VEGF Signaling Pathway: Receptor Lineage, Activation Mechanisms, and Biological Effects
VEGF Signaling Pathway: Receptor Lineage, Activation Mechanisms, and Biological Effects
The VEGF (vascular endothelial growth factor) signaling pathway is one of the central molecular networks in angiogenesis research. Its role is not limited to promoting endothelial cell proliferation. Rather, it coordinates multiple processes, including angiogenesis, vascular permeability, lymphangiogenesis, and tissue microenvironment remodeling, through the integrated regulation of ligand repertoire, receptor subtypes, co-receptor participation, and downstream signaling branches.
Keywords: VEGF; VEGFR; angiogenesis; vascular permeability; lymphangiogenesis; PI3K-AKT; MAPK; endothelial cells
1 VEGF Family and Receptor System
1.1 VEGF Ligand Family
The VEGF family primarily includes VEGF-A, VEGF-B, VEGF-C, VEGF-D, and PlGF (placental growth factor). Among these ligands, VEGF-A is the core ligand in classical angiogenesis research; VEGF-C and VEGF-D are more closely associated with lymphangiogenesis; and PlGF together with VEGF-B is more often involved in vascular regulation and tissue adaptation under specific pathological conditions.
Because different ligands do not share an identical receptor spectrum, the VEGF pathway should not be viewed as a single ligand driving a single linear route. Instead, it is a functional network composed of multiple ligand–receptor combinations.
1.2 VEGF Receptor Family
VEGF signaling is mainly mediated by three receptor tyrosine kinases:
(1) VEGFR1, also known as FLT1.
(2) VEGFR2, also known as KDR/Flk1.
(3) VEGFR3, also known as FLT4.
Among these receptors, VEGFR2 is the principal effector receptor for classical angiogenic and vascular permeability signaling; VEGFR1 exerts regulatory and buffering functions in certain contexts; and VEGFR3 primarily participates in lymphangiogenesis as well as selected angiogenic processes.
1.3 Co-Receptor System
Neuropilin-1 (NRP1) and Neuropilin-2 (NRP2) are important co-receptors in the VEGF pathway. Although they do not possess classical tyrosine kinase activity themselves, they can modulate VEGF signal intensity and directionality by enhancing ligand binding, altering receptor clustering, and influencing the composition of membrane-proximal signaling complexes.
2 Fundamental Mechanisms of VEGF Receptor Activation
2.1 Ligand Binding and Receptor Dimerization
VEGF ligands usually exist as dimers. Upon ligand binding, VEGFRs are induced to form homodimers or, under certain conditions, heterodimers, followed by activation of the intracellular kinase domains and trans-phosphorylation of multiple key tyrosine residues.
The essence of this process is not simply receptor switching, but the establishment of multiple downstream docking platforms through dimerization and site-specific phosphorylation.
2.2 Central Role of VEGFR2
In most classical angiogenesis models, VEGFR2 is the dominant signaling output node. After VEGF-A binds VEGFR2, it efficiently activates signaling pathways associated with proliferation, migration, survival, and permeability. VEGFR2 is therefore generally regarded as the major effector receptor of the VEGF pathway.
2.3 Regulatory Role of VEGFR1
VEGFR1 has high affinity for VEGF-A, but its kinase output is usually weaker than that of VEGFR2. Accordingly, in some settings, VEGFR1 functions more as a node for ligand competition and signal modulation rather than as the strongest direct effector receptor. For this reason, VEGFR1 may promote, constrain, or redirect VEGF signaling depending on the biological system.
Table 1. Major VEGF Family Ligands and Their Corresponding Receptors
Ligand | Major Receptor(s) | Functional Bias |
VEGF-A | VEGFR1, VEGFR2 | Angiogenesis, permeability regulation |
VEGF-B | VEGFR1 | Tissue adaptation and vascular regulation |
PlGF | VEGFR1 | Inflammation and pathological vascular responses |
VEGF-C | VEGFR3, and in part VEGFR2 | Predominantly lymphangiogenesis |
VEGF-D | VEGFR3, and in part VEGFR2 | Lymphangiogenesis and vascular remodeling |
3 Major Downstream Signaling Branches
3.1 PLCγ-PKC-MAPK Axis
Upon VEGFR2 activation, PLCγ can initiate PKC signaling and further connect to the RAF-MEK-ERK cascade. This pathway is mainly associated with endothelial cell proliferation, migration, and sprout growth, and represents one of the major output branches underlying the pro-angiogenic effect of VEGF.
