Genomes and Genes
Gene Symbol: Jun
Description: jun proto-oncogene
Alias: AP-1, Junc, c-jun, transcription factor AP-1, AH119, AP1, Jun oncogene, V-jun avian sarcoma virus 17 oncogene homolog, activator protein 1, immediate early, jun A, proto-oncogene c-jun
Publications170 found, 100 shown here
- Induction of proto-oncogene JUN/AP-1 by serum and TPAW W Lamph
Molecular Biology and Virology Laboratory, Salk Institute, San Diego, California 92138
Nature 334:629-31. 1988..Prominent among these so-called 'immediate early' or 'competence' genes are the nuclear oncogenes fos and myc...
- c-Jun NH2-terminal kinase (JNK)1 and JNK2 have similar and stage-dependent roles in regulating T cell apoptosis and proliferationK Sabapathy
Research Institute of Molecular Pathology, Vienna A 1030, Austria
J Exp Med 193:317-28. 2001Apoptotic and mitogenic stimuli activate c-Jun NH2-terminal kinases (JNKs) in T cells...
- JNK1 modulates osteoclastogenesis through both c-Jun phosphorylation-dependent and -independent mechanismsJean Pierre David
Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
J Cell Sci 115:4317-25. 2002Phosphorylation of the N-terminal domain of Jun by the Jun kinases (JNKs) modulates the transcriptional activity of AP-1, a dimeric transcription factor typically composed of c-Jun and c-Fos, the latter being essential for osteoclast ..
- Insulin-mediated activation of activator protein-1 through the mitogen-activated protein kinase pathway stimulates collagenase-1 gene transcription in the MES 13 mesangial cell lineJ E Ayala
Department of Molecular Physiology and Biophysics, 761 PRB MRB II, Vanderbilt University Medical School, Nashville, Tennessee 37232 0615, USA
J Mol Endocrinol 33:263-80. 2004..In MES 13 cells, the AP-1 motif is bound by Fra-1, Fra-2, Jun B and Jun D...
- Nuclear factor kappaB and activating protein 1 are involved in differentiation-related resistance to oxidative stress in skeletal muscle cellsM Valeria Catani
Department of Experimental Medicine and Biochemical Sciences, University of Rome Tor Vergata, Rome, Italy
Free Radic Biol Med 37:1024-36. 2004..In conclusion, the two cell lines, although similar in terms of growth and differentiation, displayed significant heterogeneity in terms of redox homeostasis...
- The LIM protein, Limd1, regulates AP-1 activation through an interaction with Traf6 to influence osteoclast developmentYunfeng Feng
Department of Medicine, Washington University, St Louis, Missouri 63110, USA
J Biol Chem 282:39-48. 2007..These results implicate Limd1 as a potentially important regulator of osteoclast development under conditions of stress...
- TNF-alpha induces TGF-beta1 expression in lung fibroblasts at the transcriptional level via AP-1 activationDeborah E Sullivan
Department of Microbiology and Immunology, Biomedical Sciences Graduate Program, Tulane University School of Medicine, New Orleans, LA, USA
J Cell Mol Med 13:1866-76. 2009..TNF-alpha induced increased levels of c-Jun and C-Fos in the nucleus accompanied by phosphorylation of c-Jun...
- Essential role of Jun family transcription factors in PU.1 knockdown-induced leukemic stem cellsUlrich Steidl
Harvard Institutes of Medicine, Harvard Medical School and Harvard Stem Cell Institute, Boston, Massachusetts 02115, USA
Nat Genet 38:1269-77. 2006..1-knockdown HSCs') to identify transcriptional changes preceding malignant transformation. Transcription factors c-Jun and JunB were among the top-downregulated targets...
- Jun and JunD-dependent functions in cell proliferation and stress responseA Meixner
Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria
Cell Death Differ 17:1409-19. 2010b>Jun is essential for fetal development, as fetuses lacking Jun die at mid-gestation with multiple cellular defects in liver and heart...
- AP1 factor inactivation in the suprabasal epidermis causes increased epidermal hyperproliferation and hyperkeratosis but reduced carcinogen-dependent tumor formationE A Rorke
Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
Oncogene 29:5873-82. 2010Activator protein one (AP1) (jun/fos) factors comprise a family of transcriptional regulators (c-jun, junB, junD, c-fos, FosB, Fra-1 and Fra-2) that are key controllers of epidermal keratinocyte survival and differentiation, and are ..
- H2O2-dependent activation of GCLC-ARE4 reporter occurs by mitogen-activated protein kinase pathways without oxidation of cellular glutathione or thioredoxin-1Young Mi Go
Department of Medicine, Division of Cardiology, School of Medicine, Emory University, Atlanta, Georgia 30322, USA
J Biol Chem 279:5837-45. 2004..H2O2 signaling to ARE4 was mediated by activation of both the c-Jun N-terminal kinase and ERK1/2 pathways modulated by Ras...
- Basic fibroblast growth factor-induced neuronal differentiation of mouse bone marrow stromal cells requires FGFR-1, MAPK/ERK, and transcription factor AP-1Haijie Yang
Research Laboratories, National Neuroscience Institute, Singapore 308433
J Biol Chem 283:5287-95. 2008..the immediate-early transcription factors AP-1 and NF-kappaB and have found that phospholipase C-gamma-dependent c-Jun and ERK-dependent c-fos, but not the NF-kappaB, are strongly activated by bFGF, which in turn regulates the ..
