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Validated All-in-One™ qPCR Primer for KDR(NM_002253.3) Search again
Product ID:
HQP101431
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD309, FLK1, VEGFR, VEGFR2
Gene Description:
kinase insert domain receptor
Target Gene Accession:
NM_002253.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- vitronectin increased the presence of all four growth factor receptors and most notably, VEGFR-1; in contrast, fibrin decreased all four receptors, especially FGFR-1 and FGFR-2
- A potential mechanism involved in hemangioma formation is the alteration of the FLK1 signaling pathway in endothelial and/or pericytic cells.
- green tea catechins are novel inhibitors of VEGFR-2 activity.
- Involvement of VEGFR-2 (kdr/flk-1) but not VEGFR-1 (flt-1) in VEGF-A and VEGF-C-induced tube formation by human microvascular endothelial cells in fibrin matrices in vitro.
- In this study we give evidence of Flt-1 and KDR receptors in platelets.
- Constitutive activation of Stat3alpha in brain tumors: localization to tumor endothelial cells and activation by the endothelial tyrosine kinase receptor (VEGFR-2)
- CLL B cells consistently express VEGFR2 mRNA; co-expression of angiogenic molecules and receptors suggest autocrine pathways of stimulation.
- Expression of vascular endothelial growth factor receptor Flk1/KDR is induced by shear stress through the CT-rich Sp1 binding site.
- KDR plays a key role in regulating the proliferation of HGCC and HVEC.
- findings implicate altered VEGF and KDR signaling in pituitary tumorigenesis; PTTG stimulation of FGF-2 and VEGF expression in the presence of up-regulated growth factor receptors may account for angiogenic growth and progression of human pituitary tumor
- The binding of VEGF to its receptor, KDR, is necessary and sufficient to induce the gene expression profile induced by VEGF.
- The expression of vascular endothelial growth factor and its receptors KDR and Flt-1 by gastric carcinoma tissues and cell lines was detected to elucidate the molecular mechanism of this growth factor in promoting tumor growth.
- VEGFR-2 has a role in regulating angiogenesis-related functions [review]
- transcriptional activation of Flk-1 in endothelial cells requires the interaction between HIF-2alpha and Ets-1
- A set of loop-1 and -3 structures in the novel vascular endothelial growth factor (VEGF) family member, VEGF-ENZ-7, is essential for the activation of this protein's signaling.
- Fluid shear stress induced upregulation requires Sp1 transcription factor binding to specific response elements in the 5' regulatory region
- Staining for the receptors VEGFR-1 and VEGFR-2 was positive in large lymphoid cells in stage IV non-Hodgkin lymphoma.
- Gq/11 proteins mediate KDR tyrosine phosphorylation and KDR-mediated HUVEC proliferation through interaction with KDR.
- These data indicate that activation of vascular endothelial growth factor receptor-2 prevents endothelial cell apoptosis by inhibiting p38 MAP kinase phosphorylation and reducing caspase-3 activity.
- in humans: 1) VEGF, KDR, and Flt-1 mRNA are increased by acute systemic exercise; 2) the time course of the VEGF, KDR, and Flt-1 mRNA responses are different from those previously reported in rats
- TNF induces transactivation between Etk and VEGFR2, and Etk directly activates PI3K-Akt angiogenic signaling independent of VEGF-induced VEGFR2-PI3K-Akt signaling pathway.
- Altered expression of vascular endothelial growth factor and FLK-1 receptor in chronically hypoxic carotid body.
- VEGF, VEGFR-1 and VEGFR-2 are concomitantly expressed in pre-B ALL cells. Expression of the receptors is limited to the intra-cytoplasmic compartment and may suggest either internalization or a block in trafficking of the receptor to the surface.
- changing of transcriptional activity of VEGF gene and its receptor FLK-1 indicates an autocrine mechanism of regulation of angiogenic gene activity in the first step of carcinogenesis--low-grade intraepithelial lesions of the uterine cervix
- Specific VEGFR2 expression, examined in 27 B-CLL samples, was positive in 26 of them. The VEGF transduction pathway may be very active in CLL cells. Both its paracrine & autocrine pathways may contribute to their enhanced survival.