3.2 PI3K-AKT-eNOS Axis
The PI3K-AKT pathway is an important module through which VEGF maintains endothelial cell survival and regulates vasodilatory function. Activated AKT promotes eNOS phosphorylation and enhances nitric oxide production, thereby influencing vascular tone, endothelial stability, and local perfusion status.
3.3 SRC and Permeability-Associated Signaling
VEGF can also affect endothelial junctional stability through SRC family kinases, the VE-cadherin complex, and cytoskeletal remodeling, thereby increasing vascular permeability. This branch is particularly important in inflammatory exudation, tumor vessel leakage, and retinal vascular disorders.
Table 2. Major Downstream Branches of the VEGF Pathway and Their Functional Bias
Downstream Pathway | Core Nodes | Major Functional Bias |
PLCγ-PKC-ERK | PLCγ, PKC, ERK | Endothelial proliferation, sprout growth, migration |
PI3K-AKT | PI3K, AKT | Survival, anti-apoptosis |
AKT-eNOS | AKT, eNOS, NO | Vasodilation, perfusion regulation |
SRC-associated branch | SRC, VE-cadherin | Increased permeability, junctional remodeling |
4 Functions of VEGF Signaling in Angiogenesis
4.1 Endothelial Cell Activation
Following activation of the VEGF pathway, quiescent endothelial cells shift from a stable state to an activated state characterized by enhanced proliferation, increased migratory capacity, and cytoskeletal reorganization. This transition is a prerequisite for the initiation of angiogenesis.
4.2 Sprout Growth and Branch Formation
During angiogenesis, a subset of endothelial cells acquires stronger tip cell-like characteristics and migrates along the VEGF gradient, while following endothelial cells contribute to elongation and lumen formation. Thus, VEGF not only promotes vessel growth, but also participates in the establishment of branching patterns and spatial vascular organization.
4.3 Limits of Neovessel Maturation
Although the VEGF pathway is critical for vessel initiation and expansion, whether newly formed vessels become mature also depends on pericyte recruitment, basement membrane reconstruction, and coordination with other growth factor systems. In other words, strong VEGF signaling does not necessarily mean vascular maturation; excessive VEGF activity may instead generate structurally unstable and highly leaky abnormal vessels.
5 Vascular Permeability and Lymphangiogenesis
5.1 Regulation of Vascular Permeability
VEGF was initially recognized for its activity as a vascular permeability factor. VEGF-A can rapidly influence endothelial junctions, cytoskeletal organization, and transendothelial transport, thereby facilitating plasma extravasation. This effect is highly relevant in acute inflammation, elevated tumor interstitial pressure, and retinal edema.
5.2 Lymphangiogenesis
VEGF-C and VEGF-D drive lymphatic endothelial cell proliferation and migration primarily through VEGFR3 and are key ligands in lymphangiogenesis research. Compared with the classical VEGF-A-VEGFR2 axis, the VEGF-C/D-VEGFR3 axis is more strongly associated with lymphatic system remodeling, although it may also participate in angiogenesis and metastasis-related microenvironmental changes under certain pathological conditions.
6 Dysregulation of the VEGF Pathway in Disease
6.1 Tumor Angiogenesis
Tumor tissues frequently undergo hypoxia-induced upregulation of HIF-1α, which in turn enhances VEGF-A expression and promotes neovascularization. These tumor vessels often exhibit disorganized architecture, high permeability, and uneven perfusion. Thus, in tumors, VEGF not only supports blood supply but also reshapes drug delivery and immune cell infiltration.
6.2 Ocular Neovascularization and Leakage-Associated Disorders
In diseases such as age-related macular degeneration and diabetic retinopathy, abnormal activation of the VEGF pathway can induce pathological neovascularization and retinal leakage. Accordingly, VEGF inhibition remains of sustained importance in therapeutic research for ophthalmic disorders.
6.3 Inflammation and Ischemic Repair
In ischemic tissues, VEGF can facilitate reperfusion and vascular regeneration. In inflammatory settings, however, excessive VEGF may aggravate leakage and tissue edema. Therefore, VEGF is neither purely detrimental nor purely beneficial; its significance depends on tissue stage, expression magnitude, and the accompanying microenvironmental context.
