Gene Symbol: c-Jun
Description: Jun proto-oncogene, AP-1 transcription factor subunit
Alias: AP-1, AP1, c-Jun, p39, transcription factor AP-1, Jun activation domain binding protein, activator protein 1, enhancer-binding protein AP1, jun oncogene, proto-oncogene c-Jun, v-jun avian sarcoma virus 17 oncogene homolog, v-jun sarcoma virus 17 oncogene homolog
Species: human
Products:     c-Jun

Top Publications

  1. Tournier C, Whitmarsh A, Cavanagh J, Barrett T, Davis R. Mitogen-activated protein kinase kinase 7 is an activator of the c-Jun NH2-terminal kinase. Proc Natl Acad Sci U S A. 1997;94:7337-42 pubmed
    ..Expression of MKK7 in cultured cells causes activation of the JNK signal transduction pathway. MKK7 is therefore established to be a novel component of the JNK signal transduction pathway. ..
  2. Seldeen K, McDonald C, Deegan B, Farooq A. Coupling of folding and DNA-binding in the bZIP domains of Jun-Fos heterodimeric transcription factor. Arch Biochem Biophys. 2008;473:48-60 pubmed publisher
    ..Our data corroborate the notion that the DNA-induced protein structural changes are a general feature of the bZIP family of transcription factors. ..
  3. Yuan G, Qian L, Song L, Shi M, Li D, Yu M, et al. Heregulin-beta promotes matrix metalloproteinase-7 expression via HER2-mediated AP-1 activation in MCF-7 cells. Mol Cell Biochem. 2008;318:73-9 pubmed publisher
    ..The data indicate a close link among HRG-beta stimulation, HER signaling, and AP-1 activation. Our data suggest that HRG-beta-induced MMP-7 expression was regulated by HER2-mediated AP-1 activation in MCF-7 cells. ..
  4. Mishra A, Bharti A, Saluja D, Das B. Transactivation and expression patterns of Jun and Fos/AP-1 super-family proteins in human oral cancer. Int J Cancer. 2010;126:819-29 pubmed publisher
    ..Thus, this study demonstrates differential expression and activation of AP-1 super-family proteins in relation to severity of lesion and their crucial role in human oral carcinogenesis. ..
  5. Gonsalves C, Kalra V. Endothelin-1-induced macrophage inflammatory protein-1beta expression in monocytic cells involves hypoxia-inducible factor-1alpha and AP-1 and is negatively regulated by microRNA-195. J Immunol. 2010;185:6253-64 pubmed publisher
    ..These studies provide what we believe are new avenues, based on targets of HIF-1? and microRNAs, for ameliorating inflammation in SCD. ..
  6. Shan Z, Lin Q, Yang M, Zhang B, Zhu J, Mai L, et al. Transcription factor Ap-1 mediates proangiogenic MIF expression in human endothelial cells exposed to Angiotensin II. Cytokine. 2011;53:35-41 pubmed publisher
    ..Our results suggest that AP-1 mediates Ang II-induced MIF expression which contributes to atherosclerotic plaque destabilization in human endothelial cells. ..
  7. Kudo K, Gavin E, Das S, Amable L, Shevde L, Reed E. Inhibition of Gli1 results in altered c-Jun activation, inhibition of cisplatin-induced upregulation of ERCC1, XPD and XRCC1, and inhibition of platinum-DNA adduct repair. Oncogene. 2012;31:4718-24 pubmed publisher
    ..In all, inhibition of Gli1 by a specific shRNA inhibits the upregulation of c-jun Ser63/73, and also inhibits the upregulation of three genes essential to NER (ERCC1, XPD) and base excision repair (XRCC1). ..
  8. Aguilera C, Nakagawa K, Sancho R, Chakraborty A, Hendrich B, Behrens A. c-Jun N-terminal phosphorylation antagonises recruitment of the Mbd3/NuRD repressor complex. Nature. 2011;469:231-5 pubmed publisher
    AP-1 (activator protein 1) activity is strongly induced in response to numerous signals, including growth factors, cytokines and extracellular stresses...
