anti-FLT1 (FLT1) Antikörper

Human Fms-Related tyrosine Kinase 1 (Vascular Endothelial Growth Factor/vascular Permeability Factor Receptor) (FLT1) Interaktionspartner

1. The expressions of VEGF receptors and their ligands significantly differed between malignant ovarian tumors and paired distant metastases. VEGF-A, VEGF-D, and VEGFR1 protein expressions seem to be higher in distant metastases than in the primary high grade serous ovarian cancer lesions.

2. treating primary cytotrophoblasts with therapeutics which have been previously found to reduce sFlt-1 secretion, either reduced EGFR signaling (esomeprazole and statins) or perturbed mitochondrial function (esomeprazole, resveratrol, and metformin). Additionally, targeting both pathways simultaneously produced additive reductions in sFlt-1 secretion

3. RA suppresses sFLT1 expression in DSCs independently of cellular decidualization. These findings suggest that reduced decidual RA levels may contribute to preeclampsia pathogenesis by allowing sFLT1 accumulation at the maternal-fetal interface.

4. male fetal sex is associated with lower FLT levels in preeclamptic women

5. Complement activation plays a major role in both the expression and secretion of sFLT1 from syncytial trophoblast cells. The terminal membrane attack complex is involved in its secretion. Increased levels of sFLT1 in pre-eclampsia patients may be due to complement-induced upregulation and secretion.

6. The current study demonstrates a pro-angiogenic role of Fzd5, which was shown to be involved in endothelial tubule formation, cell cycle progression and migration, and partly does so by repression of PKC/Ets1-mediated transcription of Flt1 and Angpt2.

7. Hypoxia-induced elevation of sFlt-1 secretion from the cytotrophoblasts was inhibited by silencing the HIF-2alpha, but not HIF-1alpha mRNA.

8. Studies focusing on the ratio of serum fms related tyrosine kinase 1 (FLT1) and serum placental growth factor (PLGF)in first and second trimester as possible biomarkers for preeclampsia.

9. This review describes preeclampsia and intra-uterine growth restriction (IUGR), focusing on sFlt-1 and PGF, their sources during and outside pregnancy and the application of these markers in diseases outside pregnancy.

10. In human fetoplacental endothelial cells, FLT1 ablation unexpectedly increased cell proliferation. FLT1 knock-down significantly impaired wound scratch closure and tube formation. FLT1 effects on cell motility were Akt and ERK-independent.

11. sFlt-1 is linked to cardiovascular remodeling and was demonstrated to be elevated in patients with Heart Failure. Additionally, it was suggested as a potential biomarker of Cardiovascular risk.

12. Our results demonstrated that simultaneous blockade of VEGFR1/VEGFR2 is an effective strategy to fight solid tumors by targeting a wider range of mediators involved in tumor angiogenesis, growth, and metastasis.

13. plasma level not related to HMOX1 polymorphism

14. VEGFR TKIs have clinical activity in metastatic renal cell carcinoma (mRCC) refractory to immune-based combination therapy, possibly impacted by the mechanism of prior combination therapy.

15. Genetic predisposition to pre-eclampsia was found to be associated with single nucleotide polymorphisms near the FLT1 gene.

16. This study performed FLT1 and transcriptome-wide polyadenylation site (PAS) analysis in preeclampsia. Consistent with soluble Flt1 overproduction being a significant driver of clinical symptoms, placental Flt1 mRNA levels strongly correlate with maternal blood pressure.

17. The inhibition of FLT1 ectodomain cleavage by VEGF-A is dependent neither on receptor activation nor on internalization.

18. This is the first study to demonstrate that the ratio of sFlt-1/PlGF can both predict and serve as a diagnostic factor for preeclampsia in pregnant women from different populations within the Xinjiang region of China.

19. Results find the expression of Flt-1 was 48% higher in the frontal cortex and 72% higher in the basal ganglia of congenital heart disease fetuses compared with controls.

20. Our findings indicate a mechanism by which the VEGF and the sVEGFR-1 production by immune cells regulates local VEGF signalling.