- Inhibition of myoblast differentiation by tumor necrosis factor alpha is mediated by c-Jun N-terminal kinase 1 and leukemia inhibitory factorJoel Alter
Department of Biochemistry, Technion Israel Institute of Technology, Haifa 31096, Israel
J Biol Chem 283:23224-34. 2008..In the present study, the role of c-Jun N-terminal kinase (JNK), a mediator of TNFalpha, was investigated in differentiating myoblast cell lines...
- Inhibition of AP-1 transcriptional activity blocks the migration, invasion, and experimental metastasis of murine osteosarcomaVirna D Leaner
Cell and Cancer Biology Department, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Am J Pathol 174:265-75. 2009..This study shows that differences in metastatic activity can be due to AP-1 activation. The inhibition of AP-1 activity may serve as a therapeutic tool in the management of osteosarcoma...
- Low doses of lipopolysaccharide and minimally oxidized low-density lipoprotein cooperatively activate macrophages via nuclear factor kappa B and activator protein-1: possible mechanism for acceleration of atherosclerosis by subclinical endotoxemiaPhilipp Wiesner
Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA 92093 0682, USA
Circ Res 107:56-65. 2010..In addition, low-level but persistent metabolic endotoxemia is often found in diabetic and obese subjects and is induced in mice fed a high-fat diet...
- Induction of protooncogene c-jun by serum growth factorsK Ryder
Howard Hughes Medical Institute Laboratory, Baltimore, MD
Proc Natl Acad Sci U S A 85:8464-7. 1988..We have previously reported that one of the genes that is rapidly induced in mouse 3T3 cells by serum growth factors (jun-B) encodes a protein related to the onco-protein v-jun...
- FoxP3 maintains Treg unresponsiveness by selectively inhibiting the promoter DNA-binding activity of AP-1Sang Myeong Lee
Department of Otolaryngology Head and Neck Surgery, University of Missouri Columbia School of Medicine 65212, USA
Blood 111:3599-606. 2008..binding is not the result of the decreased nuclear translocation of AP-1 family transcription factors, including c-Jun, JunB, and c-Fos...
- SIRT1 suppresses activator protein-1 transcriptional activity and cyclooxygenase-2 expression in macrophagesRan Zhang
National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China
J Biol Chem 285:7097-110. 2010..Here we demonstrate that SIRT1 directly interacts with the basic leucine zipper domains of c-Fos and c-Jun, the major components of AP-1, by which SIRT1 suppressed the transcriptional activity of AP-1...
- A novel mouse c-fos intronic promoter that responds to CREB and AP-1 is developmentally regulated in vivoVincent Coulon
Institut de Genetique Moleculaire de Montpellier, Centre National de la Recherche Scientifique, Universite Montpellier 2, Universite Montpellier 1, Montpellier, France
PLoS ONE 5:e11235. 2010..Innumerable studies have focused on the canonical promoter, located upstream from the transcriptional start site. However, several regulatory sequences have been found in the first intron...
- Ethanol-induced HO-1 and NQO1 are differentially regulated by HIF-1alpha and Nrf2 to attenuate inflammatory cytokine expressionSamantha M Yeligar
Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA
J Biol Chem 285:35359-73. 2010..Furthermore, livers of ethanol-fed c-Jun(fl/fl) mice showed reduced levels of mRNA for HO-1 but not of NQO1 compared with ethanol-fed control rats, ..
- Macrophage-derived BAFF induces AID expression through the p38MAPK/CREB and JNK/AP-1 pathwaysHyun A Kim
Institute of Bioscience and Biotechnology, Kangwon National University, Chuncheon 200 701, Republic of Korea
J Leukoc Biol 89:393-8. 2011..Our findings suggest that macrophage-derived BAFF stimulates B cells to express AID through BCMA and at least two different pathways, including the p38MAPK/CREB and the JNK/AP-1 pathways...
- c-jun is essential for sympathetic neuronal death induced by NGF withdrawal but not by p75 activationM Palmada
Department of Biology, University of California, San Diego, 92138, USA
J Cell Biol 158:453-61. 2002..transcription-dependent apoptotic response, which is suggested to require activation of the transcription factor c-Jun. Similarly, apoptosis can also be induced by selective activation of the p75 neurotrophin receptor...
- IKKbeta couples hepatocyte death to cytokine-driven compensatory proliferation that promotes chemical hepatocarcinogenesisShin Maeda
Laboratory of Gene Regulation and Signal Transduction, University of California, San Diego, 9500 Gilman Drive MC 0723, La Jolla, California 92093, USA
Cell 121:977-90. 2005..IKKbeta, therefore, orchestrates inflammatory crosstalk between hepatocytes and hematopoietic-derived cells that promotes chemical hepatocarcinogenesis...
- The FGF-BMP signaling axis regulates outflow tract valve primordium formation by promoting cushion neural crest cell differentiationJue Zhang
Center for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, Texas A and M Health Science Center, Houston, TX 77030 3303, USA
Circ Res 107:1209-19. 2010..Disruption of the fibroblast growth factor (FGF) signaling axis impairs morphogenesis of the outflow tract (OFT). Yet, whether FGF signaling regulates OFT valve formation is unknown...
- Embryonic stem (ES) cells lacking functional c-jun: consequences for growth and differentiation, AP-1 activity and tumorigenicityF Hilberg
Research Institute of Molecular Pathology IMP, Vienna, Austria
Oncogene 7:2371-80. 1992The proto-oncogene c-jun encodes the major component of the transcription factor AP-1 and is thought to have important functions in cell proliferation and differentiation as well as in the cellular response to a variety of external ..
