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FOS — RB1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of FOS-JUN → Complex of JUN-RB1 (increases)
  Evidence: RB1&CEBPB^taof(CEBPB) Hypophosphorylated pRb binds c-Jun, JunD, and JunB (Nead et al., 1998). This enhances the binding of the Jun family members to c-Fos and stimulates transcriptional activation by the Fos:Jun complexes. A region (amino acids 612?657) in the B-pocket of pRb and a region in the C-pocket can independently bind c-Jun. The binding site in c-Jun is in the leucine zipper region.

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: FOS — RB1 (direct interaction, pull down) Nead et al., EMBO J 1998*
• IRef Hprd Interaction: FOS — RB1 (in vivo) Udvadia et al., Proc Natl Acad Sci U S A 1993*
• IRef Ophid Interaction: FOS — RB1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

David et al., J Clin Invest 2005 (Bone Diseases, Metabolic...) : However, in the absence of RSK2, c-Fos dependent osteosarcoma formation is impaired ... Therefore, RSK2 dependent stabilization of c-Fos is essential for osteosarcoma formation in mice and may also be important for human osteosarcomas
Xiong et al., Diabetes 2010 (Hyperglycemia...) : This inhibitory effect on feeding may be mediated by central mechanisms because Rb1 stimulated c-Fos expression in brain areas involved in energy homeostasis
Cheng et al., Food Chem Toxicol 2012 (MAP Kinase Signaling System) : Taken together, our data suggest that ginsenoside Rb1 is one of the effective components of GSS for the anti-osteoporosis activity and can inhibit osteoclastogenesis by suppressing RANKL induced activation of both JNK and p38 MAPKs and NF-?B pathways, and consequently down regulating the gene expression of c-Fos and NFATc1 in osteoclast precursors
Sunters et al., Dev Genet 1998 (Bone Neoplasms...) : Control of cell cycle gene expression in bone development and during c-Fos induced osteosarcoma formation ... Prolonged activation of c-Fos resulted in osteosarcoma formation wherein the levels of cyclin D1, cyclin E, and CDKs 2, 4, and 6 were high in a wide spectrum of malignant cell types, especially in transformed osteoblasts