Transcription Factor AP-1

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  Subject Areas on Research

  • A direct HDAC4-MAP kinase crosstalk activates muscle atrophy program. 
  • A genomic regulatory element that directs assembly and function of immune-specific AP-1-IRF complexes. 
  • A novel basal promoter element is required for expression of the rat tyrosine hydroxylase gene. 
  • A polymorphism of the human matrix gamma-carboxyglutamic acid protein promoter alters binding of an activating protein-1 complex and is associated with altered transcription and serum levels. 
  • A small interfering RNA screen for modulators of tumor cell motility identifies MAP4K4 as a promigratory kinase. 
  • Activation of src-family tyrosine kinases by LPS regulates cytokine production in dendritic cells by controlling AP-1 formation. 
  • Activation of the 9E3/cCAF chemokine by phorbol esters occurs via multiple signal transduction pathways that converge to MEK1/ERK2 and activate the Elk1 transcription factor. 
  • Activation of transcription factors activator protein-1 and nuclear factor-kappaB by 2,3,7,8-tetrachlorodibenzo-p-dioxin. 
  • Activator protein-1 has an essential role in pancreatic cancer cells and is regulated by a novel Akt-mediated mechanism. 
  • CYLD inhibits melanoma growth and progression through suppression of the JNK/AP-1 and β1-integrin signaling pathways. 
  • CYLD inhibits tumorigenesis and metastasis by blocking JNK/AP1 signaling at multiple levels. 
  • Characterization of murine BATF: a negative regulator of activator protein-1 activity in the thymus. 
  • Characterization of short range DNA looping in endotoxin-mediated transcription of the murine inducible nitric-oxide synthase (iNOS) gene. 
  • Context-dependent activation kinetics elicited by soluble versus outer membrane vesicle-associated heat-labile enterotoxin. 
  • Cooperation between core binding factor and adjacent promoter elements contributes to the tissue-specific expression of interleukin-3. 
  • Cooperation between transcription factor AP-1 and NF-kappaB in the induction of interleukin-8 in human pancreatic adenocarcinoma cells by hypoxia. 
  • Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines. 
  • Dehydroepiandrosterone and analogs inhibit DNA binding of AP-1 and airway smooth muscle proliferation. 
  • Differential osteopontin expression in phenotypically distinct subclones of murine breast cancer cells mediates metastatic behavior. 
  • Differential regulation of hepatocyte DNA synthesis by cAMP in vitro in vivo. 
  • Erythroid AP-1/NF-E2 elements vary in their response to NF-E2. 
  • Essential role for Smad3 in regulating MCP-1 expression and vascular inflammation. 
  • Functional Toll-like receptor 4 mutations modulate the response to fibrinogen. 
  • Genetic Correction of SOD1 Mutant iPSCs Reveals ERK and JNK Activated AP1 as a Driver of Neurodegeneration in Amyotrophic Lateral Sclerosis. 
  • Identification of the sequences within the human complement 3 promoter required for estrogen responsiveness provides insight into the mechanism of tamoxifen mixed agonist activity. 
  • Intracellular CMTM2 negatively regulates human immunodeficiency virus type-1 transcription through targeting the transcription factors AP-1 and CREB. 
  • JunB promotes Th17 cell identity and restrains alternative CD4+ T-cell programs during inflammation. 
  • LAT is required for TCR-mediated activation of PLCgamma1 and the Ras pathway. 
  • Microparticles stimulate the synthesis of prostaglandin E(2) via induction of cyclooxygenase 2 and microsomal prostaglandin E synthase 1. 
  • Molecular mechanism of fibronectin gene activation by cyclic stretch in vascular smooth muscle cells. 
  • Molecular regulation of constitutive expression of interleukin-8 in human pancreatic adenocarcinoma. 
  • NF-kappaB and AP-1 connection: mechanism of NF-kappaB-dependent regulation of AP-1 activity. 
  • NF-κB- and AP-1-mediated DNA looping regulates osteopontin transcription in endotoxin-stimulated murine macrophages. 
  • Negative regulation of mTOR activation by diacylglycerol kinases. 
  • Novel nuclear target for thrombin: activation of the Elk1 transcription factor leads to chemokine gene expression. 
  • Overexpression of tropomysin-related kinase B in metastatic human pancreatic cancer cells. 
  • Oxidative stress activates anion exchange protein 2 and AP-1 in airway epithelial cells. 
  • Patterns of regulatory activity across diverse human cell types predict tissue identity, transcription factor binding, and long-range interactions. 
  • Peptide antagonists of the human estrogen receptor. 
  • Phosphorylation of tumor necrosis factor receptor 1 (p55) protects macrophages from silica-induced apoptosis. 
  • Regulation of T cell receptor-induced activation of the Ras-ERK pathway by diacylglycerol kinase zeta. 
  • Regulation of interleukin-8 expression by cellular pH in human pancreatic adenocarcinoma cells. 
  • Retinoids and mouse embryonic development. 
  • Role of AP-1 complex in angiotensin II-mediated transforming growth factor-beta expression and growth of smooth muscle cells: using decoy approach against AP-1 binding site. 
  • S-nitrosylation in the regulation of gene transcription. 
  • Smad3-Smad4 and AP-1 complexes synergize in transcriptional activation of the c-Jun promoter by transforming growth factor beta. 
  • Smads bind directly to the Jun family of AP-1 transcription factors. 
  • Suppression of the c-Jun N-terminal kinase pathway by 17beta-estradiol can preserve human islet functional mass from proinflammatory cytokine-induced destruction. 
  • The activity of a highly promiscuous AP-1 element can be confined to neurons by a tissue-selective repressive element. 
  • Transcription factor decoy. 
  • Tumor necrosis factor receptor 1/c-Jun-NH2-kinase signaling promotes human neoplasia. 
  • Tumor necrosis factor-alpha induces c-jun during the regenerative response to liver injury. 
  • Tumor suppressor Smad4 is a transforming growth factor beta-inducible DNA binding protein. 
  • Unusual Rel-like architecture in the DNA-binding domain of the transcription factor NFATc. 
  • c-Jun promotes whereas JunB inhibits epidermal neoplasia. 
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  Keywords of People

  • Ciofani, Maria, Associate Professor of Immunology, Immunology
  • McDonnell, Donald Patrick, Glaxo-Wellcome Distinguished Professor of Molecular Cancer Biology, in the School of Medicine, Duke Innovation & Entrepreneurship