- Cloning of the human glycine transporter type 1: molecular and pharmacological characterization of novel isoform variants and chromosomal localization of the gene in the human and mouse genomesK M Kim
Howard Hughes Medical Institute Research Laboratories, Department of Cell Biology and Medicine, Duke University Medical Center, Durham, North Carolina 27710
Mol Pharmacol 45:608-17. 1994..These variants point to regions of the glycine transporter that might be important in the processing or transport function of this protein...
- The Wnt antagonist Dickkopf-1 is regulated by Bmp signaling and c-Jun and modulates programmed cell deathLars Grotewold
Entwicklungs und Molekularbiologie der Tiere, Heinrich Heine Universitat, D 40225 Dusseldorf, Germany
EMBO J 21:966-75. 2002..We further show that normal expression of Dkk-1 is dependent on the Ap-1 family member c-Jun and that overexpression of Dkk-1 enhances Bmp-triggered apoptosis in the vertebrate limb...
- The response of c-jun/AP-1 to chronic hypoxia is hypoxia-inducible factor 1 alpha dependentKeith R Laderoute
Pharmaceutical Discovery Division, SRI International, Menlo Park, California 94025, USA
Mol Cell Biol 22:2515-23. 2002..Prolonged or chronic hypoxia stimulates expression of the stress-inducible transcription factor gene c-jun and transient activation of protein kinase and phosphatase activities that regulate c-Jun/AP-1 activity...
- AP-1 transrepressing retinoic acid does not deplete coactivators or AP-1 monomers but may target specific Jun or Fos containing dimersKazumi Suzukawa
Gene Regulation Section, Basic Research Laboratory, National Cancer Institute at Frederick, Frederick, Maryland 21702 1201, USA
Oncogene 21:2181-90. 2002..induced AP-1 activation nor did a GST pull down experiment implicate direct binding, thus rendering unlikely both a Jun/Fos-RA-RAR direct interaction and a Jun/Fos sequestration mechanism...
- Simulated microgravity suppresses osteoblast phenotype, Runx2 levels and AP-1 transactivationC Ontiveros
Department of Physiology, Michigan State University, 2201 Biomedical Physical Science Bldg, East Lansing 48824, USA
J Cell Biochem 88:427-37. 2003..Taken together, our results indicate that simulated microgravity may suppress osteoblast differentiation through decreased runx2 and AP-1 activities...
- Erk pathway and activator protein 1 play crucial roles in FGF2-stimulated premature cranial suture closureHyun Jung Kim
Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, Korea
Dev Dyn 227:335-46. 2003..FGF2 treatment also induced fos and jun mRNAs and later increased the nuclear levels of activator protein 1 (AP1)...
- The gonadotropin releasing hormone (GnRH) receptor activating sequence (GRAS) is a composite regulatory element that interacts with multiple classes of transcription factors including Smads, AP-1 and a forkhead DNA binding proteinBuffy S Ellsworth
Animal Reproduction and Biotechnology Laboratory, Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
Mol Cell Endocrinol 206:93-111. 2003..We suggest that GRAS is a composite regulatory element whose functional activity is dependent on the organization of a multi-protein complex consisting of Smads, AP-1 and a member of the forkhead family of DNA binding proteins...
- The interaction between GATA proteins and activator protein-1 promotes the transcription of IL-13 in mast cellsAkio Masuda
Division of Host Defense, Center for Neural Disease and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan
J Immunol 173:5564-73. 2004..The results of the present study have shown that direct interaction between AP-1 and GATA proteins plays an important role in IL-13 transcription in mast cells...
- Increased keratinocyte proliferation by JUN-dependent expression of PTN and SDF-1 in fibroblastsLore Florin
Division of Signal Transduction and Growth Control, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany
J Cell Sci 118:1981-9. 2005..The AP-1 transcription factor subunit JUN plays a crucial role in this mesenchymal-epithelial interplay by regulating the expression of two critical ..
- A role for c-fos/activator protein 1 in B lymphocyte terminal differentiationYusuke Ohkubo
Department of Developmental Genetics H2, Graduate School of Medicine, Chiba University, Chiba, Japan
J Immunol 174:7703-10. 2005..Thus, although c-Fos is not essential for Blimp-1 expression, c-Fos/AP-1 positively regulates Blimp-1 expression and terminal differentiation of activated B cells...
- Treatment of experimental asthma by decoy-mediated local inhibition of activator protein-1Christophe Desmet
Laboratoire de Physiologie, Faculte de Medecine Veterinaire, Centre de Thérapie Cellulaire et Moléculaire, Universite de Liege, Belgium
Am J Respir Crit Care Med 172:671-8. 2005....
- Increased expression of interleukin-6 by vasoactive intestinal peptide is associated with regulation of CREB, AP-1 and C/EBP, but not NF-kappaB, in mouse calvarial osteoblastsEmma Persson
Department of Oral Cell Biology, Umea University, SE 901 87 Umea, Sweden
Bone 37:513-29. 2005..The mRNA expressions of C/EBPbeta, C/EBPdelta, C/EBPgamma, c-Jun, JunB, c-Fos, Fra-1 and IkappaBalpha and protein level of IkappaBalpha were all unaffected by VIP...
