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DDIT3 — JUN

Pathways - manually collected, often from reviews:

• FastForward regulation: JUN → DDIT3 (transcriptional regulation, increase) Guyton et al., Biochem J 1996*
  Evidence: PROMACTIVITY, DNABINDING

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: DDIT3 — JUN (direct interaction, fluorescent resonance energy transfer) Reinke et al., Science 2013
• IRef Biogrid Interaction: DDIT3 — JUN (direct interaction, pull down) Ubeda et al., Mol Cell Biol 1999*
• IRef Biogrid Interaction: DDIT3 — JUN (physical association, affinity chromatography technology) Ubeda et al., Mol Cell Biol 1999*
• IRef Hprd Interaction: DDIT3 — JUN (in vivo) Ubeda et al., Mol Cell Biol 1999*
• IRef Ophid Interaction: DDIT3 — JUN (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: DDIT3 — JUN (aggregation, confirmational text mining) Ubeda et al., Mol Cell Biol 1999*

Text-mined interactions from Literome

Ubeda et al., Mol Cell Biol 1999 : Thus, CHOP not only is a negative or a positive regulator of C/EBP target genes but also, when tethered to AP-1 factors, can activate AP-1 target genes
Frigo et al., J Nutr 2002 : Chalcone was the only phytochemical that activated all three transcription factors [ Elk-1, 2.7-fold ( P < 0.001 ) ; c-Jun, 2.7-fold ( P = 0.025 ) ; CHOP, 3.0-fold ( P = 0.002 ) ], whereas apigenin stimulated CHOP ( 3.9-fold ; P < 0.001 ), but inhibited phorbol myristoyl acetate induced c-Jun activity ( 71 % ; P = 0.006 )
Singh et al., J Mol Biol 2008 (Adenocarcinoma...) : We report a novel mechanistic role of CHOP in the inhibition of Wnt/TCF signaling and stimulation of c-Jun and sucrase-isomaltase reporter activity in intestinal colon cancer cells