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However, expression of the cell cycle regulatory machinery including cyclin-dependent kinases (CDKs) and CDK inhibitors (CDKIs) persists into adulthood .
The growth, differentiation, and survival of HSC have been shown to depend on the relative basal expression level of cyclins, cyclin-dependent kinases (cdks), and cdk-inhibitors (cdkis) [25,44].
Despite requiring phosphorylation, CDK-cyclin complexes are kept inactivated by binding to a CDK inhibitor (CDKI).
Aparte de la determinacion del tamano telomerico y el metodo de senescencia asociada a la enzima [beta]-gal (SA-[beta]Gal) actualmente se emplean otro tipo de marcadores clasificados en: elementos de las vias de transduccion de senales que mantienen fenotipos senescentes, como las proteinas reguladoras de CDKIs: p16 o p21; marcadores de estres genotoxico; secrecion de citoquinas inflamatorias, entre otros (Campisi, 2005; Campisi y d'Adda di Fagagna, 2007; Jeyapalan y Sedivy, 2008), pero estos no son tan especificos y requieren de otros ensayos que los soporten.
We sought to examine the expression of the cyclin-dependent kinase inhibitors (CDKIs) [p21.sup.WAF1] and [p27.sup.KIP1], to determine the extent of their expression by immunohistochemistry and their possible association with histologic subtype.
Other studies in U251 GBM cells show that p53 expression is upregulated by curcumin treatment, as were CDKi [p21.sup.Waf1/Cip1] (p21) and ING4--a tumor suppressor gene that has been found to be suppressed in gliomas [36,37].
In stomach carcinoma cell model, an ethanol extract of Rhus verniciflua Stokes significantly inhibited [G.sub.1] cell cycle progression via [p27.sup.Kip1] CDKI upregulation and induced mitochondrial apoptosis through the increment of Bax expression, the inhibition of Bcl-2 expression, the release of cytochrome c, and the activation of caspase-3 and caspase9 cascade, and this mechanism by Rhus verniciflua Stokes was an enhanced inhibition of the PI3K-Akt/PKB survival pathway [11,13].
In addition, IGF-IR can also down-regulate the transcription of the cyclin dependent kinase (CDK) inhibitor (CDKI) p27KIP1 or alter its processing and nuclear localization through a PI-3 K/Akt and phosphatase and tensin homologous on chromosome 10 (PTEN)-dependent mechanism (Samani et al., 2007).
More recent data have shown that CDK inhibitors (CDKi) drive granulocyte apoptosis and resolve inflammation by downregulating Mcl-1 and upregulating proapoptotic proteins such as Bim [24, 26, 27, 29-31].
The cyclin dependent kinases (CDKs) are important components of the cell cycle machinery, and are positively regulated by cyclins and negatively regulated by cyclin dependent kinase inhibitors (CDKIs) .
The SA-miRNAs control cell transition, mainly through the [G.sub.1]/S checkpoint during cell cycle progression by targeting the components of cell cycle including cyclin-dependent kinases (CDKs) and cyclin-dependent kinase inhibitors (CDKIs) .
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- CDK4 gene
- CDK4 gene
- CDK4 inhibitor p16-INK4, INK4a
- CDK4B inhibitor
- CDK5-Binding Protein
- CDK6 inhibitor p18
- CDK8 protein kinase
- CDK8-like cyclin-dependent kinase
- CDK9-associated C-type protein