Ask about this productRelated genes to: PTPN12 Blocking Peptide
- Gene:
- PTPN12 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 12
- Previous symbol:
- -
- Synonyms:
- PTPG1, PTP-PEST
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2019-02-14
Related products to: PTPN12 Blocking Peptide
Related articles to: PTPN12 Blocking Peptide
- Microfracture (MF) is widely used for cartilage repair, but it often yields limited clinical benefit because it predominantly induces fibrocartilage formation. However, the mechanisms underlying this fibrocartilaginous repair remain insufficiently defined. In this study, temporal histopathological profiling and integrative bioinformatic analyses of post-microfracture specimens revealed that early extracellular iron accumulation was positively associated with ferroptosis severity. Single-cell RNA sequencing further delineated a bifurcating differentiation trajectory of bone marrow mesenchymal stem cells (BMSCs) toward either hyaline-like chondrocytes or fibrocartilaginous chondrocytes, with ferroptosis acting as a critical regulator at the branch point. Given the antioxidant and ferroptosis-modulating activity of curcumin-derived components, we hypothesized that curcuma-derived extracellular vesicles (CDEVs) could suppress ferroptosis and bias the differentiation of BMSCs toward hyaline cartilage. Mechanistically, in vitro assays identified Pvu-miR-159 in CDEVs as a key functional cargo that attenuates ferroptosis via the PTPN12-ERK1/2-ATF4-GPX4 pathway. To enhance its translational potential, we developed an injectable reactive oxygen species (ROS)-responsive hydrogel enabling sustained CDEVs delivery, which effectively reduced ferroptosis and promoted cartilage regeneration in vivo. Together, these findings uncover a ferroptosis-driven mechanism contributing to suboptimal microfracture repair and support a plant-vesicle-based, ROS-responsive delivery strategy to reprogram BMSCs toward improved regenerative outcomes. - Source: PubMed
Publication date: 2026/05/22
Mu YuhaoLi HaoZhang RuiyangLi RunmengMa KeLi FakaiYang YongkangRen YimingGuo ZhengGao TianzeWang ChaoMiao JiafengYan QinlinGuan JuanLiu ShuyunGuo Quanyi - Peters anomaly is an anterior segment dysgenesis and a leading cause of congenital corneal opacity. Here, we show that loss of ABL kinases restores lens induction in the absence of FGF signaling but induces Peters anomaly type II independently of ERK signaling, a phenotype also observed with elevated FGF-Ras activity. This defect is rescued by allelic deletion of the ABL substrates CRK and CRKL. Contrary to prevailing models, ABL kinases do not act through direct phosphorylation of CRK proteins; instead, they phosphorylate PTPN12, suppressing p130CAS phosphorylation and CRK recruitment required for RHO GTPase activation. ABL kinase deficiency reduces actomyosin contractility in the lens vesicle and genetically interacts with RHOA inhibition, whereas RAC1 inhibition ameliorates disease phenotypes. These findings define an ABL-PTPN12-p130CAS pathway that controls cytoskeletal tension during lens vesicle separation and suggest that modulation of this process may offer a therapeutic approach for Peters anomaly type II. - Source: PubMed
Publication date: 2026/05/13
Wu HaoMao YingyuWang QianYu HonglianBouaziz MichaelMakrides NeoklisWang EnpengDing ZhipengKoleske Anthony JRadice Glenn LHsu JerryZhang Xin - Protein tyrosine phosphatase non-receptor type 12 (PTPN12), a crucial enzymatic protein involved in cellular signaling, remains understudied in colorectal cancer (CRC). This study investigates this biological macromolecule's potential as a biomarker, examining its protein-protein interactions, therapeutic relevance, and immunomodulatory functions in CRC. - Source: PubMed
Publication date: 2026/04/20
Qian SiyiGong HanZhang PeihePan YimingZhang BinLiu Qiang - Cholangiocarcinoma is a highly malignant tumor of the biliary system with a poor prognosis. The epigenetic molecular mechanisms underlying its occurrence and progression remain unclear, and no effective molecular targets for clinical treatment have been identified. - Source: PubMed
Publication date: 2026/04/06
Qiu RongfangXu ZiweiMeng HuiWang YishanWu QinqqingZeng LuluZhao HaixiaMao ZianWeng QiaoyouTu JianfeiZhao ZhongweiChen MinjiangYang YangJi Jiansong - To construct and validate a diagnostic model for osteonecrosis of the femoral head (ONFH) based on alcohol exposure-related genes using machine learning methods. - Source: PubMed
Tao HongchengLiang FukaiHuang WenboFan SiqiZeng Ping