| Attributes | Values |
|---|
| rdf:type
| |
| 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. (en)
|
| 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 (en)
|
| 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 (en)
|
| skos:notation
| - RIV/61989592:15310/08:00005285!RIV13-MSM-15310___
|
| http://linked.open...avai/riv/aktivita
| |
| http://linked.open...avai/riv/aktivity
| - P(GA204/08/0511), Z(AV0Z50380511), Z(MSM6198959216)
|
| 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/61989592:15310/08:00005285
|
| http://linked.open...riv/jazykVysledku
| |
| http://linked.open.../riv/klicovaSlova
| - Cyclin-dependent kinase, cancer, roscovitine, cell cycle, inhibitor, p53 (en)
|
| http://linked.open.../riv/klicoveSlovo
| |
| http://linked.open...ontrolniKodProRIV
| |
| http://linked.open...i/riv/mistoVydani
| |
| http://linked.open...i/riv/nazevZdroje
| - Trends in Cell Cycle Research
|
| http://linked.open...in/vavai/riv/obor
| |
| http://linked.open...ichTvurcuVysledku
| |
| http://linked.open...v/pocetStranKnihy
| |
| http://linked.open...cetTvurcuVysledku
| |
| http://linked.open...vavai/riv/projekt
| |
| http://linked.open...UplatneniVysledku
| |
| http://linked.open...iv/tvurceVysledku
| - Kryštof, Vladimír
- Węsierskia-Gądek, Józefa
- Komina, Oxana
- Krammer, Matthias
- Maurer, Margarita
- Schmid, Gerald
- Wandl, Stefanie
|
| http://linked.open...n/vavai/riv/zamer
| |
| number of pages
| |
| http://purl.org/ne...btex#hasPublisher
| |
| https://schema.org/isbn
| |
| http://localhost/t...ganizacniJednotka
| |
| 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)