◀ Back to JUN

FOSL1 — JUN

Pathways - manually collected, often from reviews:

• FastForward regulation: JUN → FOSL1 (transcriptional regulation, increase) Smith et al., Oncogene 1999*
  Evidence: REG
• NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2: Fra1 (FOSL1) → JUN (JUN) (modification, collaborate) Young et al., Mol Cell Biol 2002*, Kovary et al., Mol Cell Biol 1992*, Burch et al., Mol Cell Biol 2004*, Chalmers et al., Cell Signal 2007*, Basbous et al., Mol Cell Biol 2007*, Ryseck et al., Oncogene 1991, Suzuki et al., Nucleic Acids Res 1991, Malnou et al., J Biol Chem 2010*, Talotta et al., Oncogene 2010*, Cohen et al., Genes Dev 1989*, Rauscher et al., Science 1988*, Gruda et al., Oncogene 1994*, Treinies et al., Mol Cell Biol 1999*, Cook et al., Mol Cell Biol 1999*
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2: Fra1 (FOSL1) → Fra1/JUN complex (FOSL1-JUN) (modification, collaborate)
  Young et al., Mol Cell Biol 2002*, Kovary et al., Mol Cell Biol 1992*, Burch et al., Mol Cell Biol 2004*, Chalmers et al., Cell Signal 2007*, Basbous et al., Mol Cell Biol 2007*, Ryseck et al., Oncogene 1991, Suzuki et al., Nucleic Acids Res 1991, Malnou et al., J Biol Chem 2010*, Talotta et al., Oncogene 2010*, Cohen et al., Genes Dev 1989*, Rauscher et al., Science 1988*, Gruda et al., Oncogene 1994*, Treinies et al., Mol Cell Biol 1999*, Cook et al., Mol Cell Biol 1999*
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2: JUN (JUN) → Fra1/JUN complex (FOSL1-JUN) (modification, collaborate)
  Young et al., Mol Cell Biol 2002*, Kovary et al., Mol Cell Biol 1992*, Burch et al., Mol Cell Biol 2004*, Chalmers et al., Cell Signal 2007*, Basbous et al., Mol Cell Biol 2007*, Ryseck et al., Oncogene 1991, Suzuki et al., Nucleic Acids Res 1991, Malnou et al., J Biol Chem 2010*, Talotta et al., Oncogene 2010*, Cohen et al., Genes Dev 1989*, Rauscher et al., Science 1988*, Gruda et al., Oncogene 1994*, Treinies et al., Mol Cell Biol 1999*, Cook et al., Mol Cell Biol 1999*
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2: Fra1/FIAT complex (FOSL1-TXLNG) → Fra1/JUN complex (FOSL1-JUN) (transcription, inhibits)
  Farzaneh-Far et al., J Biol Chem 2001*, Eferl et al., EMBO J 2004*, Julien et al., J Bone Miner Res 2009*, St-Arnaud et al., Ann N Y Acad Sci 2010*
  Evidence: reporter gene, physical interaction
• NCI Pathway Database AP-1 transcription factor network: Fra1 (FOSL1) → JUN (JUN) (modification, collaborate) Young et al., Mol Cell Biol 2002*, Malnou et al., J Biol Chem 2010*, Talotta et al., Oncogene 2010*, Cohen et al., Genes Dev 1989*, Gruda et al., Oncogene 1994*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: Fra1 (FOSL1) → Fra1/JUN complex (FOSL1-JUN) (modification, collaborate)
  Young et al., Mol Cell Biol 2002*, Malnou et al., J Biol Chem 2010*, Talotta et al., Oncogene 2010*, Cohen et al., Genes Dev 1989*, Gruda et al., Oncogene 1994*
  Evidence: physical interaction
• NCI Pathway Database AP-1 transcription factor network: JUN (JUN) → Fra1/JUN complex (FOSL1-JUN) (modification, collaborate)
  Young et al., Mol Cell Biol 2002*, Malnou et al., J Biol Chem 2010*, Talotta et al., Oncogene 2010*, Cohen et al., Genes Dev 1989*, Gruda et al., Oncogene 1994*
  Evidence: physical interaction
• NCI Pathway Database Validated transcriptional targets of AP1 family members Fra1 and Fra2: Fra1/FIAT complex (FOSL1-TXLNG) → Fra1/JUN complex (FOSL1-JUN) (transcription, inhibits)
  Chandrasekar et al., J Biol Chem 2006*, St-Arnaud et al., Ann N Y Acad Sci 2010*
  Evidence: reporter gene, physical interaction
• WikiPathways Wnt Signaling Pathway and Pluripotency: EP300 → Complex of 11 proteins (activation)
• WikiPathways Wnt Signaling Pathway and Pluripotency: ZBTB33 → Complex of 11 proteins (mim-inhibition)

