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ATF3 — JUN

Pathways - manually collected, often from reviews:

• NCI Pathway Database AP-1 transcription factor network: JUN (JUN) → JUN/ATF3 complex (JUN-ATF3) (modification, collaborate)
  Hai et al., Proc Natl Acad Sci U S A 1991, Filén et al., J Immunol 2010*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUN (JUN) → ATF3 (ATF3) (modification, collaborate) Hai et al., Proc Natl Acad Sci U S A 1991, Filén et al., J Immunol 2010*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUN/ATF3 complex (JUN-ATF3) → ATF3 (ATF3) (modification, collaborate) Hai et al., Proc Natl Acad Sci U S A 1991, Filén et al., J Immunol 2010*
  Evidence: physical interaction
• NCI Pathway Database ATF-2 transcription factor network: JUN/ATF2 complex (JUN-ATF2) → ATF3 (ATF3) (transcription, activates) Kool et al., Oncogene 2003*, Yuan et al., Mol Cell Biol 2009*, Chaveroux et al., Mol Cell Biol 2009*
  Evidence: assay, reporter gene

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: ATF3 — JUN Newman et al., Science 2003
• IRef Bind_translation Interaction: ATF3 — JUN (array technology) Newman et al., Science 2003
• IRef Biogrid Interaction: ATF3 — JUN (physical association, affinity chromatography technology) Pearson et al., Brain Res Mol Brain Res 2003*
• IRef Biogrid Interaction: ATF3 — JUN (physical association, affinity chromatography technology) Filén et al., J Immunol 2010*
• IRef Biogrid Interaction: ATF3 — JUN (physical association, affinity chromatography technology) Chen et al., Mol Cell Biol 1996*
• IRef Biogrid Interaction: ATF3 — JUN (direct interaction, pull down) Hai et al., Proc Natl Acad Sci U S A 1991
• IRef Biogrid Interaction: ATF3 — JUN (direct interaction, fluorescent resonance energy transfer) Reinke et al., Science 2013
• IRef Dip Interaction: ATF3 — JUN (physical association, coimmunoprecipitation) Hai et al., Proc Natl Acad Sci U S A 1991
• IRef Hprd Interaction: ATF3 — JUN (in vitro) Pearson et al., Brain Res Mol Brain Res 2003*, Hagmeyer et al., Oncogene 1996*
• IRef Hprd Interaction: ATF3 — JUN (in vivo) Pearson et al., Brain Res Mol Brain Res 2003*, Hagmeyer et al., Oncogene 1996*
• IRef Intact Interaction: ATF3 — JUN (physical association, coimmunoprecipitation) Duyndam et al., Oncogene 1999*
• IRef Ophid Interaction: ATF3 — JUN (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: ATF3 — JUN (aggregation, confirmational text mining) Pearson et al., Brain Res Mol Brain Res 2003*

Text-mined interactions from Literome

Mao et al., J Immunol 2001 : Furthermore, the bZip elements of the two promoters bind different transcription factors, as the GL epsilon promoter binds and is activated by AP-1 , whereas the gamma1 promoter binds and is activated by activating transcription factor 2
Nobori et al., J Mol Cell Cardiol 2002 : DOX rapidly activated JNK and c-Jun and induced ATF3 at both mRNA and protein level
Lindwall et al., Mol Cell Neurosci 2004 : Peripheral severance of the vagus or the sciatic nerve resulted in a massive and rapid, but transient increase of the activated JNK ( p-JNK ) in neuronal nuclei, followed by c-Jun phosphorylation and activating transcription factor-3 (ATF3) induction ... JNK inhibition by the selective JNK inhibitors SP600125 and ( D ) -JNKI1 did not affect neuronal survival in explanted or dissociated ganglia, but dramatically reduced axonal outgrowth, c-Jun activation, and ATF3 induction
Seijffers et al., Mol Cell Neurosci 2006 (Peripheral Nerve Injuries) : ATF-3 overexpression did not increase c-Jun expression
Lu et al., J Dermatol 2013 : Importantly, JUN may regulate activating transcription factor 3 expression to involve cell proliferation process ; STAT1 and STAT3 can inhibit tissue inhibitor of metalloproteinases-3 expression to modulate the cell adhesion molecule pathway ; NF-?B and E2F1 can downregulate cyclin D1, but upregulate proliferating cell nuclear antigen expression to promote the cell cycle pathway
Suk et al., Anticancer Res 2013 (Adenocarcinoma...) : The up-regulation of ATF3 was blocked by a c-JUN N-terminal kinase (JNK) or p38 inhibitor
Hagmeyer et al., Oncogene 1996 : Altered AP-1/ATF complexes in adenovirus-E1 transformed cells due to EIA dependent induction of ATF3