PTP4A2 Antibody
- Known as:
- PTP4A2 Antibody
- Catalog number:
- XW-7842
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTP4A2 Antibody
Related genes to: PTP4A2 Antibody
- Gene:
- PTP4A2 NIH gene
- Name:
- protein tyrosine phosphatase 4A2
- Previous symbol:
- PTP4A
- Synonyms:
- HU-PP-1, PTPCAAX2, OV-1, ptp-IV1a, PRL-2, PRL2
- Chromosome:
- 1p35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-14
- Date modifiied:
- 2019-02-14
Related products to: PTP4A2 Antibody
Related articles to: PTP4A2 Antibody
- Non-small cell lung cancer (NSCLC) is a major subtype of lung cancer and accounts for a large proportion of cancer-related deaths worldwide. Despite extensive research progress in recent years, the diagnosis and treatment of lung cancer remain insufficient. There is an urgent need to deepen the mechanistic understanding of lung cancer, develop early diagnostic strategies, and explore novel therapeutic targets. In this study, qRT-PCR was used to detect the expression of circPTP4A2 (circular RNA PTP4A2) in tumor and adjacent normal tissues from 50 NSCLC patients. CircPTP4A2 was significantly upregulated in tumor tissues and was closely associated with patient survival and prognosis. In vitro silencing of circPTP4A2 in NSCLC cell lines SPCA1 and H1299 significantly inhibited cell proliferation and malignant metastatic potential. Moreover, modulating the expression of miR-127-5p and SMC3 effectively reversed the phenotypic changes induced by circPTP4A2 knockdown. In conclusion, circPTP4A2 is upregulated in NSCLC and promotes tumorigenesis and progression through the miR-127-5p/SMC3 signaling axis. - Source: PubMed
Publication date: 2026/05/07
Feng YaliHong JiangYang ChanggangCheng ChunXue YujieZhang JiaqiLu YuCao XiangJiang GengxiChong Xiaodan - Acute myeloid leukemia (AML) is an aggressive hematological malignancy that is sustained by leukemia-initiating cells (LICs). While PTP4A2 phosphatase, as known as PRL2, is highly expressed in AML, the mechanisms by which PTP4A2 promotes leukemogenesis are largely unexplored. In this study, we demonstrate that PTP4A2 promotes AML by inhibiting the p53 tumor suppressor pathway in LICs. Using KMT2A-MLLT3-driven AML as a model, we found that PTP4A2 deficiency activates p53 and induces LIC apoptosis and senescence, thereby extending the survival of recipient mice repopulated with Ptp4a2-/- LICs. Mechanistically, PTP4A2 directly interacts with p53 and dephosphorylates it at serine 392, decreasing p53 stability and activity to enhance LIC proliferation and survival. Collectively, our findings identify p53 as a potential PTP4A2 substrate in leukemia cells and uncover a novel mechanism by which PTP4A2 enhances LIC maintenance. - Source: PubMed
Publication date: 2026/04/15
Xiao ShiyuKopbayashi MichihiroBai YunpengCai WenjieBarajas SergioAmin Mohammed AbdullahelVemula SasidharYao ChonghuaYang YuxiaBorchers ChristopherMays Tiffany MSotelo MagdalenaPan HaoJia YuzhiShen JianHu Sophie Kimiko KuriyamaAli MoiezVeranga SophiaOgino JaymeEggleston Sydney GLiu HuipingPerlman HarrisLi LorettaAltman Jessica KAbaza YasminEklund Elizabeth AJi PengZhang Christine RKhan IrumMayo Lindsey DMulloy James CSukhanova MadinaDou YaliPlatanias Leonidas CZhang Zhong-YinChen HongxiaLiu Yan - Premature ovarian insufficiency (POI) profoundly compromises female reproductive health through accelerated follicle depletion and endocrine disruption. Emerging evidence highlights the therapeutic potential of mesenchymal stem cell-derived exosomes (MSC-Exs), particularly when their function is enhanced by hypoxic preconditioning. In this study, the ability of hypoxia-preconditioned MSC-Exs (H-Exs) to ameliorate oxidative damage to granulosa cells (GCs) and restore ovarian function, was systematically evaluated, and a POI rat model was used to investigate the underlying mechanism. - Source: PubMed
Publication date: 2026/01/22
Zhu XiaolanShi XuyanLu JingjingLi WenxinLiu YueqinJiang LinLv Yanting - Ovarian cancer (OC) has the highest mortality rate of all gynaecological malignancies, partly attributable to its propensity for chemotherapy resistance. The most common subtype of OC is serous, of which high-grade serous ovarian cancer (HGSOC) is the most lethal subtype. Protein tyrosine phosphatase 4A3 (PTP4A3) overexpression is implicated in tumour cell invasion and metastasis by upregulating the PI3K/Akt/mTORC1 axis. Previously, we reported that PTP4A3 increased the survival of non-serous OC cells by activating the autophagy pathway. Here, we investigated the impact of PTP4A3 on cell proliferation, autophagy and chemoresistance in HGSOC cells and whether targeting PTP4A3 in HGSOC cells that overexpress this phosphatase would sensitise them to existing chemotherapeutic drugs. Gene silencing of PTP4A3 resulted in the upregulation of compensatory mechanisms that overcame the loss of PTP4A3 expression, but this was mitigated by pan-PTP4A inhibition with JMS-053 in HGSOC cells. Moreover, shRNA-mediated silencing of PTP4A3 sensitised HGSOC cells to clinically relevant chemotherapeutic drugs. Overall, we show that compensatory mechanisms from PTP4A1 and PTP4A2 can arise when specifically targeting PTP4A3 in HGSOC and that pan-PTP4A inhibition can overcome those effects. - Source: PubMed
Publication date: 2025/07/14
López-Garza AnaJames DavidCreagh EmmaMurray James T - Hepatocellular carcinoma (HCC) is a highly aggressive malignancy. As a specific immune cell subpopulation, FGFBP2 NK cells play a crucial part in immune surveillance of HCC progression. This study set out to identify prognostic signature related to FGFBP2 NK cell in HCC. - Source: PubMed
Publication date: 2025/05/20
Wu YinbingPeng HuanjunChen GuangkangTu YinuoYu Xinpei