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• W2045685311 abstract "Induction of cyclin D2 is essential for mediating cell cycle entry in B cells activated by BCR cross-linking. In the present study we show that, like B lymphocytes lacking cyclin D2, the p85α subunit of phosphatidylinositol 3-kinase (PI3K) or other components of the B cell signalosome, p110δ-null B cells fail to induce cyclin D2 and enter early G1 but not S phase of the cell cycle. The inhibitors of PI3K activity, LY294002 and Wortmannin, also abrogate cyclin D2 induction by BCR cross-linking, confirming that the class IA PI3K is necessary for cyclin D2 induction in response to BCR stimulation. Furthermore, using both p85α-null and p110δ-null B cells and inhibitors of PI3K, this study demonstrates for the first time, that BCR cross-linking induces cyclin D2 mRNA expression via transcriptional activation of the cyclin D2 promoter and that this transcriptional activation of cyclin D2 requires PI3K activity. Moreover, we identify a region between nucleotides -1624 and -1303 of the cyclin D2 promoter containing elements responsive to anti-IgM, which are PI3K dependent. Further characterisation of signalling intermediates downstream of the BCR revealed a perturbation of MAPK signalling pathways in p85α-null and p110δ-null B cells, and our data suggests that cross-talk exists between the PI3K and JNK pathways." @default.
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• W2045685311 date "2005-09-01" @default.
• W2045685311 modified "2023-09-26" @default.
• W2045685311 title "Phosphatidylinositol 3-kinase is required for the transcriptional activation of cyclin D2 in BCR activated primary mouse B lymphocytes" @default.
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• W2045685311 doi "https://doi.org/10.1002/eji.200425812" @default.
• W2045685311 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16114097" @default.
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