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Cyclin D1 is indispensable for normal hematopoiesis; in its absence, cyclins D2 and D3 are also not expressed, preventing hematopoietic cell division and differentiation at its earliest stage. The results demonstrate that not all functions of individual D cyclins are redundant, and highlight a master role of cyclin D1 in hematopoiesis.
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These results suggest that progesterone receptor overexpression in endometrial stromal cells, likely due to high progesterone levels, triggers cyclin D3 and Hoxa-10 overexpression, which may be involved in the pathological mechanisms of the mouse uterine decidual reaction.
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the activation of TLR7 increased CCND3 expression via the downregulation of miR-15b in B cells.
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immature B and T cells use lymphocyte lineage- and developmental stage-specific mechanisms to inhibit Cyclin D3 protein levels.
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we suggest that proper regional decidualization and polyploidy development requires FoxM1 signaling downstream of Hoxa10 and cyclin D3.
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Cyclin D3 protein that drives immature T cell proliferation is essential for transformation of Atm-deficient thymocytes
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DYRK1A has a role in lymphopoiesis; Cyclin D3 protein stability is negatively regulated during exit from the proliferative phases of B and T cell development
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inactivation of Ccnd3 leads to increased frequencies of lymphocytes with biallelic expression of IgH or TCRbeta genes.
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FGF2 signaling results in the phosphorylation of Erk1/2, and activation of c-Fos and c-Jun that lead to elevated cyclin D mRNA levels.
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Results indicate that cyclin D3 plays a cell-autonomous and nonredundant function in regulating the dynamic balance between proliferation, differentiation, and self-renewal that normally establishes an appropriate pool size of adult satellite cells.
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Investigated the expression of GABA and GABPR in the early-pregnancy mouse uterus. Cyclin D3 was measured in cultured stromal cells artificially induced to undergo decidualization, by GABA and a GABA A-type receptor agonist or antagonist.
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Subnuclear compartmentalization enables cyclin D3 to drive cell cycle progression and repress V gene accessibility, thereby ensuring coordination of proliferation with immunoglobulin recombination.
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cyclin D3 expression influences a host of genes involved in decidualization and can improve decidualization in Hoxa-10(-/-) mice.
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CCND3 gene product cyclin D3 regulates the number of cell divisions that erythroid precursors undergo during terminal differentiation
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Simultaneous ablation of cyclin D1 and downregulation of cyclin D2 via cyclin D3 expression resulted in a robust reduction in ras-mediated skin tumorigenesis.
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Cyclin D3 primes myoblasts for differentiation by enhancing muscle specific gene expression and cell cycle exit.
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Bcl2, Myc and Ccnd1 or Bcl2, Myc and CCND3 synergistically transformed mouse primary B cells into aggressive malignant cells.
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Ccnd3(-/-) mice exhibit a B-cell-intrinsic defect in germinal center maturation and fail to generate an affinity-matured IgG response. The defect resulted from failed proliferative expansion of GL7(+) IgD(-) PNA(+) B cells.
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Stimulating mitogenesis of Swiss 3T3 cells with phorbol esters or forskolin can induce divergent responses in the expression levels, localization and activation state of cyclin D1 and cyclin D3.
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coordinate expression and functional association of cyclin D3 with cdk4 suggest a role for proliferation and, that of cyclin D3 with p21 and cdk6 is consistent with the development of polyploidy during stromal cell decidualization