7 Experimental Investigation of the VEGF Pathway and Common Readouts
7.1 Receptor-Level Readouts
Common indicators include total VEGFR1, VEGFR2, and VEGFR3 protein levels as well as their phosphorylation states. Among these, p-VEGFR2 is typically a key initiating readout in classical angiogenic stimulation experiments.
7.2 Downstream-Level Readouts
Frequently used indicators include p-ERK, p-AKT, p-eNOS, and SRC-related molecular states, which are useful for determining whether VEGF signaling is biased toward proliferation, survival, or permeability regulation.
7.3 Functional Readouts
Common functional assays related to VEGF include:
(1) Endothelial cell proliferation assays.
(2) Migration or chemotaxis assays.
(3) Tube formation assays.
(4) Permeability measurements.
(5) Analysis of lymphangiogenesis-related markers.
Table 3. Common Experimental Readouts for the VEGF Pathway
Research Level | Common Indicators | Primary Significance |
Receptor level | VEGFR1/2/3, p-VEGFR2 | Assessment of receptor activation status |
Downstream level | p-ERK, p-AKT, p-eNOS, SRC-related indicators | Assessment of signaling bias |
Cellular functional level | Proliferation, migration, tube formation, permeability | Assessment of endothelial responses |
Tissue level | Microvessel density, lymphatic markers, leakage readouts | Assessment of in vivo vascular responses |
8 Products Related to the VEGF Signaling Pathway
Table 4. Recombinant VEGF Ligand and Receptor Products
Product Category | Catalog No. | Name | Grade and Purity | Applicable Research Direction / Use |
VEGF-A ligand protein | Recombinant Human VEGF 165 GMP Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,≥97%(SDS-PAGE&SEC-HPLC) | For classical VEGF-A stimulation and establishment of high-standard angiogenesis models | |
VEGF-A ligand protein | Recombinant Human VEGF 165 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,sterile,His Tag,PBS Only,≥98%(SDS-PAGE) | For VEGF165 stimulation, receptor activation, and endothelial functional assays | |
VEGF-A ligand protein | Recombinant Human VEGF Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,≥95%(SDS-PAGE) | For classical VEGF signaling activation studies | |
VEGF-A ligand protein | Recombinant Human VEGFA-165 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,His Tag,≥95%(SDS-PAGE),See COA | For VEGFA-165 isoform stimulation and VEGFR2 response studies | |
VEGF-B ligand protein | Recombinant Human VEGFB Protein | ≥97%(SDS-PAGE) | For studies of the VEGFB-VEGFR1 branch | |
VEGF-C ligand protein | Recombinant Human VEGFC Protein | ≥90%(SDS-PAGE) | For studies of the VEGFC-VEGFR3 axis and lymphangiogenesis | |
VEGF-D ligand protein | Recombinant Human VEGF-D Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,His Tag,≥95%(SDS-PAGE),See COA | For studies of the VEGFD-VEGFR3 axis and lymphangiogenesis | |
VEGFR1 receptor protein | Recombinant Human VEGFR1 Protein | ≥97%(SDS-PAGE) | For VEGFR1 binding and receptor function studies | |
VEGFR1 receptor protein | Recombinant Human VEGFR1/Flt-1 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,His Tag,≥95%(SDS-PAGE),expressed in HEK293; See COA | For VEGFR1/Flt-1 binding and competition assays | |
VEGFR2 receptor protein | Recombinant Human VEGFR2 Protein | ≥95%(SDS-PAGE) | For VEGFR2 receptor binding and activation studies | |
VEGFR2 receptor protein | Recombinant Human VEGFR2/KDR Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,High Performance,His Tag,PBS Only,≥95%(SDS-PAGE) | For VEGFR2/KDR binding and functional validation | |
VEGFR3 receptor protein | Recombinant Human VEGFR3/Flt-4 Protein | Animal Free,Carrier Free,His Tag,≥95%(SDS-PAGE) | For VEGFR3/Flt-4 binding and lymphatic signaling studies | |
Mouse VEGF ligand protein | Recombinant Mouse VEGF 164 Protein | Animal Free,Carrier Free,Bioactive,ActiBioPure™,Azide Free,High Performance,His Tag,≥95%(SDS-PAGE) | For mouse VEGF164 stimulation models | |
