AP-1 as a regulator of cell life and death
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Summary
Interestingly, the growth-promoting activity of c-Jun is mediated by repression of tumour suppressors, as well as upregulation of positive cell cycle regulators, whereas JunB has the converse effect.
- Type
- review
- Published
- 2002-05-01
- Cited by
- 2,979
- References
- 98
- OpenAlex
- https://openalex.org/W1994219871
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:34337538
Keywords
JUNB, Regulator, Downregulation and upregulation, Cell biology, Transcription factor
References
- Induction of apoptosis by the transcription factor c‐Jun
- Fos Family Members Induce Cell Cycle Entry by Activating Cyclin D1
- Bcl-3 Expression Promotes Cell Survival following Interleukin-4 Deprivation and Is Controlled by AP1 and AP1-Like Transcription Factors
- Serum‐regulated transcription by serum response factor (SRF): a novel role for the DNA binding domain.
- Cell proliferation and cell cycle progression are not impaired in fibroblasts and ES cells lacking c-Fos.
- Regulation of Fra-1 and Fra-2 phosphorylation differs during the cell cycle of fibroblasts and phosphorylation in vitro by MAP kinase affects DNA binding activity.
- Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation
- Expression and involvement of c-fos and c-jun protooncogenes in programmed cell death induced by growth factor deprivation in lymphoid cell lines.
- Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
- Induction of c‐fos expression through JNK‐mediated TCF/Elk‐1 phosphorylation.
- Lasting N-Terminal Phosphorylation of c-Jun and Activation of c-Jun N-Terminal Kinases after Neuronal Injury
- Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling
- c-fos expression induces bone tumors in transgenic mice.
- The jun and fos protein families are both required for cell cycle progression in fibroblasts
- Rapid and preferential activation of the c-jun gene during the mammalian UV response
- Cellular transformation and malignancy induced by ras require c-jun
- Targeted disruption of the murine junD gene results in multiple defects in male reproductive function.
- A c-Jun dominant negative mutant protects sympathetic neurons against programmed cell death.
- Dominant-negative c-Jun promotes neuronal survival by reducing BIM expression and inhibiting mitochondrial cytochrome c release.
- Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis
Cited by
- Characterization of putative regulators of the small GTPase, Rac, in Drosophila
- Double lethal effects of fusion gene of wild-type p53 and JunB on hepatocellular carcinoma cells
- Early nuclear exclusion of the transcription factor max is associated with retinal ganglion cell death independent of caspase activity
- Kinetics of Senescence-associated Changes of Gene Expression in an Epithelial, Temperature-sensitive SV40 Large T Antigen Model
- Aberrant Polycystin-1 Expression Results in Modification of Activator Protein-1 Activity, whereas Wnt Signaling Remains Unaffected*
- Identification of target genes involved in the antiproliferative effect of glucocorticoids reveals a role for nuclear factor-(kappa)B repression.
- Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury
- Fucoidan Extracted From Cladosiphon Okamuranus Tokida Induces Apoptosis of Human T-Cell Leukemia Virus Type 1-Infected T-Cell Lines and Primary Adult T-Cell Leukemia Cells
- Arachidonic acid-induced gene expression in colon cancer cells.
- Electrokinetic measurements of dielectric properties of membrane for apoptotic HL-60 cells on chip-based device
- Nf-kappab and AP-1 activation is associated with late lumen loss after porcine coronary angioplasty and antiproliferative beta-irradiation.
- Interleukin (IL) 1β Induction of IL-6 Is Mediated by a Novel Phosphatidylinositol 3-Kinase-dependent AKT/IκB Kinase α Pathway Targeting Activator Protein-1*
- Additive Inhibitory Effect of Experimentally Induced Hepatic Cirrhosis by Agonists of Peroxisome Proliferator Activator Receptor γ and Retinoic Acid Receptor
- Prevention of hepatocarcinogenesis and increased susceptibility to acetaminophen-induced liver failure in transaldolase-deficient mice by N-acetylcysteine.
- Regulation of Expression of the Rat Orthologue of Mouse Double Minute 2 (MDM2) by H2O2-induced Oxidative Stress in Neonatal Rat Cardiac Myocytes
- NPM-ALK and the JunB transcription factor regulate the expression of cytotoxic molecules in ALK-positive, anaplastic large cell lymphoma.
- In Situ Proximity Ligation Detection of c-Jun/AP-1 Dimers Reveals Increased Levels of c-Jun/Fra1 Complexes in Aggressive Breast Cancer Cell Lines in Vitro and in Vivo*
- Molecular cloning and characterization of novel human JNK2 (MAPK9) transcript variants that show different stimulation activities on AP-1.
- The Function of Heterodimeric AP-1 Comprised of c-Jun and c-Fos in Activin Mediated Spemann Organizer Gene Expression
- Upregulation of Nuclear Factor-Related Kappa B Suggests a Disorder of Transcriptional Regulation in Minimal Change Nephrotic Syndrome
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