- The expression of VEGF and KDR correlates highly with the normal ocular vascularization in humans
- Intact caveolae are required for the VEGF/VEGFR-2-mediated MEK/ERK signaling cascade.
- phosphorylation of Y1214 on VEGFR2 is required to trigger the sequential activation of Cdc42 and SAPK2/p38 and to drive the SAPK2/p38-mediated actin remodeling in stress fibers in endothelial cells exposed to VEGF
- KDR is constitutively phosphorylated and located at the nucleus of VEGF-producing leukemias; a KDR-specific intracellular inhibitor failed to block KDR nuclear IMPORT, but inhibited the constitutive activation of MAPK/Erk and PI3-kinase/AKT pathways
- the level of sVEGFR-2 is lower in active systemic lupus erythematosus than in inactive disease
- maximal P-selectin translocation and subsequent neutrophil adhesion was mediated by VEGF-A(165) on the activation of VEGFR-2/NRP-1 complex and required PAF synthesis.
- Our data support a role for KDR in oviduct angiogenesis.
- VEGF receotor signaling regulates survival signals in CLL cells and that interruption of this autocrine pathway results in caspase activation and subsequent leukemic cell death.
- Tgf-beta mediated repression of flk-1/KDR and mediated repression of flk-1/KDR and VEGF signaling involves the inducible formation of inhibitory Hex-GATA signaling Hex-GATA involves the formation of Hex-GATA complexes.
- Shb binds to tyrosine 1175 in the VEGFR-2, which regulates VEGF-induced formation of focal adhesions and cell migration, of which the latter occurs in a phosphatidylinositol 3-kinase-dependent manner
- Nedd4-mediated vascular endothelial growth factor receptor-2 degradation is prevented by Grb10
- Data suggest that periostin-mediated angiogenesis derives in part from the up-regulation of the vascular endothelial growth factor receptor Flk-1/KDR by endothelial cells through an integrin alpha(v)beta(3)-focal adhesion kinase signaling pathway.
- PPARgamma1 has bifunctional properties in the regulation of KDR gene expression mediated via interaction with both Sp1 and Sp3
- vascular endothelial growth factor (VEGF) is strongly expressed in villous cytotrophoblast cells and subsequently in Hofbauer cells while its receptors Flt-1 and Flk-1 are found on vasculogenic and angiogenic precursor cells
- In chronic lower limb ischemia, growth factor-1 (IGF-1) and IGF-2, were upregulated in atrophic and regenerating myocytes together with attenuated HIF, VEGF, and VEGFR-2 expression in the same cells.
- Increased expression of KDR is associated with an aggressive angiogenic phenotype in melanoma.
- activation of the P2Y(2)R induced rapid tyrosine phosphorylation of vascular endothelial growth factor receptor (VEGFR)-2 in human coronary artery endothelial cells
- VEGFR2 initiates a clonogenic response in myeloid leukemia cells that is PI3-kinase dependent.
- VEGFR2 mediated phosphorylation of focal adhesion kinase is regulated by heat shock protein 90 and Src kinase activities
- Inhibition by flk-1 kinase inhibitor SU1498 and failure of placental growth factor (PlGF) to up-regulate DAF confirmed the role of VEGF-R2 in VEGF-mediated DAF up-regulation.
- VEGF(165)-induced phosphorylation of KDR and PLCgamma was partially inhibited by PF-4
- VEGF and its receptor, KDR, genes contributed to the development of coronary artery lesions in Kawasaki disease patients.
- VEGFR-3 needs to be associated to VEGFR-2 to induce ligand-dependent cellular responses
- there was no significant correlation between VEGF and VEGF-R2 expression. VEGF-R2 expression was significantly increased on endothelial cell (
- The VEGFR2, through interaction with VEGF, regulated adhesive and migratory properties of the cancer cells.
- Axl stimulation by GAS6 results in inhibition of the ligand-dependent activation of vascular endothelial growth factor (VEGF) receptor 2 and the consequent activation of an angiogenic program in vascular endothelial cells
- NRP-1 modulates VEGFR-2 signaling-dependent mitogenic functions of VEGF and regulates endothelial cell adhesion to extracellular matrix proteins independently of VEGFR-2.
