PTP4A3 Antibody
- Known as:
- PTP4A3 Antibody
- Catalog number:
- XW-7843
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTP4A3 Antibody
Related genes to: PTP4A3 Antibody
- Gene:
- PTP4A3 NIH gene
- Name:
- protein tyrosine phosphatase 4A3
- Previous symbol:
- -
- Synonyms:
- PRL-3, PRL-R, PRL3
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-09
- Date modifiied:
- 2019-02-14
Related products to: PTP4A3 Antibody
Related articles to: PTP4A3 Antibody
- Diabetic retinopathy (DR) is a common microvascular complication of diabetes mellitus and an important cause of acquired blindness among working-age populations globally. Endothelial cell dysfunction is involved in the elevated diabetic retinal vascular leakage and pathological neovascularization. This study aimed to elucidate the impact of PTP4A3 in endothelial cell dysfunction in DR-related models. PTP4A3 expression was significantly increased in human diabetic retinopathy, and the streptozotocin-induced diabetic (STZ) model and oxygen-induced retinopathy (OIR) model. PTP4A3 overexpression led to excessive proliferation and migration of endothelial cell. Furthermore, PTP4A3 overexpression disrupted endothelial cell barrier function through decreasing Occludin and Claudin-5 expression. The PTP4A3 inhibitor reversed endothelial cell dysfunction induced by PTP4A3 overexpression in vitro, and ameliorated retinal vascular leakage and pathological neovascularization in vivo. Inhibition of PI3K or AKT partly alleviated endothelial cell dysfunction induced by PTP4A3 overexpression. Overall, PTP4A3 contributes to the enhanced proliferation, migration, and permeability of endothelial cells, which is associated with PI3K-AKT signaling pathway activation, thereby promoting retinal vascular leakage and pathological neovascularization. - Source: PubMed
Publication date: 2026/03/18
Gui Yong-KunYan Zhi-XinRen Rui-FangZhu Rui-RuiZhu De-WeiSun Yu-YingZhang Ping - Acute myeloid leukemia (AML)'s treatment and remission remains unsatisfactory. A prognostic risk-scoring model containing seven signature genes (POU3F1, RPGR, PTP4A3, SOCS1, FAM83G, GREB1 and COL2A1), was developed by LASSO-Cox regression analysis. In the training set, the test group, area under the curve values of 1, 3, and 5 years were 0.876, 0.877, 0.937, and 0.974, 0.878, 0.976 respectively, which indicates a good predictive efficacy. In the two external GEO (GSE71014 and GSE6891) datasets, area under the curve values of 1, 3, 5 years were 0.847, 0.857, 0.822, and 0.830, 0.863, 0.891 respectively. Our seven signature genes containing risk-scoring model performed excellently in evaluating the OS of AML patients. - Source: PubMed
Publication date: 2025/12/26
Liu BinZhang JianWang JingWang QianLiu XiaomanSun Hui - This study aims to examine the pro-apoptotic and anti-migratory effects of Berberine in KB-1 oral cancer cells and its role in ferroptosis via glutathione peroxidase4/six-transmembrane epithelial antigen of prostate3 (GPX4/STEAP3) signaling pathway. - Source: PubMed
Publication date: 2025/11/01
Alassiri Saeed - - Source: PubMed
Publication date: 2025/12/04
Greenstein Sarah JRamlogan-Steel Charmaine AWise Ingrid AWilson Rebecca JSteel Jason C - Acute myeloid leukemia (AML), a biologically heterogeneous malignancy, requires improved prognostic models, particularly for patients with intermediate-risk profiles and lacking definitive genetic markers. Therefore, this study aims to identify biologically coherent and clinically informative gene signatures using a novel prognostic modeling approach integrating gene expression profiles with protein–protein interaction networks. - Source: PubMed
Publication date: 2025/12/03
Song Jong KeonKim HyeryHwang Sang-Hyun