| Attributes | Values |
|---|
| rdf:type
| |
| Description
| - Byly studovány mechanismy seleničitanem vyvolané buněčné smrti u nádorové linie HeLa Hep-2 odvozené z karcinomu děložního čípku. Seleničitan v koncentracích 5 a 50 mol/l během 24 hodin vyvolal poškození DNA a aktivaci na p53 zavislé signální dráhy. Následně seleničitan aktivoval p38, ale jeho vliv na JNK byl minimální. Závěrem, seleničitan vyvolal na kaspázách nezávislou apoptózu, ale jiné mechanismy hrály také úlohu. (cs)
- The mechanisms of sodium selenite-induced cell death in cervical carcinoma cells were studied during 24 h of exposure in the HeLa Hep-2 cell line. Selenite at the employed concentrations of 5 and 50 mikro mol/L produced time- and dose-dependent suppression of DNA synthesis and induced DNA damage which resulted in phosphorylation of histone H2A.X. These effects were influenced by pretreatment of cells with the SOD/catalase mimetic MnTMPyP or glutathione-depleting buthionine sulfoximine, suggesting the significant role of selenite-generated oxidative stress. Following the DNA damage, selenite activated p53-dependent pathway as evidenced by the appearance of phosphorylated p53 and accumulation of p21 in the treated cells. Concomitantly, selenite activated p38 pathway but its effect on JNK was very weak. p53- and p38-dependent signaling led to the accumulation of Bax protein, which was preventable by specific inhibitors of p38 (SB 203580) and p53 (Pifithrin-alpha).
- The mechanisms of sodium selenite-induced cell death in cervical carcinoma cells were studied during 24 h of exposure in the HeLa Hep-2 cell line. Selenite at the employed concentrations of 5 and 50 mikro mol/L produced time- and dose-dependent suppression of DNA synthesis and induced DNA damage which resulted in phosphorylation of histone H2A.X. These effects were influenced by pretreatment of cells with the SOD/catalase mimetic MnTMPyP or glutathione-depleting buthionine sulfoximine, suggesting the significant role of selenite-generated oxidative stress. Following the DNA damage, selenite activated p53-dependent pathway as evidenced by the appearance of phosphorylated p53 and accumulation of p21 in the treated cells. Concomitantly, selenite activated p38 pathway but its effect on JNK was very weak. p53- and p38-dependent signaling led to the accumulation of Bax protein, which was preventable by specific inhibitors of p38 (SB 203580) and p53 (Pifithrin-alpha). (en)
|
| Title
| - Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells
- Seleničitan aktivuje na p53 a p38 závislé dráhy a vyvolává na kaspázách nezávislou smrt u nádorových buněk karcinomu děložního čípku (cs)
- Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells (en)
|
| skos:prefLabel
| - Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells
- Seleničitan aktivuje na p53 a p38 závislé dráhy a vyvolává na kaspázách nezávislou smrt u nádorových buněk karcinomu děložního čípku (cs)
- Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells (en)
|
| skos:notation
| - RIV/00179906:_____/08:00001286!RIV09-MSM-00179906
|
| http://linked.open...avai/riv/aktivita
| |
| http://linked.open...avai/riv/aktivity
| |
| http://linked.open...iv/cisloPeriodika
| |
| http://linked.open...vai/riv/dodaniDat
| |
| http://linked.open...aciTvurceVysledku
| |
| http://linked.open.../riv/druhVysledku
| |
| http://linked.open...iv/duvernostUdaju
| |
| http://linked.open...titaPredkladatele
| |
| http://linked.open...dnocenehoVysledku
| |
| http://linked.open...ai/riv/idVysledku
| - RIV/00179906:_____/08:00001286
|
| http://linked.open...riv/jazykVysledku
| |
| http://linked.open.../riv/klicovaSlova
| - selenite; cell death, cervical carcinoma; p53; MAPK (en)
|
| http://linked.open.../riv/klicoveSlovo
| |
| http://linked.open...odStatuVydavatele
| |
| http://linked.open...ontrolniKodProRIV
| |
| http://linked.open...i/riv/nazevZdroje
| - Cell Biology and Toxicology
|
| http://linked.open...in/vavai/riv/obor
| |
| http://linked.open...ichTvurcuVysledku
| |
| http://linked.open...cetTvurcuVysledku
| |
| http://linked.open...UplatneniVysledku
| |
| http://linked.open...v/svazekPeriodika
| |
| http://linked.open...iv/tvurceVysledku
| - Rudolf, Emil
- Rudolf, Kamil
- Červinka, Miroslav
|
| http://linked.open...ain/vavai/riv/wos
| |
| http://linked.open...n/vavai/riv/zamer
| |
| issn
| |
| number of pages
| |
| is http://linked.open...avai/riv/vysledek
of | |
![[RDF Data]](/fct/images/sw-rdf-blue.png)
![[cxml]](/fct/images/cxml_doc.png)
![[csv]](/fct/images/csv_doc.png)
![[text]](/fct/images/ntriples_doc.png)
![[turtle]](/fct/images/n3turtle_doc.png)
![[ld+json]](/fct/images/jsonld_doc.png)
![[rdf+json]](/fct/images/json_doc.png)
![[rdf+xml]](/fct/images/xml_doc.png)
![[atom+xml]](/fct/images/atom_doc.png)
![[html]](/fct/images/html_doc.png)