ArticleThe Journal of biological chemistry2013
Signal transducer and activator of transcription 3 (STAT3) degradation by proteasome controls a developmental switch in neurotrophin dependence.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- The antioxidative effect of STAT3 involved in cellular vulnerability to isoflurane.BMC neuroscience · 2024Article
- The Warburg micro syndrome protein RAB3GAP1 modulates neuronal morphogenesis and interacts with axon elongation end ER-Golgi trafficking factors.Neurobiology of disease · 2023Article
- Phosphorylation of STAT3 at Tyr705 contributes to TFEB-mediated autophagy-lysosomal pathway dysfunction and leads to ischemic injury in rats.Cellular and molecular life sciences : CMLS · 2023Article
- STAT3 in medulloblastoma: a key transcriptional regulator and potential therapeutic target.Molecular biology reports · 2022Review
- Targeting EphA2 suppresses hepatocellular carcinoma initiation and progression by dual inhibition of JAK1/STAT3 and AKT signaling.Cell reports · 2021Article
- Targeting Aberrant Expression of STAT3 and AP-1 Oncogenic Transcription Factors and HPV Oncoproteins in Cervical Cancer byFrontiers in pharmacology · 2021Article
- Stress-induced dynamic regulation of mitochondrial STAT3 and its association with cyclophilin D reduce mitochondrial ROS production.Science signaling · 2017Article
- Lysophosphatidic acid counteracts glucagon-induced hepatocyte glucose production via STAT3.Scientific reports · 2017Article
- Quantitative liver proteomics identifies FGF19 targets that couple metabolism and proliferation.PloS one · 2017Article
- mRNA and microRNA expression profiles of radioresistant NCI-H520 non-small cell lung cancer cells.Molecular medicine reports · 2015Article
- Inducible STAT3 NH2 terminal mono-ubiquitination promotes BRD4 complex formation to regulate apoptosis.Cellular signalling · 2014Article
- A new model for developmental neuronal death and excitatory/inhibitory balance in hippocampus.Molecular neurobiology · 2014Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Neonatal brains develop through a program that eliminates about half of the neurons. During this period, neurons depend on neurotrophins for their survival. Recently, we reported that, at the conclusion of the naturally occurring death period, neurons become neurotrophin-independent and, further, that this developmental switch is achieved by the emergence of a second survival pathway mediated by signal transducer and activator of transcription 3 (STAT3). Here I show that calcineurin plays a key role in controlling the developmental switch in mouse hippocampal neurons. Calcineurin promotes the degradation of STAT3 via the ubiquitin-proteasome pathway. Inhibition of calcineurin acutely increases total levels of STAT3 as well as its activated forms, resulting in decreased levels of the tumor suppressor p53 and its proapoptotic target, Bax. In vivo and in vitro, calcineurin regulates levels of STAT3 and neurotrophin dependence. TMF/ARA 160 (TATA element modulatory factor/androgen receptor co-activator 160), the key mediator of STAT3 ubiquitination, is required for calcineurin-dependent STAT3 degradation. Thus, these results show that the ubiquitin-proteasome pathway controls the critical developmental switch of neurotrophin dependence in the newborn hippocampus.
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