  9. Gray L, Fong K, Pavelitz T, Weiner A. Tethering of the conserved piggyBac transposase fusion protein CSB-PGBD3 to chromosomal AP-1 proteins regulates expression of nearby genes in humans. PLoS Genet. 2012;8:e1002972 pubmed publisher

More Information


  1. Worrall J, Mason J. Thermodynamic analysis of Jun-Fos coiled coil peptide antagonists. FEBS J. 2011;278:663-72 pubmed publisher
    ..By contrast, the wild-type cJun-cFos complex is dominated by a favourable entropic contribution, owing partially to a decrease in buried hydrophobic groups from cFos core residues and an increase in the conformational freedom. ..
  2. Shi M, Liu D, Duan H, Han C, Wei B, Qian L, et al. Catecholamine up-regulates MMP-7 expression by activating AP-1 and STAT3 in gastric cancer. Mol Cancer. 2010;9:269 pubmed publisher
    ..Up-regulation of MMP-7 expression through ?2-AR-mediated signaling pathway is involved in invasion and metastasis of gastric cancer. ..
  3. González Ramos M, Mora I, de Frutos S, Garesse R, Rodriguez Puyol M, Olmos G, et al. Intracellular redox equilibrium is essential for the constitutive expression of AP-1 dependent genes in resting cells: studies on TGF-?1 regulation. Int J Biochem Cell Biol. 2012;44:963-71 pubmed publisher
    ..for the steady state intracellular ROS concentration, where the compartmentalized, different systems involved in the intracellular ROS production, could be essential for the expression of constitutive AP1-dependent genes, as TGF-?1.
  4. Dey N, Liu T, Garofalo R, Casola A. TAK1 regulates NF-?B and AP-1 activation in airway epithelial cells following RSV infection. Virology. 2011;418:93-101 pubmed publisher
  5. Rajagopalan K, Qiu R, Mooney S, Rao S, Shiraishi T, Sacho E, et al. The Stress-response protein prostate-associated gene 4, interacts with c-Jun and potentiates its transactivation. Biochim Biophys Acta. 2014;1842:154-63 pubmed publisher
    ..To our knowledge, this is the first report demonstrating crosstalk between a CTA and a proto-oncogene. Disrupting PAGE4/c-Jun interactions using small molecules may represent a novel therapeutic strategy for PCa. ..
  6. Xu Y, Zhu F, Cho Y, Carper A, Peng C, Zheng D, et al. Extracellular signal-regulated kinase 8-mediated c-Jun phosphorylation increases tumorigenesis of human colon cancer. Cancer Res. 2010;70:3218-27 pubmed publisher
    ..The interaction between ERK8 and c-Jun seems to increase the tumorigenic properties of HCT15 colorectal cancer cells. Thus, ERK8-regulated signaling might serve as a potential therapeutic target in colorectal cancer...
  7. Nookala A, Shah A, Noel R, Kumar A. HIV-1 Tat-mediated induction of CCL5 in astrocytes involves NF-?B, AP-1, C/EBP? and C/EBP? transcription factors and JAK, PI3K/Akt and p38 MAPK signaling pathways. PLoS ONE. 2013;8:e78855 pubmed publisher
    ..This was further confirmed at transcriptional level that AP-1, C/EBP? and C/EBP? were involved in CCL5 up-regulation. ..
  8. Gangwani M, Noel R, Shah A, Rivera Amill V, Kumar A. Human immunodeficiency virus type 1 viral protein R (Vpr) induces CCL5 expression in astrocytes via PI3K and MAPK signaling pathways. J Neuroinflammation. 2013;10:136 pubmed publisher
    ..Furthermore, this effect was observed to be mediated by transcription factors NF-?B and AP-1 and involved the p38-MAPK and PI3K/Akt pathway. ..
  9. Zugowski C, Lieder F, Müller A, Gasch J, Corvinus F, Moriggl R, et al. STAT3 controls matrix metalloproteinase-1 expression in colon carcinoma cells by both direct and AP-1-mediated interaction with the MMP-1 promoter. Biol Chem. 2011;392:449-59 pubmed publisher
    ..This finding supports the notion that the combination of inappropriate STAT3 and AP-1 activities drives elevated MMP-1 expression and tissue invasion in colorectal cancer and is of clinical relevance. ..
  10. Ahmed S, Milner J. Basal cancer cell survival involves JNK2 suppression of a novel JNK1/c-Jun/Bcl-3 apoptotic network. PLoS ONE. 2009;4:e7305 pubmed publisher
    ..This information also opens new avenues for therapeutic intervention in human proliferative disease states including cancer. ..