Zebrafish Fms-Related tyrosine Kinase 1 (Vascular Endothelial Growth Factor/vascular Permeability Factor Receptor) (FLT1) Interaktionspartner

1. sFlt1 role in the venous sprouting and spinal cord vascularization.

2. we determined that radial glia control this process via the Vegf decoy receptor sFlt1: sflt1 mutants exhibit the venous over-sprouting observed in radial glia-ablated larvae, and sFlt1 overexpression rescues it. Genetic mosaic analyses show that sFlt1 function in trunk endothelial cells can limit their over-sprouting.

3. Flt1-tyrosine kinase (TK) activity contributed significantly in endothelial cells survival and vascular development during embryo angiogenesis in zebrafish by engaging PI3K/Akt pathway.

4. Elevated Notch signaling downstream of perturbed VEGF signaling contributes to aberrant flt-1(-/-) blood vessel formation.

5. Data indicate that the increase in FLT1/sFLT1 protein levels upon miR-10 knockdown inhibited the angiogenic behavior of endothelial cells largely by antagonizing vascular endothelial growth factor receptor 2 signaling.

Mouse (Murine) Fms-Related tyrosine Kinase 1 (Vascular Endothelial Growth Factor/vascular Permeability Factor Receptor) (FLT1) Interaktionspartner

1. Report the physiological functions of VEGFR1 in the modulation of adipose angiogenesis, obesity, and global metabolism. Pharmacological inhibition and genetic deletion of endothelial VEGFR1 augmented adipose angiogenesis and browning of subcutaneous white adipose tissue, leading to elevated thermogenesis.

2. excessive sFlt1 and lack of eNOS synergistically induce hepatic dysfunction and thrombocytopenia, suggesting a novel role for VEGF and nitric oxide signaling in hepatocyte-endothelial cross-talk in health and in liver injury states.

3. Motor neurons control blood vessel patterning by an autocrine mechanism that titrates motor neuron-derived VEGF via their own expression of sFlt1.

4. inducible endothelial genetic deletion of Neuropilin1 (Nrp1) and Vascular endothelial growth factor receptor 1 (Vegfr1; also known as Flt1) renders mice resistant to diet-induced obesity.

5. findings identified a novel function of the VEGFR1 signaling in avoiding over-expression of Arginase 1 potentially to maintain the proper innate immune response.

6. Results show that Flt1 heterozygosity causes embryonic edema with enhanced vascular permeability. It can also be a risk factor for embryonic lethality in combination with other mutations causing non-lethal vascular phenotype.

7. Our study suggests that "migration" of the placenta is derived from placental degeneration at the caudal part of the placenta, and sFlt-1 plays a role in this placental degeneration.

8. This is the first report demonstrating the spatiotemporal expression patterns of Flk1 and Flt1 in the coronary vascular system during development and after MI; thus, this study suggests that these factors have distinct and important functions in coronary angiogenesis.

9. sFlt-1 overexpression in Padi4(-/-) mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation.

10. endothelial dysfunction due to high circulating sFLT1 may be the primary event leading to enhanced vasoconstrictor sensitivity that is characteristic of preeclampsia

11. Flt1 has a role in blood vessel anastomosis during angiogenesis

12. Esomeprazole decreased blood pressure in a transgenic mouse model where human sFlt-1 was overexpressed in placenta. PPIs upregulated endogenous antioxidant defenses and decreased cytokine secretion from placental tissue and endothelial cells.

13. First-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 were constructed and successfully validated in an orthotopic murine tumor model.

14. these results suggest that VEGFR1 signaling plays a role in regulating the balance between macrophage phenotypes in streptozotocin -induced diabetic wounds, prevents impaired diabetic wound healing, and promotes angiogenesis/lymphangiogenesis.

15. These data therefore support a tightly controlled, paracrine signaling mechanism of VEGF-B to VEGFR1.

16. Flt1/VEGF-A signalling has stage-specific effects on vascular morphogenesis.

17. IL-35 treatment reduced collagen-induced arthritis via inhibiting vascular endothelial growth factor and its receptors

18. the VEGFR-1 tyrosine kinase signaling has an effect on angiogenesis.

