ArticleCell death and differentiation2008
Analysis of Ret knockin mice reveals a critical role for IKKs, but not PI 3-K, in neurotrophic factor-induced survival of sympathetic neurons.
Article in Cell death and differentiation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Sprouty1 is a broad mediator of cellular senescence.Cell death & disease · 2024Article
- Regulation of Survival Motor Neuron Protein by the Nuclear Factor-Kappa B Pathway in Mouse Spinal Cord Motoneurons.Molecular neurobiology · 2018Article
- 7-dehydrocholesterol efficiently supports Ret signaling in a mouse model of Smith-Opitz-Lemli syndrome.Scientific reports · 2016Article
- RAS and downstream RAF-MEK and PI3K-AKT signaling in neuronal development, function and dysfunction.Biological chemistry · 2016Review
- Secreted herpes simplex virus-2 glycoprotein G modifies NGF-TrkA signaling to attract free nerve endings to the site of infection.PLoS pathogens · 2015Article
- Sprouty1 induces a senescence-associated secretory phenotype by regulating NFκB activity: implications for tumorigenesis.Cell death and differentiation · 2014Article
- Protein tyrosine phosphatase receptor type O inhibits trigeminal axon growth and branching by repressing TrkB and Ret signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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- Synergistic growth inhibition of cancer cells harboring the RET/PTC1 oncogene by staurosporine and rotenone involves enhanced cell death.Journal of biosciences · 2011Article
- The canonical nuclear factor-κB pathway regulates cell survival in a developmental model of spinal cord motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- RET modulates cell adhesion via its cleavage by caspase in sympathetic neurons.The Journal of biological chemistry · 2011Article
- Differential expression of c-Ret in motor neurons versus non-neuronal cells is linked to the pathogenesis of ALS.Laboratory investigation; a journal of technical methods and pathology · 2011Article
- The Gata3 transcription factor is required for the survival of embryonic and adult sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Pro-survival role for Parkinson's associated gene DJ-1 revealed in trophically impaired dopaminergic neurons.PLoS biology · 2010Article
- Organotypic specificity of key RET adaptor-docking sites in the pathogenesis of neurocristopathies and renal malformations in mice.The Journal of clinical investigation · 2010Article
- Intracellular signalling pathways in dopamine cell death and axonal degeneration.Progress in brain research · 2010Article
- Loss of Sprouty1 rescues renal agenesis caused by Ret mutation.Journal of the American Society of Nephrology : JASN · 2009Article
- Angiotensin II-induced activation of c-Ret signaling is critical in ureteric bud branching morphogenesis.Mechanisms of developmentArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
We analyzed the survival responses and downstream signaling elicited by GDNF on sympathetic neurons from different Ret knockin mice. Lack of tyrosine 1062, a multidocking site in Ret, completely prevented GDNF-mediated survival. Importantly, lack of tyrosine 981, although abrogating Akt phosphorylation, had no effect on neuronal survival, indicating that the PI 3-K/Akt pathway is not necessary for survival of sympathetic neurons. In contrast, silencing of B-Raf completely prevented not only GDNF-mediated but also NGF-mediated cell survival, independently of MEK-1/2. We identified IKKs as the main effectors of the protective effects of B-Raf. First, B-Raf interacted with and activated IKKs. Second, knockdown of IKKs reversed the protection afforded by a constitutively active form of B-Raf. Third, knockdown of IKKs prevented both NGF- and GDNF-mediated survival. In conclusion, our data delineate a novel survival pathway for sympathetic neurons linking B-Raf to IKKs, independently of both PI 3-K and MEK-1/2 pathways.
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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.