p53AIP1 Antibody
- Known as:
- p53AIP1 Antibody
- Catalog number:
- 2449
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- p53AIP1 Antibody
Related genes to: p53AIP1 Antibody
- Gene:
- TP53AIP1 NIH gene
- Name:
- tumor protein p53 regulated apoptosis inducing protein 1
- Previous symbol:
- -
- Synonyms:
- p53AIP1
- Chromosome:
- 11q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-09
- Date modifiied:
- 2016-04-25
Related products to: p53AIP1 Antibody
Related articles to: p53AIP1 Antibody
- Peutz-Jeghers syndrome (PJS) is a rare autosomal dominant disorder hallmarked by mucocutaneous melanocytic macules and gastrointestinal hamartomatous polyposis associated with germline/somatic pathogenic variants in the tumor suppressor . PJS is clinically heterogeneous; however, the relationship between clinical phenotype and genotype remains elusive. Here, we report a family with PJS that harbors a heterozygous whole gene deletion combined with a heterozygous variant in that segregates with mucocutaneous pigmentation in the family. RNA-seq analysis followed by qRT-PCR confirmed that the expression of , , and and a large fraction of p53 signaling pathway components are significantly reduced, while Wnt signaling pathway effectors are upregulated in cells from an affected individual. Our findings shed light on transcriptome-level pathway dysregulation in PJS with germline deletion of . Further evaluation of mutational burden across relevant signaling pathways can likely inform disease prognosis. - Source: PubMed
Publication date: 2025/08/15
Khan Tahir NLiu ChunyuYap Kai LeeSatti Humayoon ShafiqueKhan AyazSafeer MuhammadKhan SherazMalik Naveed AltafZhang FengTariq MuhammadDavis Erica E - This paper studies the toxic effect of micron-sized quartz silica particles on primary human airway epithelial cells (AECs) and the molecular mechanism of its induction of apoptosis. Studies have found that micron-sized quartz silica particles cause AECs damage by activating cell apoptosis. By constructing a competitive endogenous RNA (ceRNA) network, it was identified that three circRNAs (hsa_circ_0052203, hsa_circ_0022429, hsa_circ_0052264) and four key miRNAs (hsa-miR-4646-5p, hsa-miR-150-3p, hsa-miR-6798-3p, hsa-miR-6756-5p) play key roles in regulating apoptosis. In addition, seven mRNAs (LMNB1, TP53AIP1, CASP10, BCL2, LMNB2, CFLAR and ITPR1) were significantly associated with the apoptosis. Functional enrichment analysis indicated that these genes were involved in biological processes such as nuclear lysis, hypoxia response and DNA damage. This study has for the first time revealed the role of the ceRNA network in the apoptosis of AECs induced by micron-sized quartz silica particles, providing new molecular targets and therapeutic ideas for the early pathogenesis of silicosis. - Source: PubMed
Publication date: 2025/08/14
Ma JiaziHan BingYang YongZhang YuCao MaoCao WenyueZhang WeiCheng MengjieCui GuanqunDu ZhongjunChen Shangya - Curcumin, a major phytochemical derived from Curcuma longa, has been shown to enhance the efficacy of chemotherapeutic agents such as doxorubicin, 5-fluorouracil, and cisplatin by overcoming drug resistance, making it a promising adjunct in the treatment of glioblastoma. However, the global gene-expression changes triggered by curcumin in glioblastoma remain underexplored. In this study, we investigated the effects of curcumin on human glioblastoma (U87 MG) cells, where it significantly reduced cell viability and proliferation in a dose- and time-dependent manner and induced apoptosis without affecting senescence. Transcriptomic analysis revealed 5036 differentially expressed genes, with pathway enrichment identifying 13 dysregulated cancer-associated pathways. Notably, curcumin modulated several key regulators involved in