VEGF_D
- Known as:
- VEGF_D
- Catalog number:
- 000280A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- VEGF_D
Related genes to: VEGF_D
- Gene:
- VEGFD NIH gene
- Name:
- vascular endothelial growth factor D
- Previous symbol:
- FIGF
- Synonyms:
- VEGF-D
- Chromosome:
- Xp22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-27
- Date modifiied:
- 2016-10-05
Related products to: VEGF_D
13.6 kDa protein,C-X-C motif chemokine 17,Cxcl17,Mouse,Mus musculus,Vcc1,VEGF co-regulated chemokine 1A-human VEGF IgG fr mon 100µgABT-869 ABT-869(Linifanib) is a structurally novel, potent RTK and VEGF and PDGF receptor families inhibitor with IC50 of 0.2, 2, 4, and 7 nM for human endothelial cells, PDGFR-beta, KDR, and CSF-1R,Anti- VEGF-Apan AntibodyAnti- VEGF-Apan antibodyAnti-bovine VEGF (164aa), liquid (PAB), Source: Polyclonal Rabbit, PABAnti-bovine VEGF (164aa), liquid (PAB), Source: Polyclonal Rabbit, PABAnti-Bovine VEGF-A (RABBIT) Antibody TRIAL SIZE (25ul)Anti-bovine VEGF-A PAbAnti-bovine VEGF-A PAbAnti-equine VEGF-A PAbanti-FLK1 (VEGF-R2) (FLK-6)anti-FLK1 (VEGF-R2) (FLK-6)anti-FLK1 (VEGF-R2) (FLK-6) type: Primary antibodies host: Mouseanti-FLT4 VEGF Receptor 3 (AFL4) Related articles to: VEGF_D
- The temporal relationship between hepatic decompensation and portal vein thrombosis (PVT) in compensated advanced chronic liver disease (cACLD) remains unclear. We investigated their temporal sequence, prognostic significance, and molecular signatures and developed a biologically grounded predictive model for decompensation. - Source: PubMed
Publication date: 2026/08/29
Villa EricaCritelli Rosina MariaDonghia RossellaShahini EndritMilosa FabiolaScianò FilippoDituri FrancescoGiannelli Gianluigi - Increased peripheral inflammation and astrogliosis, as assessed by glial fibrillary acidic protein (GFAP) associates with worse cognition. GFAP, however, does not provide brain spatial information. F-SMBT-1, a tracer that binds to overexpressed MAO-B in reactive astrogliosis, may help overcome this limitation. Neuroprotective growth factors (e.g. BDNF, VGF, VEGFA, VEGFD, IGF1R and IGFBP7) usually accompany astrogliosis and could mediate the pathways between AD pathology and cognitive impairment. We evaluated the relationships among peripheral inflammatory markers, growth factors, astrogliosis, and cognitive function and explored whether the relationship of astrogliosis with cognition could be mediated by these growth factors. - Source: PubMed
Publication date: 2026/07/31
Ramirez-Tirado Laura-AlejandraCohen Ann DLopresti Brian JIkonomovic Milos DGogola AlexandraMatan CristyZeng XuemeiKarikari Thomas KLopez Oscar LSnitz Beth EShaaban C ElizabethVillemagne Victor L - Traditional therapeutic strategies for coronary artery disease (CAD) primarily focus on arterial perfusion, largely overlooking the critical role of the cardiac lymphatic system in maintaining myocardial fluid, lipid, and immune homeostasis. The vascular endothelial growth factor C (VEGF-C) and VEGF-D/VEGF receptor-3 (VEGFR3) signaling axes are the primary drivers of lymphangiogenesis. However, recent clinical and mechanistic insights suggest that these two homologous ligands exert highly distinct and divergent pathophysiological roles under ischemic stress. This review synthesizes the current clinical, epidemiological, and preclinical evidence evaluating the distinct temporal and spatial dynamics of the VEGF-C/D axis. Large-scale clinical cohorts have revealed a striking prognostic divergence: while elevated circulating VEGF-D levels independently predict incident heart failure, atrial fibrillation, and mortality, low serum VEGF-C levels independently predict mortality. Mechanistically, adventitial lymphatics actively govern scavenger receptor class B type I (SR-BI)-dependent reverse cholesterol transport and macrophage trafficking. Preclinical large animal validation and phase 1/2 clinical trials (such as KAT301 and ReGenHeart) have demonstrated that timely, localized pro-lymphangiogenic interventions-leveraging modified mRNA, lipid nanoparticles, or sequential growth factor delivery kinetics-effectively resolve myocardial edema, suppress adverse remodeling, and improve the myocardial perfusion reserve. In conclusion, VEGF-C and VEGF-D represent a complex molecular dualism in CAD. Transitioning from non-specific growth factor overproduction to cell-specific, sequentially timed lymphatic therapeutics is a new frontier in halting the progression of adverse ventricular remodeling and chronic heart failure. - Source: PubMed
Publication date: 2026/08/19
Wada HiromichiKotani KazuhikoIguchi MoritakeHasegawa Koji - Autologous hematopoietic stem cell transplantation (ASCT) remains a cornerstone therapy for eligible patients with multiple myeloma. Cryopreservation of hematopoietic grafts provides logistical flexibility but may increase procedure-related toxicity and resource utilization. - Source: PubMed
Publication date: 2026/07/22
Sarmiento MauricioMacanas-Pirard PatriciaBroekhuizen Aart J FGavilán Rosales CarolinaDíaz JavierSalinas Snr José EmilioGutiérrez CatherineJara VerónicaRivera ElizabethAlcalde-Mellado PatriciaGarcia Culebras MartaEscamilla-Gomez VirginiaChiclana-Rodríguez BeatrizPérez-Simón José Antonio - Gallbladder cancer (GBC), the most common malignancy of the biliary tract, exhibits a high propensity for lymphatic system invasion. However, the mechanisms underlying lymphatic metastasis in GBC remain poorly understood. Here, we demonstrate that C-C motif chemokine ligand 21 (CCL21) is significantly upregulated in GBC and positively correlates with lymphatic vessel density and lymph node metastasis. Both in vivo and in vitro experiments confirm that CCL21/CCR7 axis promotes lymphangiogenesis and lymphatic metastasis in GBC. Mechanistically, CCL21/CCR7 modulates Vascular Endothelial Growth Factor-D (VEGF-D) mRNA N6-Methyladenosine (mA) modification in an AlkB homolog 5 (ALKBH5)-dependent manner, thereby regulating VEGF-D protein expression. Site-directed mutagenesis experiments reveal that mA modification sites in the coding sequence (CDS) region of VEGF-D mRNA are critical for VEGF-D protein regulation. Collectively, our findings highlight that CCL21/CCR7 regulates VEGF-D expression via mA modification, driving lymphatic metastasis in GBC. - Source: PubMed
Publication date: 2026/07/24
Wu ZhenhengCai XinranJiang LeiLin BinPan WeiLin ShengzheChen YanlingHong Haijie