ArticleOncogene2000
A genetic screen to identify genes that rescue the slow growth phenotype of c-myc null fibroblasts.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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
25 citing papers in PubMed.
- Photobiomodulation by Near-Infrared 980-nm Wavelengths Regulates Pre-Osteoblast Proliferation and Viability through the PI3K/Akt/Bcl-2 Pathway.International journal of molecular sciences · 2021Article
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- Mechanisms Underlying Recurrent Genomic Amplification in Human Cancers.Trends in cancer · 2020Review
- N-Myc overexpression increases cisplatin resistance in neuroblastoma via deregulation of mitochondrial dynamics.Cell death discovery · 2016Article
- A MEK/PI3K/HDAC inhibitor combination therapy for KRAS mutant pancreatic cancer cells.Oncotarget · 2015Article
- Article
- Article
- AP4 directly downregulates p16 and p21 to suppress senescence and mediate transformation.Cell death & disease · 2013Article
- c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells.Cell · 2012Article
- Myc, mondo, and metabolism.Genes & cancer · 2010Article
- Enigmatic MYC Conducts an Unfolding Systems Biology Symphony.Genes & cancer · 2010Article
- Targeting c-Myc as a novel approach for hepatocellular carcinoma.World journal of hepatology · 2010Article
- c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.Nature · 2009Article
- AP4 encodes a c-MYC-inducible repressor of p21.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- The oncogene c-Myc coordinates regulation of metabolic networks to enable rapid cell cycle entry.Cell cycle (Georgetown, Tex.) · 2008Article
- N-Myc and the cyclin-dependent kinase inhibitors p18Ink4c and p27Kip1 coordinately regulate cerebellar development.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Myc confers androgen-independent prostate cancer cell growth.The Journal of clinical investigation · 2003Article
- Loss of protooncogene c-Myc function impedes G1 phase progression both before and after the restriction point.Molecular biology of the cell · 2003Article
- Novel retroviral vectors to facilitate expression screens in mammalian cells.Nucleic acids research · 2002Article
- A functional screen for Myc-responsive genes reveals serine hydroxymethyltransferase, a major source of the one-carbon unit for cell metabolism.Molecular and cellular biology · 2002Article
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.
Funding
Abstract
The c-myc gene is frequently over-expressed in human cancers and is involved in regulation of proliferation, differentiation and apoptosis. c-Myc is a transcription factor that acts primarily by regulating the expression of other genes. However, it has been very difficult to identify bona fide c-Myc target genes that explain its diverse biological activities. The recent generation of c-myc deficient Rat1A fibroblasts with a profound and stable growth defect provides a new system to search for genes that can substitute for c-myc in proliferation. In this study, we have attempted to identify genes that rescue the slow growth phenotype of c-myc null cells through introduction of a series of potent cell cycle regulatory genes and several retroviral cDNA expression libraries. None of the candidate genes tested, including SV40 T-antigen and adenovirus E1A, caused reversal of the c-myc null growth defect. Furthermore, extensive screens with high-complexity retroviral cDNA libraries from three different tissue sources revealed that only c-myc and N-myc rescued the c-myc null slow-growth phenotype. Our data support the notion that there are no functional equivalents of the myc family of proto-oncogenes and also suggest that there are no c-Myc-activated genes that alone can substitute for c-Myc in control of cell proliferation.
Indexed as
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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.