Linked Life Data

12049936

Source:http://linkedlifedata.com/resource/pubmed/id/12049936

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-6-6
pubmed:abstractText
Calcium/calmodulin-dependent protein kinase II (CaMKII) is thought to be a critical mediator of neuronal plasticity that links transiently triggered Ca(2+) signals to persistent changes in neuronal physiology. In one of its roles, CaMKII is an essential player in the N-methyl-D-aspartate receptor-mediated increase in conductance at glutamatergic synapses, a process described as long-term potentiation, which serves as a common model for neuronal plasticity and memory. Recent studies have used genetic, biochemical, live cell imaging and mathematical modeling approaches to investigate neuronal CaMKII and have led to a model of the molecular steps of CaMKII translocation and activation that can explain its role in neuronal plasticity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0959-4388
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
293-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Molecular mechanisms of CaMKII activation in neuronal plasticity.
pubmed:affiliation
Stanford University, Department of Molecular Pharmacology, CCSR Building, Room 3230, 269 Campus Drive, Stanford, California 94305, USA. cfink@stanford.edu
pubmed:publicationType
Journal Article, Review