  11. Maritz M, van der Watt P, Holderness N, Birrer M, Leaner V. Inhibition of AP-1 suppresses cervical cancer cell proliferation and is associated with p21 expression. Biol Chem. 2011;392:439-48 pubmed publisher
    ..Our results suggest a role for AP-1 in the proliferation, G(2)/M progression and inhibition of p21 expression in cervical cancer. ..
  12. Zhang H, Yan B, Li X, Fan L, Zhang Y, Wu G, et al. PAX2 protein induces expression of cyclin D1 through activating AP-1 protein and promotes proliferation of colon cancer cells. J Biol Chem. 2012;287:44164-72 pubmed publisher
    ..Taken together, these results suggest that PAX2 promotes proliferation of colon cancer cells through AP-1. ..
  13. Ju S, Goh A, Kwon D, Youn G, Kwon H, Bae Y, et al. Extracellular HIV-1 Tat induces human beta-defensin-2 production via NF-kappaB/AP-1 dependent pathways in human B cells. Mol Cells. 2012;33:335-41 pubmed publisher
    ..Taken together, our results indicate that HIV-1 Tat can up-regulate the expression of hBD-2 via JNK-NF-?B/AP-1-dependent pathways in human B cells. ..
  14. Yang C, Luo S, Hsieh H, Chi P, Lin C, Wu C, et al. Interleukin-1beta induces ICAM-1 expression enhancing leukocyte adhesion in human rheumatoid arthritis synovial fibroblasts: involvement of ERK, JNK, AP-1, and NF-kappaB. J Cell Physiol. 2010;224:516-26 pubmed publisher
    ..These results suggest that in human RASFs, activation of ERK, JNK, AP-1, and NF-kappaB are essential for IL-1beta-induced ICAM-1 expression and leukocyte adhesion. ..
  15. Jiao X, Katiyar S, Willmarth N, Liu M, Ma X, Flomenberg N, et al. c-Jun induces mammary epithelial cellular invasion and breast cancer stem cell expansion. J Biol Chem. 2010;285:8218-26 pubmed publisher
    ..CCL5 rescued the c-Jun-deficient breast tumor cellular invasion phenotype. SCF rescued the c-Jun-deficient mammosphere production. Endogenous c-Jun thus contributes to ErbB2-induced mammary tumor cell invasion and self-renewal. ..
  16. Khattar E, Kumar V. Mitogenic regulation of p27(Kip1) gene is mediated by AP-1 transcription factors. J Biol Chem. 2010;285:4554-61 pubmed publisher
    ..Collectively, our studies present the first evidence demonstrating the role of the AP-1 complex in transcriptional down-regulation of the p27(Kip1) gene following mitogenic stimulation. ..
  17. Jin J, Ke H, Hall R, Zhang J. c-Jun promotes whereas JunB inhibits epidermal neoplasia. J Invest Dermatol. 2011;131:1149-58 pubmed publisher
    Deregulation of the activator protein 1 (AP1) family gene regulators has been implicated in a wide range of diseases, including cancer...
  18. Polytarchou C, Hatziapostolou M, Papadimitriou E. Hydrogen peroxide stimulates proliferation and migration of human prostate cancer cells through activation of activator protein-1 and up-regulation of the heparin affin regulatory peptide gene. J Biol Chem. 2005;280:40428-35 pubmed
  19. Mehic D, Bakiri L, Ghannadan M, Wagner E, Tschachler E. Fos and jun proteins are specifically expressed during differentiation of human keratinocytes. J Invest Dermatol. 2005;124:212-20 pubmed
    b>Activator protein 1 (AP-1) proteins play key roles in the regulation of cell proliferation and differentiation...
  20. Hayakawa J, Mittal S, Wang Y, Korkmaz K, Adamson E, English C, et al. Identification of promoters bound by c-Jun/ATF2 during rapid large-scale gene activation following genotoxic stress. Mol Cell. 2004;16:521-35 pubmed
    ..Thus, the genotoxic stress response occurs at least partly via activation of ATF2 and c-Jun, leading to large-scale coordinate gene expression dominated by genes of DNA repair. ..
