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B cell antigen receptor-mediated activation of cyclin-dependent retinoblastoma protein kinases and inhibition by co-cross-linking with Fc gamma receptors
D. Tanguay, S. Pavlovic, MJ. Piatelli, J. Bartek, TC. Chiles,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.
NLK
Free Medical Journals
from 1998 to 1 year ago
Freely Accessible Science Journals
from 1998-01-01 to 1 year ago
Open Access Digital Library
from 1998-01-01
PubMed
10477583
Knihovny.cz E-resources
- MeSH
- Enzyme Activation immunology MeSH
- B-Lymphocytes enzymology immunology metabolism MeSH
- Cell Differentiation immunology MeSH
- Cyclin D MeSH
- Cyclin E antagonists & inhibitors biosynthesis MeSH
- Cyclin-Dependent Kinase 2 MeSH
- Cyclin-Dependent Kinase 4 MeSH
- Cyclin-Dependent Kinase 6 MeSH
- Cyclin-Dependent Kinase 9 MeSH
- Cyclin-Dependent Kinases antagonists & inhibitors biosynthesis metabolism MeSH
- Cyclins antagonists & inhibitors biosynthesis MeSH
- DNA antagonists & inhibitors biosynthesis MeSH
- Phosphorylation MeSH
- G1 Phase immunology MeSH
- Holoenzymes biosynthesis MeSH
- Immunoglobulin Fab Fragments pharmacology MeSH
- Cyclin-Dependent Kinase Inhibitor p27 MeSH
- CDC2-CDC28 Kinases * MeSH
- Mice, Inbred BALB C MeSH
- Mice MeSH
- Tumor Suppressor Proteins * MeSH
- Protein Serine-Threonine Kinases antagonists & inhibitors biosynthesis metabolism MeSH
- Microtubule-Associated Proteins biosynthesis MeSH
- Cell Cycle Proteins * MeSH
- Antibodies, Anti-Idiotypic pharmacology MeSH
- Proto-Oncogene Proteins * MeSH
- Receptors, Antigen, B-Cell antagonists & inhibitors immunology metabolism physiology MeSH
- Receptors, IgG metabolism MeSH
- Retinoblastoma Protein antagonists & inhibitors metabolism MeSH
- RNA antagonists & inhibitors biosynthesis MeSH
- Up-Regulation immunology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, U.S. Gov't, Non-P.H.S. MeSH
- Research Support, U.S. Gov't, P.H.S. MeSH
Cross-linking the B cell Ag receptor (BCR) to surface Fc receptors for IgG (Fc gamma R) inhibits G1-to-S progression; the mechanism by which this occurs is not completely known. We investigated the regulation of three key cell cycle regulatory components by BCR-Fc gamma R co-cross-linking: G1-cyclins, cyclin-dependent kinases (Cdks), and the retinoblastoma gene product (Rb). Rb functions to suppress G1-to-S progression in mammalian cells. Rb undergoes cell-cycle-dependent phosphorylation, leading to its inactivation and thereby promoting S phase entry. We demonstrate in this paper for the first time that BCR-induced Rb phosphorylation is abrogated by co-cross-linking with Fc gamma R. The activation of Cdk4/6- and Cdk2-dependent Rb protein kinases is concomitantly blocked. Fc gamma R-mediated inhibition of Cdk2 activity results in part from an apparent failure to express Cdk2 protein. By contrast, inhibition of Cdk4/6 activities is not due to suppression of Cdk4/6 or cyclins D2/D3 expression or inhibition of Cdk-activating kinase activity. Cdk4- and Cdk6-immune complexes recovered from B cells following BCR-Fc gamma R co-cross-linking are devoid of coprecipitated D-type cyclins, indicating that inhibition of their Rb protein kinase activities is due in part to the absence of bound D-type cyclin. Thus, BCR-derived activation signals that up-regulate D-type cyclin and Cdk4/6 protein expression remain intact; however, Fc gamma R-mediated signals block cyclin D-Cdk4/6 assembly or stabilization. These results suggest that assembly or stabilization of D-type cyclin holoenzyme complexes 1) is an important step in the activation of Cdk4/6 by BCR signals, and 2) suffice in providing a mechanism to account for inhibition of BCR-stimulated Rb protein phosphorylation by Fc gamma R.
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