- These data support the involvement in melanoma growth and survival of a VEGF-dependent internal autocrine loop mechanism, at least in vitro.
- The majority of embryonic stem cells with the potential to differentiate into osteoclasts expressed Flk-1.
- 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 parallel activation of VEGFR-1 or -2 homodimers with corresponding agonists [VEGFR2]
- Blood levels correlate with lymph node involvement in colorectal cancer.
- regulatory mechanisms involved in the attenuation of VEGFR-2 activation is mediated by nonclassical Protein Kinase C and the presence of serine sites in the carboxyl terminal of VEGFR-2
- VEGFR2 may be involved in the transcriptional regulation of T-cell lymphoma.
- VEGFR-2 expression, co-localized in the cytoplasmic and nuclear membrane, is associated with progression towards invasive melanoma
- Phosphorylated ERK1/2 was further associated with the presence of VEGFR2 (cohorts II and III) and the degree of phosphorylated Ets-2, indicating in vivo, a signalling cascade from VEGFR2 via ERK1/2 to Ets-2 phosphorylation
- Targeting the release of VEGF from tumor epithelial cells as well as blocking interactions between VEGF and VEGFR-2 on both endothelial and tumor epithelial cells may facilitate the development of antiangiogenic therapies for breast tumors.
- human VEGFR-2 promoter is functionally counter-regulated by TFII-I and TFII-IRD1.
- key role of KDR in megakaryopoiesis
- decrease in expression is caused by C-reactive protein
- KLF2 is a regulator of VEGFR2/KDR and has a role in regulating angiogenesis
- role in modulating tumor neovascularization in conjunction with interleukin-3 receptor
- dynamin-2 regulates KDR expression and function and hence plays an important role in VPF/VEGF mediated angiogenesis
- assessed the role of VEGF and its receptors in osteoclastogenesis, in vitro, by culturing osteoclast precursors in the presence of VEGF, VEGF receptor-specific ligands, and blocking antibodies to VEGF receptors
- Up-regulation of VEGF-A receptor VEGFR-2 in capillaries in menorrhagia could be involved in abnormal endometrial vascular structure and permeability.
- An immunohistochemical analysis of VEGFR2 in pituitary adenomas was made.
- Blockade of either VEGF or its receptors with neutralizing antibodies significantly reduced cell viability and increased apoptosis levels of the VEGFR-positive thyroid tumour cell line.
- vascular endothelial growth factor receptor-2 phosphorylation is inhibited by delphinidin
- LPC-induced Flk-1/KDR transactivation via c-Src may have important implications for the progression of atherosclerosis
- Type I collagen limits VEGFR-2 signaling by a SHP2 protein-tyrosine phosphatase-dependent mechanism 1.
- Regulation of VEGF(165) signaling through the VEGFR-2 complex in response to cigarette smoke exposure in vivo, and in smokers with and without chronic obstructive pulmonary disease.
- New VEGFR2 containing cell subpopulation,which is apparently a precursor classical endothelial progenitor cells more potent with respect too homing and vasscular repair.
- We conclude that neoplastic cells show a variable expression of total and phosphorylated KDR in the nucleus.
- This study describes the first specific antagonist of VEGF-A165 binding to NP-1 and demonstrate that NP-1 is essential for optimum KDR activation and intracellular signaling.
- We conclude that IL-6 triggers VEGF-induced angiogenic activity through increasing VEGF release, up-regulates KDR expression and phosphorylation through activating ERK1/2 signaling, and stimulates MMP-9 overexpression.
- Phosphorylated KDR expression was significantly associated with poor prognosis.
- Sp3 and Sp4 cooperatively interact with ERalpha to activate VEGFR2
- In conclusion, EC death induced by high shear stress and VEGFR blockade leads to the production of factors, in particular TGF-beta1, that activate VSMC proliferation.
- haplotype analysis showed that atopy prevalence was strongly associated with a haplotype (AGAG) of VEGFR2
- Immunohistochemical staining showed that VEGF-R2 were expressed in epithelial, stromal and endothelial cells.
