ArticleThe EMBO journal1998
Bax-mediated cell death by the Gax homeoprotein requires mitogen activation but is independent of cell cycle activity.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 48 citations in OpenAlex.
- Considerations for feature selection using gene pairs and applications in large-scale dataset integration, novel oncogene discovery, and interpretable cancer screening.BMC medical genomics · 2020Article
- miRNA screening reveals a new miRNA family stimulating iPS cell generation via regulation of Meox2.EMBO reports · 2011Article
- Vitamin D receptor-dependent 1 alpha,25(OH)2 vitamin D3-induced anti-apoptotic PI3K/AKT signaling in osteoblasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2008Article
- Functional role of Meox2 during the epithelial cytostatic response to TGF-beta.Molecular oncology · 2007Article
- The homeobox gene GAX activates p21WAF1/CIP1 expression in vascular endothelial cells through direct interaction with upstream AT-rich sequences.The Journal of biological chemistry · 2007Article
- Constitutively activated Akt-1 is vital for the survival of human monocyte-differentiated macrophages. Role of Mcl-1, independent of nuclear factor (NF)-kappaB, Bad, or caspase activation.The Journal of experimental medicine · 2001Article
- Macrophages require constitutive NF-kappaB activation to maintain A1 expression and mitochondrial homeostasis.Molecular and cellular biology · 2000Article
- Effect of percutaneous adenovirus-mediated Gax gene delivery to the arterial wall in double-injured atheromatous stented rabbit iliac arteries.Gene therapy · 2000Article
- Gene therapy for restenosis.Current cardiology reports · 2000Review
- FLICE-inhibitory protein expression during macrophage differentiation confers resistance to fas-mediated apoptosis.The Journal of experimental medicine · 1999Article
- Regulation of smooth muscle cell migration and integrin expression by the Gax transcription factor.The Journal of clinical investigation · 1999Article
- Distinct glucocorticoid receptor transcriptional regulatory surfaces mediate the cytotoxic and cytostatic effects of glucocorticoids.Molecular and cellular biology · 1999Article
- Adenovirus-mediated delivery of the Gax transcription factor to rat carotid arteries inhibits smooth muscle proliferation and induces apoptosis.Gene therapy · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Tissues with the highest rates of proliferation typically exhibit the highest frequencies of apoptosis, but the mechanisms that coordinate these processes are largely unknown. The homeodomain protein Gax is down-regulated when quiescent cells are stimulated to proliferate, and constitutive Gax expression inhibits cell proliferation in a p21(WAF/CIP)-dependent manner. To understand how mitogen-induced proliferation influences the apoptotic process, we investigated the effects of deregulated Gax expression on cell viability. Forced Gax expression induced apoptosis in mitogen-activated cultures, but quiescent cultures were resistant to cell death. Though mitogen activation was required for apoptosis, neither the cdk inhibitor p21(WAF/CIP) nor the tumor suppressor p53 was required for Gax-induced cell death. Arrest in G1 or S phases of the cell cycle with chemical inhibitors also did not affect apoptosis, further suggesting that Gax-mediated cell death is independent of cell cycle activity. Forced Gax expression led to Bcl-2 down-regulation and Bax up-regulation in mitogen-activated, but not quiescent cultures. Mouse embryonic fibroblasts homozygous null for the Bax gene were refractive to Gax-induced apoptosis, demonstrating the functional significance of this regulation. These data suggest that the homeostatic balance between cell growth and death can be controlled by mitogen-dependent pathways that circumvent the cell cycle to alter Bcl-2 family protein expression.
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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.