ReviewThe Journal of physiology2010
Kinase regulation of Na+-K+-2Cl- cotransport in primary afferent neurons.
Review in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed.
- Sphingosine-1-phosphate-induced nociceptor excitation and ongoing pain behavior in mice and humans is largely mediated by S1P3 receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Trial
- NKCC1, an Elusive Molecular Target in Brain Development: Making Sense of the Existing Data.Cells · 2020Review
- Differential expression of NaScientific reports · 2020Article
- Expression and effect of sodium-potassium-chloride cotransporter on dorsal root ganglion neurons in a rat model of chronic constriction injury.Neural regeneration research · 2020Article
- Sodium Transporters in Human Health and Disease.Frontiers in physiology · 2020Review
- Interactions between Membrane Resistance, GABA-A Receptor Properties, Bicarbonate Dynamics and ClInternational journal of molecular sciences · 2019Article
- A patient with multisystem dysfunction carries a truncation mutation in humanCold Spring Harbor molecular case studies · 2016Article
- Article
- Sphaeropsidin A shows promising activity against drug-resistant cancer cells by targeting regulatory volume increase.Cellular and molecular life sciences : CMLS · 2015Article
- NKCC1 and NKCC2: The pathogenetic role of cation-chloride cotransporters in hypertension.Genes & diseases · 2015Article
- Syndrome of severe pain associated with a continuous bumetanide infusion.International journal of cardiology · 2014Article
- Mechanism and synergism in epithelial fluid and electrolyte secretion.Pflugers Archiv : European journal of physiology · 2014Review
- In silico analysis and experimental verification of OSR1 kinase - Peptide interaction.Journal of structural biology · 2014Article
- Article
- Direct control of Na(+)-K(+)-2Cl(-)-cotransport protein (NKCC1) expression with aldosterone.American journal of physiology. Cell physiology · 2014Article
- Parkinson's disease-implicated kinases in the brain; insights into disease pathogenesis.Frontiers in molecular neuroscience · 2014Review
- Molecular transport machinery involved in orchestrating luminal acid-induced duodenal bicarbonate secretion in vivo.The Journal of physiology · 2013Article
- Regulation of synaptic transmission at the photoreceptor terminal: a novel role for the cation-chloride co-transporter NKCC1.The Journal of physiology · 2013Article
- The WNK/SPAK and IRBIT/PP1 pathways in epithelial fluid and electrolyte transport.Physiology (Bethesda, Md.) · 2012Review
- Molecular and functional expression of cation-chloride cotransporters in dorsal root ganglion neurons during postnatal maturation.Journal of neurophysiology · 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
2 authors.
Funding
Abstract
The Na(+)-K(+)-2Cl(-) cotransporter NKCC1 is expressed in sensory neurons where it accumulates intracellular Cl(-) and facilitates primary afferent depolarization. Depolarization of primary afferent fibre terminals interferes with the gating of incoming sensory signals to the spinal cord. The cotransporter belongs to a family of ion transporters which are sensitive to changes in cell volume. Cell shrinkage, through mechanisms that are still unknown, leads to the phosphorylation and activation of NKCC1. Similarly, axotomy results in increased NKCC1 phosphorylation in dorsal root ganglion (DRG) neurons. This review summarizes the work on the kinases that directly mediate NKCC1 activation. These are the sterile-20-like kinases SPAK and OSR1. Upon their activation through phosphorylation by upstream kinases, SPAK and OSR1 bind to specific peptides located in the cytosolic N-terminal tail of NKCC1, phosphorylate, and stimulate cotransport activity. Expression of SPAK and OSR1 varies from tissue to tissue, but in DRG neurons and in spinal cord, SPAK and OSR1 expression levels are similar. In DRG neurons, both kinases participate in the modulation of NKCC1, as the knockdown of one kinase only results in a partial decrease of NKCC1 function, while the knockdown of both kinases is additive. The identity of the kinases (e.g. WNK kinases) that possibly act upstream of SPAK and OSR1 is also discussed.
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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.