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Statements

Subject Item
n2:RIV%2F61989592%3A15310%2F08%3A00005285%21RIV13-MSM-15310___
rdf:type
skos:Concept n16:Vysledek
dcterms:description
Cyclin-dependent kinases (CDKs) play a key role in orchestrating the coordination of cell cycle progression in proliferating cells. The escape from the proper control of the cell cycle by upregulation of cyclins or aberrant activation of CDKs leads to malignant transformation. Proteins encoded by tumor suppressor genes such as p53 and cellular inhibitors of CDKs e.g. p16INK4a, p21Waf1/Cip1/Sdi, and p27Kip1 are able to counteract the deregulated cell cycle progression and to inhibit rapid (uncontrolled) cell proliferation. However, in the majority of cancer tissues tumor suppressors are inactivated or mutated. Virally encoded proteins e.g. E6 oncoprotein inactivate p53 by its accelerated proteolytic degradation. Therefore, use of synthetic compounds that are able to inhibit the abnormally activated cyclin-CDK complexes and to reactivate p53 phosphoprotein became a new therapeutic option. The reactivation of p53 in malignant cells can inhibit cell cycle progression by multiple pathways and may additionally promote the induction of apoptosis. Considering the fact that p53 is a transcription factor, it may transactivate a number of pro-apoptotic and repress some anti-apoptotic genes. Survivin, a member of a big protein family of inhibitors of apoptosis (IAPs) has a double face: it regulates important events during mitosis and simultaneously counteracts the action of Smac/DIABLO. In this way survivin prevents mitotic cells from inducing apoptosis. Interestingly, p53 is known to repress the expression of survivin. Pharmacological inhibition of CDKs preventing phosphorylation of survivin results in its down-regulation by accelerated degradation, thereby facilitating initiation of apoptosis in cancer cells. Cyclin-dependent kinases (CDKs) play a key role in orchestrating the coordination of cell cycle progression in proliferating cells. The escape from the proper control of the cell cycle by upregulation of cyclins or aberrant activation of CDKs leads to malignant transformation. Proteins encoded by tumor suppressor genes such as p53 and cellular inhibitors of CDKs e.g. p16INK4a, p21Waf1/Cip1/Sdi, and p27Kip1 are able to counteract the deregulated cell cycle progression and to inhibit rapid (uncontrolled) cell proliferation. However, in the majority of cancer tissues tumor suppressors are inactivated or mutated. Virally encoded proteins e.g. E6 oncoprotein inactivate p53 by its accelerated proteolytic degradation. Therefore, use of synthetic compounds that are able to inhibit the abnormally activated cyclin-CDK complexes and to reactivate p53 phosphoprotein became a new therapeutic option. The reactivation of p53 in malignant cells can inhibit cell cycle progression by multiple pathways and may additionally promote the induction of apoptosis. Considering the fact that p53 is a transcription factor, it may transactivate a number of pro-apoptotic and repress some anti-apoptotic genes. Survivin, a member of a big protein family of inhibitors of apoptosis (IAPs) has a double face: it regulates important events during mitosis and simultaneously counteracts the action of Smac/DIABLO. In this way survivin prevents mitotic cells from inducing apoptosis. Interestingly, p53 is known to repress the expression of survivin. Pharmacological inhibition of CDKs preventing phosphorylation of survivin results in its down-regulation by accelerated degradation, thereby facilitating initiation of apoptosis in cancer cells.
dcterms:title
Control of the proper cell cycle progression by products of the tumor suppressor gene p53 and inhibitors of cyclin-dependent kinases. Use of pharmacological inhibitors mimicking the action of cell cycle regulators for cancer therapy Control of the proper cell cycle progression by products of the tumor suppressor gene p53 and inhibitors of cyclin-dependent kinases. Use of pharmacological inhibitors mimicking the action of cell cycle regulators for cancer therapy
skos:prefLabel
Control of the proper cell cycle progression by products of the tumor suppressor gene p53 and inhibitors of cyclin-dependent kinases. Use of pharmacological inhibitors mimicking the action of cell cycle regulators for cancer therapy Control of the proper cell cycle progression by products of the tumor suppressor gene p53 and inhibitors of cyclin-dependent kinases. Use of pharmacological inhibitors mimicking the action of cell cycle regulators for cancer therapy
skos:notation
RIV/61989592:15310/08:00005285!RIV13-MSM-15310___
n3:aktivita
n4:Z n4:P
n3:aktivity
P(GA204/08/0511), Z(AV0Z50380511), Z(MSM6198959216)
n3:dodaniDat
n8:2013
n3:domaciTvurceVysledku
n9:9961216
n3:druhVysledku
n14:C
n3:duvernostUdaju
n20:S
n3:entitaPredkladatele
n18:predkladatel
n3:idSjednocenehoVysledku
361255
n3:idVysledku
RIV/61989592:15310/08:00005285
n3:jazykVysledku
n13:eng
n3:klicovaSlova
Cyclin-dependent kinase, cancer, roscovitine, cell cycle, inhibitor, p53
n3:klicoveSlovo
n15:Cyclin-dependent%20kinase n15:cancer n15:inhibitor n15:p53 n15:roscovitine n15:cell%20cycle
n3:kontrolniKodProRIV
[8F8B1114436C]
n3:mistoVydani
Kerala, India
n3:nazevZdroje
Trends in Cell Cycle Research
n3:obor
n19:EB
n3:pocetDomacichTvurcuVysledku
1
n3:pocetStranKnihy
317
n3:pocetTvurcuVysledku
7
n3:projekt
n11:GA204%2F08%2F0511
n3:rokUplatneniVysledku
n8:2008
n3:tvurceVysledku
Kryštof, Vladimír Krammer, Matthias Schmid, Gerald Komina, Oxana Węsierskia-Gądek, Józefa Wandl, Stefanie Maurer, Margarita
n3:zamer
n7:MSM6198959216 n7:AV0Z50380511
s:numberOfPages
44
n5:hasPublisher
Research Signpost
n17:isbn
978-81-308-0274-9
n12:organizacniJednotka
15310