TP53I3

更新于：2025-05-07

基本信息

别名

NADPH:quinone reductase PIG3、p53-induced gene 3 protein、PIG3

+ [5]

简介

Catalyzes the NADPH-dependent reduction of quinones (PubMed:19349281). Exhibits a low enzymatic activity with beta-naphthoquinones, with a strong preference for the ortho-quinone isomer (1,2-beta-naphthoquinone) over the para isomer (1,4-beta-naphthoquinone). Also displays a low reductase activity for non-quinone compounds such as diamine and 2,6-dichloroindophenol (in vitro) (PubMed:19349281). Involved in the generation of reactive oxygen species (ROS) (PubMed:19349281).

关联

100 项与 TP53I3 相关的临床结果

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100 项与 TP53I3 相关的转化医学

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0 项与 TP53I3 相关的专利（医药）

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项与 TP53I3 相关的文献（医药）

2025-02-01·Molecular Genetics & Genomic Medicine

Identification and Validation of Biomarkers in Metabolic Dysfunction‐Associated Steatohepatitis Using Machine Learning and Bioinformatics

Article

作者: Zhang, Yu‐Ying ; Yu, Peng ; Liu, Shuang ; Liu, Jian‐Ping ; Luo, Yun‐Fei ; Li, Jin‐E ; Zeng, Hai‐Xia

ABSTRACTBackgroundThe incidence of metabolic dysfunction‐associated steatohepatitis (MASH) is increasing annually. MASH can progress to cirrhosis and hepatocellular carcinoma. However, the early diagnosis of MASH is challenging.AimTo screen prospective biomarkers for MASH and verify their effectiveness through in vitro and in vivo experiments.MethodsMicroarray datasets (GSE89632, GSE48452, and GSE63067) from the Gene Expression Omnibus database were used to identify differentially expressed genes (DEGs) between patients with MASH and healthy controls. Machine learning methods such as support vector machine recursive feature elimination and least absolute shrinkage and selection operator were utilized to identify optimum feature genes (OFGs). OFGs were validated using the GSE66676 dataset. CIBERSORT was utilized to illustrate the variations in immune cell abundance between patients with MASH and healthy controls. The correlation between OFGs and immune cell populations was evaluated. The OFGs were validated at both transcriptional and protein levels.ResultsInitially, 37 DEGs were identified in patients with MASH compared with healthy controls. In the enrichment analysis, the DEGs were mainly related to inflammatory responses and immune signal‐related pathways. Subsequently, using machine learning algorithms, five genes (FMO1, PEG10, TP53I3, ME1, and TRHDE) were identified as OFGs. The candidate biomarkers were validated in the testing dataset and through experiments with animal and cell models. The malic enzyme (ME1) gene (HGNC:6983) expression was significantly upregulated in MASH samples compared to controls (0.4353 ± 0.2262 vs. −0.06968 ± 0.3222, p = 0.00076). Immune infiltration analysis revealed a negative correlation between ME1 expression and plasma cells (R = −0.77, p = 0.0033).ConclusionThis study found that ME1 plays a regulatory role in early MASH, which may affect disease progression by mediating plasma cells and T cells gamma delta to regulate immune microenvironment. This finding provides a new idea for the early diagnosis, monitoring and potential therapeutic intervention of MASH.

2024-11-01·Biochemical and Biophysical Research Communications

Calreticulin exposure induced by anticancer drugs is associated with the p53 signaling pathway in colorectal cancer cells

Article

作者: Kajiwara, Taiki ; Saito, Tatsushi ; Karasawa, Hideaki ; Ono, Tomoyuki ; Naito, Satoru ; Ohnuma, Shinobu ; Nakayama, Keiko ; Funayama, Ryo ; Unno, Michiaki

Immunogenic cell death (ICD) enhances immunogenicity and activates antitumor immune responses. ICD induction by anticancer drugs may be effective against microsatellite-stable colorectal cancers (CRCs) that are less responsive to immune checkpoint inhibitors. Calreticulin (CRT) is crucial in ICD, promoting dendritic cell phagocytosis and initiating antitumor immunity. This study investigated CRT exposure mechanisms in four CRC cell lines and three human CRC organoids. Flow cytometry and immunofluorescence showed that oxaliplatin and 5-fluorouracil caused CRT exposure in all models. Despite CRT's association with endoplasmic reticulum stress, Western blot analysis showed no increase in this stress. These findings suggest alternative pathways. RNA sequencing identified enrichment of p53 signaling pathway genes, including TP53I3, TP53INP1, and YPEL3, which were confirmed by RT-qPCR. These results suggest that the p53 signaling pathway plays an important role in CRT exposure induced by anticancer drugs.

2024-10-01·Molecular Immunology

Identification and analysis of significant genes in nonalcoholic steatohepatitis-hepatocellular carcinoma transformation: Bioinformatics analysis and machine learning approach

Article

作者: Shen, Yumeng ; Zhang, Yidong ; Yu, Qiyi ; Hu, Weiwei ; Ni, Jiaping

PURPOSENonalcoholic steatohepatitis (NASH) has been an increasingly significant contributor to hepatocellular carcinoma (HCC). Understanding the progression from NASH to HCC is critical to early diagnosis and elucidating the underlying mechanisms.RESULTS5 significant prognostic genes related to NASH-HCC transformation were identified through algorithm selection, which were ME1, TP53I3, SOCS2, GADD45G and CYP7A1. A diagnostic model for NASH prediction was established (AUC=0.988). TP53I3 and SOCS2 were selected as potential critical genes in the progression of NASH-HCC by external dataset validation and in vitro experiments on NASH and HCC cell lines. Immune infiltration analysis illustrated the correlation between 5 significant prognostic genes and immune cells. Single-cell analysis identified hepatocytes related to NASH-HCC transformation markers, revealing their promoting role in the transformation from NASH to HCC.CONCLUSIONWith bulk-seq analysis and single-cell analysis, 5 significant prognostic genes related to NASH-HCC transformation were identified and validated at both dataset and in vitro experiment level. Among them, TP53I3 and SOCS2 might be potential critical genes in NASH-HCC progression. Single-cell analysis identified and revealed the critical role that NASH-HCC related hepatocytes play in NASH-HCC tansformation. Our research may introduce a new perspective to the diagnosis, treatment of NASH-related HCC.

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