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FOS — JUND

Pathways - manually collected, often from reviews:

• NCI Pathway Database AP-1 transcription factor network: JUND/FOS complex (JUND-FOS) → HIF1A (HIF1A) (transcription, activates) Abdul-Hafez et al., FASEB J 2009*
  Evidence: mutant phenotype, reporter gene, physical interaction
• NCI Pathway Database AP-1 transcription factor network: FOS (FOS) → JUND/FOS complex (JUND-FOS) (modification, collaborate)
  Ryseck et al., Oncogene 1991, Suzuki et al., Nucleic Acids Res 1991, Hirai et al., EMBO J 1989*, Nakabeppu et al., Cell 1988*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: FOS (FOS) → JUND (JUND) (modification, collaborate) Ryseck et al., Oncogene 1991, Suzuki et al., Nucleic Acids Res 1991, Hirai et al., EMBO J 1989*, Nakabeppu et al., Cell 1988*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUND/FOS complex (JUND-FOS) → JUND (JUND) (modification, collaborate) Ryseck et al., Oncogene 1991, Suzuki et al., Nucleic Acids Res 1991, Hirai et al., EMBO J 1989*, Nakabeppu et al., Cell 1988*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUND/FOS complex (JUND-FOS) → uPA (PLAU) (transcription, activates) D'Orazio et al., Gene 1997*
  Evidence: reporter gene, physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUND/FOS complex (JUND-FOS) → ANF (NPPA) (transcription, activates) McBride et al., Mol Cell Biol 1998*
  Evidence: reporter gene, physical interaction

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: FOS — JUND Newman et al., Science 2003
• IRef Bind_translation Interaction: FOS — JUND (array technology) Newman et al., Science 2003
• IRef Biogrid Interaction: FOS — JUND (physical association, affinity chromatography technology) Miyamoto-Sato et al., PloS one 2010
• IRef Biogrid Interaction: FOS — JUND (physical association, affinity chromatography technology) Kumar et al., J Biol Chem 2001*
• IRef Hprd Interaction: FOS — JUND (in vitro) Thway et al., Biol Reprod 2002*, Miyamoto-Sato et al., Genome Res 2005
• IRef Hprd Interaction: FOS — JUND (in vivo) Thway et al., Biol Reprod 2002*, Miyamoto-Sato et al., Genome Res 2005
• IRef Intact Interaction: FOS — JUND (physical association, display technology) Miyamoto-Sato et al., PloS one 2010
• IRef Intact Interaction: FOS — JUND (physical association, tandem affinity purification) Miyamoto-Sato et al., PloS one 2010
• IRef Ophid Interaction: FOS — JUND (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Srivastava et al., J Clin Invest 1999 : The consequent decrease in the nuclear levels of c-Jun and JunD leads to diminished binding of c-Jun/c-Fos and JunD/c-Fos heterodimers to the AP-1 consensus sequence in the TNF promoter and, thus, to decreased transactivation of the TNF gene
Berry et al., Biochem Pharmacol 2001 : Supershift assays demonstrated that in control cells, AP-1 binding activity was mediated by Jun D/Fra 2 heterodimers, whereas after vinblastine treatment, AP-1 complexes also containing c-Jun and Fra 1 were present, suggesting that induction of these latter proteins by vinblastine is functionally significant
Yumita et al., Int J Cancer 2003 : The translation product of the MEN1 gene, menin, has been reported to suppress JunD mediated activator protein-1 (AP-1) transactivation and inhibit Ras mediated tumor formation, but its molecular mechanisms and physiologic significance have been poorly elucidated
Yang et al., Pigment Cell Res 2004 (Melanoma) : There are progressive variations in AP-1 composition in different melanoma cell lines compared with normal melanocytes, in which c-Jun, JunD and FosB were involved in AP-1 complexes ... In w3211, c-Jun, JunD and Fra-1 were involved in AP-1 binding, while in w1205, overall AP-1 binding activity was decreased significantly and supershift binding was detected only with JunD antibodies ... In metastatic c81-46A and A375 cells, only JunD was involved in AP-1 binding activity, but in a third ( c83-2c ) c-Jun, JunD and Fra-1 were present
Ikeo et al., Endocr J 2004 (Multiple Endocrine Neoplasia Type 1) : JunD-menin interaction regulates c-Jun mediated AP-1 transactivation
Hilfiker-Kleiner et al., Cardiovasc Res 2006 (Cardiomegaly) : Over-expression of JunD in cardiomyocytes caused enhanced AP-1 protein-DNA binding, without increasing the transcriptional response from AP-1 or ANP luciferase reporter plasmids at baseline or upon PE stimulation
Parra et al., Mol Cell Biol 1997 : LFA-3 induced primarily Jun-D , Fra-1, and Fra-2, while B7-1 induced June-D-Fos complexes