Ask about this productRelated genes to: PTK2 antibody
- Gene:
- PTK2 NIH gene
- Name:
- protein tyrosine kinase 2
- Previous symbol:
- -
- Synonyms:
- FAK, FADK, FAK1, PPP1R71
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-02
- Date modifiied:
- 2014-11-18
Related products to: PTK2 antibody
Related articles to: PTK2 antibody
- Pinellia ternate has long been used to treat respiratory diseases, possessing potential anti-tumor activity and exhibiting multi-component, multi-target characteristics. This study prioritized lung cancer-related targets using the HERBGAT framework based on graph attention networks (GAT). High-quality PDB structures were retrieved, and diffusion-generative docking was performed to construct complex conformations and assess their confidence levels. Molecular dynamics simulations of representative complexes were conducted over 200 ns, and binding free energies were estimated using the MM/PBSA method. The pharmacokinetic characteristics of the bioactive compounds were evaluated using Swiss ADME and PreADMET computational tools, and density functional theory (DFT) analysis using ORCA software was combined to explore their electronic structure and properties. In this study, the potential targets of Pinellia ternata highly overlap with lung cancer pathological genes, with FGFR4, CDK2, JAK2, KDR, PAK4, PTK2 and PDGFRA being the core. Baicalein exhibits a conserved binding mode of "hinge hydrogen bond-aromatic interlayer-hydrophobic groove" at targets such as PTK2/KDR/JAK2. Energy decomposition indicates that van der Waals forces and nonpolar solvation are the main thermodynamic driving forces for complex formation. Density functional theory (DFT) analysis further reveals that the high electronic "softness" of baicalein and its sensitive response to the environment in terms of frontier orbitals and electrostatic potential may be related to its high affinity, which is ubiquitous in different pockets. This study provides a computational chain of evidence for the intervention of Pinellia ternata's active ingredient on lung cancer-related targets. The well-defined cross-target migratory pharmacophore of baicalein, consistent energy and kinetics, and the oral pharmacodynamics of ADMET indicate that it can serve as a multi-target lead compound targeting the PTK2/KDR migration-angiogenesis pathway, while also affecting JAK2 and CDK2. Given that the current evidence is based on in-silico predictions, further validation through target enzymology, binding thermodynamics, and cellular pathway experiments is needed. - Source: PubMed
Publication date: 2026/05/18
Bian GuoqiangZhang YuanbinShen YuanhaoXiao PengchengZhang DaifengXie JiadongLi XiongChen DuoHu KongfaHu Chenjun - Macroautophagy/autophagy represents a promising therapeutic target in oncology, exhibiting context-dependent roles in tumor progression. Kinase inhibitors are a large group of anti-cancer drugs, and elucidating the regulatory effects of different kinase inhibitors on autophagy offers a valuable strategy to advance our understanding of autophagy regulation in cancer and develop innovative anti-cancer therapies. In this study, we developed a drug screening platform and performed high-content screening using a kinase inhibitor library. The screening identified PTK2/FAK (protein tyrosine kinase 2) inhibitors as potent autophagy inducers. Mechanistic investigations revealed that PTK2/FAK inhibition triggers rapid autophagy flux through a non-classical mechanism dependent on PTK2/FAK expression, which is associated with the spatial redistribution of ER exit sites (ERES). Further analysis demonstrated that PTK2/FAK inhibitor (FAKi)-induced ERES-associated autophagy is not contingent upon full PREB/SEC12 and SEC16 expression, but is sensitized to TMED9 expression level. Additionally, we identified AKAP13 as a novel FAKi-responsive protein that undergoes dephosphorylation upon FAKi treatment and contributes to TMED9-mediated ERES-associated autophagy. Given that ERES-associated autophagy is initiated through membrane contact between ERES and the ER-Golgi intermediate compartment (ERGIC), we further observed enhanced TMED9-ERGIC interactions following FAKi treatment. Furthermore, functional studies confirmed that FAKi-induced autophagy promotes pancreatic ductal adenocarcinoma (PDAC) cell survival both and . Collectively, our work unveils a previously unrecognized mechanism of FAKi-mediated autophagy induction and provides new insights for developing targeted therapies against PDAC. - Source: PubMed
Publication date: 2026/05/17
Wu Ming-YueTang WanZhang Xiao-WenZhang Meng-NiXu He-DanYu Si-RuiCheng YueLi LingChen YingLiang SenPan QiongLu Jia-HongChai Jin - Lung cancer remains the predominant cause of cancer-related mortality worldwide. Piperlongumine is a natural extract that has antitumor effects. However, the mechanism of Piperlongumine on lung cancer remains to be elucidated. This study aimed to investigate the effects and potential mechanisms of Piperlongumine on non-small cell lung cancer. - Source: PubMed
Publication date: 2026/05/14
Huang QianwenChen WenXu XinHua JiaxinLi LehuiHu PingZhang WeiSun Longhua - In males, prostate cancer (PCa) is one of the frequently diagnosed forms of cancer, with high clinical variability and limited treatment options for advanced cases. This receptor, which goes by the names Coagulation Factor II Receptor (F2R) and PAR1, belongs to the family of G-protein-linked membrane proteins and plays roles in both blood clotting processes and the development of malignancies. Whereas F2R has been associated with tumor progression in various malignancies, its specific involvement in PCa is not well understood. Here, we seek to examine the expression patterns and biological functions of F2R to better understand its impact on PCa progression. - Source: PubMed
Ding XianfanWang JinrunNing JinzhuoLi HaoyongCheng Fan - Normal vascular structure and function are crucial for the homeostasis of the central nervous system (CNS), yet the regulation of CNS vasculature remains incompletely understood. Here we show that CD98 heavy chain (CD98hc), also known as SLC3A2 or 4F2hc, is essential for CNS angiogenesis and blood-brain barrier (BBB) integrity. CD98hc is selectively enriched in the CNS endothelium versus the peripheral endothelium in mice and humans. Ablation of endothelial CD98hc in mouse embryos leads to aberrant CNS angiogenesis, impaired BBB formation and cerebral hemorrhage, without affecting the peripheral vasculature. In adults, endothelial CD98hc deficiency does not impact homeostatic CNS angiogenesis but disrupts the BBB and causes neurological deficits. The mechanism involves a CNS-specific reduction in the systemic integrin-FAK pathway in endothelial cells, affecting subsequent VEGFR2 and Wnt-β-catenin pathways. Importantly, FAK activation fully rectifies the CNS vascular phenotype in CD98hc-deficient mice. These findings open promising avenues for CNS-specific vascular regulation and targeted therapy of cerebrovascular diseases. - Source: PubMed
Publication date: 2026/05/12
Hu XiaoyanYu MinYang ShilunFang ChengWei PengjuZhang XunMa YinzhongFeng ZiyingChen YukunYan JingyuWang YingQiu LinhuiSong DengpanGuo FuyouChang Junlei