  21. Cai C, Hsieh C, Shemshedini L. c-Jun has multiple enhancing activities in the novel cross talk between the androgen receptor and Ets variant gene 1 in prostate cancer. Mol Cancer Res. 2007;5:725-35 pubmed
  22. Chapuy B, Tikkanen R, Mühlhausen C, Wenzel D, von Figura K, Honing S. AP-1 and AP-3 mediate sorting of melanosomal and lysosomal membrane proteins into distinct post-Golgi trafficking pathways. Traffic. 2008;9:1157-72 pubmed publisher
  23. Morrison B, Majdzadeh N, Zhang X, Lyles A, Bassel Duby R, Olson E, et al. Neuroprotection by histone deacetylase-related protein. Mol Cell Biol. 2006;26:3550-64 pubmed
    ..Our results suggest that neuroprotection by HDRP is mediated by the inhibition of c-Jun through its interaction with JNK and HDAC1. ..
  24. Weiss C, Faust D, Dürk H, Kolluri S, Pelzer A, Schneider S, et al. TCDD induces c-jun expression via a novel Ah (dioxin) receptor-mediated p38-MAPK-dependent pathway. Oncogene. 2005;24:4975-83 pubmed
    ..These findings establish activating 'cross-talk' with MAPK signaling as a novel principle of AhR action, which is apparently independent of the AhR's function as a DNA-binding transcriptional activator. ..
  25. Kadoya T, Khurana A, Tcherpakov M, Bromberg K, Didier C, Broday L, et al. JAMP, a Jun N-terminal kinase 1 (JNK1)-associated membrane protein, regulates duration of JNK activity. Mol Cell Biol. 2005;25:8619-30 pubmed publisher
    ..Through its regulation of JNK1 activity, JAMP emerges as a membrane-anchored regulator of the duration of JNK1 activity in response to diverse stress stimuli...
  26. Benbrook D, Jones N. Heterodimer formation between CREB and JUN proteins. Oncogene. 1990;5:295-302 pubmed
    ..The interaction of members of these two families of proteins increases the repertoire of possible regulatory complexes that could play an important role in the regulation of transcription of specific cellular genes. ..
  27. Westermarck J, Weiss C, Saffrich R, Kast J, Musti A, Wessely M, et al. The DEXD/H-box RNA helicase RHII/Gu is a co-factor for c-Jun-activated transcription. EMBO J. 2002;21:451-60 pubmed
    ..These findings clarify the mechanism of c-Jun-mediated transcriptional regulation, and provide evidence for an involvement of RHII/Gu in stress response and in RNA polymerase II-catalyzed transcription in mammalian cells. ..
  28. Shen Q, Uray I, Li Y, Krisko T, Strecker T, Kim H, et al. The AP-1 transcription factor regulates breast cancer cell growth via cyclins and E2F factors. Oncogene. 2008;27:366-77 pubmed
    ..Thus, the AP-1 factor regulates the expression of cyclin D and E2F (the latter in turn regulates E2F-downstream genes), leading to cell cycle progression and breast cancer cell proliferation. ..
  29. Teng J, Wang Z, Prossnitz E, Bjorling D. The G protein-coupled receptor GPR30 inhibits human urothelial cell proliferation. Endocrinology. 2008;149:4024-34 pubmed publisher
    ..These results suggest that GPR30-mediated inhibition of urothelial cell proliferation is the result of decreased cyclin D1 by down-regulation of activation protein-1 signaling. ..
  30. Yazgan O, Pfarr C. Regulation of two JunD isoforms by Jun N-terminal kinases. J Biol Chem. 2002;277:29710-8 pubmed
    ..These results identify two distinct isoforms of JunD with differential responses to JNK signaling pathways. ..
  31. Varin A, Decrion A, Sabbah E, Quivy V, Sire J, Van Lint C, et al. Synthetic Vpr protein activates activator protein-1, c-Jun N-terminal kinase, and NF-kappaB and stimulates HIV-1 transcription in promonocytic cells and primary macrophages. J Biol Chem. 2005;280:42557-67 pubmed
    ..Therefore, our results suggest that extracellular Vpr could fuel the progression of AIDS via stimulation of HIV-1 provirus present in such cellular reservoirs as mononuclear phagocytes in HIV-infected patients. ..
