Ask about this productRelated genes to: FAK1 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: FAK1 antibody
Related articles to: FAK1 antibody
- Focal adhesion kinase (FAK) is overexpressed and hyperactivated in triple-negative breast cancer, driving tumor aggressiveness and cancer stem cell-mediated therapy resistance. Therefore, targeting FAK signalling represents a promising therapeutic strategy. In this study, a series of indole and bis-indole-1,2,4-triazoles were synthesized and evaluated as anti-TNBC agents targeting FAK. Compounds 3c, 4c, and 5c displayed potent cytotoxicity (IC₅₀ = 41-77 µg/mL) with minimal toxicity to normal cells, outperforming precursor compound 2. Wound-healing assay revealed significant inhibition of cell migration, particularly by 4c. Cell cycle analysis revealed that 4c induced S-phase arrest in MCF-7 cells and G1-phase arrest in MDA-MB-231 cells, accompanied by significant apoptosis. In MDA-MB-231 cells, 4c triggered extensive total apoptosis (90.84%) with minimal necrosis. Gene expression studies demonstrated that 4c markedly downregulated PTK2 (FAK), CCL5, and BCL2, while upregulating CASP3, highlighting its dual role as FAK inhibitor and apoptosis inducer. Importantly, 4c efficiently suppressed FAK protein expression (61.3%) in TNBC, compared to the FAK inhibitor GSK-2256098 (70.7%). In vivo toxicity assessment confirmed good tolerability in mice without profound hepatic or renal impairments, while docking and ADMET analyses confirmed strong FAK binding affinity, and favourable pharmacokinetics of 4c. Collectively, 4c emerges as a promising FAK-targeted candidate for TNBC therapy. - Source: PubMed
Publication date: 2026/04/22
Abd El Salam Hayam AAbu-Shahba NourhanIbrahim Fouad GhadhaMahmoud MarwaMostafa Eslam AAbozeid Mona A MAbo-Salem Heba MAzouz Rasha A M - Protein kinases are key components of many signaling pathways that regulate cellular activities, and some of them are indispensable for the viability of cells. We used inducible gene deletion to assess the importance of a set of putative essential protein kinases for growth and viability of the pathogenic yeast Candida albicans and to get clues about the functions of uncharacterized essential kinases. We found that bud32Δ, ctk1Δ, rio1Δ, and rio2Δ mutants were viable but grew very slowly, explaining previous failures to generate homozygous deletion mutants. PTK2 was essential, but under certain conditions ptk2Δ mutants remained viable and over time could acquire suppressor mutations in the Ptk2-dependent plasma membrane ATPase Pma1 that restored growth. Deletion of the uncharacterized orf19.5376 was lethal and the null mutants formed pseudohyphae that lacked normal septa and eventually lysed, a phenotype that was phenocopied by auxin-induced protein depletion. The mutants were defective in septin organization, indicating that the orf19.5376-encoded kinase is functionally similar to the nonessential kinase Elm1 of Saccharomyces cerevisiae, but is indispensable for viability in C. albicans. Mutants lacking orf19.3456, which does not have a homolog in S. cerevisiae, were also nonviable and grew as aseptate, sometimes multinucleate hyphae before cell death. Co-immunoprecipitation followed by liquid chromatography-mass spectrometry identified a protein, encoded by the uncharacterized orf19.193, as a candidate regulatory subunit of the orf19.3456-encoded kinase, as mutants lacking this protein exhibited the same terminal phenotype as orf19.3456 mutants. These results provide strong evidence that instead of using a mitotic exit network (MEN) with only two kinases (Cdc15 and Dbf2), as was previously thought, C. albicans regulates septum formation and cytokinesis via a septation initiation network (SIN), known from fission yeast and filamentous fungi, which contains a protein kinase cascade consisting of the upstream kinase Cdc15, the orf19.3456-encoded kinase, and the downstream kinase Dbf2. - Source: PubMed
