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
- Tumor protein p53-regulated apoptosis-inducing protein 1 (TP53AIP1) has been implicated in tumor suppression, but its role in breast cancer remains unclear. This study evaluated the expression pattern, prognostic value, immune infiltration association, methylation status, and biological function of TP53AIP1 in breast cancer using TCGA transcriptomic data, public methylation datasets, immunohistochemistry, and in vitro experiments. TP53AIP1 was significantly downregulated in breast cancer tissues and was identified as an independent prognostic factor for poor survival. TP53AIP1 expression was positively associated with transcriptome-estimated infiltration of natural killer cells, mast cells, and plasmacytoid dendritic cells. Methylation analysis showed that TP53AIP1 promoter hypermethylation was associated with reduced TP53AIP1 expression, suggesting a potential epigenetic silencing mechanism. Functionally, TP53AIP1 overexpression suppressed breast cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition and, promoted apoptosis and cell-cycle arrest. Mechanistically, TP53AIP1 overexpression reduced MEK/ERK phosphorylation, whereas MAPK pathway reactivation partially reversed its inhibitory effects on malignant phenotypes. These findings suggest that TP53AIP1 may serve as a potential prognostic biomarker and tumor-suppressive candidate in breast cancer, with its effects at least partly associated with MAPK pathway attenuation. - Source: PubMed
Publication date: 2026/07/16
Deng MeiWu XuetingBai JinhuiSong JingzhiXiong ChaoWu HuixianQin Jie - Prolactinomas are typically benign but represent a major cause of endocrine dysfunction. However, their molecular subtypes remain undefined, and clinical implications of such subtypes are unclear. The objective of this study was to characterize the genomic subtypes of prolactinomas and evaluate associated clinicopathological and immunological features. - Source: PubMed
Publication date: 2026/06/26
Wang Da PengLiu Yan TingDai Yu TingChen De ShengCheng Yi JunLin Shao JianZhang YanXue LiXie JingWu Zhe Bao - 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