ArticleMolecular biology of the cell2001
Dominant negative c-jun inhibits activation of the cyclin D1 and cyclin E kinase complexes.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 53 citations in OpenAlex.
- ZBTB7B is a permissive regulator of hepatocellular carcinoma initiation by repressing c-Jun expression and function.Cell death & disease · 2024Article
- Tanshinone IIA pretreatment promotes cell survival in human lung epithelial cells under hypoxia via AP-1-Nrf2 transcription factor.Cell stress & chaperones · 2020Article
- MicroRNA 10b promotes abnormal expression of the proto-oncogene c-Jun in metastatic breast cancer cells.Oncotarget · 2016Article
- Human TTC5, a novel tetratricopeptide repeat domain containing gene, activates p53 and inhibits AP-1 pathway.Molecular biology reports · 2013Article
- Induction of p38δ expression plays an essential role in oncogenic ras-induced senescence.Molecular and cellular biology · 2013Article
- Ras inhibition boosts galectin-7 at the expense of galectin-1 to sensitize cells to apoptosis.Oncotarget · 2013Article
- INMAP, a novel truncated version of POLR3B, represses AP-1 and p53 transcriptional activity.Molecular and cellular biochemistry · 2013Article
- Dual suppression of the cyclin-dependent kinase inhibitors CDKN2C and CDKN1A in human melanoma.Journal of the National Cancer Institute · 2012Article
- Aberrant expression of c-Jun in glioblastoma by internal ribosome entry site (IRES)-mediated translational activation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Suppression of AP1 transcription factor function in keratinocyte suppresses differentiation.PloS one · 2012Article
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- Age-related changes in redox signaling and VSMC function.Antioxidants & redox signaling · 2010Review
- Loss of E-cadherin-mediated cell-cell contacts activates a novel mechanism for up-regulation of the proto-oncogene c-Jun.Molecular biology of the cell · 2009Article
- FoxM1 regulates transcription of JNK1 to promote the G1/S transition and tumor cell invasiveness.The Journal of biological chemistry · 2008Article
- Benzo(a)pyrene-caused increased G1-S transition requires the activation of c-Jun through p53-dependent PI-3K/Akt/ERK pathway in human embryo lung fibroblasts.Toxicology letters · 2008Article
- Growth inhibition of non-small cell lung cancer cells by AP-1 blockade using a cJun dominant-negative mutant.British journal of cancer · 2008Article
- Immediate and delayed effects of E-cadherin inhibition on gene regulation and cell motility in human epidermoid carcinoma cells.Molecular and cellular biology · 2005Article
- cFos is critical for MCF-7 breast cancer cell growth.Oncogene · 2005Article
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Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AP-1 transcription factor is activated by oncogenic signal transduction cascades and its function is critical for both mitogenesis and carcinogenesis. To define the role of AP-1 in the context of a human fibrosarcoma cell line, HT1080, we expressed a dominant negative c-jun mutant fused to the green fluorescent protein in an ecdysone-inducible system. We demonstrated that high levels of this mutant, GFP-TAM67, inhibit AP-1 activity and arrest cells predominantly in the G1 phase of the cell cycle. This arrest is reversible and occurs only above a threshold concentration; low to moderate levels of GFP-TAM67 are insufficient for growth arrest. Contrary to expectations based on the literature, GFP-TAM67 does not inhibit expression of cyclin D1, cyclin E, or their respective cyclin-dependent kinases. However, pRB is hypophosphorylated in GFP-TAM67-arrested cells and the activity of both the cyclin D1:cdk and the cyclin E:cdk complexes are impaired. Both of these complexes show an increased association with p21(CIP1/WAF1), concomitantly with induction of the p21 mRNA by GFP-TAM67. These results suggest a novel function of AP-1 in the activation of the G1 cyclin:cdk complexes in human tumor cells by regulating the expression of the p21(CIP1/WAF1) gene.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.