Linked Life Data

12890701

Source:http://linkedlifedata.com/resource/pubmed/id/12890701

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2003-7-31
pubmed:abstractText
DNA microarray analyses were used to investigate the effect of cell-incorporated 35S-methionine on human colorectal carcinoma cells. This beta-radiation-induced gene expression profile was compared with that induced by external gamma-radiation. The extent of DNA fragmentation was used as a biomarker to determine the external gamma dose that was bioequivalent to that received by cells incubated in medium containing 35S-methionine. Studies showed that 35S-methionine at 100 microCi/mL induced a much more robust transcriptional response than gamma-radiation (2000 cGy) when evaluated 2 h after the labeling or irradiation period. The cellular response to internal beta-radiation was greater not only with respect to the number of genes induced, but also with respect to the level of gene induction. Not surprisingly, the induced genes overlapped with the set of gamma-responsive genes. However, a distinct beta-gene induction profile that included a large number of cell adhesion proteins was also observed. Taken together, these studies demonstrate that metabolic incorporation of a low energy beta-emitter, such as 35S-methionine, can globally influence a diverse set of cellular activities that can, in turn, affect the outcome of many experiments by altering the cell cycle, metabolic, signaling, or redox status (set point) of the cell. Additional studies of the mechanism of beta-induced proliferation arrest and cell death and of the significance of its differential gene induction/repression profile in comparison to pulsed gamma-irradiation may lead to new insights into the ways in which ionizing radiation can interact with cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1470-86
pubmed:dateRevised
2011-9-22
pubmed:meshHeading
pubmed-meshheading:12890701-Beta Particles, pubmed-meshheading:12890701-CDC2 Protein Kinase, pubmed-meshheading:12890701-Cluster Analysis, pubmed-meshheading:12890701-DNA Damage, pubmed-meshheading:12890701-Gamma Rays, pubmed-meshheading:12890701-Gene Expression, pubmed-meshheading:12890701-Gene Expression Profiling, pubmed-meshheading:12890701-Gene Silencing, pubmed-meshheading:12890701-Humans, pubmed-meshheading:12890701-Kinetics, pubmed-meshheading:12890701-Methionine, pubmed-meshheading:12890701-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:12890701-Radiation Dosage, pubmed-meshheading:12890701-Radioactive Tracers, pubmed-meshheading:12890701-Sulfur Radioisotopes, pubmed-meshheading:12890701-Tumor Cells, Cultured, pubmed-meshheading:12890701-Tumor Suppressor Protein p53, pubmed-meshheading:12890701-Up-Regulation
pubmed:year
2003
pubmed:articleTitle
Does metabolic radiolabeling stimulate the stress response? Gene expression profiling reveals differential cellular responses to internal beta vs. external gamma radiation.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, The George Washington University Medical Center, 2300 Eye St., N.W., Washington, DC 20037, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't