Mouse VEGF ligand protein | Recombinant Mouse VEGF165 Protein | ≥90%(SDS-PAGE) | For mouse VEGF165 stimulation studies | |
Mouse VEGFB ligand protein | Recombinant Mouse VEGFB Protein | ≥90%(SDS-PAGE) | For mouse VEGFB-related studies | |
Rat VEGF ligand protein | Recombinant Rat VEGF 164 Protein | ActiBioPure™, Recombinant, Animal Free, Carrier Free, High performance, ≥95%(SDS-PAGE) | For rat VEGF164 stimulation studies | |
Rat VEGF ligand protein | Recombinant Rat VEGFA Protein | ≥90%(SDS-PAGE) | For rat VEGFA-related studies |
Table 5. VEGF/VEGFR Detection and Blocking Antibody Products
Product Category | Catalog No. | Name | CAS No. | Grade and Purity | Applicable Research Direction / Use |
VEGF blocking antibody | Bevacizumab (anti-VEGF) | 216974-75-3 | Moligand™, ≥95%, ~25mg/ml(in buffer,PH6.2 | For VEGF neutralization and classical anti-angiogenesis studies | |
VEGF blocking antibody | Bevacizumab (anti-VEGF) | 216974-75-3 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGF neutralization and functional blocking assays | |
VEGFA blocking antibody | Brolucizumab (anti-VEGFA) | 1531589-13-5 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFA-specific blocking studies | |
VEGFB blocking antibody | CSL346 (anti-VEGFB) |
| Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For neutralization studies of the VEGFB branch | |
VEGFA dual-target blocking antibody | Faricimab (anti-ANG2&VEGFA) | 1607793-29-2 | Animal Free,Carrier Free,Recombinant,ExactAb™,Low Endotoxin,Azide Free,Validated,PBS Only,≥90%(SDS-PAGE&SEC-HPLC),See COA | For dual-target intervention studies on ANG2/VEGFA | |
VEGFR2 blocking antibody | Imclone 6.64 (anti-VEGFR2) |
| Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFR2 blockade and receptor-dependence validation | |
VEGFR2 blocking antibody | Olinvacimab (anti-VEGFR2) | 2095504-49-5 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFR2 blocking studies | |
VEGFR2 blocking antibody | Ramucirumab (anti-VEGFR2) | 947687-13-0 | Carrier Free, Recombinant, ExactAb™, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFR2 receptor blocking studies | |
VEGFA blocking antibody | Ranibizumab (anti-VEGFA) | 347396-82-1 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFA neutralization studies | |
VEGFC blocking antibody | VGX100 (anti-VEGFC) |
| Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFC blockade and lymphangiogenesis studies | |
VEGFA dual-target blocking antibody | Vanucizumab (anti-ANG2&VEGFA) | 1448221-05-3 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥90%(SDS-PAGE&SEC-HPLC), See COA | For dual-target intervention studies on ANG2/VEGFA | |
VEGF blocking antibody | Varisacumab (anti-VEGF) | 1610010-60-0 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGF neutralization studies | |
VEGFR2 blocking antibody | Vulinacimab (anti-VEGFR2) | 2250342-36-8 | Carrier Free, Recombinant, ExactAb™, Low Endotoxin, Azide Free, Validated, Animal Free, ≥95%(SDS-PAGE&SEC-HPLC), See COA | For VEGFR2 blocking studies | |
VEGFR1 detection antibody | Recombinant VEGF Receptor 1 Antibody |
| ExactAb™, Validated, Recombinant, 0.1 mg/mL | For VEGFR1 protein detection | |
VEGFR1 detection antibody | Recombinant VEGF Receptor 1 Antibody |
| See COA | For VEGFR1 protein detection | |
VEGFR2 detection antibody | Recombinant VEGF Receptor 2 Antibody |
| ExactAb™, Validated, Recombinant, 0.12 mg/mL | For VEGFR2 protein detection | |
VEGFR2 detection antibody | Recombinant VEGF Receptor 2 Antibody |
| Recombinant, ExactAb™, Validated, See COA | For VEGFR2 protein detection | |
VEGFA detection antibody | Recombinant VEGFA Antibody |
| ExactAb™, Validated, Carrier Free, Recombinant, 0.075 mg/mL | For VEGFA protein detection | |
VEGFD detection antibody | Recombinant VEGFD Antibody |
| ExactAb™, Validated, Recombinant, 1.5 mg/mL | For VEGFD protein detection | |
VEGFA detection antibody | VEGFA Mouse mAb |
| Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,See COA | For VEGFA protein detection | |
VEGFA detection antibody | VEGFA Mouse mAb |
| Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,See COA | For VEGFA protein detection | |
VEGFA detection antibody | VEGFA Mouse mAb |
| Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,See COA | For VEGFA protein detection |
Table 6. Small-Molecule Modulators and Degraders of the VEGF/VEGFR Pathway
Product Category | Catalog No. | Name | CAS No. | Grade and Purity | Applicable Research Direction / Use |
VEGFR inhibitor | AAL 993 | 269390-77-4 | ≥98% | For classical VEGFR small-molecule inhibition studies | |
VEGFR2 inhibitor | BMS 605541 | 639858-32-5 | ≥98%(HPLC) | For VEGFR2 inhibition studies | |
VEGFR2 inhibitor | Brivanib (BMS-540215) | 649735-46-6 | Moligand™, ≥98% | For VEGFR2 pathway inhibition studies | |
VEGFR2 inhibitor | Brivanib Alaninate (BMS-582664) | 649735-63-7 | Moligand™, ≥95% | For VEGFR2 pathway inhibition studies | |
VEGFR inhibitor | KRN-633 | 286370-15-8 | Moligand™, ≥97% | For pan-VEGFR inhibition studies | |
VEGFR2 tyrosine kinase inhibitor | Ki8751 | 228559-41-9 | ≥98% | For selective VEGFR2 inhibition studies | |
VEGFR2 degrader | PROTAC VEGFR-2 degrader-1 | 2601594-19-6 |
| For VEGFR2 protein degradation studies | |
VEGFR2 degrader | PROTAC VEGFR-2 degrader-2 | 2353417-85-1 |
| For VEGFR2 protein degradation studies | |
VEGFR2 inhibitor | SU1498 | 168835-82-3 | ≥98%(HPLC) | For classical VEGFR2 inhibition studies | |
VEGFR/PDGFR inhibitor | SU4312 | 5812-07-7 | Moligand™, ≥98% | For multi-receptor inhibition studies related to angiogenesis | |
TIE-2/VEGFR-2 dual-target inhibitor | TIE-2/VEGFR-2 kinase-IN-1 | 453590-24-4 | Moligand™, ≥98% | For dual-target intervention studies related to angiogenesis | |
TIE-2/VEGFR-2 dual-target inhibitor | TIE-2/VEGFR-2 kinase-IN-2 | 501693-48-7 | Moligand™, ≥98% | For dual-target intervention studies related to angiogenesis | |
VEGFR-2 inhibitor | UNC0064-12 (VEGFR-2-IN-5) | 1430089-64-7 | ≥98% | For VEGFR2 inhibition studies | |
VEGFR-3 inhibitor | VEGFR-3-IN-1 | 2756668-73-0 | ≥98% | For VEGFR3 and lymphangiogenesis studies | |
VEGFR inhibitor | VEGFR-IN-1 | 269390-69-4 | Moligand™, 10 mM in DMSO | For VEGFR pathway inhibition experiments | |
VEGFR2 inhibitor | VEGFR2-IN-1 | 2765224-55-1 |
| For VEGFR2 inhibition studies | |
VEGFR2 inhibitor | VEGFR2-IN-7 | 174258-31-2 | ≥99% | For VEGFR2 inhibition studies | |
VEGFR2 kinase inhibitor | VEGFR2 Kinase Inhibitor I | 15966-93-5 | Moligand™, ≥98%, (including isomers) | For VEGFR2 kinase inhibition studies | |
VEGFR2 kinase inhibitor | VEGFR2 kinase inhibitor IV | 216661-57-3 | Moligand™, ≥95% | For VEGFR2 kinase inhibition studies | |
VEGFR tyrosine kinase inhibitor | VEGFR Tyrosine Kinase Inhibitor II | 269390-69-4 | Moligand™, ≥98% | For VEGFR tyrosine kinase inhibition studies | |
VEGFR inhibitor | ZM 306416 | 690206-97-4 | Moligand™, ≥98% | For classical VEGFR inhibition studies |
Table 7. Quantitative Detection Reagents for VEGF/VEGFR
Product Category | Catalog No. | Name | Grade and Purity | Applicable Research Direction / Use |
Human ELISA | Human Vascular Endothelial Growth Factor (VEGF) ELISA Kit | BioReagent | For quantitative detection of total human VEGF | |
Human ELISA | Human Vascular Endothelial Growth Factor 121 (VEGF121) ELISA Kit | BioReagent | For quantitative detection of human VEGF121 | |
Human ELISA | Human Vascular Endothelial Growth Factor 145 (VEGF145) ELISA Kit | BioReagent | For quantitative detection of human VEGF145 | |
Human ELISA | Human Vascular Endothelial Growth Factor 165 (VEGF165) ELISA Kit | BioReagent | For quantitative detection of human VEGF165 | |
Human ELISA | Human Vascular Endothelial Growth Factor A (VEGF-A) ELISA Kit | BioReagent | For quantitative detection of human VEGF-A | |