- These results suggest that VEGFR2 cannot only be targeted by receptor tyrosine kinase inhibitors but also by drugs that downregulate Sp proteins or block Sp-dependent transactivation.
- In this study, we demonstrate that 1121B Fab is able to strongly block KDR/VEGF interaction, resulting in potent inhibition of an array of biological activities of VEGF, including activation of the receptor and its signaling pathway.
- Vascular endothelial growth factor165 (VEGF165) and semaphorin3A (SEMA3A) elicit pro- and antiangiogenic signals respectively in endothelial cells (ECs) by binding to their receptors VEGFR-2, neuropilin-1 and plexin-a.
- VEGF and VEGFR-2 may have a role in progression of gastric cancer
- NRP1 expression and its GAG modification post-transcriptionally regulate VEGFR2 protein expression.
- illuminate an important mechanism for notch/HESR1 regulation of VEGF-induced angiogenesis
- VEGFR-1 and VEGFR-2 have roles in differentiation of hepatocellular carcinoma
- Gab1 thus appears as a primary actor in coupling VEGFR-2 to PI3K/Akt, recruited through an amplification loop involving PtdIns(3,4,5)P3 and its PH domain
- REVIEW: The binding of VEGF-A to VEGFR-2 causes receptor dimerization, kinase activation and autophosphorylation of specific tyrosine residues within the dimeric complex.
- overexpression of VEGF, its receptors flt-1, KDR/flk-1 and TGF-beta interaction may play an important role in the ovarian cancer biology, with potential effects on tumor growth and angiogenesis
- VEGF receptors are found on plasma cells from all groups of patients with multiple myeloma with the lowest expression on plasma cells from normal individuals
- Thus, vascular endothelial cadherin limits cell proliferation by retaining VEGFR-2 at the membrane and preventing its internalization into signaling compartments.
- Taken together these data show that VEGF-A(165)b has attenuated signaling potential through VEGF receptor 2 defining this new member of the VEGF family as a partial receptor agonist.
- Endothelial cell tissue transglutaminase (tTG) might be involved in modulation of the cellular response to VEGF by forming an intracellular complex with VEGFR-2, and mediating its translocation into the nucleus upon VEGF stimulation.
- perlecan secreted by VEGF165-stimulated endothelial cells may be involved in the regulation of cellular behavior during angiogenesis
- VEGFR-2 expressed on HaCaT cells plays a crucial role in VEGF-mediated regulation of cell activity
- SCID mice bearing xenografts of transfected cell lines were used to assess the effect of VEGF overexpression and the effect of VEGF receptor (VEGFR) 2 inhibition on soft tissue sarcoma growth.
- VEGF regulation of angiogenesis may in part be due to enhanced proliferation of VEGFR-1 and VEGFR-2
- Signaling via VEGFR-2 is involved in prostate lymphatic endothelial cell tube formation, migration, & proliferation in vitro. Blockade of VEGFR-2 significantly reduced tumor-induced activation of LECs.
- These results suggest that the expression of VEGFRs and NRPs on keratinocytes may constitute important regulators for its activity and may possibly be responsible for the autocrine signaling in the epidermis.
- in binding VEGFR-2, furin and PC5 promote cleavage of N-and C-terminal VEGF-D propeptides, whereas PC7 promotes cleavage of the C-terminal propeptide only
- Binding of VEGF to membrane-distal immunoglobulin-like domains causes receptor dimerization and promotes further interaction between receptor monomers through the membrane-proximal immunoglobulin-like domain 7.
- Endometrial blood vessels possess a discrete morphology that is characterized by endothelial gaps, and these gaps are more pronounced in women with menorrhagia and overexpression of VEGFR2.
- corecruitment of c-Cbl and PLCgamma1 to VEGFR-2 serves as a mechanism to fine-tune the angiogenic signal relay of VEGFR-2
- Mechanisms other than genetic variation may downregulate expression or function of the VEGFR2 receptor in patients with ALS.
- Taken together, these results lend great support to use PDGFRbeta antagonists in combinations with other antitumor and/or anti-angiogenic agents in the treatment of a variety of cancers.
