Polyclonal Rabbit ADCK1 Antibody
- Known as:
- Polyclonal Rabbit ADCK1 Antibody
- Catalog number:
- KA0097
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ADCK1 Antibody
Related genes to: Polyclonal Rabbit ADCK1 Antibody
- Gene:
- ADCK1 NIH gene
- Name:
- aarF domain containing kinase 1
- Previous symbol:
- -
- Synonyms:
- FLJ39600
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2015-10-15
Related products to: Polyclonal Rabbit ADCK1 Antibody
Related articles to: Polyclonal Rabbit ADCK1 Antibody
- Primary renal small cell carcinoma (PRSCC) is a rare, poorly differentiated neuroendocrine carcinoma, and its clinicopathological features and the gene mutation spectrum associated with its pathogenesis remain to be elucidated. The present study aimed to characterize the genetic mutation spectrum associated with the pathogenesis of PRSCC, identify novel driver and predisposing genes for the disease, reveal its histopathological features associated with genetic mutations and systematically summarize the clinicopathologic characteristics and prognostic factors of PRSCC patients to provide a theoretical basis for molecularly targeted therapy and prognostic assessment of PRSCC. Whole-exome sequencing (WES) was performed on PRSCC samples to characterize the spectrum of genetic mutations and the results were validated using Sanger sequencing. Immunohistochemistry (IHC) was performed to reveal the histopathological features associated with these mutations. Furthermore, based on the published literature, a population-based study was conducted by searching PubMed and EMBASE databases to systematically summarize the clinicopathologic characteristics and prognostic factors of patients with PRSCC. WES identified 113 somatic single-nucleotide variants, 26 somatic insertions and deletions and mutations in 8 predisposing genes (DST, OR10H3, PTK2B, APOBR, ZNF606, CCN4, ADCK1, and MYH2) and 10 driver genes (KRTAP10-9, HYDIN, ZNF665, KRTAP10-2, GPAM, MUC12, KRT9, CCDC168, DUSP27 and MDC1). Sanger sequencing of germline DNA identified a germline A/G variant in the HYDIN sequence, first reported in PRSCC. Furthermore, IHC analysis indicated that PRSCC was positive for CD56, Syn, insulinoma associated protein 1, CgA and neuron specific enolase. In the population-based study, the majority of patients with PRSCC were elderly (57.92±15.75 years), with a pathological tumor (T) 3/4 stage (68.3%) and presented with lymph node involvement (51.7%) and distant metastasis (51.7%). T stage was an independent prognostic factor for overall survival in patients with PRSCC (P=0.004). Driver mutations in the HYDIN gene may be a key factor in the pathogenesis of PRSCC. HYDIN may serve as a prognostic marker and a target for immunotherapy in the management of PRSCC. However, due to the extreme rarity of PRSCC, the WES analysis in the present study was based solely on individual cases. To ensure the reliability and generalizability of genetic alterations detected by WES, additional PRSCC samples, along with cell and animal experiments, are warranted to confirm the role of these genetic variants (particularly HYDIN) in PRSCC pathogenesis. The functional role of HYDIN mutations in PRSCC pathogenesis requires further validation in future research. - Source: PubMed
Publication date: 2026/03/30
Wang YangZhang LizhiXia XueyanLi Xiancheng - Milk composition in dairy goats, an economically important trait, is coordinately governed by complex metabolic networks and genetic factors. This study employed extreme phenotype grouping and multi-omics analysis of Xinong Saanen dairy goats to systematically elucidate the metabolic and genetic regulatory mechanisms underlying milk fat, SNF, protein, and lactose. Using widely targeted metabolomics, we identified 795 milk metabolites. Differential metabolite analysis revealed 57, 94, 50, and 58 significantly altered metabolites in milk fat, SNF, protein, and lactose, respectively. Subsequent metabolomic GWAS of these metabolites demonstrated significant genetic signals for 17 milk fat-associated metabolites, annotating 330 candidate genes (e.g., JAK2, LIPC, LRP1B). Similarly, 33 SNF-associated metabolites exhibited heritable signals linked to 177 candidate genes (including DGAT2, TGFB1, and NPAS3). For the protein-associated metabolites, 9 showed significant signals corresponding to 18 candidate genes (e.g., SRP54, CABYR, PRRX1), and 6 lactose-associated metabolites carried heritable signals that were mapped to 47 key candidate genes (such as HMGCS1, RXRA, and ADCK1). Collectively, this work identifies critical metabolites and candidate genes governing distinct milk components, deciphers the genetic-metabolic regulatory network influencing milk composition traits from a multidimensional perspective, and provides novel targets for the precise molecular breeding of high-quality goat milk. - Source: PubMed
Publication date: 2026/02/20
