ArticleScience signaling2010
A kinase-independent role for unoccupied insulin and IGF-1 receptors in the control of apoptosis.
Article in Science signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 77 citations in OpenAlex.
- The Role of Insulin-like Growth Factor I in Mechanisms of Resilience and Vulnerability to Sporadic Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The neurobiology of insulin-like growth factor I: From neuroprotection to modulation of brain states.Molecular psychiatry · 2023Review
- Leucine-973 is a crucial residue differentiating insulin and IGF-1 receptor signaling.The Journal of clinical investigation · 2023Article
- Untangling IGF-I signaling in the aging brain.Aging · 2023Article
- Unique ligand and kinase-independent roles of the insulin receptor in regulation of cell cycle, senescence and apoptosis.Nature communications · 2023Article
- Glucose-dependent effect of insulin receptor isoforms on tamoxifen antitumor activity in estrogen receptor-positive breast cancer cells.Frontiers in endocrinology · 2023Article
- Differential IL18 signaling via IL18 receptor and Na-Cl co-transporter discriminating thermogenesis and glucose metabolism regulation.Nature communications · 2022Article
- Insulin regulates neurovascular coupling through astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Dependence receptors: new targets for cancer therapy.EMBO molecular medicine · 2021Review
- Insulin Receptor Isoforms Differently Regulate Cell Proliferation and Apoptosis in the Ligand-Occupied and Unoccupied State.International journal of molecular sciences · 2021Article
- Distinct signaling by insulin and IGF-1 receptors and their extra- and intracellular domains.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Nanoparticle mediated increased insulin-like growth factor 1 expression enhances human placenta syncytium function.Placenta · 2020Article
- Review
- Acquired Resistance to Drugs Targeting Tyrosine Kinases.Advances in cancer research · 2018Review
- Male Brown Fat-Specific Double Knockout of IGFIR/IR: Atrophy, Mitochondrial Fission Failure, Impaired Thermogenesis, and Obesity.Endocrinology · 2018Article
- Insulin Receptor Isoforms in Physiology and Disease: An Updated View.Endocrine reviews · 2017Review
- Domain-dependent effects of insulin and IGF-1 receptors on signalling and gene expression.Nature communications · 2017Article
- Adipocyte Dynamics and Reversible Metabolic Syndrome in Mice with an Inducible Adipocyte-Specific Deletion of the Insulin Receptor.Cell metabolism · 2017Article
- Phase I Dose-Escalation Study of Linsitinib (OSI-906) and Erlotinib in Patients with Advanced Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Acute knockdown of the insulin receptor or its substrates Irs1 and 2 in 3T3-L1 adipocytes suppresses adiponectin production.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Insulin and insulin-like growth factor 1 (IGF-1) act as antiapoptotic hormones. We found that, unexpectedly, double-knockout (DKO) cells that lacked both insulin and IGF-1 receptors (IR and IGF1R, respectively) were resistant to apoptosis induced through either the intrinsic or the extrinsic pathway. This resistance to apoptosis was associated with decreased abundance of the proapoptotic protein Bax and increases in abundance of the antiapoptotic proteins Bcl-2, Bcl-xL, XIAP, and Flip. These changes in protein abundance involved primarily posttranscriptional mechanisms. Restoration of IR or IGF1R to DKO cells also restored their sensitivity to apoptosis. Notably, expression of a catalytically inactive mutant form of the IR also restored susceptibility to apoptosis. Thus, IR and IGF1R have bidirectional roles in the control of cell survival and can be viewed as dependence receptors. Insulin and IGF-1 binding stimulates receptor tyrosine kinase activity and blocks apoptosis, whereas unliganded IR and IGF1R, acting through a mechanism independent of their catalytic activity, exert a permissive effect on cell death.
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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.