  32. Quan T, He T, Voorhees J, Fisher G. Ultraviolet irradiation induces Smad7 via induction of transcription factor AP-1 in human skin fibroblasts. J Biol Chem. 2005;280:8079-85 pubmed
    ..These data demonstrate that induction of Smad7 gene expression by UV irradiation is mediated via induction of the transcription factor AP-1 in human skin fibroblasts. ..
  33. Xia Y, Wu Z, Su B, Murray B, Karin M. JNKK1 organizes a MAP kinase module through specific and sequential interactions with upstream and downstream components mediated by its amino-terminal extension. Genes Dev. 1998;12:3369-81 pubmed
    ..These results underscore a role for the amino-terminal extension of MAPKKs in determination of response specificity. ..
  34. Vries R, Prudenziati M, Zwartjes C, Verlaan M, Kalkhoven E, Zantema A. A specific lysine in c-Jun is required for transcriptional repression by E1A and is acetylated by p300. EMBO J. 2001;20:6095-103 pubmed
    ..In addition, Lys271 is acetylated both in vitro and in vivo. These results suggest that the specific repression of the collagenase promoter by E1A involves acetylation of c-Jun. ..
  35. Zhang Y, Feng X, Derynck R. Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-beta-induced transcription. Nature. 1998;394:909-13 pubmed
    ..factors, composed of c-Jun and c-Fos, bind to and direct transcription from TREs, which are therefore known as AP1-binding sites...
  36. Vinciguerra M, Esposito I, Salzano S, Madeo A, Nagel G, Maggiolini M, et al. Negative charged threonine 95 of c-Jun is essential for c-Jun N-terminal kinase-dependent phosphorylation of threonine 91/93 and stress-induced c-Jun biological activity. Int J Biochem Cell Biol. 2008;40:307-16 pubmed
    ..Hence, our study suggests that c-Jun may sense the strength of genotoxic stress through DNA-damage dependent phosphorylation of T95, which in turn augments c-Jun transactivation by JNKs. ..
  37. Mao X, Orchard G, Mitchell T, Oyama N, Russell Jones R, Vermeer M, et al. A genomic and expression study of AP-1 in primary cutaneous T-cell lymphoma: evidence for dysregulated expression of JUNB and JUND in MF and SS. J Cutan Pathol. 2008;35:899-910 pubmed publisher
    b>Activator protein 1 (AP-1) consists of a group of transcription factors including the JUN and FOS family proteins with diverse biological functions...
  38. Zhang Y, Pu X, Shi M, Chen L, Song Y, Qian L, et al. Critical role of c-Jun overexpression in liver metastasis of human breast cancer xenograft model. BMC Cancer. 2007;7:145 pubmed
    ..The results provide further evidence that c-Jun is involved in the metastasis of breast cancer. The finding also opens an opportunity for development of anti-c-Jun strategies in breast cancer therapy. ..
  39. Newell C, Deisseroth A, Lopez Berestein G. Interaction of nuclear proteins with an AP-1/CRE-like promoter sequence in the human TNF-alpha gene. J Leukoc Biol. 1994;56:27-35 pubmed
  40. Nateri A, Spencer Dene B, Behrens A. Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer development. Nature. 2005;437:281-5 pubmed
    ..Therefore, the phosphorylation-dependent interaction between c-Jun and TCF4 regulates intestinal tumorigenesis by integrating JNK and APC/beta-catenin, two distinct pathways activated by WNT signalling. ..
  41. Qi X, Borowicz S, Pramanik R, Schultz R, Han J, Chen G. Estrogen receptor inhibits c-Jun-dependent stress-induced cell death by binding and modifying c-Jun activity in human breast cancer cells. J Biol Chem. 2004;279:6769-77 pubmed
    ..Together, our studies reveal a novel function of ER in stress response by modification of c-Jun activity. ..
  42. Yu Y, Ge N, Xie M, Sun W, Burlingame S, Pass A, et al. Phosphorylation of Thr-178 and Thr-184 in the TAK1 T-loop is required for interleukin (IL)-1-mediated optimal NFkappaB and AP-1 activation as well as IL-6 gene expression. J Biol Chem. 2008;283:24497-505 pubmed publisher
    ..Our finding is the first report that substitution of key serine/threonine residues with acidic residues mimics the phosphorylated state of TAK1 and renders TAK1 active during its induced activation. ..
