STAT1 activation by venous malformations mutant Tie2-R849W antagonizes VEGF-A-mediated angiogenic response partly via reduced bFGF production

The Molecular Balance between Receptor Tyrosine Kinases Tie1 and Tie2 Is Dynamically Controlled by VEGF and TNFα and Regulates Angiopoietin Signalling

(2012) Harprit Singh et al.   PLoS One

Cucurbitacin E, a tetracyclic triterpenes compound from Chinese medicine, inhibits tumor angiogenesis through VEGFR2-mediated Jak2-STAT3 signaling pathway

(2010) Y. Dong et al.   CARCINOGENESIS

Visfatin through STAT3 activation enhances IL-6 expression that promotes endothelial angiogenesis

(2009) Jee-Young Kim et al.   BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH

Hereditary cutaneomucosal venous malformations are caused by TIE2 mutations with widely variable hyper-phosphorylating effects

(2009) Vinciane Wouters et al.   EUROPEAN JOURNAL OF HUMAN GENETICS

Loss of Protein Inhibitors of Activated STAT-3 Expression in Glioblastoma Multiforme Tumors: Implications for STAT-3 Activation and Gene Expression

(2008) E. C. Brantley et al.   CLINICAL CANCER RESEARCH

Tie2-R849W Mutant in Venous Malformations Chronically Activates a Functional STAT1 to Modulate Gene Expression

(2008) Hsiao-Tang Hu et al.   JOURNAL OF INVESTIGATIVE DERMATOLOGY

VEGF regulates FGF-2 and TGF-β1 expression in injury endothelial cells and mediates smooth muscle cells proliferation and migration

(2008) Dongmei Li et al.   MICROVASCULAR RESEARCH

Somatic mutations in angiopoietin receptor gene TEK cause solitary and multiple sporadic venous malformations

(2008) Nisha Limaye et al.   NATURE GENETICS

STAT3: A critical transcription activator in angiogenesis

(2007) Zhong Chen et al.   MEDICINAL RESEARCH REVIEWS