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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F05%3A00001914%21RIV06-MSM-15110___
rdf:type
n10:Vysledek skos:Concept
dcterms:description
The role of microtubules (MTs) in steroid hormone-dependent human glucocorticoid receptor (hGR) activation/translocation is controversial. It was demonstrated recently that colchicine (COL) down-regulates hGR-driven genes in primary human hepatocytes by a mechanism involving inhibition of hGR translocation to the nucleus. To investigate whether inhibition of hGR translocation is the sole reason for its inactivation, we used human cervical carcinoma cells (HeLa) as a model. Herein we present evidence that perturbation of microtubules in HeLa cells leads to rapid time- and dose-dependent degradation of hGR protein. Degradation is proteasome mediated as revealed by its reversibility by proteasome inhibitor MG132. Moreover, degradation was observed for neither wt-hGR nor hGR mutants S226A and K419A in transiently transfected COS-1 cells. On the other hand, c-jun N-terminal kinase (JNK) seems not to be involved in the process because JNK inhibitor 1,9-Pyrazoloanthrone (SP600125) does not reverse hGR degrad Úloha mikrotubulů (MT) při aktivaci/translokaci lidského glukokortikoidního receptoru (hGR), která závisí na steroidních hormonech, je kontroverzní. Nedávno bylo prokázáno, že kolchicin (COL) snižuje expresi genů závislých na aktivitě hGR v primárních lidských hepatocytech mechanismem, který souvisí s inhibicí translokace hGR do jádra. Abychom zjistili, je-li inhibice translokace hGR jediným důvodem inaktivace tohoto receptoru, využili jsme buněčnou linii karcinomu lidského děložního čípku (HeLa) jako model. Zde předkládáme důkazy, že porušení mikrotubulů v HeLa buňkách vede k rychlé degradaci proteinu hGR v závislosti na čase a dávce. Degradace probíhá v proteasomu, což vyplývá z faktu, že ji lze zvrátit přídavkem inhibitoru proteasomu MG132. Navíc degradace nebyla pozorována ani v případě wt-hGR ani mutantů S226A a K419A, které byly transientně transfektovány do buněk COS-1. Na druhou stranu se ukazuje, že c-jun N-terminální kinasa (JNK) není do tohoto procesu zapojena, protože inhibitor JNK 1,9-pyr The role of microtubules (MTs) in steroid hormone-dependent human glucocorticoid receptor (hGR) activation/translocation is controversial. It was demonstrated recently that colchicine (COL) down-regulates hGR-driven genes in primary human hepatocytes by a mechanism involving inhibition of hGR translocation to the nucleus. To investigate whether inhibition of hGR translocation is the sole reason for its inactivation, we used human cervical carcinoma cells (HeLa) as a model. Herein we present evidence that perturbation of microtubules in HeLa cells leads to rapid time- and dose-dependent degradation of hGR protein. Degradation is proteasome mediated as revealed by its reversibility by proteasome inhibitor MG132. Moreover, degradation was observed for neither wt-hGR nor hGR mutants S226A and K419A in transiently transfected COS-1 cells. On the other hand, c-jun N-terminal kinase (JNK) seems not to be involved in the process because JNK inhibitor 1,9-Pyrazoloanthrone (SP600125) does not reverse hGR degrad
dcterms:title
Disruption of microtubules leads to glucocorticoid receptor degradation in HeLa cell line Porušení sítě mikrotubulů v buněčné linii HeLa vede k degradaci glukokortikoidního receptoru Disruption of microtubules leads to glucocorticoid receptor degradation in HeLa cell line
skos:prefLabel
Disruption of microtubules leads to glucocorticoid receptor degradation in HeLa cell line Disruption of microtubules leads to glucocorticoid receptor degradation in HeLa cell line Porušení sítě mikrotubulů v buněčné linii HeLa vede k degradaci glukokortikoidního receptoru
skos:notation
RIV/61989592:15110/05:00001914!RIV06-MSM-15110___
n3:strany
187-196
n3:aktivita
n16:P n16:Z
n3:aktivity
P(GP303/04/P074), Z(MSM 151100003)
n3:cisloPeriodika
2
n3:dodaniDat
n8:2006
n3:domaciTvurceVysledku
n9:2514559 n9:8069239 n9:1030957
n3:druhVysledku
n14:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n12:predkladatel
n3:idSjednocenehoVysledku
518296
n3:idVysledku
RIV/61989592:15110/05:00001914
n3:jazykVysledku
n15:eng
n3:klicovaSlova
Microtubules; glucocorticoid receptor; proteasome; degradation; translocation; c-jun N-terminal kinase; HeLa cells
n3:klicoveSlovo
n5:HeLa%20cells n5:Microtubules n5:c-jun%20N-terminal%20kinase n5:glucocorticoid%20receptor n5:translocation n5:degradation n5:proteasome
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[275CD2E87319]
n3:nazevZdroje
Cellular Signalling
n3:obor
n18:CE
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
6
n3:projekt
n17:GP303%2F04%2FP074
n3:rokUplatneniVysledku
n8:2005
n3:svazekPeriodika
17
n3:tvurceVysledku
Dvořák, Zdeněk Modrianský, Martin Ulrichová, Jitka Vilarem, Marie-Jose Pascussi, Jean-Marc Maurel, Patrick
n3:zamer
n4:MSM%20151100003
s:issn
0898-6568
s:numberOfPages
10
n13:organizacniJednotka
15110