  43. Yamaguchi K, Lantowski A, Dannenberg A, Subbaramaiah K. Histone deacetylase inhibitors suppress the induction of c-Jun and its target genes including COX-2. J Biol Chem. 2005;280:32569-77 pubmed
    ..This led, in turn, to reduced expression of several activator protein-1-dependent genes (COX-2, cyclin D1, collagenase-1). These findings provide new insights into the mechanisms underlying the antitumor activity of HDAC inhibitors. ..
  44. Derijard B, Hibi M, Wu I, Barrett T, Su B, Deng T, et al. JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain. Cell. 1994;76:1025-37 pubmed
    ..Thus, JNK1 is a component of a novel signal transduction pathway that is activated by oncoproteins and UV irradiation. These properties indicate that JNK1 activation may play an important role in tumor promotion. ..
  45. Ishitani T, Takaesu G, Ninomiya Tsuji J, Shibuya H, Gaynor R, Matsumoto K. Role of the TAB2-related protein TAB3 in IL-1 and TNF signaling. EMBO J. 2003;22:6277-88 pubmed
    ..These results suggest that TAB2 and TAB3 function redundantly as mediators of TAK1 activation in IL-1 and TNF signal transduction. ..
  46. Hu Y, Li R. JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction. Genes Dev. 2002;16:1509-17 pubmed
    ..Thus, the coiled-coil-mediated cooperation between BRCA1 and JunB may facilitate the function of these proteins in tissue-specific transcriptional regulation and tumor suppression. ..
  47. Toborek M, Lee Y, Pu H, Malecki A, Flora G, Garrido R, et al. HIV-Tat protein induces oxidative and inflammatory pathways in brain endothelium. J Neurochem. 2003;84:169-79 pubmed
    ..These changes can directly lead to disruption of the BBB. Thus, Tat can play an important role in the development of detrimental vascular changes in the brains of HIV-infected patients. ..
  48. Wu X, Sun S. Retroviral oncoprotein Tax deregulates NF-kappaB by activating Tak1 and mediating the physical association of Tak1-IKK. EMBO Rep. 2007;8:510-5 pubmed
    ..These findings show a pathological mechanism of IKK activation by Tax and provide an example for how IKK is persistently activated in cancer cells. ..
  49. Trøen G, Nygaard V, Jenssen T, Ikonomou I, Tierens A, Matutes E, et al. Constitutive expression of the AP-1 transcription factors c-jun, junD, junB, and c-fos and the marginal zone B-cell transcription factor Notch2 in splenic marginal zone lymphoma. J Mol Diagn. 2004;6:297-307 pubmed
  50. Singhirunnusorn P, Suzuki S, Kawasaki N, Saiki I, Sakurai H. Critical roles of threonine 187 phosphorylation in cellular stress-induced rapid and transient activation of transforming growth factor-beta-activated kinase 1 (TAK1) in a signaling complex containing TAK1-binding protein TAB1 and TAB2. J Biol Chem. 2005;280:7359-68 pubmed
    ..These results indicate critical roles of Thr-187 phosphorylation in the stress-induced rapid and transient activation of TAK1 in a signaling complex containing TAB1 and TAB2. ..
  51. Grondin B, Lefrancois M, Tremblay M, Saint Denis M, Haman A, Waga K, et al. c-Jun homodimers can function as a context-specific coactivator. Mol Cell Biol. 2007;27:2919-33 pubmed
  52. Fujita S, Ito T, Mizutani T, Minoguchi S, Yamamichi N, Sakurai K, et al. miR-21 Gene expression triggered by AP-1 is sustained through a double-negative feedback mechanism. J Mol Biol. 2008;378:492-504 pubmed publisher
    ..Since exogenous miR-21 expression moderately induced endogenous miR-21, an evolutionarily conserved double-negative feedback regulation would be operating as a mechanism to sustain miR-21 expression. ..
  53. Hattori K, Angel P, Le Beau M, Karin M. Structure and chromosomal localization of the functional intronless human JUN protooncogene. Proc Natl Acad Sci U S A. 1988;85:9148-52 pubmed
    ..encodes a protein that is functionally and biochemically identical to the transcription factor AP-1 (activator protein 1)...
