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Statements

Subject Item
n2:RIV%2F61389030%3A_____%2F11%3A00368596%21RIV12-AV0-61389030
rdf:type
n8:Vysledek skos:Concept
dcterms:description
Small molecule inhibitors of cyclin-dependent kinases (CDK) have been developed as anticancer drugs with cytostatic and cytotoxic properties, but some of them have also been shown to limit angiogenesis. Here, we report that the 3,5-diaminopyrazole CAN508 inhibits endothelial cell migration and tube formation. In addition, it reduces phosphorylation of the C-terminus of RNA polymerase II and inhibits mRNA synthesis in endothelial cells, in accordance with previous observations that it has high selectivity towards the positive transcriptional regulator P-TEFb. Moreover, CAN508 reduces expression of vascular endothelial growth factor by several human cancer cell lines. The findings suggest that P-TEFb may be an attractive target for anti-angiogenic therapy. (C) 2011 Elsevier Masson SAS. All rights reserved. Small molecule inhibitors of cyclin-dependent kinases (CDK) have been developed as anticancer drugs with cytostatic and cytotoxic properties, but some of them have also been shown to limit angiogenesis. Here, we report that the 3,5-diaminopyrazole CAN508 inhibits endothelial cell migration and tube formation. In addition, it reduces phosphorylation of the C-terminus of RNA polymerase II and inhibits mRNA synthesis in endothelial cells, in accordance with previous observations that it has high selectivity towards the positive transcriptional regulator P-TEFb. Moreover, CAN508 reduces expression of vascular endothelial growth factor by several human cancer cell lines. The findings suggest that P-TEFb may be an attractive target for anti-angiogenic therapy. (C) 2011 Elsevier Masson SAS. All rights reserved.
dcterms:title
The selective P-TEFb inhibitor CAN508 targets angiogenesise The selective P-TEFb inhibitor CAN508 targets angiogenesise
skos:prefLabel
The selective P-TEFb inhibitor CAN508 targets angiogenesise The selective P-TEFb inhibitor CAN508 targets angiogenesise
skos:notation
RIV/61389030:_____/11:00368596!RIV12-AV0-61389030
n8:predkladatel
n9:ico%3A61389030
n3:aktivita
n13:Z n13:P
n3:aktivity
P(ED0007/01/01), P(GA204/08/0511), P(GA301/08/1649), Z(AV0Z50380511), Z(MSM6198959216)
n3:cisloPeriodika
9
n3:dodaniDat
n20:2012
n3:domaciTvurceVysledku
n12:6978932 n12:4837177 Cankař, Petr n12:1793411 n12:9961216
n3:druhVysledku
n17:J
n3:duvernostUdaju
n7:S
n3:entitaPredkladatele
n6:predkladatel
n3:idSjednocenehoVysledku
228697
n3:idVysledku
RIV/61389030:_____/11:00368596
n3:jazykVysledku
n18:eng
n3:klicovaSlova
Angiogenesis; Cancer; Transcription; Inhibitor; Cyclin-dependent kinase 9
n3:klicoveSlovo
n14:Inhibitor n14:Cancer n14:Transcription n14:Angiogenesis n14:Cyclin-dependent%20kinase%209
n3:kodStatuVydavatele
FR - Francouzská republika
n3:kontrolniKodProRIV
[C7C8009FACBA]
n3:nazevZdroje
European Journal of Medicinal Chemistry
n3:obor
n15:CE
n3:pocetDomacichTvurcuVysledku
5
n3:pocetTvurcuVysledku
7
n3:projekt
n11:GA301%2F08%2F1649 n11:ED0007%2F01%2F01 n11:GA204%2F08%2F0511
n3:rokUplatneniVysledku
n20:2011
n3:svazekPeriodika
46
n3:tvurceVysledku
Voller, Jiří Zahler, S. Cankař, Petr Liebl, J. Jorda, Radek Kryštof, Vladimír Rárová, Lucie
n3:wos
000295237400081
n3:zamer
n4:AV0Z50380511 n4:MSM6198959216
s:issn
0223-5234
s:numberOfPages
6
n10:doi
10.1016/j.ejmech.2011.06.035