MAPK, Ras, TGF-β, Wnt, Cytokine, and TNF signaling pathways. Several apoptosis and cell cycle-associated genes, including PRKCG, GDF7, GDF9, GDF15, GDF5, FZD1, FZD2, FZD8, AIFM3, TP53AIP1, CRD14, NIBAN3, BOK, BCL2L10, BCL2L14, BNIPL, FASLG, GZMM, TNFSF10, TNFSF11, and TNFSF4, were significantly altered. Several pro-apoptotic and anti-BCL, cell-cycle-regulated genes were modulated following curcumin treatment, emphasizing its potential role in curcumin-mediated anti-tumor effects. This study provides insight into the molecular mechanisms underlying curcumin's action against glioblastoma. - Source: PubMed
Publication date: 2025/05/09
Mashozhera Nicole TendayiReddy Chinreddy SubramanyamRanasinghe Yevin NenukaNatarajan PurushothamanReddy Umesh KHankins Gerald - Cervical cancer (CC) patients have a poor prognosis and a low 1-year survival rate due to recurrence or pelvic metastasis. The GSE9750 dataset was analyzed to identify hub genes in CC. CCK-8, colony formation assay, EdU, TUNEL, Transwell assays, and western blot analysis for apoptosis-associated markers were conducted to examine CC cell malignant phenotype after different lentiviral vector treatments. Dual-luciferase assay, ChIP, and MSP were used for regulatory assays. P53-regulated apoptosis-inducing protein 1 (TP53AIP1) was lowly expressed in CC tissues and cell lines, and TP53AIP1 overexpression repressed proliferation, migration, and invasion, and induced apoptosis of CC cells by activating the p53 signaling. DNMT3A bound to the TP53AIP1 promoter and transcriptionally repressed TP53AIP1 expression. DNA-methyltransferase 3A (DNMT3A) silencing inhibited CC development and lung metastasis in vivo, but further TP53AIP1 knockdown reversed this phenomenon by disrupting p53-mediated apoptosis. In summary, DNMT3A transcriptionally repressed TP53AIP1 expression to promote CC progression and metastasis. - Source: PubMed
Publication date: 2025/03/07
Pan XiaohongDu XiuluanJia Suhong - Breast cancer ranks the first in the incidence of female cancer and is the most common cancer threatening the life and health of women worldwide.Tumor protein p53-regulated apoptosis-inducing protein 1 (TP53AIP1) is a pro-apoptotic gene downstream of p53. However, the role of TP53AIP1 in BC needs to be investigated. In vitro and in vivo experiments were conducted to assess the biological functions and associated mechanisms. Several bioinformatics analyses were made, CCK8 assay, wound healing, transwell assays, colony formation assay, EDU, flow cytometry, Immunofluorescence, qRT-PCR and Western-blotting were performed. In our study, we discovered that BC samples had low levels of TP53AIP1 expression, which correlated with a lower survival rate in BC patients. When TP53AIP1 was up-regulated, it caused a decrease in cell proliferation, migration, and invasion. It also induced epithelial-to-mesenchymal transition (EMT) and protective autophagy. Furthermore, the over-expression of TP53AIP1 suppressed tumor growth when tested in vivo. We also noticed that TP53AIP1 up-regulation resulted in decreased levels of phosphorylation in AKT and mTOR, suggesting a mechanistic role. In addition, we performed functional rescue experiments where the activation of AKT was able to counteract the impact of TP53AIP1 on the survival and autophagy in breast cancer cell lines. This suggests that TP53AIP1 acts as an oncogene by controlling the AKT/mTOR pathway. These findings reveal TP53AIP1 as a gene that suppresses tumor growth and triggers autophagy through the AKT/mTOR pathway in breast cancer cells. As a result, TP53AIP1 presents itself as a potential target for novel therapeutic approaches in treating breast cancer. - Source: PubMed
Publication date: 2024/09/02
Liu ShutianXu TingChen XiTang LiLi LongjiangZhang LiYang YongqiangHuang Jiayi