Publication date: 2026/04/21
Ramírez-Zavala BernardoKrüger InesSchwanfelder SonjaLackner JohannesKrüger ThomasKniemeyer OlafMorschhäuser Joachim - Early pregnancy is a highly coordinated process requiring precise embryo-maternal communication. Estradiol-17β (E2) is considered the primary conceptus-derived signal responsible for the maternal recognition of pregnancy in pigs. Successful pregnancy establishment requires two distinct peaks of E2 secretion by porcine conceptuses: during days 11-12 (the maternal recognition of pregnancy) and days 15-30 (implantation). Although the role of E2 in signaling to the maternal system is well established, its potential autocrine effects on conceptus development remain unclear. This study examined whether E2 regulates trophoblast function during the maternal recognition of pregnancy and implantation. We demonstrated that expression of estrogen receptors (ESR1, ESR2, GPER1) and selected pregnancy-related genes (FOXO3, GDF15, SERPINE1, ESRRB, ESRRG) changes during early pregnancy in the pig. E2 regulated the gene expression of its receptors (ESR1, ESR2, GPER1), genes involved in E2 synthesis (HSD17B1), prostaglandin synthesis (PTGS2, AKR1C4, PTGES), and key mediators of pregnancy establishment (IL1B2, SERPINE1, FOXO3, GDF15, ESRRB and ESRRG). Furthermore, E2, acting via nuclear estrogen receptors, enhanced trophoblast cell proliferation on days 12 and 15 of pregnancy, and increased adhesion as well as MAPK1/3 and PTK2 protein phosphorylation on day 15 of pregnancy. E2 stimulated cell proliferation via MAPK and PI3K/AKT/mTOR pathways, whereas E2-promoted adhesion was mediated via MAPK and PI3K/AKT signaling. Concluding, these findings indicate that E2 functions not only as a critical embryonic signal for the maternal recognition of pregnancy but also plays an autocrine role in conceptus development, regulating gene expression and trophoblast cell function during early gestation in pigs. - Source: PubMed
Publication date: 2026/04/11
Goryszewska-Szczurek EwelinaWaclawik Agnieszka - The disruption of chondrocyte homeostasis, manifesting as an anabolic/catabolic imbalance and increased apoptosis, is a hallmark of osteoarthritis (OA). While physiological mechanical stimuli are protective, the molecular mechanisms rescuing degenerative chondrocytes remain unclear. This study elucidates how cyclic tensile stress (TS) restores homeostasis using primary chondrocytes from rats with anterior cruciate ligament transection-induced OA. These degenerative chondrocytes exhibited suppressed anabolism (Acan, Col2a1 downregulation) and elevated catabolism (Mmp13, Adamts5 upregulation). Application of TS (10% strain, 0.5 Hz) significantly reversed this pathogenic phenotype, restoring cell viability and extracellular matrix synthesis. Integrated transcriptomic and proteomic analyses identified "Focal Adhesion" as the most significantly enriched pathway. Mechanistically, TS reactivated the suppressed Integrin-FAK-RhoA/ROCK2 cascade, evidenced by increased FAK phosphorylation (Y397) and RhoA/ROCK2 expression. Crucially, FAK knockdown abolished the TS-induced upregulation of RhoA and ROCK2, confirming FAK as the essential mediator. These findings demonstrate that TS rescues degenerative chondrocytes by reactivating the Integrin-FAK-RhoA/ROCK2 axis, suggesting a potential mechanobiological therapeutic target for OA. - Source: PubMed
Publication date: 2026/04/02
Yin ZuozhenXie LiangyuMa JialeYang YongmingZhang XuanshuoYu GongchangShi BinCao Shengnan - Cholecystokinin A receptor (CCKAR) has been linked to poor prognosis in colon cancer patients, but the role of CCKAR in colon cancer cell invasiveness and the underlying mechanisms remain elusive. This study aimed to explore the effect of CCKAR on the invasive potential of colon cancer cells. - Source: PubMed
Publication date: 2026/03/23
Lin Chun-ShiangHsu Ta-WenLee Hsiang-LinKao Shao-Hsuan