Ask about this productRelated genes to: TP53RK Blocking Peptide
- Gene:
- TP53RK NIH gene
- Name:
- TP53 regulating kinase
- Previous symbol:
- C20orf64
- Synonyms:
- dJ101A2.2, prpk, Nori-2p, BUD32
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-10-05
Related products to: TP53RK Blocking Peptide
Related articles to: TP53RK Blocking Peptide
- Oral squamous cell carcinoma (OSCC) is a malignant tumour with high-local invasiveness and lymph node metastasis potential. It is associated with poor prognosis and postoperative cosmetic complications. Therefore, developing molecular targets for early detection, diagnosis, and treatment is imperative. Methyltransferase-like 5 (METTL5), a newly identified N6-methyladenosine (m6A) modification writer, has been shown to exhibit tumour-promoting functions in several cancers. However, the significance of METTL5 expression in OSCC remains unexplored. - Source: PubMed
Publication date: 2026/04/21
Kajiya YukaShima KaoriShimojukkoku YudaiOku YasunobuTsuchiyama TakahiroHigashimoto KanakoKurihara-Shimomura MiyakoSasahira Tomonori - Colorectal cancer (CRC) is a leading cause of cancer-related mortality, necessitating the development of novel therapeutic strategies. In the present study, we identified TP53-regulating kinase (TP53RK) as a critical regulator of CRC cell survival and proliferation using a custom clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 library screen targeting serine/threonine kinase-related genes. TP53RK was significantly overexpressed in CRC tissues and was correlated with copy number amplification. Functional validation revealed that TP53RK depletion induced DNA replication stress, apoptosis, and cell cycle arrest, independent from p53 status. Mechanistically, TP53RK stabilized cell division cycle 7 (CDC7), a key kinase regulating DNA replication origin activation, ensuring robust minichromosome maintenance complex protein (MCM) phosphorylation and replication fork progression. Disruption of the TP53RK-CDC7 axis led to reduced MCM2 enrichment at replication origins and impaired DNA replication dynamics. Moreover, TP53RK overexpression sensitized cells to DNA replication stress (aphidicolin) and CDC7 inhibition (XL413), highlighting its potential as a therapeutic strategy. These findings establish TP53RK as a pivotal regulator of DNA replication fidelity and genomic stability, thereby providing a promising therapeutic target for CRC. - Source: PubMed
Publication date: 2025/10/16
Choi YoungheePark SeowooYang SeojinKim EunjuCho YoungwonYang Hye-JuYi Eugene CSong Sang-HyunKim Tae-You - Galloway-Mowat syndrome (GAMOS) is a rare autosomal recessive genetic disorder that is underrecognized. The phenotype is heterogeneous, but it is now widely accepted that early-onset nephrotic syndrome (SRNS) and microcephaly with brain malformation are characteristic features of Galloway-Mowat syndrome. Although the five subunits that encode the KEOPS complex, OSGEP/TP53RK/TPRKB/LAGE3/GON7, are known to cause Galloway-Mowat syndrome, the mutation of the WDR73, WDR4, NUP107, NUP133, and PRDM15 genes can lead to Galloway-Mowat syndrome, which makes the diagnosis more challenging. This review outlines current knowledge regarding Galloway-Mowat syndrome from another perspective. Starting from the history of Galloway-Mowat syndrome and reviewing the clinical details of patients with and without genetic traits, we discuss the phenotypic and genetic heterogeneity of the disease. We pay particular attention to all confounding clinical signs and symptoms that may lead to misdiagnosis. Indeed, some patients with Galloway-Mowat syndrome have a clinical condition of nephrotic range proteinuria, with or without hematuria, such as glomerular disease or chronic kidney disease of unknown origin. Although glomerular injury is frequently documented in biopsies of patients with Galloway-Mowat syndrome, there is currently no reliable evidence that renal biopsy has diagnostic or prognostic value. We reviewed published histopathological reports of renal tubule and glomerular injury in these patients and discussed the current knowledge on the role of genes that contribute to the onset of Galloway-Mowat syndrome in glomerular function. - Source: PubMed
Publication date: 2025/06/18
Huang LiminWang YanfeiZhang YingyingFu HaidongMao Jianhua - The p53 signaling pathway plays a critical role in regulating the cell cycle, apoptosis, and senescence, making it a key target in cancer research. The aim of this study was to investigate the effects of an ethanol extract from the stem of on the proliferation and expression of genes involved in the p53 pathway in MCF-7 breast cancer cells. To achieve this, real-time quantitative PCR (RT-qPCR) was used to evaluate the mRNA expression of downstream genes linked to cell cycle and senescence, including or Molecular docking simulations using Molegro Virtual Docker (MVD) were also performed to assess the potential inhibitory activity of metabolite compounds from stem against p53-regulating kinase (TP53RK. The results showed that the IC50 value of stem ethanol extract against MCF-7 cells was 38.27 ± 0.72 μg/mL. The results also revealed a reduction in the expression of downstream genes linked to cell senescence and the cell cycle: or ( = 0.011), ( = 0.008), and ( = 0.005), which was observed through RT-qPCR analysis of mRNA expression. This fact indicated that the inhibitory effects on proliferation by the ethanol extract of stem might occur via pathways associated with cell senescence and cell cycle arrest. Molecular docking results of metabolite compounds from stem suggested that squalene (Rerank score -112.70 kJ/mol), and nummularine B (Rerank score -110.68 kJ/mol) had potential as TP53RK inhibitors. These Rerank scores were smaller compared to the Rerank score of adenyl-imidodiphosphate (AMP-PNP), which was the native ligand of TP53RK, as confirmed by molecular dynamics analysis. These in silico results were confirmed by the decrease in () mRNA expression. In conclusion, the anti-proliferative effects of the ethanol extract from stem on breast cancer cells occurred by affecting cell cycle-related genes and inhibiting apoptosis protection mediated by overexpression of through p53 activity. - Source: PubMed
Publication date: 2025/02/10
Elya BernaRosmalena RosmalenaFajrin Ajeng MTedjo AryoRamadanti Nur AAzizah Norma NHashim Najihah Bm - N6-Threonylcarbamoyladenosine (tA) modification irregularities and their associated enzymes genes (OSGEP, OSGEPL1, TPRKB, GON7, TP53RK, YRDC, and LAGE3) are linked to various malignancies development, including Hepatocellular Carcinoma (HCC), yet the specific mechanisms remain obscure. This gap in knowledge is significant, as understanding the mechanisms of tA modification could reveal new insights into HCC pathogenesis and potentially identify novel therapeutic targets. - Source: PubMed
Publication date: 2025/03/16
Mui SintimShi JuanyiWen KaiYan YongcongLi HuomingWang WeidongZhou ZhenyuXiao Zhiyu