  54. Hibi M, Lin A, Smeal T, Minden A, Karin M. Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain. Genes Dev. 1993;7:2135-48 pubmed
    ..Therefore the binding of JNK to c-Jun is of regulatory importance and suggests a mechanism through which protein kinase cascades can specifically modulate the activity of distinct nuclear targets. ..
  55. Kardassis D, Papakosta P, Pardali K, Moustakas A. c-Jun transactivates the promoter of the human p21(WAF1/Cip1) gene by acting as a superactivator of the ubiquitous transcription factor Sp1. J Biol Chem. 1999;274:29572-81 pubmed
    ..In conclusion, our data support a mechanism of superactivation of Sp1 by c-Jun, which is based on physical and functional interactions between these two transcription factors on the human p21 and possibly other Sp1-dependent promoters. ..
  56. Bossis G, Malnou C, Farras R, Andermarcher E, Hipskind R, Rodriguez M, et al. Down-regulation of c-Fos/c-Jun AP-1 dimer activity by sumoylation. Mol Cell Biol. 2005;25:6964-79 pubmed
    ..This supports the idea that this modification does not constitute a final inactivation step that necessarily precedes protein degradation. ..
  57. Tanos T, Marinissen M, Leskow F, Hochbaum D, Martinetto H, Gutkind J, et al. Phosphorylation of c-Fos by members of the p38 MAPK family. Role in the AP-1 response to UV light. J Biol Chem. 2005;280:18842-52 pubmed
    ..This phosphorylation is transduced into changes in its transcriptional ability as p38-activated c-Fos enhances AP1-driven gene expression...
  58. Yang X, Chen Y, Gabuzda D. ERK MAP kinase links cytokine signals to activation of latent HIV-1 infection by stimulating a cooperative interaction of AP-1 and NF-kappaB. J Biol Chem. 1999;274:27981-8 pubmed
    ..These results define a mechanism for signal-dependent activation of HIV-1 replication in latently infected cells and suggest potential therapeutic strategies for unmasking latent reservoirs of HIV-1. ..
  59. DeNardo D, Kim H, Hilsenbeck S, Cuba V, Tsimelzon A, Brown P. Global gene expression analysis of estrogen receptor transcription factor cross talk in breast cancer: identification of estrogen-induced/activator protein-1-dependent genes. Mol Endocrinol. 2005;19:362-78 pubmed
    ..These studies demonstrate that microarrays can be used in a reverse genetics approach to predict the functional promoter structure of large numbers of genes that are regulated by multiple transcription factors. ..
  60. Zhang L, Xing G, Tie Y, Tang Y, Tian C, Li L, et al. Role for the pleckstrin homology domain-containing protein CKIP-1 in AP-1 regulation and apoptosis. EMBO J. 2005;24:766-78 pubmed
    ..CKIP-1 is the first case of a c-Jun-interacting protein that regulates AP-1 activity via caspase-3-dependent cleavage and translocation. ..
  61. Wang Y, Chang W. Induction of disease-associated keratin 16 gene expression by epidermal growth factor is regulated through cooperation of transcription factors Sp1 and c-Jun. J Biol Chem. 2003;278:45848-57 pubmed
    ..Disruption of the Sp1 site (-127 to -122 bp) and the AP1 site (-148 to -142 bp) of the keratin 16 promoter by site-directed mutagenesis significantly inhibited keratin 16 ..
  62. Wulf G, Ryo A, Wulf G, Lee S, Niu T, Petkova V, et al. Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c-Jun towards cyclin D1. EMBO J. 2001;20:3459-72 pubmed
    ..Given the crucial roles of Ras signaling and cyclin D1 overexpression in oncogenesis, our results suggest that overexpression of Pin1 may promote tumor growth. ..
  63. Vasanwala F, Kusam S, Toney L, Dent A. Repression of AP-1 function: a mechanism for the regulation of Blimp-1 expression and B lymphocyte differentiation by the B cell lymphoma-6 protooncogene. J Immunol. 2002;169:1922-9 pubmed
    ..Repression of AP-1 function by BCL-6 may be a key mechanism for how BCL-6 regulates gene expression to control inflammation, lymphocyte differentiation, and lymphomagenesis. ..
