VEGF Receptor 3 Antibody [M6F2] Datasheet

Biological Description

Specificity	VEGF Receptor 3 Antibody [M6F2] detects endogenous levels of total VEGF Receptor 3 protein.
Background	VEGF receptor 3 (VEGFR3, FLT4) is a type III receptor tyrosine kinase of the VEGF receptor family that is expressed predominantly on lymphatic endothelial cells in postnatal tissues and functions as a principal regulator of lymphangiogenesis and lymphatic vessel homeostasis through selective binding of the processed forms of VEGF‑C and VEGF‑D. The receptor contains seven extracellular immunoglobulin-like domains that engage dimeric VEGF‑C or VEGF‑D ligands, a single transmembrane segment, and an intracellular split tyrosine kinase domain with multiple regulatory tyrosines whose phosphorylation controls recruitment of signaling complexes, so ligand-induced dimerization triggers trans-autophosphorylation and converts VEGFR3 into an active signaling hub at the lymphatic endothelial surface. VEGF‑C/VEGFR3 signaling activates phosphatidylinositol 3‑kinase via direct receptor interaction and stimulates the PI3K–Akt axis, leading to phosphorylation of downstream targets including p70S6K, endothelial nitric oxide synthase, PLCγ1, and ERK1/2, and this coordinated kinase output promotes lymphatic endothelial cell survival, proliferation, migration, and tube formation, which underlies lymphatic sprouting, branching, and vessel enlargement. The same receptor–ligand system also engages the MEK–ERK pathway and modulates cytoskeletal dynamics and junctional organization, thereby shaping lymphatic vessel patterning, valve formation, and fluid transport capacity during development and in adult tissue remodeling. VEGFR3 expression, initially present on embryonic blood vascular endothelium, becomes progressively restricted to lymphatic endothelium after midgestation, and in adult tissues, VEGFR3 marks lymphatic capillaries and collecting vessels in skin, intestine, and other organs where it maintains lymphatic integrity and responds to inflammatory and tissue repair cues. In pathological contexts, upregulation of VEGFR3 and its ligands in and around tumors drives lymphangiogenesis and lymphatic vessel dilation, facilitating entry and dissemination of tumor cells to regional lymph nodes, while blockade of VEGFR3 signaling with neutralizing antibodies or soluble receptor constructs reduces tumor-associated lymphatic density and lymph node metastasis, and can also lower blood vessel density in some tumor models where VEGFR3 contributes to angiogenesis. VEGFR3 is also expressed in specialized non-lymphatic compartments, including the subventricular zone and hippocampal neural stem cells and cardiac endothelium, where VEGF‑C/VEGFR3 activation engages Akt and ERK signaling to regulate neural stem cell activation, adult neurogenesis, and aspects of cardiac lymphatic remodeling and function, linking this receptor to broader roles in tissue regeneration and organ homeostasis beyond classical lymphatic biology.

Specificity

VEGF Receptor 3 Antibody [M6F2] detects endogenous levels of total VEGF Receptor 3 protein.

Background

VEGF receptor 3 (VEGFR3, FLT4) is a type III receptor tyrosine kinase of the VEGF receptor family that is expressed predominantly on lymphatic endothelial cells in postnatal tissues and functions as a principal regulator of lymphangiogenesis and lymphatic vessel homeostasis through selective binding of the processed forms of VEGF‑C and VEGF‑D. The receptor contains seven extracellular immunoglobulin-like domains that engage dimeric VEGF‑C or VEGF‑D ligands, a single transmembrane segment, and an intracellular split tyrosine kinase domain with multiple regulatory tyrosines whose phosphorylation controls recruitment of signaling complexes, so ligand-induced dimerization triggers trans-autophosphorylation and converts VEGFR3 into an active signaling hub at the lymphatic endothelial surface. VEGF‑C/VEGFR3 signaling activates phosphatidylinositol 3‑kinase via direct receptor interaction and stimulates the PI3K–Akt axis, leading to phosphorylation of downstream targets including p70S6K, endothelial nitric oxide synthase, PLCγ1, and ERK1/2, and this coordinated kinase output promotes lymphatic endothelial cell survival, proliferation, migration, and tube formation, which underlies lymphatic sprouting, branching, and vessel enlargement. The same receptor–ligand system also engages the MEK–ERK pathway and modulates cytoskeletal dynamics and junctional organization, thereby shaping lymphatic vessel patterning, valve formation, and fluid transport capacity during development and in adult tissue remodeling. VEGFR3 expression, initially present on embryonic blood vascular endothelium, becomes progressively restricted to lymphatic endothelium after midgestation, and in adult tissues, VEGFR3 marks lymphatic capillaries and collecting vessels in skin, intestine, and other organs where it maintains lymphatic integrity and responds to inflammatory and tissue repair cues. In pathological contexts, upregulation of VEGFR3 and its ligands in and around tumors drives lymphangiogenesis and lymphatic vessel dilation, facilitating entry and dissemination of tumor cells to regional lymph nodes, while blockade of VEGFR3 signaling with neutralizing antibodies or soluble receptor constructs reduces tumor-associated lymphatic density and lymph node metastasis, and can also lower blood vessel density in some tumor models where VEGFR3 contributes to angiogenesis. VEGFR3 is also expressed in specialized non-lymphatic compartments, including the subventricular zone and hippocampal neural stem cells and cardiac endothelium, where VEGF‑C/VEGFR3 activation engages Akt and ERK signaling to regulate neural stem cell activation, adult neurogenesis, and aspects of cardiac lymphatic remodeling and function, linking this receptor to broader roles in tissue regeneration and organ homeostasis beyond classical lymphatic biology.

Usage Information

Application

WB

Dilution

WB

1:1000

Reactivity

Human

Source

Rabbit Monoclonal Antibody

MW

153 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/22745786/
https://pubmed.ncbi.nlm.nih.gov/11250889/

VEGF Receptor 3 Antibody [M6F2]

Biological Description

Usage Information

References

Application Data