- Polyinosinic acid induces TNF and NO production as well as NF-kappaB and AP-1 transcriptional activation in the monocytemacrophage cell line RAW 264.7V M Campa
Instituto Universitario de Oncología del Principado de Asturias and Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, 33071 Oviedo, Spain
Inflamm Res 54:328-37. 2005..This study evaluates the poly inosinic acid (poly I)-induced activation in the murine monocytemacrophage cell line RAW 264.7, which led to an inflammatory phenotype...
- Role of AP-1 in ethanol-induced N-methyl-D-aspartate receptor 2B subunit gene up-regulation in mouse cortical neuronsMei Qiang
Department of Pharmacology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229 3900, USA
J Neurochem 95:1332-41. 2005b>Activator protein 1 (AP-1) has been reported to regulate the gene expression in a wide variety of cellular processes in response to stimuli...
- A role for Ets1, synergizing with AP-1 and GATA-3 in the regulation of IL-5 transcription in mouse Th2 lymphocytesJun Wang
Division of Molecular Bioscience, John Curtin School of Medical Research, Australian National University, Mills Road, Acton, ACT 0200 Australia
Int Immunol 18:313-23. 2006..AP-1 (c-Fos/c-Jun) strongly induced IL-5 transcription and dominant negative AP-1 constructs confirmed that AP-1 plays an important ..
- TBP is differentially regulated by c-Jun N-terminal kinase 1 (JNK1) and JNK2 through Elk-1, controlling c-Jun expression and cell proliferationShuping Zhong
Department of Biochemistry and Molecular Biology, University of Southern California, 2011 Zonal Ave, Los Angeles, CA 90033, USA
Mol Cell Biol 27:54-64. 2007Emerging evidence supports the idea that the c-Jun N-terminal kinases (JNKs) possess overlapping but distinct functions...
- Hyperactive variants of p38alpha induce, whereas hyperactive variants of p38gamma suppress, activating protein 1-mediated transcriptionNadav Askari
Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel
J Biol Chem 282:91-9. 2007..Active mutants of p38alpha induced AP-1-driven reporter genes, as well as the c-jun and c-fos promoters. An active variant of p38gamma suppressed AP-1-mediated transcription...
- Induction of activator protein-1 and nuclear factor-kappaB as a prerequisite for disease development in susceptible SJL/J mice after theiler murine encephalomyelitisIngo Gerhauser
Department of Pathology, University of Veterinary Medicine Hannover, Hannover, Germany
J Neuropathol Exp Neurol 66:809-18. 2007..The expression of activator protein-1 (c-fos and c-jun) and nuclear factor-kappaB (p50 and p65) genes, TME virus, tumor necrosis factor-alpha, and interferon-gamma was ..
- Fast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelopeJosé María González
Laboratory of Vascular Biology, Department of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Cientificas CSIC, Valencia, Spain
J Cell Biol 183:653-66. 2008..Thus, NE-bound ERK1/2 functions as a molecular switch for rapid mitogen-dependent AP-1 activation through phosphorylation-induced release of preexisting c-Fos from its inhibitory interaction with lamin A/C...
- Viperin is required for optimal Th2 responses and T-cell receptor-mediated activation of NF-kappaB and AP-1Lian Qun Qiu
Laboratory of Gene Regulation and Inflammation, Singapore Immunology Network, Biomedical Sciences Institutes, Singapore
Blood 113:3520-9. 2009..Thus, viperin facilitates TCR-mediated GATA-3 activation and optimal Th2 cytokine production by modulating NF-kappaB and AP-1 activities...
- Effect of ultraviolet B radiation on activator protein 1 constituent proteins and modulation by dietary energy restriction in SKH-1 mouse skinBrian D Hopper
Interdepartmental Toxicology Program, Iowa State University, Ames, Iowa 50011 1123, USA
Mol Carcinog 48:843-52. 2009The study examined the timing of modulation of activator protein 1(AP-1):DNA binding and production of AP-1 constituent proteins by ultraviolet B (UVB) radiation and effect of dietary energy restriction [DER, 40% calorie reduction from ..
- Nuclear localization of c-FLIP-L and its regulation of AP-1 activityJing Zhang
Jiangsu Center of Hepatobiliary Diseases and the State Key Laboratory of Pharmaceutical Biotechnology, Affiliated Gulou Hospital, School of Life Sciences, Nanjing University, Nanjing, China
Int J Biochem Cell Biol 41:1678-84. 2009..In sum, our findings describe a novel function of c-FLIP-L involved in AP-1 activation and cell proliferation...
- Helicobacter pylori induces ERK-dependent formation of a phospho-c-Fos c-Jun activator protein-1 complex that causes apoptosis in macrophagesMohammad Asim
Division of Gastroenterology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
J Biol Chem 285:20343-57. 2010..shift assay and immunoprecipitation revealed a previously unrecognized complex of phospho-c-Fos (pc-Fos) and c-Jun in the nucleus. Fluorescence resonance energy transfer demonstrated the interaction of pc-Fos and c-Jun...
- Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblastsR P Ryseck
European Molecular Biology Laboratory, Heidelberg, FRG
Nature 334:535-7. 1988..the nucleotide sequence of a mouse cDNA clone coding for a 334 residue protein which shows 80% similarity with v-JUN and more than 98% similarity with the human c-JUN sequence...
- A gene activated by growth factors is related to the oncogene v-junK Ryder
Howard Hughes Medical Institute Laboratory, Baltimore, MD
Proc Natl Acad Sci U S A 85:1487-91. 1988..Here we report that the nucleotide sequence of a cDNA (clone 465) derived from one of these immediate early genes (hereafter called jun-B) encodes a protein homologous to that encoded by the avian sarcoma virus 17 ..
