Gene interactions and pathways from curated databases and text-mining

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IGF1R — JAK2

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: JAK2 → Complex of IGF1-IGF1R (increases) Zong et al., J Biol Chem 2000*
    Evidence: We found that STAT3, but not STAT5, was activated in response to IGF-I in 293T cells cotransfected with IGF-IR and STAT expression vectors. Moreover, tyrosine phosphorylation of STAT3, JAK1, and JAK2 was increased upon IGF-I stimulation of endogenous IGF-IR in 293T cells transfected with the respective STAT or JAK expression vector.
  • OpenBEL Selventa BEL large corpus: JAK2 → IGF1R (increases, IGF1R Activity, JAK2 Activity) Zong et al., J Biol Chem 2000*
    Evidence: tyrosine phosphorylation of STAT3, JAK1, and JAK2 was increased upon IGF-I stimulation of endogenous IGF-IR in 293T cells transfected with the respective STAT or JAK expression vector.
  • OpenBEL Selventa BEL large corpus: JAK2 → IGF1R (increases, JAK2 Activity) Gual et al., Endocrinology 1998*
    Evidence: Insulin and insulin-like growth factor-1 (IGF-1) treatment of cells overexpressing the insulin receptor or the IGF-1 receptor promotes phosphorylation and activation of Janus kinases JAK-1 and JAK-2

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *