ArticleOncogene2000
Comparative microarray analysis of gene expression during apoptosis-induction by growth factor deprivation or protein kinase C inhibition.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 36 citations in OpenAlex.
- Global gene expression profiling and senescence biomarker analysis of hESC exposed to HStem cell research & therapy · 2017Article
- A microarray analysis of full depth knee cartilage of ovariectomized rats.BMC research notes · 2011Article
- Article
- Rab7 activation by growth factor withdrawal contributes to the induction of apoptosis.Molecular biology of the cell · 2009Article
- Expression profiling via novel multiplex assay allows rapid assessment of gene regulation in defined signalling pathways.Nucleic acids research · 2003Article
- Positive feedback of protein kinase C proteolytic activation during apoptosis.The Biochemical journal · 2002Article
- A microarray-based, integrated approach to identify novel regulators of cancer drug response and apoptosis.Oncogene · 2002Article
- Microarray-based expression profiling of normal and malignant immune cells.Endocrine reviews · 2002Review
- Studying the functional genomics of stress responses in loblolly pine with the Expresso microarray experiment management system.Comparative and functional genomics · 2002Article
- DNA microarrays: a powerful genomic tool for biomedical and clinical research.Molecular medicine (Cambridge, Mass.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional response of mouse pro-B cells to two different apoptotic stimuli was investigated. First, interleukin-3 (IL-3) deprivation was used to trigger programmed cell death in IL-3 dependent FL5.12 cells. Alternatively, cells were treated with the protein kinase C (PKC) inhibitor staurosporine. The temporal pattern of gene expression was followed with cDNA microarrays, covering over 8700 different mouse cDNA sequences corresponding to approximately 7900 unique genes. Messenger RNA levels of 315 genes were found to be regulated by more than twofold upon IL-3 removal, while 125 genes reacted to staurosporine treatment. Cross-comparison revealed an intersection of 34 genes similarly regulated in both pathways and thus representing candidates for common apoptosis regulators. For many expressed sequence tags (ESTs) our data suggest for the first time functions in the control of apoptosis, stress response or the cell cycle. IL-3 removal led to the repression of genes required for proliferation and to the induction of genes, linked to apoptotic and signaling pathways. Staurosporine caused predominantly activation of genes, some of which had previously been described to be involved in inflammation. Our findings indicate that cellular responses to both apoptotic stimuli influence various physiological pathways which had not previously been known to be linked.
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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.