Human ELISA | Human Vascular Endothelial Growth Factor B (VEGF-B) ELISA Kit | BioReagent | For quantitative detection of human VEGFB | |
Human ELISA | Human Vascular Endothelial Growth Factor C (VEGF-C) ELISA Kit | BioReagent | For quantitative detection of human VEGFC | |
Human ELISA | Human Vascular Endothelial Growth Factor D (VEGF-D) ELISA Kit | BioReagent | For quantitative detection of human VEGFD | |
Human ELISA | Human Vascular Endothelial Growth Factor Receptor 1 (VEGFR-1) ELISA Kit | BioReagent | For quantitative detection of human VEGFR1 | |
Human ELISA | Human Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) ELISA Kit | BioReagent | For quantitative detection of human VEGFR2 | |
Human ELISA | Human Vascular Endothelial Growth Factor Receptor 3 (VEGFR3/FLT4) ELISA Kit | BioReagent | For quantitative detection of human VEGFR3 | |
Rat ELISA | Rat Vascular Endothelial Growth Factor (VEGF) ELISA Kit | BioReagent | For quantitative detection of total rat VEGF | |
Rat ELISA | Rat Vascular Endothelial Growth Factor 121 (VEGF121) ELISA Kit | BioReagent | For quantitative detection of rat VEGF121 | |
Rat ELISA | Rat Vascular Endothelial Growth Factor A (VEGF-A) ELISA Kit | BioReagent | For quantitative detection of rat VEGF-A | |
Rat ELISA | Rat Vascular Endothelial Growth Factor B (VEGF-B) ELISA Kit | BioReagent | For quantitative detection of rat VEGFB | |
Rat ELISA | Rat Vascular Endothelial Growth Factor C (VEGFC) ELISA Kit | BioReagent | For quantitative detection of rat VEGFC | |
Rat ELISA | Rat Vascular Endothelial Growth Factor D (VEGF-D) ELISA Kit | BioReagent | For quantitative detection of rat VEGFD | |
Rat ELISA | Rat Vascular Endothelial Growth Factor Receptor 1 (VEGFR-1) ELISA Kit | BioReagent | For quantitative detection of rat VEGFR1 | |
Rat ELISA | Rat Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) ELISA Kit | BioReagent | For quantitative detection of rat VEGFR2 | |
Rat ELISA | Rat Vascular Endothelial Growth Factor Receptor 3 (VEGFR3) ELISA Kit | BioReagent | For quantitative detection of rat VEGFR3 | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor (VEGF) ELISA Kit | BioReagent | For quantitative detection of total mouse VEGF | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor A (VEGFA) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFA | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor B (VEGFB) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFB | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor C (VEGFC) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFC | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor D (VEGFD) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFD | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor Receptor 1 (VEGFR1/Flt1) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFR1 | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFR2 | |
Mouse ELISA | Mouse Vascular Endothelial Growth Factor Receptor 3 (VEGFR-3) ELISA Kit | BioReagent | For quantitative detection of mouse VEGFR3 |
The core of VEGF signaling does not lie in merely memorizing a few ligand and receptor names, but in understanding how differences in ligand repertoire, division of labor among receptor subtypes, co-receptor participation, and downstream branch selection together determine distinct outcomes such as angiogenesis, permeability regulation, and lymphatic remodeling.
For more related articles, please see below:
[2] Wnt/β-Catenin Signaling Pathway
[4] Metabolic signaling pathway
[5] Wnt Signaling
[7] JAK-STAT Cell Signaling Pathway
[8] PD-1/PD-L1 Signaling Pathway
References
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[3] Claesson-Welsh L. Signal transduction by vascular endothelial growth factor receptors. Biochem Soc Trans. 2003;31(Pt 1):20-24.
[4] Hofer E, Schweighofer B. Signal transduction induced in endothelial cells by growth factor receptors involved in angiogenesis. Thromb Haemost. 2007;97(3):355-363.