Ask about this productRelated genes to: CTDSP2 antibody
- Gene:
- CTDSP2 NIH gene
- Name:
- CTD small phosphatase 2
- Previous symbol:
- -
- Synonyms:
- OS4, SCP2, PSR2
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-27
- Date modifiied:
- 2015-11-06
Related products to: CTDSP2 antibody
Related articles to: CTDSP2 antibody
- Cytogenetics analysis of adipocytic tumours revealed varieties of chromosomal translocations beyond MDM2 amplification, so, this report aimed to identify these translocations and recognise the altered genes with their fusion partners. - Source: PubMed
Atta I SShafek S IAbdel-Hamid M - BACKGROUND: MicroRNAs (miRNA) detection in urine samples may be a scarce invasive approach for diagnosis and monitoring prostate cancer (PCa). The role of miR-191-5p in prostate oncogenesis, as well as its function as a potential diagnostic and prognostic biomarker has been described in many cancers. However, its role as a diagnostic non-invasive indicator in PCa is still under investigated. METHODS: We performed an extracellular vesicle (EV)-based miRNA-sequencing of urine samples (n = 12/group) collected from PCa patients before (T0) and three months after (T1) radical prostatectomy, and healthy individuals. An independent cohort of PCa paired urine samples (n = 25/group) and controls (n = 22) was used to validate our sequencing data by RT-qPCR. Furthermore, we conducted comprehensive in silico analyses on urine and tissue samples extracted from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases, respectively. Receiver operator curves analysis was employed to assess the diagnostic value of miR-191-5p. To explore the role(s) of miR-191-5p in prostate carcinogenesis, we predicted miR-191-5p potential targets using four miRNA/target-gene pair databases (i.e., miRDB, miRTarBase, TarBase, and TargetScan). Finally, we corroborated the potential correlation between miR-191-5p and its targets by in silico investigation using TCGA dataset. RESULTS: Differential expression analysis revealed a significant upregulation of miR-191-5p in PCa patients compared to healthy individuals. Remarkably, urinary miR-191-5p expression levels significantly decreased after surgery in both our discovery and validation cohorts of urine samples by miRNA-seq and RT-qPCR, respectively. Bioinformatics analyses further confirmed high levels of miR-191-5p in urine and tissue samples from PCa patients compared to controls, particularly in patients with high Gleason score. Moreover, miR-191-5p showed a strong diagnostic value in urine and tissue samples. Finally, target prediction analysis identified the genes Satb1 and Ctdsp2 as potential targets of miR-191-5p. This was supported by a significant inverse correlation between the expression of miR-191-5p and these genes in TCGA PCa tissues. Moreover, both Satb1 and Ctdsp2 were downregulated in PCa tissues, and especially in high Gleason score tumors compared to normal and low Gleason score samples. CONCLUSIONS: MiR-191-5p is highly expressed in urine and tissue samples from patients with prostate cancer. Our findings, although preliminary, support miR-191-5p as a promising minimally invasive biomarker for diagnosis of PCa patients. - Source: PubMed
Publication date: 2026/01/20
De Palma Fatima Domenica ElisaCarbonnier VincentCernera GustavoGelzo MonicaNardelli CarmelaPandolfo Savio DomenicoAveta AchillePerdonà SistoImbimbo CiroCastaldo Giuseppe - Coronary artery disease (CAD) is a complex condition influenced by genetic factors, lifestyle, and other risk factors that contribute to increased mortality. This study is aimed at evaluating the diagnostic potential of genes associated with cuproptosis, ferroptosis, and pyroptosis (CFP) using network modularization and machine learning methods. CAD-related datasets GSE42148, GSE20680, and GSE20681 were sourced from the GEO database, and genes related to CFP genes were gathered from MsigDB and FerrDb datasets and literature. To identify diagnostic genes linked to these pathways, weighted gene coexpression network analysis (WGCNA) was used to isolate CAD-related modules. The diagnostic accuracy of key genes in these modules was then assessed using LASSO, SVM, and random forest models. Immunity and drug sensitivity correlation analyses were subsequently performed to investigate possible underlying