- VEGF receptor KDR was expressed in ovarian cancer cells, and CDDP-inhibited VEGF expression was linked with cellular apoptosis, which was rescued by VEGF treatment.
- These findings provide evidence for a novel cooperative interaction between VEGFR2 and RET that mediates VEGF-A functions in ureteric bud cells.
- VEGFR2 enhances VEGF(165), but not VEGF(121) binding to NRP1.
- Leukemia patients showing parallel activation of the studied proteins trended to exhibit higher incidence of fatal outcome.
- High levels of VEGFR-3 and -2 seem to contribute to the etiology of lymphangiomas.
- determined the expression pattern of VEGF splice variants in NSCLC and its correlation with the clinicopathological characteristics of tumors
- ZD6474 treatment inhibited EGFR phosphorylation and led to a dose- and time-dependent decrease in nasopharyngeal carcinoma cell
- Increased expression of Flk-1 may be involved in sinusoidal capillarization and the increased numbers of unpaired arteries in capillarized areas with increased numbers of unpaired arteries in dysplastic liver nodules.
- c-Src controls functional association between integrin alphav-beta3 and VEGFR-2 via integrin beta3 phosphorylation.
- PKA and VEGFR2 converge at the MEK/ERK1/2 pathway to protect serum starved neuronal cells from a caspase-dependent cell death.
- increase in VEGF in AR with and without asthma despite a higher Flk-1 in AR patients with asthma may be a possible explanation for the presence of angiogenesis in the airway wall in patients with asthma but not in those with pure AR.
- myoferlin forms a complex with dynamin-2 and VEGFR-2, which prevents CBL-dependent VEGFR-2 polyubiquitination and proteasomal degradation.
- KDR polymorphisms may serve as novel genetic markers for the risk of coronary heart disease.
- studied circulating CD31- and/or CD34-positive cell populations with a low to moderate VEGFR2 expression in human volunteers and cancer patients.
- Vascularization and VEGF and Flk-1 expression are significantly higher in deeply infiltrating endometriosis affecting the rectum.
- VEGF receptor Flk-1 is involved in c-kit up regulation via ERK-mediated pathway
- HARP negatively affects diverse biological activities in C6 glioma cells, mainly due to binding of HARP to VEGF, which may sequester secreted VEGF from signalling through VEGFR2.
- isolation and purification of Flk-1cells with mesenchymal stem cell characteristics from bone marrow of myeloma patients.
- points to VEGFR2 transactivation as an important signaling pathway used by chemokines such as IL-8/CXCL8
- Expression profile of total VEGF, VEGF splice variants and VEGF receptors in the myocardium and arterial vasculature of diabetic patients.
- VEGFR2 up-regulation had no effect on VEGF-induced cell proliferation, but significantly enhanced endothelial progenitor cells migration and pseudotubes formation dependent on integrin alpha(6) subunit overexpression.
- Within mdx mice, an animal model of DMD, adipose tissue-derived Flk-1(+) MSCs (AD-MSCs) homed to and differentiated into cells that repaired injured muscle tissue.
- Activation of fractalkine/CX3CR1 by vascular endothelial cells induces angiogenesis through VEGF-A/KDR.
- expressed in the microvascular endothelial cells of both primary and young permanent teeth
- Increased levels of Factor VIII occurred in the precursors of cardiac myocytes, smooth muscle and endothelial cells in normal and post-ischemic hearts.
- Support a role for NP-1 in mediating synergistic effects between VEGF-A(165) and FGF-2, which may occur in part through a contribution of NP-1 to KDR stability.
- Preeclampsia and SGA are associated with low maternal plasma concentrations of soluble vascular endothelial growth factor receptor-2 (sVEGFR-2)
- These proteins have an essential molecule required for promoting the disruption of endothelial cell-cell contacts and paracellular permeability.
- Overall, these results indicate that HDAC6 and HDAC10 play important roles in Hsp-mediated VEGFR regulation.
- a maximal bout of exercise induces a significant shift in CD34+ cells toward CD34+/KDR+ cells
- Gal-1 can directly bind to NRP1 on endothelial cells, and can promote the NRP1/VEGFR-2-mediated signaling pathway as well as NRP1-mediated biological activities.
