ArticleGenes & development1998
Autocrine growth and anchorage independence: two complementing Jun-controlled genetic programs of cellular transformation.
Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 117 citations in OpenAlex.
- Hypertonicity induces mitochondrial extracellular vesicles (MEVs) that activate TNF-α and β-catenin signaling to promote adipocyte dedifferentiation.Stem cell research & therapy · 2023Article
- Article
- Antioxidant response elements: Discovery, classes, regulation and potential applications.Redox biology · 2018Review
- MicroRNA 10b promotes abnormal expression of the proto-oncogene c-Jun in metastatic breast cancer cells.Oncotarget · 2016Article
- C-Jun N-terminal kinase (JNK) isoforms play differing roles in otitis media.BMC immunology · 2014Article
- Novel mechanism of JNK pathway activation by adenoviral E1A.Oncotarget · 2014Article
- Enhanceosomes as integrators of hypoxia inducible factor (HIF) and other transcription factors in the hypoxic transcriptional response.Cellular signalling · 2013Review
- 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
- 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 & cellular proteomics : MCP · 2010Article
- Emerging roles of ATF2 and the dynamic AP1 network in cancer.Nature reviews. Cancer · 2010Review
- The proapoptotic dp5 gene is a direct target of the MLK-JNK-c-Jun pathway in sympathetic neurons.Nucleic acids research · 2009Article
- Inhibition of ataxia telangiectasia mutated kinase activity enhances TRAIL-mediated apoptosis in human melanoma cells.Cancer research · 2009Article
- 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
- Restriction to Fos family members of Trip6-dependent coactivation and glucocorticoid receptor-dependent trans-repression of activator protein-1.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Radiosensitization of melanoma cells through combined inhibition of protein regulators of cell survival.Apoptosis : an international journal on programmed cell death · 2008Article
- Resveratrol sensitizes melanomas to TRAIL through modulation of antiapoptotic gene expression.Experimental cell research · 2008Article
- Sequential treatment by ionizing radiation and sodium arsenite dramatically accelerates TRAIL-mediated apoptosis of human melanoma cells.Cancer research · 2007Article
- Reduced levels of ATF-2 predispose mice to mammary tumors.Molecular and cellular biology · 2007Article
- JunB is required for endothelial cell morphogenesis by regulating core-binding factor beta.The Journal of cell biology · 2006Article
- Sodium arsenite accelerates TRAIL-mediated apoptosis in melanoma cells through upregulation of TRAIL-R1/R2 surface levels and downregulation of cFLIP expression.Experimental cell research · 2006Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular transformation can be achieved by constitutive activation of growth-regulatory signaling pathways, which, in turn, activate nuclear transcription factors thought to execute a transformation-specific program of gene expression. Members of the dimeric transcription factor family AP-1 are at the receiving end of such growth-regulating pathways and the viral form of the AP-1 subunit Jun establishes one important aspect of transformation in chick embryo fibroblasts (CEFs): enhanced growth in agar and in low serum. Enhanced Jun activity is likely to target several different genetic programs as Jun forms heterodimers with one of several members of the Fos and ATF2 subfamilies, resulting in transcription factors with different sequence specificities. To identify the programs relevant for transformation, we have reduced the complexity of AP-1 factors by constructing Jun bZip mutants that can efficiently dimerize and transactivate with only a restricted set of partner subunits. Upon introduction into CEFs, a Jun mutant selective for the Fos family induced anchorage-independent growth but no growth factor-independence. In contrast, a c-Jun mutant with preference for ATF2-like proteins caused growth factor-independence, but no growth in agar. Coexpression of both mutants reestablished the combined transformation program as induced by wild-type Jun. These data show that Jun-dependent cell transformation can be resolved into at least two distinct and independent processes, anchorage and growth factor independence, obviously triggered by two classes of Jun heterodimers likely regulating different sets of target genes.
Indexed as
Identifiers
What OpenQuestion holds
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.