  64. Sato N, Sadar M, Bruchovsky N, Saatcioglu F, Rennie P, Sato S, et al. Androgenic induction of prostate-specific antigen gene is repressed by protein-protein interaction between the androgen receptor and AP-1/c-Jun in the human prostate cancer cell line LNCaP. J Biol Chem. 1997;272:17485-94 pubmed
    ..This association provides a link between AP-1 and AR signal transduction pathways and may play a role in the regulation of the androgen-responsive PSA gene. ..
  65. Kallunki T, Deng T, Hibi M, Karin M. c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions. Cell. 1996;87:929-39 pubmed
    ..Substrates such as JunD can be phosphorylated by JNK through heterodimerization with docking competent partners. Therefore, heterodimerization can affect the recognition of transcription factors by signal-regulated protein kinases. ..
  66. Ito T, Yamauchi M, Nishina M, Yamamichi N, Mizutani T, Ui M, et al. Identification of SWI.SNF complex subunit BAF60a as a determinant of the transactivation potential of Fos/Jun dimers. J Biol Chem. 2001;276:2852-7 pubmed
    ..These results indicate that a specific subset of Fos/Jun dimers recruits SWI.SNF complex via BAF60a to initiate transcription. ..
  67. Laner Plamberger S, Kaser A, Paulischta M, Hauser Kronberger C, Eichberger T, Frischauf A. Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes. Oncogene. 2009;28:1639-51 pubmed publisher
    ..GLI1 and GLI2, the main transcriptional activators of the HH pathway, directly regulate expression of the activator protein 1 (AP-1) family member JUN, a transcription factor controlling keratinocyte proliferation and skin ..
  68. Holmström T, Mialon A, Kallio M, Nymalm Y, Mannermaa L, Holm T, et al. c-Jun supports ribosomal RNA processing and nucleolar localization of RNA helicase DDX21. J Biol Chem. 2008;283:7046-53 pubmed publisher
    ..Moreover, these results suggest that the phenotypes observed previously in c-Jun-depleted mouse models and cell lines could be partly due to the effects of c-Jun on rRNA processing. ..
  69. Neub A, Houdek P, Ohnemus U, Moll I, Brandner J. Biphasic regulation of AP-1 subunits during human epidermal wound healing. J Invest Dermatol. 2007;127:2453-62 pubmed
    ..b>Activator protein 1 (AP-1) subunits have been implicated in the regulation of genes important for these processes and have been ..
  70. Wei W, Jin J, Schlisio S, Harper J, Kaelin W. The v-Jun point mutation allows c-Jun to escape GSK3-dependent recognition and destruction by the Fbw7 ubiquitin ligase. Cancer Cell. 2005;8:25-33 pubmed
    ..These findings explain the enhanced stability and oncogenicity of v-Jun relative to its cellular counterpart and reveal that GSK3 and Fbw7 coordinately regulate c-Jun and c-Myc. ..
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    ..These findings provide an 'activation by de-repression' model as an explanation for the stimulatory function of JNK on c-Jun. ..
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    ..Thus, our data illustrate that NF-kappaB orchestrates immediate-early effects of LPS signaling and controls secondary AP-1 activation to mount an appropriate biological response. ..
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    ..Altogether, our findings suggest that the presence of the AP-1 signal acts as a survival factor that determines the outcome of myc-induced proliferation or apoptosis. ..
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    ..Moreover, targeting of G1 regulatory proteins and the resulting induction of G1 arrest by A3D8 may provide new insights into antiproliferative and differentiation therapy of AML. ..
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    ..Together, these data suggest that TGFbeta-mediated transcriptional activation through AP-1 sites may involve a regulated interaction between Smads and AP-1 transcription factors. ..
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    ..We also demonstrated novel interactions between coactivators and AP-1 proteins. We propose that extracellular signal-mediated coactivator exchange at AP-1 sites is mediated via protein kinase pathways. ..
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    ..In addition, the results of the present study strongly suggest that inhibition of EGFR expression is a novel mechanism by which topotecan inhibits cell proliferation in cancer therapy. ..
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    ..The genes differentially regulated by GRR488Q mutant versus the wild-type GR after 2 h of treatment seem mainly to be involved in control of transcription and cell growth. At 8 h, no such distinction could be seen. ..
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    ..Therefore, our results suggest that exogenous Nef could fuel the progression of the disease via stimulation of HIV-1 provirus present in such cellular reservoirs as mononuclear phagocytes in HIV-infected patients. ..
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