Zhang ZhenNi MengkeHuang QingyingLi YifanGong XinglongLuo XinranWang WeiLuo JunLi Cong - Hepatoblastoma is the most common malignant liver tumor of embryonic origin in children; however, its underlying etiology remains unclear. N1-methyladenosine (mA) modification is widely found in various human tissues and has been demonstrated to regulate tumorigenesis, but no studies have explored the role of in the development of hepatoblastoma. We genotyped three gene polymorphisms (rs1048147 C > A, rs6494 T > A, and rs176942 A > G) via the TaqMan method for 313 patients with hepatoblastoma and 1446 healthy subjects, after which the odds ratios (ORs), 95% confidence intervals (CIs), and values for each polymorphism were calculated. We found that all the three polymorphisms were significantly associated with hepatoblastoma susceptibility. The rs1048147 C > A was shown to reduce hepatoblastoma risk (adjusted OR = 0.72, 95% CI = 0.56–0.92, = 0.009) under dominant model, whereas rs6494 T > A (adjusted OR = 6.17, 95% CI = 1.37–27.37, = 0.018) and rs176942 A > G (adjusted OR = 2.12, 95% CI = 1.22–3.69, = 0.008) significantly increased hepatoblastoma risk under recessive model. Stratified analysis indicated that the rs1048147 CA/AA genotype decreased hepatoblastoma risk in children aged ≥ 17 months, females, and those with clinical stages I + II, whereas the rs176942 GG genotype increased the risk of hepatoblastoma in females. In addition, carriers of 2–3 risk genotypes had higher risk of tumor development, specifically among children aged ≥ 17 months, males, and those diagnosed with clinical stages I–II disease. Finally, eQTL analysis revealed that the three polymorphisms were associated with the expression levels of , , and . Overall, our findings revealed a significant association between gene polymorphisms and hepatoblastoma susceptibility. - Source: PubMed
Publication date: 2026/01/21
He ChongweiPan LinglingZeng XinhaoWang HuaYang ZhonghuaZhang JiaoLi YongLi LiLi SuhongCheng JiwenSong YalanHe JingChen Chaoyang - Wilms tumour (WT) is the most predominant renal carcinoma that affects children, and the understanding of the genetic mechanisms underlying WT development is continually evolving. The role of the demethylase ALKBH1, which is known for its association with diverse cancers, in WT has never been explored. Here, we aimed to investigate the associations between genetic variants of ALKBH1 and WT risk in Chinese children. A total of 414 WT patients and 1199 healthy controls were recruited from five centres in China. Three polymorphisms (rs1048147, rs6494 and rs176942) of the ALKBH1 gene were genotyped via the TaqMan genotyping assay. We found that rs6494 T>A was significantly associated with a reduced risk of WT [TA vs. TT: adjusted odds ratio (AOR) = 0.59, 95% confidence interval (CI) = 0.39-0.87, p = 0.009; TA/AA vs. TT: AOR = 0.61, 95% CI = 0.42-0.91, p = 0.014]. Stratification analysis revealed that the protective genotype of rs6494 (TA/AA) was significantly associated with reduced WT risk in subgroups with ages younger than 18 months, male sex and clinical stages III and III-IV. Moreover, through eQTL analysis, we observed that rs6494 T>A was associated with reduced ALKBH1 expression and elevated SNW1 and ADCK1 expression. We identified the rs6494 T>A polymorphism of the ALKBH1 gene as a WT susceptibility locus, providing valuable insights into the etiology underlying WT susceptibility. - Source: PubMed
Deng ChangmiZhou HaixiaZhang NaChen MinHua Rui-XiCheng JiwenLi SuhongZhang JiaoRuan JichenFu WenHe JingLiu Guochang - The blood-brain barrier (BBB) maintains brain homeostasis through specialized functions including tight junction formation and selective transport of brain endothelial cells (ECs). While ECs are generally thought to rely primarily on glycolysis for energy production, the transcriptional mechanisms underlying their metabolic specialization in the brain endothelium remain poorly understood, especially considering the brain's extraordinary energy demands. Through comparative transcriptomic analysis, it is demonstrated that brain endothelial cells are enriched for mitochondrial function genes, with forkhead box protein 1 (FOXQ1) being selectively expressed in cerebral vasculature. Conditional knockout of Foxq1 in endothelial cells results in severe mitochondrial dysfunction, including disrupted cristae morphology, reduced oxygen consumption, and impaired adenosine triphosphate (ATP) production. Mechanistically, FOXQ1 directly regulates two key pathways: calcium signaling through huntingtin-associated protein (HAP1)-mediated endoplasmic reticulum (ER)-mitochondrial calcium transfer, and mitochondrial structural integrity via AarF domain-containing protein kinase 1 (ADCK1)-dependent cristae organization. These findings reveal that brain endothelial cells rely on oxidative phosphorylation rather than glycolysis alone, challenging the prevailing metabolic paradigm for endothelial cells. This work establishes FOXQ1 as an important regulator of brain endothelial metabolism and provides new insights into the molecular basis of cerebrovascular specialization, with implications for understanding vascular dysfunction in neurological diseases. - Source: PubMed
Publication date: 2025/08/30
Zou WenzhengLv YuqingLi LinZhang ShukuiLiang JiaqiWu ChengchaoHuang EnyuJiao JianweiZhang Jingjing