- Tissue-specific expression of the fos-related transcription factor fra-2 during mouse developmentD Carrasco
Department of Molecular Biology, Bristol Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543 4000
Oncogene 10:1069-79. 1995..of fra-2 during mouse embryonic development and compared it to the pattern of expression of other fos and jun family members...
- A c-Jun dominant negative mutant protects sympathetic neurons against programmed cell deathJ Ham
Eisai London Research Laboratories, University College London, United Kingdom
Neuron 14:927-39. 1995..We have investigated the pattern of expression of the Jun and Fos family of transcription factors in dying sympathetic neurons using antibodies specific for each family ..
- Altered gene expression in neurons during programmed cell death: identification of c-jun as necessary for neuronal apoptosisS Estus
Department of Molecular Biology, Washington University School of Medicine, St Louis, Missouri 63110
J Cell Biol 127:1717-27. 1994..A temporal cascade of induced genes included "immediate early genes," which were remarkable in that their induction occurred hours after the initial stimulus of NGF ..
- c-jun is essential for normal mouse development and hepatogenesisF Hilberg
Research Institute of Molecular Pathology IMP, Vienna, Austria
Nature 365:179-81. 1993The proto-oncogene c-jun is the cellular homologue of v-jun, the transforming oncogene of the avian sarcoma virus 17 (ref. 1)...
- Programmed cell death in the absence of c-Fos and c-JunS Roffler-Tarlov
Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02111, USA
Development 122:1-9. 1996..factor, AP-1, in the regulation of programmed cell death, and specifically implicate the genes c-fos and c-jun, as well as some other family members...
- c-Jun regulates cell cycle progression and apoptosis by distinct mechanismsR Wisdom
Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
EMBO J 18:188-97. 1999c-Jun is a component of the transcription factor AP-1, which is activated by a wide variety of extracellular stimuli...
- JunB is essential for mammalian placentationM Schorpp-Kistner
Deutsches Krebsforschungszentrum Heidelberg, Abteilung für Signaltransduktion und Wachstumskontrolle, Im Neuenheimer Feld 280, D 69120 Heidelberg, Germany
EMBO J 18:934-48. 1999Lack of JunB, an immediate early gene product and member of the AP-1 transcription factor family causes embryonic lethality between E8.5 and E10.0...
- Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferationA Behrens
Research Institute of Molecular Pathology, Vienna, Austria
Nat Genet 21:326-9. 1999c-Jun is a major component of the heterodimeric transcription factor AP-1 and is essential for embryonic development, as fetuses lacking Jun die at mid-gestation with impaired hepatogenesis and primary Jun-/- fibroblasts have a severe ..
- The Jnk1 and Jnk2 protein kinases are required for regional specific apoptosis during early brain developmentC Y Kuan
Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
Neuron 22:667-76. 1999The c-Jun NH2-terminal kinase (Jnk) family is implicated in apoptosis, but its function in brain development is unclear. Here, we address this issue using mutant mice lacking different members of the family (Jnk1, Jnk2, and Jnk3)...
- Functions of c-Jun in liver and heart developmentR Eferl
Department of Pathology, University of Graz, A 8036 Graz, Austria
J Cell Biol 145:1049-61. 1999Mice lacking the AP-1 transcription factor c-Jun die around embryonic day E13.0 but little is known about the cell types affected as well as the cause of embryonic lethality. Here we show that a fraction of mutant E13...
- JunB can substitute for Jun in mouse development and cell proliferationEmmanuelle Passegue
Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
Nat Genet 30:158-66. 2002The Jun and JunB components of the AP-1 transcription factor are known to have antagonistic functions...
- Impaired postnatal hepatocyte proliferation and liver regeneration in mice lacking c-jun in the liverAxel Behrens
Research Institute of Molecular Pathology IMP, Dr Bohr Gasse 7, A 1030 Vienna, Austria
EMBO J 21:1782-90. 2002Mice lacking the AP-1 transcription factor c-jun die at mid-gestation showing heart defects and impaired hepatogenesis. To inactivate c-jun in hepatocytes, mice carrying a floxed c-jun allele were generated...
- A dominant negative c-jun specifically blocks okadaic acid-induced skin tumor promotionEric J Thompson
Department of Pharmacology and Toxicology, The University of Arizona, Tucson, AZ 85724, USA
Cancer Res 62:3044-7. 2002..One or more of the pathways affected by OA leads to increased signaling via the activator protein 1 (AP-1) transcription factor...
- Promoter specificity and biological activity of tethered AP-1 dimersLatifa Bakiri
Unité Expression Génétique et Maladies, CNRS URA 1644, Institut Pasteur, 75724 Paris Cedex 15, France
Mol Cell Biol 22:4952-64. 2002b>Activator protein 1 (AP-1) is a group of dimeric transcription factors composed of Jun, Fos, and ATF family proteins...
- Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53Robert Eferl
Research Institute of Molecular Pathology IMP, Dr Bohrgasse 7, A 1030, Vienna, Austria
Cell 112:181-92. 2003The transcription factor c-Jun mediates several cellular processes, including proliferation and survival, and is upregulated in many carcinomas...
- c-Jun regulates eyelid closure and skin tumor development through EGFR signalingRainer Zenz
Research Institute of Molecular Pathology IMP, A 1030, Vienna, Austria
Dev Cell 4:879-89. 2003To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated c-jun in the epidermis...