19. data suggest that sFlt-1 may have a therapeutic effect on AS, resulting from suppression of VEGF signaling-mediated recruitment of circulating monocytes/macrophages

20. that Flt-1 plays a critical role in cardiac hypertrophy induced by pressure overload via the activation of AKT

Cow (Bovine) Fms-Related tyrosine Kinase 1 (Vascular Endothelial Growth Factor/vascular Permeability Factor Receptor) (FLT1) Interaktionspartner

1. There is a possibility that steatosis can be suppressed by the CC genotype in VEGFR1.

2. These results suggest that non-dominant follicles maintain a greater concentration of the mRNA expression of both membrane and soluble VEGF receptors; but follicular dominance is related to a reduction in the mRNA expression of sVEGFR1 and sVEGFR2.

3. VEGFR-1 negatively regulates primary bovine retinal pericytes survival, and its blockade protects the blood-brain barrier integrity.

4. The changes of sVEGFR-1 and sVEGFR-2 with the age of the bovine dominant follicle indicate a physiological role in its growth and atresia.

5. gamma-Secretase and presenilin mediate cleavage and phosphorylation of vascular endothelial growth factor receptor-1

6. VEGFR1 mRNA expression was lower at estrus and at the early I and early II luteal stages than at the other stages, whereas VEGFR1 protein expression did not change significantly throughout the estrous cycle (P<0.05)

7. Alterations in the expression of VEGF-A and bFGF systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.

8. inhibition of VEGFR-1 results in decrease in number of capillary connections indicating VEGFR-1 ligands promote branching angiogenesis.

9. TGF-beta1 induction of VEGFR-1 in endothelial cells explains pericyte protection of vessels and the selective vulnerability of neonatal vessels to oxygen(VEGFR-1)

10. the activation of VEGFR-1 and VEGFR-2 heterodimer (VEGFR-1/R-2) is essential for PGI(2) synthesis mediated by VEGF-A(165) and VEGF-A(121), which cannot be reproduced by the parallel activation of VEGFR-1 and VEGFR-2 homodimers with corresponding agonists

11. PEDF and VEGFR-1 have roles in the negative regulation of angiogenesis

Pig (Porcine) Fms-Related tyrosine Kinase 1 (Vascular Endothelial Growth Factor/vascular Permeability Factor Receptor) (FLT1) Interaktionspartner

1. FLT-1 differentially methylated region was hypermethylated in parthenogenetic placenta.

2. we analyzed the expression and cellular distribution of Flt-1(VEGFR-1) and Flk-1 (KDR/VEGFR-2)in newborn piglet brain

3. data shows that members of the VEGF-VEGFR system are temporally and spatially well localized for playing key roles during umbilical cord formation and its intensive growth observed after day 75 of pregnancy

4. The VEGFR1 was stably expressed during the whole lifespan of mesonephric glomeruli, and VEGFR1 is important for the maintenance of endothelial fenestrations.

5. increased placental expression of the VEGF receptor system is associated with increased placental vascular density observed with the advancement of gestation in the pig.

6. EGFR, VEGFR and FGFR are expressed in porcine oviduct and endometrium during the time of implantation [review]

7. VEGF ligand-receptor system may play an important role in the development and maintenance of the corpus luteum in pigs.

8. VEGF/Flk-1/Flt-1 system is activated during myocardial ischemia reperfusion injury.

9. Hemodialysis graft placement leads to early increases in wall shear stress, VEGF-A, pro-MMP-9, MMP-2, VEGFR-1, VEGFR-2, and TIMP-1, which may contribute to the development of venous stenosis.

10. in experimental intervertebral disc degeneration, VEGF receptors were expressed in the damaged disc and paradiscal tissues

11. Luteal sVEGFR-1 may be involved in the maintenance of corpus luteal function whenever pregnancy occurs in pigs.