Carbon nanoparticle induced cytotoxicity in human mesenchymal stem cells through upregulation of TNF3, NFKBIA and BCL2L1 genes.
Riyadh, Saudi Arabia. In Chemosphere, Feb 2016
Furthermore, the expression of genes involved in both cell death (e.g., P53, TNF3, CDKN1A, TNFRSF1A, TNFSF10, NFKBIA, BCL2L1) and cell cycle regulation (e.g., PCNA, EGR1, E2F1, CCNG1, CCND1, CCNC, CYCD3) were assessed using qPCR.
Mediator kinase module and human tumorigenesis.
San Antonio, United States. In Crit Rev Biochem Mol Biol, 2014
In humans, MED13, MED12, CDK8 and Cyclin C (CycC) comprise a four-subunit "kinase" module that exists in variable association with a 26-subunit Mediator core.
Targeting cell cycle regulators in hematologic malignancies.
Phoenix, United States. In Front Cell Dev Biol, 2014
The present review focuses on selected cell cycle kinases with recent emerging key functions in hematopoiesis and in hematopoietic malignancies, such as CDK6 and its role in MLL-rearranged leukemia and acute lymphocytic leukemia, CDK1 and its regulator WEE-1 in acute myeloid leukemia (AML), and cyclin C/CDK8/CDK19 complexes in T-cell acute lymphocytic leukemia.
Cyclin C surprises in tumour suppression.
Madrid, Spain. In Nat Cell Biol, 2014
Cyclin C and its associated kinases Cdk3, Cdk8 and Cdk19 are now shown to function as tumour suppressors in haematopoietic malignancies by inhibiting the Notch1 pathway.
Involvement of Mediator complex in malignancy.
Napoli, Italy. In Biochim Biophys Acta, 2014
Particularly, the role of MED1, MED28, MED12, CDK8 and Cyclin C in cancer is well documented, although several studies have recently reported a possible association of other subunits with malignancy.
Dysregulation of CDK8 and Cyclin C in tumorigenesis.
Lafayette, United States. In J Genet Genomics, 2011
Here we focus our discussion on two subunits of the Mediator complex, cyclin-dependent kinase 8 (CDK8) and its regulatory partner Cyclin C (CycC), because they are either mutated or amplified in a variety of human cancers.
Cyclin C/cdk3 promotes Rb-dependent G0 exit.
Boston, United States. In Cell, 2004
A cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and this phosphorylation is required for cells to exit G0 efficiently.
TFIIH is negatively regulated by cdk8-containing mediator complexes.
United States. In Nature, 2000
Mammalian cdk8 and cyclin C, and their respective yeast homologues, Srb10 and Srb11, are components of the RNA polymerase II holoenzyme complex where they function as a protein kinase that phosphorylates the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II (ref.