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FOS — FOSL2

Pathways - manually collected, often from reviews:

• BioCarta bone remodeling: c-FOS (FOS) → FRA2 (FOSL2) (modification, activates)
• NCI Pathway Database AP-1 transcription factor network: JUN/FOS complex (FOS-JUN) → Fra2 (FOSL2) (transcription, activates) Sonobe et al., Oncogene 1995*, Ng et al., EMBO J 1997*
  Evidence: physical interaction

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: FOSL2 — FOS Newman et al., Science 2003
• IRef Bind_translation Interaction: FOSL2 — FOS (array technology) Newman et al., Science 2003
• IRef Dip Interaction: Complex of JUN-FOSB-MECOM-JUNB-YY1-FOS-FOSL2 (anti bait coimmunoprecipitation) Bard-Chapeau et al., Proc Natl Acad Sci U S A 2012
• IRef Ophid Interaction: FOSL2 — FOS (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Won et al., Mol Pharmacol 2000 : In AP-1, the basal expression of Fra-2 and c-Jun proteins and AP-1 DNA binding activity in the adrenal medulla was higher than other tissues tested, but CHX reduced these protein levels and AP-1 DNA binding activity
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
Erdem et al., J Appl Physiol 2002 (Body Weight) : We conclude that 1 ) SET elicits a pretranslational stimulatory effect on adrenomedullary CA biosynthetic enzymes, 2 ) another immediate early mRNA product, rather than FRA-2 , may contribute to the increase in AP-1 binding activity in response to SET, and 3 ) SET increases NPY mRNA expression
Roy et al., Cardiovasc Res 2010 (Disease Models, Animal...) : Knockdown of Fra-2 significantly blunted O ( 2 ) -induced expression of TGFbeta1 as well as TGFbeta3 in CF. Knockdown of Ask-1 blunted hyperoxia induced Fra-2 gene expression and nuclear localization in CF. Collectively, these observations point towards a central role of Ask-1 and Fra-2 in O ( 2 ) -inducible AP-1 activation and induction of TGFbeta
Suzuki et al., J Virol 1994 (Cell Transformation, Neoplastic) : We further showed that Fra-2-c-Jun heterodimer is mainly responsible for the elevated AP-1 DNA binding activity in these transformed cells, and we propose that this heterodimer play a crucial role in the transformation induced by these oncogenes
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
Rutberg et al., Oncogene 1997 : Exogenous expression of Fra-2 repressed AP-1 transcriptional activity in TPA treated keratinocytes, while c-Fos expression activated the AP-1 sequence in calcium treated keratinocytes
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