overexpression into the elite cultivar Zhengdan958 confirmed its breeding potential. Furthermore, its rice homologue OsMYB20 also plays a conserved role in endosperm filling. Our findings establish ZmMYB127 as a promising target for grain improvement without trade-offs for precision breeding. - Source: PubMed
Publication date: 2026/03/19
Shi JianLi ZhiqiangWang ZeyuPan ShuxingWu XuWang XiYe YafengXu ZhuopingHe JunjunZhang Zhiyong - Olfactory dysfunction not only diminishes quality of life but also serves as an early biomarker for neurodegenerative diseases. However, the molecular mechanisms underlying age-related olfactory dysfunction remain poorly understood. In this study, we profiled the dynamics of mA epitranscriptomics in mouse olfactory bulbs (OBs) throughout postnatal development, adulthood, and aging, revealing the dynamic remodeling of mA methylation during the aging process. Our findings indicate that mA modifications regulate various physiological processes in a stage-specific manner. Notably, in aged OBs, mA methylation is enriched in genes associated with the Wnt signaling pathway. Furthermore, we identified a Wnt pathway involving Wnt, Ror2, and Nkd1 that may contribute to disrupted glutamate metabolism responses linked to age-related alterations in glutamatergic neuron function. This disruption is accompanied by significant reductions in glutamate and its related metabolites, suggesting an imbalance in neurotransmitter levels and impaired mitochondrial function—factors that may lead to olfactory dysfunction. Additionally, we identified METTL3 as a key mA methyltransferase that drives age-related declines in olfactory function. Conditional knockdown of Mettl3 in aged OBs restores both olfactory function and activity within glutamatergic neurons. Our study provides valuable insights into the mA-mediated mechanisms governing OB aging and highlights potential therapeutic targets for mitigating neur odegenerative-associated olfactory deficits. - Source: PubMed
Publication date: 2026/02/27
Hu WenWang Xiao-YiZhan Xiao-JunPei PeiKong Ya-RuJi JieLiu JiaWang ShanTai Jun - To mine single-cell sequencing data for colorectal cancer (CRC), identify CRC epithelial cell subtypes, and explore the heterogeneity of epithelial cells and their impact on the tumor microenvironment (TME). The GSE201348 dataset, including normal, colorectal adenoma, high-grade colorectal intraepithelial neoplasia, and CRC tumor tissue samples, was downloaded from the Gene Expression Omnibus. The Seurat package of R software was used for data quality control, data integration, normalization, and clustering. The Feature Plot and the Recode function were executed to annotate and group the epithelial cells. Finally, genetic differences, copy number variant heterogeneity, pseudotime, cell-cell communication, and Gene Set Variation Analysis (GSVA) were further conducted. In total, 26,335 gene matrices from 263,872 cells were obtained for subsequent analyses. Four cell clusters, including immune cells, fibroblasts, endothelial cells, and epithelial cells, were identified. Epithelial cells were further divided into 11 subgroups characterized by MKI67, SLC27A6, PLCE1, NKD1, KCNMA1, GDA, CLCA4, BEST4, LRMP, ACTG2, and ASPM. GSVA enrichment analysis suggested a role of the "P53 pathway," "Wnt-β-catenin signaling," and "MYC targets V1" pathways in epithelial cells during the malignant progression of tumors. Survival analysis indicated that downregulation of KCNMA1 and upregulation of MKI67 were associated with poor prognosis. Cell-cell communication analysis suggested a bidirectional regulatory role between epithelial and fibroblast subsets. This study analyzed the gene expression characteristics of 11 types of epithelial cells during the malignant progression of CRC. KCNMA1 and MKI67 epithelial subpopulations are important indicators for the malignant progression of CRC. - Source: PubMed
Publication date: 2026/02/05
Chen QianqianYuan YaoqianTian ShuaiZhou JiayanLv KunmingLinghu Enqiang - Sugarcane smut, caused by , severely limits global sugarcane yield. Although auxin manipulation is a recognized virulence mechanism in plant-pathogen interactions, biological basis and mechanisms in orchestrating host colonization within the sugarcane-smut pathosystem remain elusive. This knowledge gap constrains a mechanistic understanding of auxin-mediated pathogenesis, thereby limiting opportunities to design auxin-based control strategies. Through integrated approaches combining exogenous hormone treatment, physiological profiling, and spatiotemporal gene expression analysis in susceptible and resistant genotypes, we aim to reveal how IAA coordinates an early host-pathogen dialogue. Our findings showed that IAA promoted infection in a dose-dependent manner: it reprogrammed host physiology at low concentrations in planta while inhibiting fungal growth at higher levels in vitro. IAA-mediated susceptibility involved disrupted redox homeostasis through suppressed activities of and , altered flavonoid metabolism, and upregulation of fungal effector genes such as and . Expression analysis further revealed temporally and genotype-dependent regulation of IAA-biosynthetic genes, with strong late-stage induction of and exclusively in susceptible plants. The resistant genotype demonstrated a superior ability to maintain redox balance and sustain flavonoid accumulation, underscoring the importance of constitutive host defense in limiting disease progression. Together, this study establishes auxin signaling as a key virulence module in , synchronizing fungal IAA production, host immunity suppression, and effector deployment. These insights advance our understanding of smut disease mechanisms and propose fungal IAA pathway elements as candidate targets for future resistance breeding. - Source: PubMed
Publication date: 2026/01/24
Hu XinLuo ZhengyingRen ShenglinZhang JingXu ChaohuaLi ChunjiaLiu Xinlong