Source:http://linkedlifedata.com/resource/pubmed/id/15259032
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
|
pubmed:dateCreated |
2004-7-19
|
pubmed:abstractText |
BACKGROUND: In utero rubella virus (RV) infection of a fetus can result in birth defects that are often collectively referred to as congenital rubella syndrome (CRS). In extreme cases, fetal death can occur. In spite of the availability of a safe and effective vaccine against rubella, recent worldwide estimates are that more than 100,000 infants are born with CRS annually. RECENT PROGRESS: Recently, several significant findings in the field of cell biology, as well as in the RV replication and virus-cell interactions, have originated from the authors' laboratory, and other researchers have provided insights into RV teratogenesis. It has been shown that 1) an RV protein induces cell-cycle arrest by generating a subpopulation of tetraploid nuclei (i.e., 4N DNA) cells, perhaps representative of the tetraploid state following S phase in the cell cycle, due to its interaction with citron-K kinase (CK); 2) RV infection induces apoptosis in cell culture, and 3) CK functional perturbations lead to tetraploidy, followed by apoptosis, in specific cell types. CONCLUSIONS: Based on several similarities between known RV-associated fetal and cellular manifestations and CK deficiency-associated phenotypes, it is reasonable to postulate that P90-CK interaction in RV-infected cells interferes with CK function and induces cell-cycle arrest following S phase in a subpopulation, perhaps representative of tetraploid stage, which could lead to subsequent apoptosis in RV infection. Taking all these observations to the fetal organogenesis level, it is plausible that P90-CK interaction could perhaps be one of the initial steps in RV infection-induced apoptosis-associated fetal birth defects in utero.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Retinoblastoma Protein,
http://linkedlifedata.com/resource/pubmed/chemical/citron-kinase
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jul
|
pubmed:issn |
1542-0752
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
70
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
431-7
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:15259032-Apoptosis,
pubmed-meshheading:15259032-Cell Cycle,
pubmed-meshheading:15259032-Congenital Abnormalities,
pubmed-meshheading:15259032-Female,
pubmed-meshheading:15259032-Fetus,
pubmed-meshheading:15259032-Humans,
pubmed-meshheading:15259032-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:15259032-Pregnancy,
pubmed-meshheading:15259032-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15259032-Retinoblastoma Protein,
pubmed-meshheading:15259032-Rubella,
pubmed-meshheading:15259032-Rubella virus
|
pubmed:year |
2004
|
pubmed:articleTitle |
Rubella virus and birth defects: molecular insights into the viral teratogenesis at the cellular level.
|
pubmed:affiliation |
Section of Viral Pathogenesis and Vaccine Adverse Reactions, Division of Viral Products, Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Bethesda, Maryland, USA. atreya@cber.fda.gov
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review
|