- A role for MEK kinase 1 in TGF-beta/activin-induced epithelium movement and embryonic eyelid closureLin Zhang
Department of Environmental Health, University of Cincinnati Medical Center, Cincinnati, OH 45267, USA
EMBO J 22:4443-54. 2003..fibers in wild-type mice, but compact cell contacts, lack of polymerized actin and a concomitant impairment in c-Jun N-terminal phosphorylation in MEKK1-deficient mice...
- Expression of dominant negative c-jun inhibits ultraviolet B-induced squamous cell carcinoma number and size in an SKH-1 hairless mouse modelSimon J Cooper
Department of Radiation Oncology, Arizona Cancer Center, College of Public Health, The University of Arizona, Tucson, AZ, USA
Mol Cancer Res 1:848-54. 2003..the hypothesis that AP-1 activation plays a role in the promotion of UVB-induced skin tumors, a dominant negative c-jun (TAM67) mutant transgene was expressed in the epidermis of SKH-1 hairless mice and bred with mice expressing an AP-..
- Krox-20 inhibits Jun-NH2-terminal kinase/c-Jun to control Schwann cell proliferation and deathDavid B Parkinson
Department of Anatomy and Developmental Biology, University College London, Gower Street, London, WC1E 6BT UK
J Cell Biol 164:385-94. 2004..Significantly, a major function of Krox-20 is to suppress the c-Jun NH2-terminal protein kinase (JNK)-c-Jun pathway, activation of which is required for both proliferation and death...
- DCX, a new mediator of the JNK pathwayAmos Gdalyahu
Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel
EMBO J 23:823-32. 2004..Here we demonstrate that DCX is a substrate of JNK and interacts with both c-Jun N-terminal kinase (JNK) and JNK interacting protein (JIP)...
- The AP-1 transcription factor c-Jun is required for efficient axonal regenerationGennadij Raivich
Perinatal Brain Repair Group, Department of Obstetrics and Gynaecology, University College London, 86 96 Chenies Mews, London WC1E 6HX, United Kingdom
Neuron 43:57-67. 2004..c-Jun is a component of the heterodimeric AP-1 transcription factor, and c-Jun is highly expressed in response to ..
- The c-Jun NH2-terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesisClaire R Weston
Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Proc Natl Acad Sci U S A 101:14114-9. 2004The c-Jun NH(2)-terminal kinase (JNK) group of mitogen-activated protein kinases is activated in response to a wide array of cellular stresses and proinflammatory cytokines...
- c-Jun-deficient cells undergo premature senescence as a result of spontaneous DNA damage accumulationAnn MacLaren
Beatson Institute for Cancer Research, Bearsden, UK
Mol Cell Biol 24:9006-18. 2004Mouse embryo fibroblasts deficient for the c-Jun proto-oncogene (c-Jun-/- MEF) undergo p53-dependent premature senescence in conventional culture...
- Phosphorylation of c-Fos by members of the p38 MAPK family. Role in the AP-1 response to UV lightTamara Tanos
Laboratorio de Fisiologia y Biologia Molecular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, IFIBYNE CONICET, 1428 Buenos Aires, Argentina
J Biol Chem 280:18842-52. 2005..This phosphorylation is transduced into changes in its transcriptional ability as p38-activated c-Fos enhances AP1-driven gene expression...
- Differential inhibition of UVB-induced AP-1 and NF-kappaB transactivation by components of the jun bZIP domainSimon Cooper
Arizona Cancer Center, Tucson, Arizona 85724, USA
Mol Carcinog 43:108-16. 2005..of both these ultraviolet light B (UVB)-induced transcription factors has been shown with the dominant-negative c-jun mutant, TAM67; however, its mechanism of action has not yet been determined...
- Interaction of phosphorylated c-Jun with TCF4 regulates intestinal cancer developmentAbdolrahman S Nateri
Mammalian Genetics Laboratory, CR UK London Research Institute, Lincoln s Inn Fields Laboratories, 44 Lincoln s Inn Fields, London WC2A 3PX, UK
Nature 437:281-5. 2005The proto-oncoprotein c-Jun is a component of the AP-1 transcription factor, the activity of which is augmented in many tumour types...
- Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteinsRainer Zenz
Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
Nature 437:369-75. 2005..We propose that the abrogation of JunB/activator protein 1 (AP-1) in keratinocytes triggers chemokine/cytokine expression, which recruits neutrophils and macrophages ..
- c-Jun promotes cellular survival by suppression of PTENK Hettinger
Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore
Cell Death Differ 14:218-29. 2007Activation of c-Jun, a component of the AP-1 family of transcription factors, leads to either promotion or prevention of apoptosis. However, the molecular determinants of c-Jun-mediated cell survival are still unclear...
- c-Jun/AP-1 controls liver regeneration by repressing p53/p21 and p38 MAPK activityEwa Stepniak
Research Institute of Molecular Pathology IMP, A 1030 Vienna, Austria
Genes Dev 20:2306-14. 2006The AP-1 transcription factor c-Jun is a key regulator of hepatocyte proliferation. Mice lacking c-Jun in the liver (c-jun (Deltali*)) display impaired liver regeneration after partial hepatectomy (PH)...
