Ask about this productRelated genes to: CGI-121 antibody
- Gene:
- TPRKB NIH gene
- Name:
- TP53RK binding protein
- Previous symbol:
- -
- Synonyms:
- CGI-121, CGI121
- Chromosome:
- 2p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-02
- Date modifiied:
- 2016-07-01
Related products to: CGI-121 antibody
Related articles to: CGI-121 antibody
- 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 - - Source: PubMed
Publication date: 2026/02/14
Kaur NamanpreetShirsat KhushbuBhat VivekanandaYeole MayuriFarooqui SheebaLimaye SanketRadhakrishnan PeriyasamySiddiqui ShahyanNarayanan Dhanya LakshmiShenoy RathikaShukla Anju - 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 - 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 - N6-methyladenosine (mA) modification plays an important role in RNA molecular functions, therefore affecting the initiation and development of hepatocellular carcinoma (HCC). Herein, multiple datasets were applied to conduct a comprehensive analysis of DEGs within HCC and the analysis revealed significant dysregulation of numerous genes. Functional and signaling pathway enrichment analyses were performed. Further, TP53RK binding protein (TPRKB) emerged as a significant factor, exhibiting high expression level within HCC tissue samples and cells which could predict HCC patients' poor OS. Knockdown investigations of TPRKB in vitro demonstrated the effect of TPRKB knockdown on attenuating the aggressiveness of HCC cells by suppressing the viability, colony formation, invasive ability, and migratory ability, inducing cell cycle arrest, and facilitating the apoptosis of HCC cells. Investigations in vivo revealed that TPRKB knockdown significantly suppressed tumor growth in mice model. Additionally, the study identified methyltransferase 5, N6-adenosine (METTL5) as a potential regulator of TPRKB expression via mA modification, positively regulating TPRKB expression by enhancing TPRKB mRNA stability. The dynamic effects of METTL5 and TPRKB upon the phenotypes of HCC cells further confirmed that TPRKB overexpression partially abolished the anti-cancer effects of METTL5 knockdown upon the aggressiveness of HCC cells. Conclusively, our findings uncover that TPRKB, significantly overexpressed in HCC, exerts a critical effect on promoting tumor aggressiveness, and its expression shows to be positively regulated by METTL5 via mA methylation. These insights deepen the understanding of HCC pathogenesis and open new avenues for targeted therapies, highlighting that METTL5-TPRKB axis is an underlying new therapeutic target in HCC management. - Source: PubMed
Publication date: 2024/08/23
Luo MingLuo XiongSun JichunAo XiangHan HaoyanYang Xin