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| Description
| - Bylo popsáno že narušení mikrotubulů způsobuje potlačení inducibility hlavních cytochromů P450 (CYP) přes některé jaderné receptory. Testovali jsme účinky strukturně odlišných klinicky využívaných látek interferujících s mikrotubuly (MIAs), jako je kolchicin colchicine, vinkristin, vinblastin, nokodazol a taxol na signální dráhu aryluhlovodíkového receptoru v lidských hepatocytech. Ukazujeme, že testované MIAs inhibují 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducibilní expresi CYP1A2 mRNA a zamezují TCDD-závislé jaderné translokaci aryl uhlovodíkového receptoru. Na druhou stranu, tyto MIAs zvyšovaly obsah AhR proteinu a mRNA transkripčním mechanismem. Ukazujeme, že MIAs aktivují c-jun-N-terminální kinasu (JNK), částečně p38 ale ne extracellulárně-regulovanou protein kinasu (ERK). Konzistentně, sorbitol, modelový aktivátor JNK, inhiboval TCDD-závislou indukci CYP1A2 mRNA a down-reguloval tyrosinaminotransferasu (mRNA), tj. cílový gen glukokortikoidního receptoru. Dexamethason měl opačný účinek na s (cs)
- Disruption of microtubules has been shown to cause suppression of inducibility of major cytochromes P450 (CYP) through several nuclear receptors. Here we tested the effects of structurally different clinically used microtubules-interfering agents (MIAs), such as colchicine, vincristine, vinblastine, nocodazole and taxol on aryl hydrocarbon receptor signaling pathway in human hepatocytes. We show that tested MIAs inhibit 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible expression of CYP1A2 mRNA and restrict TCDD-dependent nuclear translocation of aryl hydrocarbon receptor. On the other hand, these MIAs increased the content of aryl hydrocarbon receptor protein and mRNA by transcriptional mechanism. We show that the MIAs activate c-Jun -N-terminal kinase (JNK), partly p38 but not extracellular-regulated protein kinase (ERK). Consistently, sorbitol, a model activator of JNK, inhibited TCDD-mediated induction of CYP1A2 mRNA and down-regulated tyrosine aminotransferase mRNA - a target gene of glucocort
- Disruption of microtubules has been shown to cause suppression of inducibility of major cytochromes P450 (CYP) through several nuclear receptors. Here we tested the effects of structurally different clinically used microtubules-interfering agents (MIAs), such as colchicine, vincristine, vinblastine, nocodazole and taxol on aryl hydrocarbon receptor signaling pathway in human hepatocytes. We show that tested MIAs inhibit 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible expression of CYP1A2 mRNA and restrict TCDD-dependent nuclear translocation of aryl hydrocarbon receptor. On the other hand, these MIAs increased the content of aryl hydrocarbon receptor protein and mRNA by transcriptional mechanism. We show that the MIAs activate c-Jun -N-terminal kinase (JNK), partly p38 but not extracellular-regulated protein kinase (ERK). Consistently, sorbitol, a model activator of JNK, inhibited TCDD-mediated induction of CYP1A2 mRNA and down-regulated tyrosine aminotransferase mRNA - a target gene of glucocort (en)
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| Title
| - Microtubules-interfering agents restrict aryl hydrocarbon receptor-mediated CYP1A2 induction in primary cultures of human hepatocytes via c-jun-N-terminal kinase and glucocorticoid receptor.
- Microtubules-interfering agents restrict aryl hydrocarbon receptor-mediated CYP1A2 induction in primary cultures of human hepatocytes via c-jun-N-terminal kinase and glucocorticoid receptor. (en)
- Látky interferující s mikrotubuly omezují aryl uhlovodíkovým receptorem zprostředkovanou indukci CYP1A2 v primárních kulturách lidských hepatocytů přes c_Jun-N-terminální dinasu a glukokortikoidní receptor. (cs)
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| skos:prefLabel
| - Microtubules-interfering agents restrict aryl hydrocarbon receptor-mediated CYP1A2 induction in primary cultures of human hepatocytes via c-jun-N-terminal kinase and glucocorticoid receptor.
- Microtubules-interfering agents restrict aryl hydrocarbon receptor-mediated CYP1A2 induction in primary cultures of human hepatocytes via c-jun-N-terminal kinase and glucocorticoid receptor. (en)
- Látky interferující s mikrotubuly omezují aryl uhlovodíkovým receptorem zprostředkovanou indukci CYP1A2 v primárních kulturách lidských hepatocytů přes c_Jun-N-terminální dinasu a glukokortikoidní receptor. (cs)
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| skos:notation
| - RIV/61989592:15110/08:00006988!RIV09-MSM-15110___
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
| - P(GA303/07/0128), Z(MSM6198959216)
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| http://linked.open...iv/cisloPeriodika
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
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| http://linked.open...ai/riv/idVysledku
| - RIV/61989592:15110/08:00006988
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| http://linked.open...riv/jazykVysledku
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| http://linked.open.../riv/klicovaSlova
| - Aryl hydrocarbon receptor; Cytoskeleton; Human hepatocytes; MAPK kinases; Glucocorticoid receptor (en)
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| http://linked.open.../riv/klicoveSlovo
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| http://linked.open...odStatuVydavatele
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| http://linked.open...ontrolniKodProRIV
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| http://linked.open...i/riv/nazevZdroje
| - European Journal of Pharmacology
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| http://linked.open...in/vavai/riv/obor
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| http://linked.open...ichTvurcuVysledku
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| http://linked.open...cetTvurcuVysledku
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| http://linked.open...vavai/riv/projekt
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| http://linked.open...UplatneniVysledku
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| http://linked.open...v/svazekPeriodika
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| http://linked.open...iv/tvurceVysledku
| - Dvořák, Zdeněk
- Ulrichová, Jitka
- Vrzal, Radim
- Maurel, Patrick
- Pascussi, Jean-Marc
- Daujat-Chavanieu, Martine
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| http://linked.open...n/vavai/riv/zamer
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| issn
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| number of pages
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| http://localhost/t...ganizacniJednotka
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