Source:http://linkedlifedata.com/resource/pubmed/id/11753682
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
55
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pubmed:dateCreated |
2001-12-25
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pubmed:abstractText |
IEX-1, an immediate early gene, is widely expressed in epithelial and endothelial tissues, and is altered by a variety of growth regulatory factors. We have shown that expression of IEX-1 in keratinocytes increases the growth rate of these cells. The effects of IEX-1 on apoptosis, however, are unclear. To clarify the effects of IEX-1 on apoptosis, we investigated the effects of IEX-1 expression in keratinocytes (HaCaT cells) in the basal state and after the induction of cellular stress. Under normal, non-stressed conditions, both control (HaCaT) and IEX-1-transfected (IEX-HaCaT) cell lines showed no significant differences in the activity of a key apoptotic enzyme, caspase 3 despite significantly higher levels of IEX-1 expression. IEX-HaCaT cells grew faster than HaCaT cells. When both cell lines were irradiated with ultraviolet B radiation, caspase 3 activity increased to a greater extent in the IEX-HaCaT cells than in HaCaT cells. Camptothecin increased caspase 3 activity twice as much in the IEX-HaCaT cells when compared to HaCaT cells. When histone-complex DNA fragments were measured in IEX-HaCaT or HaCaT cells following UVB irradiation or treatment with camptothecin, significantly higher amounts of nucleosomes were seen in the IEX-HaCaT transfected cells. Likewise, serum deprivation induced higher degrees of apoptosis in IEX-HaCaT cells than in HaCaT cells. We conclude that overexpression of IEX-1 in HaCaT keratinocytes increases the growth rate of cells under basal conditions; in the basal state the rate of apoptosis is unchanged. However, the rate of apoptosis increases in IEX-1 overexpressing HaCaT keratinocytes after cells are subjected to stress.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/CASP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Camptothecin,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/IER3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Immediate-Early Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
29
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7992-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11753682-Apoptosis,
pubmed-meshheading:11753682-Apoptosis Regulatory Proteins,
pubmed-meshheading:11753682-Camptothecin,
pubmed-meshheading:11753682-Caspase 3,
pubmed-meshheading:11753682-Caspases,
pubmed-meshheading:11753682-Cell Adhesion,
pubmed-meshheading:11753682-Cell Division,
pubmed-meshheading:11753682-Enzyme Activation,
pubmed-meshheading:11753682-Genes, Immediate-Early,
pubmed-meshheading:11753682-Humans,
pubmed-meshheading:11753682-Immediate-Early Proteins,
pubmed-meshheading:11753682-Keratinocytes,
pubmed-meshheading:11753682-Membrane Glycoproteins,
pubmed-meshheading:11753682-Membrane Proteins,
pubmed-meshheading:11753682-Neoplasm Proteins,
pubmed-meshheading:11753682-Protein Transport,
pubmed-meshheading:11753682-RNA, Messenger,
pubmed-meshheading:11753682-Transfection,
pubmed-meshheading:11753682-Tumor Cells, Cultured,
pubmed-meshheading:11753682-Ultraviolet Rays
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pubmed:year |
2001
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pubmed:articleTitle |
IEX-1, an immediate early gene, increases the rate of apoptosis in keratinocytes.
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pubmed:affiliation |
Department of Medicine, Mayo Clinic and Foundation, Rochester, Minnesota, MN 55905, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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