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: FOSL1 — JUN Newman et al., Science 2003
• IRef Bind_translation Interaction: FOSL1 — JUN (array technology) Newman et al., Science 2003
• IRef Biogrid Interaction: FOSL1 — JUN (direct interaction, fluorescent resonance energy transfer) Reinke et al., Science 2013
• IRef Biogrid Interaction: FOSL1 — JUN (direct interaction, two hybrid) Pognonec et al., Oncogene 1997*
• IRef Biogrid Interaction: FOSL1 — JUN (direct interaction, pull down) Pognonec et al., Oncogene 1997*
• IRef Biogrid Interaction: FOSL1 — JUN (physical association, affinity chromatography technology) Kumar et al., J Biol Chem 2001*
• IRef Hprd Interaction: FOSL1 — JUN (in vitro) Udalova et al., Biochem Biophys Res Commun 2001*, Jardine et al., J Biol Chem 2002*
• IRef Hprd Interaction: FOSL1 — JUN (in vivo) Udalova et al., Biochem Biophys Res Commun 2001*, Jardine et al., J Biol Chem 2002*
• IRef Ophid Interaction: FOSL1 — JUN (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: FOSL1 — JUN (aggregation, confirmational text mining) Udalova et al., Biochem Biophys Res Commun 2001*

Text-mined interactions from Literome

Young et al., Mol Cell Biol 2002 (Cell Transformation, Neoplastic) : These observations suggest that ERK dependent activation of Fra-1 is required for AP-1 transactivation in JB6 cells
Adiseshaiah et al., J Biol Chem 2003 : In particular, coexpression of c-Jun , Jun-D, and Fra-2 up-regulated fra-1 transcription
Vial et al., J Cell Sci 2003 (Colonic Neoplasms) : We show that c-JUN and FRA-1 expression is dependent on ERK activity and that different thresholds of ERK activity control the expression of FRA-1
Yang et al., Pigment Cell Res 2004 (Melanoma) : 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
Myhrstad et al., Nutr Cancer 2006 (Carcinoma, Hepatocellular...) : Fra-1 is a member of the activator protein 1 (AP-1) family of transcription factors and, due to the lack of transactivation domain Fra-1, can suppress activation of AP-1
Camalier et al., Cancer prevention research (Philadelphia, Pa.) 2010 (Cell Transformation, Neoplastic...) : Supplementation of medium with phosphate increased anchorage independent transformation and proliferation of BALB/c mouse JB6 epidermal cells, activation of N-ras, ERK1/2, and activator protein-1 , and increased gene expression of Fra-1 , COX-2, and osteopontin in a dose dependent manner
Yoshioka et al., Proc Natl Acad Sci U S A 1995 : Furthermore, Fra-1 repressed AP-1 activity induced by either TPA or expression of c-Jun and c-Fos
Bergers et al., Mol Cell Biol 1995 (Cell Transformation, Neoplastic) : Transcriptional activation of the fra-1 gene by AP-1 is mediated by regulatory sequences in the first intron ... Constitutive expression of c-Fos, FosB, Fra-1, or c-Jun in rat fibroblasts leads to up-regulation of the immediate-early gene fra-1 ... Using the posttranslational FosER induction system, we demonstrate that this AP-1 dependent stimulation of fra-1 expression is rapid, depends on a functional DNA binding domain of FosER, and is a general phenomenon observed in different cell types ... In vitro mutagenesis and functional analysis of the rat fra-1 gene in stably transfected Rat-1A-FosER fibroblasts indicated that basal and AP-1 regulated expression of the fra-1 gene depends on regulatory sequences in the first intron which comprise a consensus AP-1 site and two AP-1-like elements
Schreiber et al., Oncogene 1997 (Osteosclerosis) : Absence of c-Fos leads to significantly reduced serum stimulation of fra-1 expression in gene targeted mouse fibroblasts, demonstrating that mitogen induction of fra-1 is partially mediated by c-Fos/AP-1
Casamassimi et al., Cancer Res 1998 : Fra-1 and c-jun were induced by p53, resulting in increased AP-1 levels
Kustikova et al., Mol Cell Biol 1998 (Adenocarcinoma...) : We found that the enhanced level of AP-1 in CSML100 cells was due to high expression of Fra-1 and Fra-2 proteins, which were undetectable in CSML0 nuclear extracts
Cook et al., Mol Cell Biol 1999 : c-Fos, c-Jun , and JunB are induced rapidly in response to LPA stimulation, whereas Fra-1 and Fra-2 are induced after a significant lag ... In cells expressing a conditionally active form of Raf-1 ( DeltaRaf-1 : ER ), we observed that selective, sustained activation of Raf-MEK-MAPK was sufficient to induce expression of Fra-1 , Fra-2, and JunB but, interestingly, induced little or no c-Fos or c-Jun