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
- The effect of dietary phytoestrogens such as genistein (GNT) is controversial. While some of its properties may be desirable in oncological contexts, in healthy tissues GNT may compromise health by affecting reproductive efficiency. This study aimed to investigate the effect of GNT on the functionality of bovine oviductal epithelial cells (BOEC) and to determine the effect on the adhesion and migratory potential of BOEC in culture. BOEC were treated with GNT at concentrations ranging from 0.1 to 10 μM, and viability, adhesion, and migration were subsequently assessed. Cell viability remained close to 100% in most treatments and decreased only to 73% at the highest concentration (10 μM), confirming that GNT does not exert cytotoxic effects. However, adhesion to type I collagen was significantly reduced, even at the lowest concentration; this inhibitory effect became more pronounced at higher doses. Furthermore, in the migration assay, GNT at 1 μM and 5 μM severely inhibited cell migration. This was consistent with a significant downregulation in the mRNA levels of Focal Adhesion Kinase (PTK2) and Paxillin (PXN) with GNT, key genes encoding proteins involved in focal adhesion formation. These findings provide clear evidence of a molecular and cellular mechanism by which GNT impairs normal oviductal cell function, which may consequently compromise cattle fertility. - Source: PubMed
Publication date: 2026/04/30
Vella Milda AlejandraDe Boeck MaximilianoGarcía Daniela CelesteValdecantos Pablo AlbertoRoldán-Olarte Mariela - Atherosclerosis (AS) is a major global health burden. Sodium nitrite, a common environmental and dietary contaminant, has been implicated in promoting AS, but its systematic molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/05/05
Yang HaoBoYu YunFengZhang YongHuiBai YaNanShi YaRuJian WeiXiong - Quercetin (QCT) and luteolin (LTL) are anticancer herbal compounds. However, their combined effects on colon cancer metastasis remain unknown. This study explored the effects and mechanisms of QCT and LTL against colon cancer metastasis using network pharmacology and experimental validation. We systematically screened 74 QCT and LTL targets from the TCMSP, HERB, SwissTargetPrediction, TCGA, and GeneCards databases, which intersected with colon cancer metastasis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed to investigate the biological processes and pathways of QCT and LTL. These analyses revealed that QCT and LTL modulate 119 pathways, and that of these, the PTK2/PI3K/Akt pathway was associated with resistance to colorectal cancer metastasis. Experimental validation demonstrated that the combination of QCT and LTL inhibited the anchorage-independent growth, adhesion, migration, and invasion of CT26 cells. The combined treatment also induced caspase-dependent anoikis in CT26 cells. In addition, QCT and LTL synergistically inhibited the lung metastasis of CT26 colon cancer . Furthermore, Western blot analysis and immunohistochemical detection identified that QCT and LTL inhibited the phosphorylation of PTK2/PI3K/Akt. These findings provide a basis for the application of QCT and LTL for the treatment of colon cancer metastasis. - Source: PubMed
Publication date: 2026/04/30
Wu Shi-WeiChen Jin-FangShi Zi-ManDing Min-RuiHu Bing - Cardiac fibrosis is a defining pathological feature of diabetic cardiomyopathy (DCM), and excessive activation of cardiac fibroblasts plays a critical role in regulating cardiomyocyte function through paracrine signaling. CCN1 (cellular communication network factor 1), an extracellular matrix protein involved in intercellular communication, has been suggested to influence cardiac remodeling, although its specific impact on cardiomyocytes in DCM has remained unclear. In this study, we found that CCN1 expression was markedly elevated in cardiac tissues from DCM mouse models and in insulin-resistant cell models, with fibroblasts serving as the primary source. Proteomic analysis and co-culture experiments demonstrated that CCN1 suppressed cardiomyocyte macroautophagy/autophagy. To determine its role in vivo, we generated fibroblast-specific knockout mice and established a DCM model, demonstrating that deletion ameliorated cardiac dysfunction and restored autophagic activity. We further identified ITGAV-ITGB1/integrin αvβ1 as the receptor mediating CCN1 signaling in cardiomyocytes. Molecular dynamics simulations and co-immunoprecipitation experiments confirmed that CCN1 engaged ITGAV-ITGB1/integrin αvβ1 through its cysteine-knot-containing (CT) domain. Mechanistically, this interaction activated the downstream PTK2/FAK-MTOR signaling pathway, leading to inhibition of cardiomyocyte autophagy. Together, these findings reveal a previously unrecognized fibroblast-cardiomyocyte signaling axis in which fibroblast-derived CCN1 drives DCM progression by suppressing autophagy through ITGAV-ITGB1/integrin αvβ1-dependent signaling. This work provides mechanistic insight into the pathogenesis of DCM and identifies CCN1 as a potential therapeutic target for mitigating disease onset and progression. - Source: PubMed
Publication date: 2026/04/29
Hu Bo-AngZhang LeiSong MingKong Yan-RuJiao Ya-QiongJia XuZhu PingLi Yu-LinTi YunZhang WeiWang Zhi-HaoZhong Ming - Colorectal cancer (CRC) is a major global cause of death, with metastases and chemotherapy resistance contributing to poor outcomes. To identify natural compounds with anticancer potential against CRC and elucidate their action mechanisms, the cytotoxicity of 37 natural compounds was evaluated against the HCT116, leading to the identification of conferone as the lead candidate. Its anti-migratory and anti-invasive effects were evaluated in HCT116, Colo205, and SW480 cells. The interactions between conferone and focal adhesion kinase (FAK) were assessed through protein expression analysis and molecular docking. Glutaminolysis regulation was determined by LC-MS/MS, and related enzyme levels were detected by western blotting. Conferone inhibited migration and invasion in all three CRC cell lines, though it showed limited anti-proliferative activity. At 10 μM, conferone reduced FAK and p-FAK (Tyr397) protein levels, reversing the epithelial-mesenchymal transition. Docking analysis confirmed direct FAK binding and predicted inhibition of its phosphorylation, with greater affinity than the FAK inhibitor 1,2,4,5-benzene tetramine tetrahydrochloride. Conferone also downregulated glutaminase and glutamate-ammonia ligase, increasing glutamine and decreasing glutamic acid. Additionally, it suppressed c-raf phosphorylation and reduced c-Myc expression, blocking glutaminolysis-driven metabolism. These findings highlight conferone as a potential therapeutic agent that targets FAK, alters metabolic reprogramming, and impedes CRC progression. - Source: PubMed
Ong Hien Thi MyAtes EdaJung JaeyongSung Jeong SooPyun Jae-ChulKang Min-Jung