mechanisms. The function of a potential gene, STK17B, was analyzed through western blot and transwell assays. Two CAD-related modules with strong correlations were identified and validated. The SVM model outperformed LASSO and random forest models, demonstrating superior discriminative power (AUC = 0.997 in the blue module and AUC = 1.000 in the turquoise module), with nine key genes identified: CTDSP2, DHRS7, NLRP1, MARCKS, PELI1, RILPL2, JUNB, STK17B, and SLC40A1. Knockdown of STK17B inhibited cell migration and invasion in human umbilical vein endothelial cells. In summary, our findings suggest that CFP genes hold potential as diagnostic biomarkers and therapeutic targets, with STK17B playing a role in CAD progression. - Source: PubMed
Publication date: 2025/03/15
Zhang YongyiGuo ZhehanLai RenkuiZou XuMa LiulingCai TianjinHuang JingyiHuang WenxiangZou BingchengZhou JinmingLi Jinxin - Amino acids and ammonia serve as sources of nitrogen for cell growth and were previously thought to have similar effects on yeast. Consistent with this idea, depletion of either of these two nitrogen sources inhibits the target of rapamycin complex 1 (TORC1), leading to induction of macroautophagy/autophagy and inhibition of cell growth. In this study, we show that Whi2 and the haloacid dehalogenase (HAD)-type phosphatases Psr1 and Psr2 distinguish between these two nitrogen sources in , as the Whi2-Psr1-Psr2 complex inhibits TORC1 in response to low leucine but not in the absence of nitrogen. In contrast, a parallel pathway controlled by Npr2 and Npr3, components of the Seh1-associated complex inhibiting TORC1 (SEACIT), suppress TORC1 under both low leucine- and nitrogen-depletion conditions. Co-immunoprecipitations with mutants of Whi2, Psr1, Psr2 and fragments of Tor1 support the model that Whi2 recruits Psr1 and Psr2 to TORC1. In accordance, the interaction between Whi2 and Tor1 appears to increase under low leucine but decreases under nitrogen-depletion conditions. Although the targets of Psr1 and Psr2 phosphatases are not known, mutation of their active sites abolishes their inhibitory effects on TORC1. Consistent with the conservation of HAD phosphatases across species, human HAD phosphatases CTDSP1 (CTD small phosphatase 1), CTDSP2, and CTDSPL can functionally replace Psr1 and Psr2 in yeast, restoring TORC1 inhibition and autophagy activation in response to low leucine conditions. - Source: PubMed
Publication date: 2025/03/27
Wang YitaoPing YangZhou RuiWang GuiqinZhang YuYang XueyuZhao MingjunLiu DongshengKulkarni MadhuraLamb HeatherNiu QingweiHardwick J MarieTeng Xinchen - Non-small cell lung cancer (NSCLC) is driven by a diverse array of somatic mutations. The vast majority of literature on NSCLC is based on targeted assays or small sample sizes, limiting the ability to provide a comprehensive view of NSCLC mutation profiles. Here, we analyzed genome-wide screen data (including whole genome sequencing and whole exome sequencing) from 1,874 NSCLC subjects to identify molecular subtypes and putative driver genes and to explore the effect of intrinsic and extrinsic factors on somatic mutation profiles. We showed that genome-wide screen data support existing knowledge, such as the TP53:KRAS mutation co-occurrence pattern as a key distinctive feature, but do not reveal additional broad molecular subtypes. In contrast, we demonstrated that low-frequency molecular subtypes or potential driver genes continue to be identified. Using driver gene identification algorithms, we found 50 potential driver genes including ANG, CDK10, CTDSP2, HOXA5, RBP4, and SPHK2, which show evidence of positive selection in NSCLC. Finally, we provided insights into the intrinsic and extrinsic covariates associated with the NSCLC somatic mutation landscape, while confirming associations with ethnicity (TP53 and EGFR), NSCLC subtype (14 genes including KRAS, NFE2L2, and STK11), and smoking history (KRAS, CSMD3, and TP53), we dismissed gene-level associations with sex when other covariates are controlled for. The results presented here represent a concise up-to-date summary of variation in the somatic mutation landscape and carry importance for NSCLC geneticists, medical practitioners, and drug discovery scientists. - Source: PubMed
Publication date: 2025/02/24
Pathak VaibhaviTazaki KoichiÇalışkan Minal