- The c-Jun N-terminal kinase activator dual leucine zipper kinase regulates axon growth and neuronal migration in the developing cerebral cortexSyu ichi Hirai
Department of Molecular Biology, Graduate School of Medical Science, Yokohama City University, Yokohama 236 0004, Japan
J Neurosci 26:11992-2002. 2006..Dual leucine zipper kinase (DLK) induces activation of c-Jun N-terminal kinase (JNK), a molecule that regulates morphogenesis in various organisms...
- Cyclooxygenase-2 gene transcription in a macrophage model of inflammationYeon Joo Kang
Cell and Molecular Biology Program, Michigan State University, East Lansing, MI 48824, USA
J Immunol 177:8111-22. 2006..In support of this concept, we found, using inhibitors of Jun kinase and NF-kappaB p50 nuclear localization, that COX-2 gene transcription was completely dependent on phospho-c-..
- Somatic excision demonstrates that c-Jun induces cellular migration and invasion through induction of stem cell factorSanjay Katiyar
Departments of Cancer Biology and Medical Oncology, The Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, PA 19107, USA
Mol Cell Biol 27:1356-69. 2007Cancer cells arise through sequential acquisition of mutations in tumor suppressors and oncogenes. c-Jun, a critical component of the AP-1 complex, is frequently overexpressed in diverse tumor types and has been implicated in promoting ..
- c-Jun supports ribosomal RNA processing and nucleolar localization of RNA helicase DDX21Tim H Holmström
Centre for Biotechnology, University of Turku and Abo Akademi University, 20520 Turku, Finland
J Biol Chem 283:7046-53. 2008The molecular mechanisms by which the AP-1 transcription factor c-Jun exerts its biological functions are not clearly understood...
- c-Jun is a negative regulator of myelinationDavid B Parkinson
Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, England, UK
J Cell Biol 181:625-37. 2008..We report that c-Jun is an important regulator of this plasticity...
- Restriction to Fos family members of Trip6-dependent coactivation and glucocorticoid receptor-dependent trans-repression of activator protein-1Markus Diefenbacher
Institut für Toxikologie und Genetik, Forschungszentrum Karlsruhe, Hermann von Helmholtz Platz 1, D 76344 Eggenstein Leopoldshafen, Germany
Mol Endocrinol 22:1767-80. 2008..activator protein (AP)-1 describes homodimeric and heterodimeric transcription factors composed of members of the Jun, Fos, and cAMP response element-binding protein (CREB)/activating transcription factor (ATF) families of proteins...
- Ezh2 orchestrates gene expression for the stepwise differentiation of tissue-specific stem cellsElena Ezhkova
Howard Hughes Medical Institute, Laboratory of Mammalian Cell Biology and Development, The Rockefeller University, New York, NY 10065, USA
Cell 136:1122-35. 2009..the Ink4A-Ink4B locus and tempers the developmental rate of differentiation by preventing premature recruitment of AP1 transcriptional activator to the structural genes that are required for epidermal differentiation...
- FGF-regulated BMP signaling is required for eyelid closure and to specify conjunctival epithelial cell fateJie Huang
Department of Ophthalmology and Visual Sciences, Washington University, St Louis, MO 63130, USA
Development 136:1741-50. 2009..c-Jun, another key regulator of eyelid closure, was present and phosphorylated in eyelid periderm cells at the time of ..
- Fra-1/AP-1 impairs inflammatory responses and chondrogenesis in fracture healingToru Yamaguchi
Department of Orthopedic Surgery, School of Medicine, Keio University, Shinjuku ku, Tokyo, Japan
J Bone Miner Res 24:2056-65. 2009..These data suggest that the Fra-1-containing transcription factor AP-1 inhibits fracture-induced endochondral ossification and bony bridge formation presumably through suppression of inflammation-induced chondrogenesis...
- Akt-dependent Pp2a activity is required for epidermal barrier formation during late embryonic developmentRyan F L O'Shaughnessy
Centre for Cutaneous Research, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, UK
Development 136:3423-31. 2009..Akt signaling increased as the barrier wave crossed epidermis and Jun was transiently dephosphorylated...
- BMP7 promotes proliferation of nephron progenitor cells via a JNK-dependent mechanismUlrika Blank
Department of Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME 04074, USA
Development 136:3557-66. 2009..find that BMP7 directly and rapidly activates JNK signaling in nephron progenitors resulting in phosphorylation of Jun and ATF2 transcription factors...
- TNFalpha shedding and epidermal inflammation are controlled by Jun proteinsJuan Guinea-Viniegra
Cancer Cell Biology Programme, Centro Nacional de Investigaciones, Oncológicas CNIO, E 28029 Madrid, Spain
Genes Dev 23:2663-74. 2009Inducible epidermal deletion of JunB and c-Jun in adult mice causes a psoriasis-like inflammatory skin disease. Increased levels of the proinflammatory cytokine TNFalpha play a major role in this phenotype...
- Systemic anti-VEGF treatment strongly reduces skin inflammation in a mouse model of psoriasisHelia B Schonthaler
Banco Bilbao Vizcaya Argentaria BBVA Foundation, Cancer Cell Biology Programme, Centro Nacional de Investigaciones Oncologicas, 28029 Madrid, Spain
Proc Natl Acad Sci U S A 106:21264-9. 2009..Simultaneous deletion of JunB and c-Jun (DKO*) in the epidermis of adult mice leads to a psoriasis-like phenotype with hyper- and parakeratosis and ..
