VEGF Receptor 2 Antibody

About the Target

VEGF Receptor 2 encoded by the KDR gene, also known as Flk-1 (fetal liver kinase 1), and CD309, is a type V receptor tyrosine kinase that serves as the primary mediator of vascular endothelial growth factor (VEGF) signaling, driving endothelial cell proliferation, migration, and survival. Structurally, VEGFR-2 consists of seven extracellular immunoglobulin (Ig)-like domains, a single transmembrane helix, and a split intracellular tyrosine kinase domain with a unique kinase insert region. Depending on the literature source, KDR may also be discussed as VEGF Receptor 2 and CD309.

Reported cellular context includes cell junction, cell membrane, cytoplasm, and cytoplasmic vesicle, which can matter when signal is compared across treatments or changing cell states. Following KDR across matched perturbations can help separate abundance effects from shifts in localization, complex assembly, or pathway state.

Research Context

KDR is commonly interpreted in the context of cancer, cardiovascular, and angiogenesis research, and readouts are often stronger when a study separates expression changes from compartment-level redistribution. When reported signal spans cell junction, cell membrane, and cytoplasm, a defined reference condition can make comparisons more interpretable across perturbations, passages, or replicate sets.

Consider these angles when interpreting target-level changes:

• apparent redistribution between cell junction, cell membrane, and cytoplasm across matched conditions
• changes associated with proliferative state, oncogenic signaling, or treatment response
• changes linked to vascular, contractile, or hemodynamic cell-state cues
• differences related to endothelial activation, vessel remodeling, or growth-factor exposure

Variant Considerations

If your project spans exploratory questions, the regular version offers a balanced option for establishing baseline signal behavior for KDR. This can help when protocols evolve over time and the goal is to compare experiments using a stable reference workflow.

Standardize sampling time, control choice, and downstream analysis thresholds so apparent differences in KDR reflect biology rather than handling. When interpreting KDR, it is often useful to decide early whether the main question is overall abundance, compartmental enrichment, or context-dependent redistribution.

For multi-run studies, a shared reference condition can keep KDR trends easier to compare across datasets. That kind of consistency is especially helpful when follow-up work expands to new perturbations, model systems, or longitudinal collections.