VEGF receptor signal transduction.

By M. Cross, J. Dixelius, Taro Matsumoto, L. Claesson‐Welsh. Science's STKE : signal transduction knowledge environment, 2003

967 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/02e86127795480ab7fd330fbc27152d53c7d240c

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Citations in the corpus

Reactive oxygen species and angiogenesis: NADPH oxidase as target for cancer therapy. (2008, background): “The mitogenic and chemotactic effects of VEGF in ECs are mediated mainly through VEGFR2 [4] which is activated through autophosphorylation of tyrosine residues in the cytoplasmic kinase domain.”
The roles of vascular endothelial growth factor in bone repair and regeneration (2016, background): “VEGF belongs to a family of homodimeric proteins consisting of at least 6 members: VEGF-A (VEGF), VEGF-B, VEGF-C, VEGF-D, VEGF-E and Placental growth factor (PlGF) [14, 15].”
Vascular Endothelial Growth Factor and Angiogenesis (2004, background): “VEGFR-2 also activates phosphatidylinositol 3 -kinase (PI3K), which results in an increase of the lipid phosphatidylinositol (3,4,5)P3, leading to activation of protein kinase B (Akt/PKB), endothelial nitric oxide synthase, and the small GTP-binding protein Rac.”
A longitudinal study of angiogenic (placental growth factor) and anti-angiogenic (soluble endoglin and soluble vascular endothelial growth factor receptor-1) factors in normal pregnancy and patients destined to develop preeclampsia and deliver a small for gestational age neonate (2008, background): “The function of VEGF is to promote survival, migration, and differentiation of endothelial cells, as well as mediate vascular permeability [55,56].”
VEGF controls endothelial-cell permeability by promoting the β-arrestin-dependent endocytosis of VE-cadherin (2006, background): “VEGF is essential for vasculogenesis (the establishment of a primitive network of blood vessels during embryonic development) and for the subsequent formation of new vessels from pre-existing ones, a process known as angiogenesi”
Chronic stress in the adult dentate gyrus reduces cell proliferation near the vasculature and VEGF and Flk‐1 protein expression (2005, background): “Firstly, VEGF binding to Flk-1 is known to activate specific intracellular signaling cascades, which involve a.o. phosphatidyllinositol 3-kinase (PI3K) and MAPK/ERK kinase extracellular signal-regulated kinase (ERK) (Thakker et al., 1999; Matsuzaki et al., 2001; Cross et al., 2003).”