- Microtubule stabilization by bone morphogenetic protein receptor-mediated scaffolding of c-Jun N-terminal kinase promotes dendrite formationMonika Podkowa
Department of Biochemistry and Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, Ontario M5S 3E1, Canada
Mol Cell Biol 30:2241-50. 2010..BMP7 rapidly activates c-Jun N-terminal kinases (JNKs), known regulators of microtubule dynamics, and we show that JNKs associate with the ..
- A dominant-negative c-jun mutant inhibits lung carcinogenesis in miceJay W Tichelaar
Department of Surgery, The Alvin J Siteman Cancer Center, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
Cancer Prev Res (Phila) 3:1148-56. 2010..We then used a transgenic mouse model directing conditional expression of the dominant-negative c-jun mutant TAM67 in lung epithelial cells to determine the effect of AP-1 inhibition on mouse lung tumorigenesis...
- C-jun inhibits mammary apoptosis in vivoSanjay Katiyar
Department of Cancer Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
Mol Biol Cell 21:4264-74. 2010c-jun, which is overexpressed in a number of human cancers encodes a critical component of the AP-1 complex. c-jun has been shown to either induce or inhibit cellular apoptosis...
- Fbw7 controls neural stem cell differentiation and progenitor apoptosis via Notch and c-JunJoerg D Hoeck
Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, London, UK
Nat Neurosci 13:1365-72. 2010..accumulation of two SCF(Fbw7) substrates, the transcription factors active Notch1 and N-terminally phosphorylated c-Jun. Genetic and pharmacological rescue experiments identified c-Jun as a key substrate of Fbw7 in controlling ..
- c-JUN promotes BCR-ABL-induced lymphoid leukemia by inhibiting methylation of the 5' region of Cdk6Karoline Kollmann
Institute of Pharmacology, Center of Biomolecular Medicine and Pharmacology, Medical University of Vienna, Vienna, Austria
Blood 117:4065-75. 2011The transcription factor c-JUN and its upstream kinase JNK1 have been implicated in BCR-ABL-induced leukemogenesis...
- DLK induces developmental neuronal degeneration via selective regulation of proapoptotic JNK activityArundhati Sengupta Ghosh
Neurodegeneration Laboratories, Department of Neuroscience, Genentech, Inc, South San Francisco, CA 94080, USA
J Cell Biol 194:751-64. 2011The c-Jun N-terminal kinase (JNK) signaling pathway is essential for neuronal degeneration in multiple contexts but also regulates neuronal homeostasis...
- c-Jun is essential for the induction of Il-1β gene expression in in vitro activated Bergmann glial cellsLidia Albanito
Institut for Clinical Neurobiology, University of Wurzburg, D 97078 Wurzburg, Germany
Glia 59:1879-90. 2011In the central nervous system (CNS), the c-Jun transcription factor has been mainly studied in neuronal cells and coupled to apoptotic and regenerative pathways following brain injury...
- The transcription factor c-Jun protects against sustained hepatic endoplasmic reticulum stress thereby promoting hepatocyte survivalMatthias Fuest
Department of Medicine II, University Hospital Freiburg, Freiburg, Germany
Hepatology 55:408-18. 2012..ER stress results in the activation of several intracellular signaling pathways including Jun N-terminal kinase (JNK)...
- Neuronal c-Jun is required for successful axonal regeneration, but the effects of phosphorylation of its N-terminus are moderateCrystal A Ruff
Perinatal Brain Repair Group, Inst Women s Health, University College London, London, UK
J Neurochem 121:607-18. 2012Although neural c-Jun is essential for successful peripheral nerve regeneration, the cellular basis of this effect and the impact of c-Jun activation are incompletely understood...
- FORMAL METHODS APPLIED TO BIOLOGICAL SIGNALING NETWORKSKeith Laderoute; Fiscal Year: 2006..abstract_text> ..
- HYPOXIC STRESS MECHANISMS IN RADIATION AND CHEMOTHERAPYKeith Laderoute; Fiscal Year: 2009..An understanding of these MTF-1-dependent properties should aid in the development of novel prognostic and new modalities for neoplastic diseases. ..
- ROLE OF AMPK IN TUMOR DEVELOPMENT AND THERAPYKeith R Laderoute; Fiscal Year: 2010..Ultimately, we intend to determine whether the AMPK "emergency stress response" can be exploited for the therapy or prognosis of human cancer. ..
- IRON, CALCIUM AND OXIDATIVE STRESS IN LUNG INJURYXi Huang; Fiscal Year: 2001..By determining the role of calcite, it is possible to propose alternative methods for lung disease prevention. ..
- REGULATION OF REPRODUCTIVE PROCESSESDOUGLAS STOCCO; Fiscal Year: 2003..abstract_text> ..
- Poly (ADP-Ribose) synthetase in expression of endotheliaBasilia Zingarelli; Fiscal Year: 2003..abstract_text> ..
- MEKK2/3-MEK5 Interaction/Activation/ERK5 Pathway(RMI)BRUCE CUEVAS; Fiscal Year: 2005....
- Role of Estrogen and Iron in Breast CancerXi Huang; Fiscal Year: 2008..We expect to show that iron plays an important role in estrogen-dependent BC and this new direction of research may greatly benefit the health of female baby- boomers. [unreadable] [unreadable] [unreadable]..
- Utilization of calcite for the reduction of coal mine dust toxicityXi Huang; Fiscal Year: 2010..This innovative dust mitigation strategy to reduce dust toxicity does not require sophisticated engineering breakthrough and could prevent occupational lung diseases in underground coal workers. ..