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
- 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 - Tetranychus evansi is an invasive spider mite pest of solanaceous crops worldwide. Its rapid global spread and ability to develop acaricide resistance highlight the need for robust genomic resources and functional genetic tools for custom control strategies. Here, we present a genome assembly and establish efficient CRISPR/Cas9 editing in T. evansi to enable mechanistic studies of host adaptation and pesticide resistance. Using an inbred line and Oxford Nanopore Technologies long-read sequencing, we assembled an 89 Mb genome into 13 contigs (N50 = 18.6 Mb) and annotated 14,246 protein-coding genes. Manual curation of detoxification gene families (P450s, CCEs, GSTs, UGTs, ABC transporters and DOGs), revealed smaller repertoires than in the polyphagous relative Tetranychus urticae. To enable reverse genetics, we adapted SYNCAS for maternal delivery of CRISPR/Cas9 in T. evansi. Targeting the phytoene desaturase (PD) pigmentation marker produced reliable knockouts with visible lack of red pigmentation and editing efficiencies of ∼10-15%, allowing the efficient creation of stable mutant lines. We further applied precision gene editing to knock-in (KI) the M918T and M918L substitutions into the voltage-gated sodium channel (VGSC). While M918L was lethal in T. evansi, we generated multiple homozygous lines for M918T (KI efficiency ∼ 4.4%). Bioassays demonstrated that while the mutation caused extremely high levels of bifenthrin resistance (RR = 345-645), this was less so for β-cyfluthrin (RR = 113-127), deltamethrin (RR = 58.2-65.6) and tau-fluvalinate (RR = 87.7-98), revealing the specific role of M918T in pyrethroid resistance. Collectively, these resources establish T. evansi as a tractable system for reverse genetic analysis and provide a reference for future comparative and population genomics. - Source: PubMed
Publication date: 2026/05/20
Amezian DriesDe Graeve FemkeMettumpurath Sasi RohithVanhaecht LotteMocchetti AntonioVillacis Perez ErnestoKant Merijn RDe Rouck SanderVan Leeuwen Thomas - Maternal nutritional restriction during gestation impairs placental vascular development; however, the underlying mechanisms in goats are still not fully understood. This study investigated the effects of feed restriction (70 % of ad libitum intake) from day 50 of gestation until parturition on placental vascular morphometry and the expression of key angiogenic factors. Placentas from control goats (C, n = 5) and feed-restricted goats (PFR, n = 5) were analyzed using immunohistochemistry, histomorphometry, and RT-qPCR. Nutritional restriction significantly reduced the number of blood vessels while increasing their mean area and perimeter, without affecting vascular density. Immunohistochemistry revealed a marked reduction in FGF2 and ANGPT2 expression, accompanied by a compensatory increase in ANGPT1 and CD31. Transcriptional analysis showed an upward trend in the expression of genes such as KDR, while ANGPT1 expression was significantly increased. Overall, these findings indicate that maternal undernutrition induces adaptive vascular remodeling, characterized by fewer but larger vessels and selective modulation of angiogenic pathways, suggesting a compensatory mechanism aimed at preserving placental function under nutrient stress. - Source: PubMed
Publication date: 2026/05/12
Fiorimanti Mariana RCristofolini Andrea LGómez Keisy PMoreira-Espinoza María JBarbeito Claudio GMerkis Cecilia I - A recent study reported that endothelial PAS domain protein 1 (EPAS1; hypoxia-inducible factor 2α) acts downstream of PGC-1α to regulate the slow-twitch muscle fiber program in mice, yet its role in human physiology and exercise adaptation remains unclear. The aim of this study was threefold: (1) to investigate EPAS1 gene expression in human skeletal muscle and its association with muscle fiber composition and the expression of endurance-related genes; (2) to determine how EPAS1 expression responds to aerobic training; and (3) to examine whether EPAS1 genetic variation is linked to aerobic capacity, hemoglobin, and athletic status. The study involved 1234 subjects, including 943 athletes and 291 untrained individuals. EPAS1 gene expression was significantly higher in endurance athletes compared with power athletes (p = 0.011) and was positively associated with the proportion of slow-twitch muscle fibers in the vastus lateralis of untrained subjects (p = 0.0008) and athletes (p = 0.0033). EPAS1 expression was higher in females (p = 0.0028) and negatively associated with smoking status (p = 0.0007). Moreover, EPAS1 expression showed positive association with endurance-related genes, including ANGPT2, CKM, CPT1B, EPOR, FNDC5, HIF1A, KDR, MYBPC3, NFATC4, NOS3, PPARA, PPARD, PPARGC1A, UCP2, and VEGFA. Analysis of 24 publicly available skeletal muscle transcriptomic datasets demonstrated that EPAS1 expression increased significantly (meta-analysis p = 9.2 × 10) following aerobic training. Finally, genetically predicted higher EPAS1 expression (i.e., carriage of the EPAS1 rs6756667 A allele) was positively associated with endurance athlete status in both sexes (p = 0.0004) and with VO₂max (p = 0.046) and hemoglobin (p = 0.041) in male athletes. These findings potentially identify EPAS1 as an important genetic factor associated with muscle fiber composition, endurance-related phenotypes, and adaptation to aerobic training. - Source: PubMed
Dautova Albina ZValeeva Elena VSemenova Ekaterina AMavliev Fanis AZverev Alexey ANazarenko Andrey SJohn GeorgeZhelankin Andrey VLarin Andrey KKulemin Nikolay ASultanov Rinat IGenerozov Edward VAhmetov Ildus I