Ask about this productRelated genes to: UTP14A antibody
- Gene:
- UTP14A NIH gene
- Name:
- UTP14A small subunit processome component
- Previous symbol:
- SDCCAG16
- Synonyms:
- NY-CO-16, Utp14
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-25
- Date modifiied:
- 2019-01-22
Related products to: UTP14A antibody
Related articles to: UTP14A antibody
- Cerebral palsy (CP) is a neurodevelopmental disorder with a significant male predisposition, yet the underlying genetic mechanisms driving this sex-specific risk remain poorly understood. Given the hemizygous state of X-linked variants in males, we hypothesized that X-chromosomal genetic variations may contribute to CP susceptibility in male patients. - Source: PubMed
Publication date: 2026/07/03
Su YuWang YangongCheng YeXu YiranQiao YimengXia LeiSong JuanLi YunqianZhang JunjieSun HongyuanWang XiaoyangZhu ChanglianXing Qinghe - The profitability of the beef industry is directly influenced by the fertility rate and reproductive performance of both males and females, which can be improved through selective breeding. When performing genomic analyses, genetic markers located on the X chromosome have been commonly ignored despite the X chromosome being one of the largest chromosomes in the cattle genome. Therefore, the primary objectives of this study were to: (1) estimate variance components and genetic parameters for eighteen male and five female fertility and reproductive traits in Nellore cattle including X chromosome markers in the analyses; and (2) perform genome-wide association studies and functional genomic analyses to better understand the genetic background of male and female fertility and reproductive performance traits in Nellore cattle. - Source: PubMed
Publication date: 2025/01/10
de Carvalho Felipe EFerraz José Bento SPedrosa Victor BMatos Elisangela CEler Joanir PSilva Marcio RGuimarães José DBussiman FernandoSilva Barbara C AMulim Henrique ARocha Artur OliveiraAraujo Andre CWen HuiCampos Gabriel SBrito Luiz F - P16 expression is inversely associated with RB1 expression in cancer cells, and P16 inhibits CDK4-catalyzed RB1 phosphorylation. How P16 and RB1 coordinately express and regulate the cell cycle remains to be studied. In the present study, we found that P16 upregulated the E3 ligase UTP14A, which led to the ubiquitination of RB1 at K810 and RB1 degradation. P16 loss consistently disrupted the UTP14A-mediated degradation of RB1 and caused RB1 accumulation. Functionally, P16 loss inhibited RB1 ubiquitination in a cell cycle progression-independent fashion and inhibited proteome-scale ubiquitination in a cell cycle progression-dependent manner. Our findings indicate that there is a negative feedback loop between P16 and RB1 expression and that disruption of this loop may partially rescue the biological outcomes of P16 loss. We also revealed a hitherto unknown function for in regulating proteome-scale ubiquitination by inhibiting cell proliferation, which may be useful for the development of anticancer drugs. - Source: PubMed
Publication date: 2024/09/03
Weng WenjieZhang BaozhenDeng Dajun - We studied the gene-expression patterns in specimens of tumor and peritumor tissue biopsies of 26 patients with head and neck carcinomas depending on smoking status. Histological and immunohistochemical examinations verified that all tumors belonged to the "classical" subgroup of head and neck carcinomas, and the HPV-negative tumor status was confirmed. The expression of 28 tumor-associated genes determined by RT-PCR was independent of patients' sex or age, TNM status, degree of differentiation, or tissue localization. Moreover, in peritumor tissue, none of the 28 genes were differentially expressed between the groups of smoking and nonsmoking patients. During oncotransformation in both studied groups, there were similar processes typical for HNSCC progression: the expression levels of paired keratins 4 and 13 were reduced, while the expression levels of keratin 17 and were significantly increased. However, further investigation revealed some distinctive features: the expression of the genes and increased significantly only in the nonsmoking group, and the expression of , , , and genes changed only in the smoking group. In addition, correlation analysis identified several clusters within which genes displayed correlations in their expression levels. The largest group included 10 genes: , , , , , , , , , and . The genetic signatures associated with smoking habits that we have found may serve as a prerequisite for the development of diagnostic panels/tests predicting responses to different therapeutic strategies for HNSCC. - Source: PubMed
Publication date: 2024/03/21
Soboleva AnnaArutyunyan IrinaJumaniyazova EnarVishnyakova PolinaZarubina DariaNimatov EldarElchaninov AndreyFatkhudinov Timur - The mRNA markers identified using microarray assay and diffusion tensor magnetic resonance imaging (DTI) were applied to elucidate the pathophysiology of attention-deficit hyperactivity disorder (ADHD). First, we obtained total RNA from leukocytes from three children with ADHD and three healthy controls for analysis with microarray assays. Subsequently, we applied real-time quantitative polymerase chain reaction (qRT‒PCR) assays to validate the differential expression of 7 genes (COX7B, CYCS, TFAM, UTP14A, ZNF280C, IFT57 and NDUFB5) between 130 ADHD patients and 70 controls, and we built an ADHD prediction model based on the ΔCt values of aforementioned seven genes (AUROC = 0.98). Finally, in a validation group (28 patients with ADHD and 27 healthy controls), mRNA expression of the above seven genes also significantly differentiated ADHD patients from controls (AUROC value = 0.91). The DTI analysis showed increased fractional anisotropy (FA) of the forceps minor, superior corona radiata, posterior corona radiata and anterior corona radiata in ADHD patients. Moreover, the FA of the right superior corona radiata tract was positively correlated with ΔCt levels of the COX7B gene and the IFT57 gene. The results shed a new light on a genetic profile of ADHD that may help in deciphering the white matter microstructural features in disease pathogenesis. - Source: PubMed
Publication date: 2024/02/21
Wang Liang-JenLi Sung-ChouChou Wen-JiunKuo Ho-ChangLee Sheng-YuLin Wei-Che