- The expression of VEGF-C and VEGF receptors is regulated specifically in HL-60 cells during macrophage differentiation.
- Surveillance of VEGFR-2 levels to predict chemotherapy response is not useful.
- the temporal expression of TNF is critical: it delays angiogenesis initially by blocking signaling through VEGFR2, and by inducing a tip cell phenotype through an NFkappaB-dependent pathway, it concomitantly primes ECs for sprouting
- Found in normal and neoplastic thymus tissue.
- Intensity of VEGFR-2 in odontoblasts increases from cap stage to late bell stage.
- VEGF is considered as an important factor in the pathogenesis of macular edema. VEGF induces the rupture of the blood retinal barrier and may also influence the retinal pigment epithelial (RPE) outer retinal barrier.
- complex interaction between sphingosine-1-phosphate and VEGFR-2 in ML-1 thyroid follicular cancer cells, particularly in regulating migratory responses
- the 167-181 region of VEGFR-2 has an important role in the stimulation of CD4(+) T cell responses to VEGFR-2 protein
- VEGFR-2 levels were associated with poor tumor differentiation in patients with gastric adenocarcinoma
- binding of Neuropilin-1 to VEGFR-2 requires the PDZ-binding domain of neuropilin-1
- vascular endothelial growth factor, receptor KDR and p53 protein are expressed in transitional cell carcinoma of the bladder
- PTHrP (107-139) interacts with VEGFR-2 to promote human osteoblastic cell survival by a mechanism involving Runx2 activation.
- sVEGFR-2 levels were not significantly increased in patients with liver cirrhosis.
- These results are consistent with a potential autocrine role of the VEGF-VEGFR2 (KDR) interplay as a factor contributing to malignant astrocytoma growth and radioresistance.
- The tumor uptake of 64Cu-DOTA-VEGF measured by small-animal PET imaging reflects tumor VEGFR-2 expression level in vivo.
- VEGF-A stimulates ADAM17-dependent shedding of VEGFR2 and crosstalk between VEGFR2 and ERK signaling.
- matrix-controlled TCPTP phosphatase activity can inhibit VEGFR2 signalling, and the growth, migration and differentiation of human endothelial cells
- VEGF-R2 expression is significantly increased in port-wine stains, suggesting that VEGF-R2 could contribute to the pathogenesis of PWS by inducing vessel proliferation, vasodilation, or both.
- Normalization of the constitutive VEGFR2 signaling in hemangioma endothelial cells with soluble VEGFR1 or antibodies that neutralize VEGF or stimulate beta1 integrin
- correlation between expression of VEGF and p27(Kip1) was observed in bone marrows from patients with acute myeloid leukemia
- Achieving optimal therapeutic outcomes, the scheduling of radiotherapy and antiangiogenic therapy requires patient-specific post-treatment monitoring of the VEGFR2 pathway.
- glioma cells enhance EPC angiogenesis via VEGFR-2, not VEGFR-1, mediated by the MMP-9, Akt and ERK signal pathways
- LDH5 is highly upregulated in B-cell non-Hodgkin lymphomas and is in direct relation to factor HIF1alpha and HIF2alpha expression. LDH5 expression is linked with activated VEGFR2/KDR expression
- Results show a significant positive correlation between the concentrations of tissue VEGF and its receptor VEGFR2 in primary breast neoplasms during neoadjuvant therapy, and suggest that VEGFR2 levels may indicate the level of lymphatic metastasis.
- a distinct VEGFR-2-mediated pathway promoting tumor growth through autocrine mechanisms.
- VEGFR2 was significantly decreased in human colonic microvascular endothelial cells under hypoxia. In contrast, the responses of VEGFR2 levels to hypoxia in human umbilical vein endothelial cells were variable, that is, either unchanged or up-regulated.
- No significant correlations between the levels of VEGFR2 in the blood and renal cancer tissue were found.
- In malignant pleural mesothelioma cells, plexin-A1 and VEGF-receptor 2 (VEGF-R2) are associated in a complex which are involved in survival pathways.