PTK2 & APC Protein Protein Interaction Antibody Pair
- Known as:
- PTK2 & Antigen presenting cellular Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0052
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PTK2 & APC Protein Interaction Antibody Pair
Related genes to: PTK2 & APC Protein Protein Interaction Antibody Pair
- 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 & APC Protein Protein Interaction Antibody Pair
Related articles to: PTK2 & APC Protein Protein Interaction Antibody Pair
- This study aimed to elucidate the therapeutic mechanisms of Chai Gui Zexie Decoction against non-small cell lung cancer (NSCLC) through an integrated approach combining metabolomics, network pharmacology, and experimental validation. A subcutaneous NSCLC metastasis model was established in C57BL/6 mice using Lewis lung cancer cells. Mice were randomly assigned to model, low-dose, and high-dose Chai Gui Zexie Decoction groups (n = 6 per group). Tumor growth was monitored over 18 days. Serum metabolomics analysis using liquid chromatography-tandem mass spectrometry was performed to identify differential metabolites and blood-absorbed components. Network pharmacology was employed to predict therapeutic targets, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Western blotting was conducted to validate the expression of core targets (IGF1R, PTK2, SRC) in tumor tissues. High-dose Chai Gui Zexie Decoction significantly inhibited tumor growth compared to the model group (P < 0.05). Metabolomics identified 13 blood-absorbed components, primarily enriched in phenylalanine metabolism. Network pharmacology revealed 195 overlapping targets between the decoction and NSCLC, with 10 core targets identified, including SRC, PTK2, and IGF1R. KEGG analysis implicated key pathways such as PI3K-Akt signaling, EGFR TKI resistance, and Ras/MAPK signaling. Western blot validation confirmed that high-dose treatment significantly downregulated IGF1R, PTK2, and SRC protein expression in tumor tissues (P < 0.05). Chai Gui Zexie Decoction exerts therapeutic effects against NSCLC through a multi-component, multi-target mechanism involving the regulation of RTK signaling pathways and phenylalanine metabolism. These findings provide a scientific basis for its clinical application and highlight potential therapeutic targets for NSCLC treatment. - Source: PubMed
Publication date: 2026/07/21
Lin ManbianZhao AipingChen BishanZhuang SudanLiu Xinyao - Breast cancer (BRCA) is a major health threat to women and often carries a poor prognosis. Succinylation is closely associated with cancer metabolism; however, research on succinylation-related genes (SRGs) in BRCA remains relatively limited. This study first identified differentially expressed genes between normal and BRCA groups in the TCGA cohort and intersected them with known SRGs to obtain differentially expressed SRGs (DE-SRGs). Univariate Cox and LASSO Cox regression analyses were used to screen the DE-SRGs, followed by multivariate Cox regression to develop a succinylation-related prognostic model. Subsequently, patients were categorized into high and low succinylation-related risk score (SRS) groups according to the median score. Two groups were then compared for differences in immune microenvironment characteristics, somatic mutation burden, and drug sensitivity. Additionally, the expression levels of the signature genes were validated via qRT-PCR. This study developed a prognostic risk model for BRCA patients based on 13 SRGs (ACOT4, ALDH3A1, B3GALT1, IFNG, MMP1, NFKB2, PCSK6, PTK2, SERPINA1, SHMT2, SIRT7, ST3GAL1, and SUCLA2). A markedly elevated infiltration of immune cells was observed in the low-SRS group, including B cells, Mast cells, and Macrophages. The tumor mutational burden was notably lower in the low-SRS group. Drug sensitivity analysis suggested that the high-SRS BRCA patients might be more susceptible to FTI-277 and GNF-2. qRT‑PCR results showed that ACOT4, IFNG, MMP1, NFKB2, PCSK6, PTK2, SHMT2, SIRT7, and ST3GAL1 were significantly upregulated in human BRCA cell lines, while ALDH3A1, B3GALT1, and SUCLA2 were significantly downregulated. Our findings highlight the prognostic value of SRGs in BRCA, laying the groundwork for its potential use in guiding personalized treatment. - Source: PubMed
Publication date: 2026/07/17
Chen ZhifengHu Mi - Pancreatic ductal adenocarcinoma (PDAC) is driven by oncogenic KRAS in roughly 90% of cases, and KRAS-pathway inhibition has finally become clinically active. Durable benefit, however, will require identifying the adaptive and baseline vulnerabilities that shape response to KRAS inhibition. Two resistance mechanisms have been proposed separately in the literature - receptor-tyrosine-kinase bypass of KRAS, and dependence on the adhesion kinase FAK - but whether they are one target class or two, and which should partner a KRAS inhibitor, is unresolved. We integrate public perturbation, dependency, and survival data to nominate them as candidate combination partners. Two findings define the separation. First, KRAS loss increases ERBB2/3 receptor expression. This appeared in both an inducible genetic KRAS-extinction model and, independently, in five PDAC lines treated with pharmacological KRAS-G12C/D inhibitors, while MAPK output collapsed as expected. The signal was clearest for ERBB2 and in the genetic model; in the small pharmacological cohort the effect was modest and its confidence intervals crossed zero, so we treat ERBB2/3 up-regulation as a candidate adaptive response - ERBB2-dominant and ERBB3-compatible - not a proven resistance mechanism. Second, focal adhesion kinase (FAK/PTK2) is the top-ranked standing druggable dependency within the KRAS/Src/RTK/adhesion network we examined (essential in 58% of pancreatic lines), yet it is induced by KRAS shutdown. FAK dependency is present at baseline and, in DepMap, is statistically independent of a line's KRAS dependency (Spearman ρ = +0.05, n.s.) - a genuinely standing vulnerability rather than a KRAS-rebound effect. The candidate adaptive response and the standing dependency are not positively co-regulated across the perturbed lines (pooled Spearman ρ = -0.43, but n = 8 and n.s., so this cannot by itself establish independence); we therefore treat them as separable on mechanistic grounds - each nominated by different data and engaged by a different drug - rather than as statistically demonstrated independent programs. A Src-centered signaling-landscape analysis associates patient prognosis with the coordinated invasion-and-RTK program these nodes organize, rather than with any single transcript; this program remains prognostic after adjustment for a conventional EMT/stromal signature, which does not (Src-neighborhood per-standard-deviation OS hazard ratio 1.9, p ≈ 3 × 10⁻⁵; EMT signature null on adjustment). Together these results motivate a concrete, testable hypothesis: that FAK inhibition (a standing dependency) and ERBB inhibition (a candidate induced adaptive response) are candidate partners for a KRAS inhibitor, best evaluated as distinct arms of a biomarker-stratified platform. They also clarify why single-agent Src inhibition - a non-oncogene dependency tested as monotherapy, without a KRAS backbone, in advanced rather than micro-metastatic disease - was not positioned to surface either mechanism. No protein-level, phospho-signaling, or combination-response validation is performed here; all findings are computational nominations that require experimental validation before any clinical inference. - Source: PubMed
Publication date: 2026/07/10
Chen Jake YSaghapour EhsanKurmachalam NikhilOishe GeetanjaliSembay Zhandos - Hepatocellular Carcinoma (HCC) is a matter of great global public health importance; however, its current therapeutic effectiveness is deemed inadequate, and the range of therapeutic targets is limited. This study aimed to explore the efficacy of Bosutinib (BOS) in HCC and the underlying molecular mechanism. - Source: PubMed
Lu CuipingCao TiantianLi ZirongLai Fobao - Vasculogenic mimicry (VM) is a non-endothelial mode of tumor vascularization in which aggressive cancer cells form vessel-like networks that support microcirculation, metastasis, and resistance to anti-angiogenic therapies. VM is particularly prominent in triple-negative breast cancer (TNBC), but its molecular regulators remain incompletely understood. Focal adhesion kinase (FAK) and its paralog, proline-rich tyrosine kinase 2 (Pyk2), are closely related non-receptor tyrosine kinases implicated in epithelial-to-mesenchymal transition (EMT), invasion, and metastasis in TNBC. However, their roles in VM have not been defined. Here we perform transcriptomic analysis of FAK and Pyk2 clinical expression patterns using TNMplot V2, DepMap, and patient cohort datasets to systematically dissect the distinct contributions of FAK and Pyk2 to VM in TNBC. Our in vitro tube formation assay shows that in TNBC cells, knockdown of FAK, but not Pyk2, results in failure to form robust 3D vessel-like networks in Matrigel. Similarly, overexpression of Pyk2, but not FAK, in TNBC cells results in poor vessel-like network formation. Consistent with these findings, analysis of two independent patient cohorts (TCGA-BRCA and METABRIC) revealed selective upregulation of FAK in TNBC, while Pyk2 was inversely associated with vasculogenic-mimicry-associated gene expression, supporting the opposing roles of the two kinases in patient tumors. Taken together, these findings establish that FAK and Pyk2 govern VM through non-redundant, kinase-specific, and functionally opposed mechanisms: FAK acting as a positive regulator of VM, and Pyk2 as a context dependent suppressor of VM at elevated levels. These results nominate FAK as a candidate target for suppressing VM-driven tumor perfusion in TNBC and suggest that dual FAK/Pyk2 inhibition warrants caution hypotheses that remain to be tested pharmacologically. - Source: PubMed
Publication date: 2026/07/06
Madhavan-Kadali ShilpaSneh TalBloch NaamahRosenblatt Joseph DSamson Abraham OGil-Henn Hava