Ask about this productRelated genes to: TP53INP1 antibody
- Gene:
- TP53INP1 NIH gene
- Name:
- tumor protein p53 inducible nuclear protein 1
- Previous symbol:
- -
- Synonyms:
- DKFZp434M1317, FLJ22139, P53DINP1, SIP, TP53INP1A, TP53INP1B, Teap
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-21
- Date modifiied:
- 2016-10-25
Related products to: TP53INP1 antibody
Related articles to: TP53INP1 antibody
- [This retracts the article DOI: 10.2147/OTT.S193097.]. - Source: PubMed
Publication date: 2026/05/04
- Epstein-Barr virus (EBV) is associated with a subset of gastric carcinomas characterized by latency programs that promote survival of infected cells. EBV-encoded H I A rightward transcript (BART) microRNAs contribute to apoptosis resistance in infected epithelial cells. This study investigated whether dasatinib, a Src family kinase (SFK) inhibitor, selectively targets EBV-positive gastric epithelial cells and examined the molecular mechanisms underlying this effect. EBV-positive and EBV-negative gastric epithelial cell models were analyzed to evaluate cell viability, apoptosis induction, signaling pathways, and viral gene regulation. BART miRNA expression was quantified by RT-qPCR, and promoter activity was examined using luciferase reporter assays. Downstream target gene expression was analyzed at both the transcript and protein levels. Recombinant EBV lacking BZLF1 or LMP2A was used to assess the contributions of lytic activation and LMP2A-associated signaling. Dasatinib preferentially reduced viability and induced apoptosis in EBV-positive gastric epithelial cells compared with EBV-negative counterparts. Treatment suppressed phosphorylation of Src and ERK and reduced expression of the anti-apoptotic proteins BCL-xL and MCL1. Apoptosis was also observed in cells infected with LMP2A-deficient EBV, suggesting that the effect cannot be fully explained by inhibition of LMP2A-associated signaling. Dasatinib inhibited BART miRNA promoter activity and reduced pri-, pre-, and mature miR-BART levels, accompanied by increased expression of pro-apoptotic target genes including , , , , and . In parallel, dasatinib suppressed BZLF1 promoter activity without evidence of lytic reactivation. Dasatinib promotes apoptosis in EBV-positive gastric epithelial cells in association with coordinated suppression of SFK signaling and EBV-encoded BART miRNA expression, accompanied by derepression of pro-apoptotic cellular genes. These findings reveal a previously underappreciated vulnerability of EBV-positive epithelial cells and suggest that targeting host kinase signaling pathways that regulate viral microRNAs may represent a potential therapeutic strategy for EBV-associated malignancies. - Source: PubMed
Publication date: 2026/03/26
Liu YuxinTumurgan ZolzayaWai Aung PhyoAkter MoushumiWadi Afifah Fatimah Azzahra AhmadMizukami YoichiWada MasamiOkada ShunpeiNiino DaisukeMurata TakayukiIizasa HisashiYoshiyama Hironori - Chemotherapy can compromise the fertility of boys with cancer, yet no standard protocols exist to preserve their reproductive potential. Before puberty, germ cells are almost exclusively spermatogonia that can be the target of anticancer drugs. Doxorubicin (DXO), a widely used anthracycline in pediatric oncology, has been associated with infertility in adulthood, but its immediate effects on prepubertal germ cells remain poorly understood. In the present study, a preclinical rat model of prepubertal DXO exposure was developed to characterize the mechanisms underlying immediate DXO-induced germ cell damage. Six-day-old pups, received a single intraperitoneal injection of DXO (5 mg/kg) and effects were measured after 24 or 48 h. DXO exposure significantly reduced relative testis weight from 24 h and significantly increased apoptosis and germ cell loss at 48 h, while circulating testosterone remained unchanged, suggesting a selective germline effect. RNA-seq was done on GFP-positive germ cells purified at 24 h. Transcriptomic analysis confirmed the enrichment in spermatogonial stem cells (SSCs) in the GFP-sorted population. Moreover, DXO induced 51 differentially expressed genes (49 upregulated, 2 down regulated) that were mostly related the p53-dependant apoptosis pathway. Pro-apoptotic genes (Cdkn1a, Bbc3/Puma, Tp53inp1, Fas) and oxidative stress regulators (Sesn2, Eda2r, Abhd4) were induced, whereas DNA repair genes (Mgmt, Xrcc1, Polh, Gadd45α, …) were not activated. Our data revealed the DXO-induced immediate transcriptomic response after 24 h, leading to germ cell death observed by histology at 48 h. These findings suggest that SSCs respond to DXO by favoring apoptosis and stress regulation, a strategy that may preserve germline integrity and reduce the risk of transmitting genetic damage to the next generation. - Source: PubMed
Publication date: 2026/02/28
Beaud HermanceHug ElisaScott-Boyer Marie-PierRwigemera ArletteTremblay AmélieDroit ArnaudDelbes Géraldine - - Source: PubMed
Publication date: 2026/01/06
Gu JingwenChen TianpingGao ShanLong Tengfei - Sleep disorders are multifactorial conditions influenced by genetic and environmental factors. However, the causal roles of specific cellular senescence-related genes in distinct sleep disorders subtypes remain unclear. This study aimed to dissect these relationships by integrating multi-omics data to identify potential causal pathways in sleep apnea and insomnia. - Source: PubMed
Publication date: 2026/01/05
Li JinyingDing SuchunZhang XingboTang LiJiang Wanwei