ArticleMolecular and cellular biology1998
Akt, a target of phosphatidylinositol 3-kinase, inhibits apoptosis in a differentiating neuronal cell line.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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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Who cites it
51 citing papers in PubMed, 191 citations in OpenAlex.
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- Endogenous Cyclin D1 Promotes the Rate of Onset and Magnitude of Mitogenic Signaling via Akt1 Ser473 Phosphorylation.Cell reports · 2020Article
- The Glycosyltransferase ST6Gal-I Protects Tumor Cells against Serum Growth Factor Withdrawal by Enhancing Survival Signaling and Proliferative Potential.The Journal of biological chemistry · 2017Article
- Apoptotic cells activate AMP-activated protein kinase (AMPK) and inhibit epithelial cell growth without change in intracellular energy stores.The Journal of biological chemistry · 2015Article
- Article
- Influenza virus induces apoptosis via BAD-mediated mitochondrial dysregulation.Journal of virology · 2013Article
- Recognition-dependent signaling events in response to apoptotic targets inhibit epithelial cell viability by multiple mechanisms: implications for non-immune tissue homeostasis.The Journal of biological chemistry · 2012Article
- Protein tyrosine kinase 6 directly phosphorylates AKT and promotes AKT activation in response to epidermal growth factor.Molecular and cellular biology · 2010Article
- Nerve growth factor blocks thapsigargin-induced apoptosis at the level of the mitochondrion via regulation of Bim.Journal of cellular and molecular medicine · 2008Article
- BAD: undertaker by night, candyman by day.Oncogene · 2008Review
- Age-related changes of calcineurin and Akt1/protein kinase Balpha (Akt1/PKBalpha) immunoreactivity in the mouse hippocampal CA1 sector: an immunohistochemical study.Metabolic brain disease · 2008Article
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- Insulin and insulin-like growth factor resistance in alcoholic neurodegeneration.Alcoholism, clinical and experimental research · 2008Article
- Protective effect of ultra low molecular weight heparin on glutamate-induced apoptosis in cortical cells.Yonsei medical journal · 2008Article
- The phosphoinositide 3-kinase pathway in human cancer: genetic alterations and therapeutic implications.Current genomics · 2007Article
- Exercise-induced neuroprotection in SMA model mice: a means for determining new therapeutic strategies.Molecular neurobiology · 2007Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Phosphatidylinositol (PI) 3-kinase has been suggested to mediate cell survival. Consistent with this possibility, apoptosis of conditionally (simian virus 40 Tts) immortalized rat hippocampal H19-7 neuronal cells was increased in response to wortmannin, an inhibitor of PI 3-kinase. Downstream effectors of PI 3-kinase include Rac1, protein kinase C, and the serine-threonine kinase Akt (protein kinase B). Here, we show that activation of Akt is one mechanism by which PI 3-kinase can mediate survival of H19-7 cells during serum deprivation or differentiation. While ectopic expression of wild-type Akt (c-Akt) does not significantly enhance survival in H19-7 cells, expression of activated forms of Akt (v-Akt or myristoylated Akt) results in enhanced survival which can be comparable to that conferred by Bcl-2. Conversely, expression of a dominant-negative mutant of Akt accelerates cell death upon serum deprivation or differentiation. Finally, the results indicate that Akt can transduce a survival signal for differentiating neuronal cells through a mechanism that is independent of induction of Bcl-2 or Bcl-XL or inhibition of Jun kinase activity.
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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 Socratic graph.