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CCND1 — FOS

Pathways - manually collected, often from reviews:

• KEGG Pathways in cancer: FOS → CCND1 (gene expression, expression)
• KEGG Colorectal cancer: FOS → CCND1 (protein-protein, expression)
• NCI Pathway Database AP-1 transcription factor network: JUN/FOS/RACO-1 complex (JUN-FOS) → Cyclin D1 (CCND1) (transcription, activates) Davies et al., Nat Cell Biol 2010, Wisdom et al., EMBO J 1999*
  Evidence: assay, physical interaction

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

Studies that report less than 10 interactions are marked with *

• IRef Innatedb Interaction: FOS — CCND1 (unknown, -) Toualbi et al., Oncogene 2007

Text-mined interactions from Literome

Balmanno et al., Oncogene 1999 : This suggests that both early and late AP-1 gene expression is regulated by the same Gi-mediated, MEK dependent MAPK signalling pathway but that expression of late AP-1 genes and cyclin D1 requires that this pathway be persistently activated
Ino et al., J Neurosci 2001 : Although KA administration causes prolonged c-Fos expression in the vulnerable regions that preceded the induction of neuronal apoptosis, the CDK4 or cyclin D1 antisense oligonucleotides exhibited no suppressive effect on c-Fos levels
Zhao et al., Biochem Biophys Res Commun 2002 (Liver Cirrhosis, Experimental) : In conclusion, downregulation of cyclin -D1 , -E, and -A expression, which may be induced by impaired activities of C/EBP and AP-1 , is responsible for the decreased regenerative capacity of cirrhotic liver after partial hepatectomy
Kim et al., Mol Cells 2002 : These results suggest that merlin inhibits abnormal cell proliferation which is activated via Ras by repressing Rb phosphorylation, blocking the increase of the cyclin D1 protein level, and inhibiting the activation of AP-1- and E2F-1 dependent transcription in NIH3T3 cells
Soh et al., J Biol Chem 2003 : A dominant negative mutant of c-Jun inhibited activation of the cyclin D1 promoter in a concentration dependent manner, providing further evidence that AP-1 activity is required for activation of the cyclin D1 promoter by PKC-alpha and PKC-epsilon
Chu et al., J Biol Chem 2005 (MAP Kinase Signaling System) : AP-1 is required for activation of the cyclin D1 promoter
Kim et al., J Environ Pathol Toxicol Oncol 2005 (Cell Transformation, Neoplastic) : We concluded that the inhibitory effect of eupatilin on p21waf1/Cip1 expression is likely to be associated with the downregulation of cyclin D1 expression and AP-1 activation , which play an important role in the cell cycle arrest of ras transformed breast epithelial cells
Yao et al., Mol Carcinog 2006 (Urinary Bladder Neoplasms) : Unexpectedly, neither TAM67 or JNK inhibition, nor forced c-jun expression had a significant impact on cyclin D1 induction by PEITC, indicating that c-jun/AP-1 does not play an important role in cyclin D1 induction by PEITC
Ranjan et al., Antioxid Redox Signal 2006 : In mouse lung epithelial cells that express Nox1, Nox2, Nox4, p22(phox), p47(phox), p67(phox), and Noxo1, overexpression of Nox1 delayed cell cycle withdrawal by maintaining AP-1 dependent expression of cyclin D1 in low serum conditions
Zhang et al., Toxicol Appl Pharmacol 2009 : Collectively, our results demonstrate that c-Jun/AP-1 mediated cyclin D1 expression is at least one of the key events implicated in cell transformation upon low dose arsenite exposure
Parrales et al., J Cell Physiol 2010 (Vitreoretinopathy, Proliferative) : Thrombin stimulates RPE cell proliferation by promoting c-Fos mediated cyclin D1 expression ... Analysis of thrombin activated PAR-1 downstream effectors demonstrated that c-Fos expression by the sustained activation of ERK and c-fos transcription triggers the expression and nuclear translocation of cyclin D1 , a key regulator of cell cycle G1/S phase progression leading to proliferation
Li et al., Int J Mol Med 2010 : Pre-treatment of NS3 protein expressing cells with ERK inhibitor, PD98059, blocked the activation of AP-1 and NF-kappaB, and inhibited cyclin D1 expression and cell proliferation
Ming et al., Cancer Immunol Immunother 2012 (Carcinoma, Non-Small-Cell Lung...) : We found that, in lung cancer cell lines and in nude mice, Interleukin-7/Interleukin-7 receptor increased the expression of cyclin D1 and phosphorylation of c-Fos/c-Jun, induce c-Fos and c-Jun heterodimer formation, and enhanced c-Fos/c-Jun DNA binding activity to regulate cyclin D1
Kreuzer et al., Free Radic Biol Med 1998 : The Fos protein forms the heterodimer AP-1 with the Jun protein and regulates the cell cycle by inducing cyclin D1
Sunters et al., Dev Genet 1998 (Bone Neoplasms...) : These in vivo observations suggest that cyclin D1 may be a target for c-Fos action and that elevation of cyclin D1 in osteoblasts which already express cyclin E/CDK2 and the cyclin D1 partners CDKs-4 and 6, may predispose cells to uncontrolled cell growth leading to osteosarcoma development
Brown et al., Mol Cell Biol 1998 : Although definitive evidence that c-Fos and FosB directly induce cyclin D1 transcription will require further analysis, these findings raise the possibility that c-Fos and FosB are either direct or indirect transcriptional regulators of the cyclin D1 gene and may function as a critical link between serum stimulation and cell cycle progression