ReviewCell calcium2011
Analysis of CaM-kinase signaling in cells.
Review in Cell calcium, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 121 citations in OpenAlex.
- CaMK4-dependent activation of AKT/mTOR and CREM-α underlies autoimmunity-associated Th17 imbalance.The Journal of clinical investigation · 2014Trial
- An Ancestral Mechanism of Calmodulin Binding to Cds1 Kinase Inhibits Catalytic Activity.IUBMB life · 2026Article
- A Constellation of Fluorescent Biosensors to Illuminate the Galaxy of Protein Kinases.Chembiochem : a European journal of chemical biology · 2026Review
- Loss of p300/CBP-associated factor aggravates cardiac remodeling via regulation of CAMKK2 acetylation.Experimental & molecular medicine · 2026Article
- Kinase Inhibitors for Targeted Cancer Therapy.Current topics in medicinal chemistry · 2026Review
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- Impact and Significance of Viral Vectors for siRNA Delivery in the Treatment of Alzheimer's Disease.Current pharmaceutical biotechnology · 2026Review
- Nuclear CaMKII Isoforms as Regulators of Transcription: From Developmental to Pathological Persistence.Medical sciences (Basel, Switzerland) · 2025Review
- CaCurrent biology : CB · 2025Article
- Article
- Allicin ameliorates acute myocardial infarction in rats by modulating calcium homeostasis in cardiomyocytes through the induction of hydrogen sulfide production.Frontiers in pharmacology · 2025Article
- Conducting polymer hydrogels for biomedical application: Current status and outstanding challenges.APL bioengineering · 2024Review
- The CaMK Family Differentially Promotes Necroptosis and Mouse Cardiac Graft Injury and Rejection.International journal of molecular sciences · 2024Article
- Involvement of calmodulin-dependent protein kinase I in the regulation of the expression of connexin 43 in MA-10 tumor Leydig cells.Molecular and cellular biochemistry · 2023Article
- Porcine reproductive and respiratory syndrome virus infection triggers autophagy via ER stress-induced calcium signaling to facilitate virus replication.PLoS pathogens · 2023Article
- Defining the Biologically Plausible Taxonomic Domain of Applicability of an Adverse Outcome Pathway: A Case Study Linking Nicotinic Acetylcholine Receptor Activation to Colony Death.Environmental toxicology and chemistry · 2023Article
- Calcium-dependent transcriptional changes in human pancreatic islet cells reveal functional diversity in islet cell subtypes.Diabetologia · 2022Article
- Glucagon, cyclic AMP, and hepatic glucose mobilization: A half-century of uncertainty.Physiological reports · 2022Review
- SERCA2a-phospholamban interaction monitored by an interposed circularly permutated green fluorescent protein.American journal of physiology. Heart and circulatory physiology · 2021Article
- CaJournal of cellular immunology · 2021Article
10 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
A change in intracellular free calcium is a common signaling mechanism that modulates a wide array of physiological processes in most cells. Responses to increased intracellular Ca(2+) are often mediated by the ubiquitous protein calmodulin (CaM) that upon binding Ca(2+) can interact with and alter the functionality of numerous proteins including a family of protein kinases referred to as CaM-kinases (CaMKs). Of particular interest are multifunctional CaMKs, such as CaMKI, CaMKII, CaMKIV and CaMKK, that can phosphorylate multiple downstream targets. This review will outline several protocols we have used to identify which members and/or isoforms of this CaMK family mediate specific cellular responses with a focus on studies in neurons. Many previous studies have relied on a single approach such as pharmacological inhibitors or transfected dominant-negative kinase constructs. Since each of these protocols has its limitations, that will be discussed, we emphasize the necessity to use multiple, independent approaches in mapping out cellular signaling pathways.
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.