Linked Life Data

8922669

Source:http://linkedlifedata.com/resource/pubmed/id/8922669

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-3-11
pubmed:abstractText
The roles of protein kinase C and its substrates in development are poorly understood. Recently, we disrupted the mouse gene for a major cellular substrate for protein kinase C, the MARCKS protein (Proc. Natl. Acad. Sci. USA, 92, 944-948, 1995). The resulting phenotype consisted of universal perinatal lethality, agenesis of the corpus callosum and other forebrain commissures, and neuronal ectopia and other cortical and retinal lamination disturbances. These mice also had high frequencies of exencephaly (25% overall, 35% in females). In the present study, we have examined the normal expression of MARCKS and the various isozymes of protein kinase C at the time of cranial neural tube closure, in an attempt to correlate MARCKS expression in time and anatomical location with the exencephaly characteristic of MARCKS deficiency. Failure of neural tube closure occurred at various sites in the cranial neural tube, suggesting a cellular functional defect that was not limited to a specific location. Non-exencephalic MARCKS-deficient embryos appeared to be anatomically normal on embryonic day (E) 8.5-9.5. MARCKS and PKC alpha were expressed at the plasma membrane of the neuroepithelial cells comprising the future neural tube, as well as in the surface ectoderm and underlying mesenchyme. Endogenous protein kinase C species, comprising either or both alpha and delta, were capable of phosphorylating MARCKS in intact E8.5 embryos. Thus, MARCKS is expressed at the plasma membranes of the specific cell types involved in cranial neurulation; its deficiency presumably results in a still-to-be-elucidated functional defect in these cells that leads to exencephaly in a high proportion of cases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0165-3806
pubmed:author
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
96
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
62-75
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:8922669-Animals, pubmed-meshheading:8922669-Embryonic and Fetal Development, pubmed-meshheading:8922669-Gene Expression Regulation, Developmental, pubmed-meshheading:8922669-Gene Expression Regulation, Enzymologic, pubmed-meshheading:8922669-Immunohistochemistry, pubmed-meshheading:8922669-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:8922669-Isoenzymes, pubmed-meshheading:8922669-Membrane Proteins, pubmed-meshheading:8922669-Mice, pubmed-meshheading:8922669-Mice, Inbred C57BL, pubmed-meshheading:8922669-Mice, Transgenic, pubmed-meshheading:8922669-Nerve Tissue Proteins, pubmed-meshheading:8922669-Neural Tube Defects, pubmed-meshheading:8922669-Phosphorylation, pubmed-meshheading:8922669-Protein Kinase C, pubmed-meshheading:8922669-Proteins, pubmed-meshheading:8922669-Recombinant Fusion Proteins, pubmed-meshheading:8922669-beta-Galactosidase
pubmed:year
1996
pubmed:articleTitle
Developmental expression of MARCKS and protein kinase C in mice in relation to the exencephaly resulting from MARCKS deficiency.
pubmed:affiliation
Howard Hughes Medical Institute Laboratories, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't