ArticleOncogene2002
Cell transformation by v-Jun deactivates ERK MAP kinase signalling.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- 17-β Estradiol Rescued Immature Rat Brain against Glutamate-Induced Oxidative Stress and Neurodegeneration via Regulating Nrf2/HO-1 and MAP-Kinase Signaling Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Systemic inflammation suppresses spinal respiratory motor plasticity via mechanisms that require serine/threonine protein phosphatase activity.Journal of neuroinflammation · 2021Article
- Mathematical model of a telomerase transcriptional regulatory network developed by cell-based screening: analysis of inhibitor effects and telomerase expression mechanisms.PLoS computational biology · 2014Article
- An approach to investigate intracellular protein network responses.Chemical research in toxicology · 2014Article
- MEKK2 kinase association with 14-3-3 protein regulates activation of c-Jun N-terminal kinase.The Journal of biological chemistry · 2013Article
- Crosstalk and signaling switches in mitogen-activated protein kinase cascades.Frontiers in physiology · 2012Article
- Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3.Molecular cancer · 2005Article
- p75-Ras-GRF1 is a c-Jun/AP-1 target protein: its up regulation results in increased Ras activity and is necessary for c-Jun-induced nonadherent growth of Rat1a cells.Molecular and cellular biology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that v-Jun accelerates G1 progression and enables cells to sustain S phase entry in the absence of serum growth factors. Since growth factor-dependent ERK MAP kinase signalling plays an important role in regulating the G1/S transition, we investigated whether aberrant ERK regulation might contribute to cell cycle deregulation by v-Jun. Contrary to expectation, we find that cells transformed by v-Jun exhibit a profound reduction in the basal level of active, dual-phosphorylated ERK. In addition, ERK becomes refractory to stimulation by a subset of agonists including serum, LPA, and EGF, but remains partially responsive to the phorbol ester, TPA. Biochemical analysis indicates that these defects are attributable to a combination of inefficient signal propagation between Ras and Raf within the ERK pathway and increased tonic deactivation by MAP kinase phosphatases. Taken together, these results demonstrate that cell transformation by v-Jun induces alterations in cell physiology which antagonize ERK signalling at multiple levels. The potential significance of this phenotype for oncogenesis by v-Jun is discussed.
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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.