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