ArticleMolecular and cellular neurosciences2007
CaMKII and CaMKIV mediate distinct prosurvival signaling pathways in response to depolarization in neurons.
Article in Molecular and cellular neurosciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
41 citing papers in PubMed, 78 citations in OpenAlex.
- Proteomic analysis of central amygdala systems regulated by mifepristone in the context of alcohol dependence.Neuropharmacology · 2026Article
- Article
- GlyT1 Inhibition by NFPS Promotes Neuroprotection in Amyloid-β-Induced Alzheimer's Disease Animal Model.Neurochemical research · 2024Article
- Effects ofNutrients · 2024Article
- Article
- Study of spatiotemporal regulation of kinase signaling using genetically encodable molecular tools.Current opinion in chemical biology · 2022Review
- Antenatal low-intensity pulsed ultrasound reduces neurobehavioral deficits and brain injury following dexamethasone-induced intrauterine growth restriction.Brain pathology (Zurich, Switzerland) · 2021Article
- The local translation ofAging · 2019Article
- Cyclin-dependent kinase 5 regulates proliferation, migration, tyrosinase activity, and melanin production in B16-F10 melanoma cells via the essential regulator p-CREB.In vitro cellular & developmental biology. Animal · 2019Article
- Treatment duration affects cytoprotective efficacy of positive allosteric modulation of α7 nAChRs after focal ischemia in rats.Pharmacological research · 2018Article
- Reduced Cytosolic Calcium as an Early Decisive Cellular State in Parkinson's Disease and Synucleinopathies.Frontiers in neuroscience · 2018Review
- Autonomous CaMKII Activity as a Drug Target for Histological and Functional Neuroprotection after Resuscitation from Cardiac Arrest.Cell reports · 2017Article
- Electroacupuncture improves cognitive ability following cerebral ischemia reperfusion injury via CaM-CaMKIV-CREB signaling in the rat hippocampus.Experimental and therapeutic medicine · 2016Article
- The Role of the Neuroprotective Factor Npas4 in Cerebral Ischemia.International journal of molecular sciences · 2015Review
- Calcium/calmodulin-dependent kinase II and Alzheimer's disease.Molecular brain · 2015Review
- CaMKII Controls Whether Touch Is Painful.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Regulation of voltage-gated Ca(2+) currents by Ca(2+)/calmodulin-dependent protein kinase II in resting sensory neurons.Molecular and cellular neurosciences · 2014Article
- Article
- Article
- Sisters Acts: Converging Signaling Between CaMKII and CaMKIV, Two Members of the Same Family.Translational medicine @ UniSa · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
By fusing the CaMKII-inhibitory peptide AIP to GFP, we constructed a specific and effective CaMKII inhibitor, GFP-AIP. Expression of GFP-AIP and/or dominant-inhibitory CaMKIV in cultured neonatal rat spiral ganglion neurons (SGNs) shows that CaMKII and CaMKIV act additively and in parallel to mediate the prosurvival effect of depolarization. Depolarization or expression of constitutively active CaMKII functionally inactivates Bad, indicating that this is one means by which CaMKII promotes neuronal survival. CaMKIV, but not CaMKII, requires CREB to promote SGN survival, consistent with the exclusively nuclear localization of CaMKIV and indicating that the principal prosurvival function of CaMKIV is activation of CREB. Consistent with this, a constitutively active CREB construct that provides a high level of CREB activity promotes SGN survival, although low levels of CREB activity did not do so. Also, in apoptotic SGNs, activation of CREB by depolarization is disabled, presumably as part of a cellular commitment to apoptosis.
Indexed as
Identifiers
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.