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FOXO3 — TSC22D3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: TSC22D3 → FOXO3 (directlyIncreases, TSC22D3 Activity) Asselin-Labat et al., Blood 2004*
  Evidence: IL-2 deprivation leads to expression of GILZ in T lymphocytes. We then characterized the human gilz promoter and showed that FoxO3 (Forkhead box class O3) binding to the Forkhead responsive elements identified in the promoter is necessary for induction of gilz expression upon IL-2 withdrawal

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

Studies that report less than 10 interactions are marked with *

• MIPS Negatome - no physical interaction between proteins Interaction: TSC22D3 — FOXO3 (Absence of interaction, coimmunoprecipitation) Latré de Laté et al., J Biol Chem 2010*

Text-mined interactions from Literome

Asselin-Labat et al., Blood 2004 : We then characterized the human gilz promoter and showed that FoxO3 ( Forkhead box class O3 ) binding to the Forkhead responsive elements identified in the promoter is necessary for induction of gilz expression upon IL-2 withdrawal ... Furthermore, GILZ inhibits FoxO3 transcriptional activity that leads to inhibition of Bim expression but also to down-regulation of GILZ itself
Asselin-Labat et al., Mol Endocrinol 2005 : Furthermore, overexpression of the Forkhead transcription factor FoxO3 enhances GC-induced gilz mRNA expression
Latré de Laté et al., J Biol Chem 2010 : GILZ inhibits FOXO1, FOXO3 , and FOXO4 transcriptional activities measured with natural or synthetic FOXO-responsive promoters in HL-60 cells