Ask about this productRelated genes to: PYK2 antibody
- Gene:
- PTK2B NIH gene
- Name:
- protein tyrosine kinase 2 beta
- Previous symbol:
- FAK2
- Synonyms:
- CAKB, PYK2, RAFTK, PTK, CADTK
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-22
- Date modifiied:
- 2017-12-06
Related products to: PYK2 antibody
Related articles to: PYK2 antibody
- Residual feed intake (RFI) is an indicator of feed efficiency that reflects variation in nutrient utilization independent of growth. This study characterized physiological traits and multi-omics profiles associated with divergent RFI in small-sized meat ducks. From an initial population of 500 1-day-old ducks, a total of 420 healthy ducks were individually housed from 21 to 42 d to record feed intake, and ducks with low RFI (LRFI) and high RFI (HRFI) were identified for further analyses. During the experiment, 30 ducks per group for growth performance, 15 ducks per group for plasma biochemical and 5 per group for multi-omics. Compared with HRFI ducks, LRFI ducks showed lower feed intake, lower feed conversion ratio (FCR), and lower plasma triglyceride concentrations, whereas body weight gain did not differ between groups. Shotgun metagenomic analysis showed that LRFI ducks were enriched in Bacteroides-related lineages and had higher predicted capacities for complex carbohydrate degradation, lipid and energy metabolism, and cofactor synthesis, whereas HRFI ducks were enriched in taxa including Subdoligranulum variabile and Clostridioides difficile. Untargeted cecal metabolomics revealed distinct lipid- and bile acid-related metabolic profiles between the 2 groups, including differences in long-chain lipid species and bile acid-associated metabolites. Hypothalamic transcriptomic analysis identified differentially expressed genes related to neuropeptide signaling, serotonin biosynthesis, intracellular signaling, and inflammatory regulation, including NMUR2, TPH1, and PTK2B. Correlation analysis integrating microbial taxa, metabolites, and hypothalamic transcripts further revealed coordinated associations among these features in small-sized meat ducks with divergent RFI. Overall, variation in feed efficiency in ducks was associated with differences in cecal microbiota, metabolite profiles, and hypothalamic gene expression, and these results highlight candidate microbial taxa, metabolites, and genes for further validation. - Source: PubMed
Publication date: 2026/06/17
Geng DandanDing YifanJiang YongWang ZhixiuChen GuohongChang GuobinBai Hao - In the developing human placenta, three subtypes of trophoblast cells, cytotrophoblasts (CTBs), extravillous trophoblasts (EVTs), and syncytiotrophoblasts (STBs), mediate critical functions essential for a successful pregnancy. CTBs constitute the stem/progenitor compartment and differentiate into STBs and EVTs within the floating and anchoring villi, respectively. STBs establish the maternal-fetal exchange interface and secrets human chorionic gonadotropin (hCG), a hormone vital for the maintenance of early pregnancy. EVTs anchor the maternal endometrium and invade the uterine tissue to remodel maternal cells, supporting implantation and progression of pregnancy. In this study, we used human trophoblast stem cells (hTSCs) as a model system and performed quantitative, label-free liquid chromatography tandem Mass Spectrometry (LC/MS/MS) to profile proteome and phosphoproteome in TSC stem state (analogous to undifferentiated CTBs) and following their differentiation to STBs and EVTs. Through a multiomics approach, we integrated our proteomics data with global gene expression profiles to correlate cell type specific gene and protein expression during human trophoblast development. We also identified global phosphoproteome and analyzed kinases that are specifically active in hTSC stem state, as well as in differentiated STBs and EVTs. We experimentally validated specific kinases, such as BUB1B, PAK6, PKYMT1 and TNIK are essential for maintaining the hTSC stem state. Additionally, atypical protein kinase C isoforms PKC zeta is essential for STB development, while PTK2B, SRC, TRIO and LYN are important for EVT development. Our findings highlight key kinases uniquely required for specific stages of trophoblast development during human placentation and suggest that pharmacological inhibition of these kinases could negatively impact the placentation process during pregnancy. - Source: PubMed
Publication date: 2026/07/24
Kumar RajnishDasgupta PurbasaRay SomaPaul Soumen - 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 - BRAF mutation is one of the most common oncogenic drivers in gliomas, sharing the highest incidence in pediatric low-grade gliomas (~ 20%) and being frequently associated with poor prognosis. Although combination therapies targeting both BRAF and downstream MAPK signaling have been developed, their efficacy is substantially limited by acquired drug resistance. Consequently, identifying the underlying mechanisms of resistance and novel therapeutic vulnerabilities remains an urgent need. - Source: PubMed
Publication date: 2026/07/13
Wang MinXu ChengyanXie ShanshanJin JichenZhang PengqiLiu JiyongWu ChengXi YongmeiYang Xiaohang - Ovarian cancer is a highly lethal gynecologic malignancy, with metabolic reprogramming being a key contributor to its progression and therapeutic resistance. Although Secreted Frizzled-Related Protein 2 (SFRP2) has been implicated in various cancers, its functional role and molecular mechanisms in ovarian cancer, particularly in regulating metabolic pathways, remain poorly defined. - Source: PubMed
Publication date: 2026/06/23
Sheng JindongXing YiwenLuan JingLiu XiangyuSong HualinSun LuYu MinFu XinWu HuijuanChen YingLiu WenxinWang Ke