Ask about this productRelated genes to: NUCKS1 antibody
- Gene:
- NUCKS1 NIH gene
- Name:
- nuclear casein kinase and cyclin dependent kinase substrate 1
- Previous symbol:
- -
- Synonyms:
- NUCKS
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-11
- Date modifiied:
- 2016-06-08
Related products to: NUCKS1 antibody
Related articles to: NUCKS1 antibody
- Astrocytes critically regulate states of consciousness, yet their molecular profiles across wake, sleep, and general anesthesia remain unclear. This study conducted proteomic and phosphoproteomic analyses of rat cortical astrocytes across these states using sevoflurane. Data quality was validated using principal component analysis (PCA) and Pearson correlation coefficient (PCC). Proteomics showed state-specific signatures: sleep and anesthesia shared similar changes (downregulated structural proteins, upregulated membrane transport complexes) but diverged in molecular expression. Anesthesia specifically suggested potential activation of cellular differentiation/structural plasticity-related pathways but implied potential disruption of metabolism and molecular clearance processes compared to sleep. Phosphoproteomics revealed the unique phosphorylation changes during general anesthesia compared to wake and normal sleep: downregulated phosphorylation of nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) at Ser188, suggesting the potential suppression of nuclear transcription and/or cell cycle activity, which may act as a potential molecular signature associated with the anesthetic state. Clustering analysis showed that sleep was associated with upregulated mRNA processing, while anesthesia indicated potential enhancement of synaptic signaling and suggested possible suppression of development-related programs. In summary, astrocytes undergo extensive molecular reprogramming during transitions of consciousness; while they share common features in morphological remodeling, sleep and anesthesia differ fundamentally in astrocytic molecular outcomes, offering new insights into astrocytic roles in unconsciousness. - Source: PubMed
Publication date: 2026/02/25
Su MengchanLi QingranLiao PingLei FanLi XinDeng LiyunYang JuexiLu FanZhou BinJiang Ruotian - Numerous studies have identified a close association between visceral adipose tissue mass (VAT) and neuropsychiatric disorders (NPDs). Both VAT and NPDs exhibit high heritability, yet their shared genetic architecture remains unclear. - Source: PubMed
Publication date: 2026/02/02
Xia JiangweiLi JiajianChen SiqiChang TianpengQian YuWu OuWu YangZhao YinanHao JunweiZhong Lianmei - Hand grip strength is a crucial indicator of muscle strength and quality. Yet, there remain significant knowledge gaps in our understanding of the genetic factors that influence hand grip strength and its impact on digestive disorders. - Source: PubMed
Publication date: 2026/01/27
Jiang PanFang YanfeiLiu ZhengyeDu HanzeBai XiaoyinChen HaotianMi Jiarui - Pulmonary arterial hypertension (PAH) is a pulmonary disease associated with alterations in gut microbiota. We aimed to identify potential diagnostic genes causally associated with gut microbiota and PAH. Mendelian randomization (MR) was performed to screen gut microbiota causally associated with PAH and to identify gut microbiota-related genes. A regulatory network was constructed to reveal the relationships among genes, gut microbiota and PAH. Diagnostic genes were screened and used to construct a diagnostic model for PAH. Characteristics of immune infiltration and diagnostic gene expression in each cell type were evaluated at the transcriptome and single-cell levels. Family. Porphyromonadaceae and genus. Eubacteriumfissicatena were risk factors for PAH, whereas phylum. Actinobacteria, class. Bacilli, genus. Erysipelatoclostridium, and genus. Ruminococcaceae were protective factors for PAH. The gene-gut microbiota-PAH network showed causal associations among six gut microbiota taxa, 13 PAH-associated genes and PAH. Copper metabolism MURR1 domain (COMMD) containing 10 (COMMD10), FES proto-oncogene, tyrosine kinase (FES), nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1), solute carrier family 22 member 4 (SLC22A4), and synaptogyrin 1 (SYNGR1) were identified as diagnostic genes, with Area Under Curve (AUC) values ranging from 0.79 to 0.99. The abundances of activated B cells, activated CD8 T cells, eosinophils, mast cells, and T helper cells were increased, whereas the abundances of activated dendritic cells (DCs), gamma delta T cells, MDSCs, macrophages, neutrophils, plasmacytoid DCs, and regulatory T cells were decreased in PAH. NUCKS1 was expressed in each cell type and was lower in T/NK and NK cells. The study deepens the understanding of PAH pathogenesis, and may provide diagnostic targets for PAH. - Source: PubMed
Publication date: 2025/12/02
Sun MingWu Song - Cellular responses after oxidative stress-induced deoxyribonucleic acid (DNA) damage (e.g., DNA double-strand break) control tumor cell proliferation, senescence, and apoptosis. The nuclear ubiquitous casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) ensures replication feasibility by modulating double-strand break repair necessary to regulate tumor cell proliferation. However, the regulatory mechanism of NUCKS1 in oxidative stress-induced melanoma cell apoptosis is not well characterized. In this study, we reported reduced phosphorylation of NUCKS1 during oxidative stress-mediated melanoma A375 and A875 cell apoptosis, and silencing of NUCKS1 obviously promoted A375 and A875 cell apoptosis. Mechanistically, cyclin-dependent kinase 13 (CDK13) was identified as a major upstream kinase to phosphorylate NUCKS1 and downregulated via ataxia telangiectasia mutated (ATM)/checkpoint kinase 2 (Chk2)/cell division cycle 25C (Cdc25C) axis during the process of oxidative stress-induced apoptosis. Moreover, we found that p-NUCKS1 could bind to tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein Zeta (YWHAZ) and subsequently regulate the level of BCL2-associated X (Bax), thereby leading to melanoma A375 and A875 cell apoptosis. Furthermore, we found that p-NUCKS1 was highly expressed in tumor specimens from melanoma patients, and silencing of NUCKS1 inhibited tumor growth in melanoma A375 and A875-bearing mouse models. Therefore, p-NUCKS1 could act as a potential target for melanoma treatment by mediating oxidative stress-induced apoptosis. - Source: PubMed
Publication date: 2025/09/25
Pan ZhaohaiGe HengJiang PanShi DanYang ZihuiZhang XinHuang JieLiang ChaoLu JunXie QiZheng QiushengLi Defang