Ask about this productRelated genes to: VEGFR2 antibody
- Gene:
- KDR NIH gene
- Name:
- kinase insert domain receptor
- Previous symbol:
- -
- Synonyms:
- FLK1, VEGFR, VEGFR2, CD309
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2019-04-23
Related products to: VEGFR2 antibody
Related articles to: VEGFR2 antibody
- Physical-layer key generation (PLKG) is a technique that produces symmetric encryption keys by exploiting the inherent characteristics of wireless channels. It offers advantages including high physical-layer security, elimination of pre-shared keys, dynamic upgradability, and resistance to quantum attacks, making PLKG a promising security solution for next-generation (6G) networks. However, satellite communication channels exhibit high dynamics and long propagation delays. Characteristics such as large Doppler shifts, short coherence times, and orbital predictability pose severe challenges to PLKG, including reciprocity degradation, low key generation rate (KGR), and susceptibility to channel-prediction attacks. This work proposes a delay-Doppler domain time-hopping key generation scheme (KE-DD-TH) based on Orthogonal Time Frequency Space (OTFS) modulation for high-speed links between Low-Earth-Orbit (LEO)/Medium-Earth-Orbit (MEO) satellites and ground terminals in Ka/Ku bands. The scheme performs non-uniform sampling on the DD domain grid of OTFS symbols using an ephemeris-driven pseudo-random time-hopping sequence generated by cascaded linear feedback shift registers (LFSRs) and a nonlinear matrix transformation. Both legitimate parties estimate the channel only at time-hopping instants and multiply two adjacent estimates to construct an "equivalent channel" matrix, yielding a random source with high entropy, high reciprocity, and low predictability. The eavesdropper's key disagreement rate (KDR) remains close to 0.5 under all signal-to-noise ratio (SNR) conditions, corresponding to the ideal random-guessing baseline. This indicates that Eve obtains negligible mutual information, i.e., I(KA;KE)≈0. By contrast, the conventional KE-DD scheme allows Eve's KDR to degrade to 0.014 at 30 dB SNR, indicating near-complete key recovery. The generated keys pass all 12 randomness tests of the NIST SP 800-22 statistical test suite. - Source: PubMed
Publication date: 2026/05/20
Li WeiBai ZhendieWang JikangXu XiaofanZhu Xianggeng - Pharmacophore hybridization is a well-established strategy for developing novel anticancer agents with improved biological profiles. In this study, a new series of ()-4-(4-acrylamidophenoxy)--methylpicolinamide derivatives has been rationally designed by hybridizing key structural features of sorafenib with cinnamide pharmacophores and subsequently synthesized. The antiproliferative activities of the synthesized compounds were evaluated against a panel of human cancer cell lines, including A549 (lung), DU-145 (prostate), SKOV3 (ovarian), and HepG2 (liver), along with non-cancerous Hek293T cells. In comparison with the standard drug sorafenib, most of the ()-4-(4-acrylamidophenoxy)--methylpicolinamides demonstrated significant antiproliferative activity, with specificity toward the HepG2 (liver cancer) cell line, and no effect on the noncancerous cells (Hek293T). Among them, compound , the derivative containing a trifluoromethyl-substituted cinnamoyl moiety was identified as the lead candidate, exhibiting an IC of 5.3 µM towards HepG2 (liver) cancer cells, comparable to the reference drug sorafenib. Enzyme inhibition studies showed that compound inhibited both b-Raf and VEGFR-2 with IC values of 1.45 and 0.37 µM, respectively. Furthermore, compound suppressed angiogenesis in vitro and in vivo, as evidenced by the tube formation assay using HUVECs and in transgenic zebrafish Tg(fli1a:EGFP) models, respectively. Mechanistic studies indicated that compound induced apoptosis in HepG2 cells through mitochondrial membrane depolarization and increased ROS generation. Molecular docking studies supported experimental findings and showed that can interact with catalytically active residues via hydrogen-bonding interactions. Overall, these results highlight the potential of compound as a promising dual target therapeutic lead with dual direct anticancer and antiangiogenic properties. - Source: PubMed
Publication date: 2026/05/20
Velma Ganga ReddyTelukutla Srinivasa ReddyVankudoth JayaramGrewal Ajmer SinghPrivér StevenYedla PoornachandraAkunuri RavikumarWlodkowic DonaldPabbaraja SrihariBhargava Suresh KPlebanski MagdalenaKamal Ahmed - Aging, especially after menopause, reduces the quantity and function of adult stem cells. Estrogen deficiency impairs proliferation, differentiation, and regenerative capacity. This study evaluated whether estrogen enhances endothelial differentiation of adipose-derived stromal cells (ADSCs) and improves therapeutic efficacy in critical limb ischemia (CLI). - Source: PubMed
Publication date: 2026/05/12
Chiang Hsin-JuHsiao Chang-ChunLeu Steve - Infectious diseases exacerbate atherosclerosis-associated morbidity and mortality by inducing sustained inflammatory responses characterized by elevated IL-6, TNF-α, IFN-γ, and CXCL10. Persistent CXCL10-driven recruitment of CXCR3⁺ immune cells promotes endothelial dysfunction and atherosclerotic progression. Although mesenchymal stem cells (MSCs) respond to inflammatory cues and secrete CXCL10, the contribution of CXCL10/CXCR3 signaling to intrinsic MSC immunomodulatory programming remains poorly understood. The objective of this study is to investigate whether CXCL10 signaling can modulate MSC-mediated immunoregulation. To address this, Wharton's jelly-derived MSCs (WJ-MSCs) were genetically engineered to express a membrane-anchored CXCL10-Lactadherin C1/C2 fusion protein (CXCL10-LACTC1/C2). This strategy was designed to recapitulate physiological, localized, and sustained CXCL10 signaling, enabling spatially restricted chemokine presentation that more closely mimics cell-associated CXCL10 in inflammatory microenvironments compared with soluble CXCL10. The Lactadherin C1/C2 domain was selected to achieve stable, physiological membrane anchoring without introducing artificial transmembrane domains or compromising CXCL10 bioactivity. CXCL10-LACTC1/C2-expressing MSCs exhibited increased expression of key immunoregulatory mediators, including IDO1, TGF-β1, and IL4I1. Furthermore, conditioned medium derived from these MSCs attenuated TNF-α-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs), as indicated by the modulation of endothelial activation and homeostasis markers (ICAM-1, PECAM-1, KDR, vWF, and NRF2) and improvement of cell viability. Collectively, these findings provide mechanistic insight into CXCL10-mediated MSC immunoregulation and support further investigation of MSC-based and cell-free therapeutic strategies aimed at mitigating CXCL10-driven endothelial inflammation in infection-associated vascular injury and atherosclerotic disease progression. - Source: PubMed
Publication date: 2026/05/22
Molo KayaEge RukenAti̇k KübraÇıtak ElifÇulcuoğlu OrçunDarıcı HakanOrdu Emel - This study aimed to assess the ability of diosgenin and its derivatives to suppress three angiogenic receptor tyrosine kinases-VEGFR2, FGFR1, and PDGFRA-through comprehensive in silico screening, molecular docking, and molecular dynamics simulations. - Source: PubMed
Publication date: 2026/05/01
Jyotishi CharmiPatel MansiPrajapati SureshGupta Reeshu