Linked Life Data

21752935

Source:http://linkedlifedata.com/resource/pubmed/id/21752935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2011-7-27
pubmed:abstractText
Intracellular Ca²? signals influence gastrulation, neurogenesis and organogenesis through pathways that are still being defined. One potential Ca²? mediator of many of these morphogenic processes is CaMK-II, a conserved calmodulin-dependent protein kinase. Prolonged Ca²? stimulation converts CaMK-II into an activated state that, in the zebrafish, is detected in the forebrain, ear and kidney. Autosomal dominant polycystic kidney disease has been linked to mutations in the Ca²?-conducting TRP family member PKD2, the suppression of which in vertebrate model organisms results in kidney cysts. Both PKD2-deficient and CaMK-II-deficient zebrafish embryos fail to form pronephric ducts properly, and exhibit anterior cysts and destabilized cloacal cilia. PKD2 suppression inactivates CaMK-II in pronephric cells and cilia, whereas constitutively active CaMK-II restores pronephric duct formation in pkd2 morphants. PKD2 and CaMK-II deficiencies are synergistic, supporting their existence in the same genetic pathway. We conclude that CaMK-II is a crucial effector of PKD2 Ca²? that both promotes morphogenesis of the pronephric kidney and stabilizes primary cloacal cilia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1477-9129
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
138
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3387-97
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
CaMK-II is a PKD2 target that promotes pronephric kidney development and stabilizes cilia.
pubmed:affiliation
Nephrology Division, Massachusetts General Hospital, Charlestown, MA 02129, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't