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after irradiation, loss of p27 is associated to accumulation of residual DNA damage and increased number of mitotic aberration. We show that p27 expression is necessary to preserve genomic integrity and for correct recognition and clearing-out of aberrant cells.
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Although expressed in all retinal cell types, p27 is required to maintain the quiescence of specific cell types including bipolar cells, Muller glia, and cones while it is dispensable for preventing cell cycle reentry in other cell types
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Findings demonstrate functional interplay between a transcriptional regulator and p27(kip1) to mediate neuroprogenitor cell cycle exit, as well as to promote radial migration through a molecular mechanism consistent with suppression of RhoA signaling.
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Specifically, the proteins p18INK4C, p21CIP1 and p27KIP1 seem to play an outstanding role in the maintenance of the differentiated state of adipocytes.
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Data show that both bone marrow-derived and gastric epithelial cells contribute to the increased gastric cancer susceptibility of p27-deficient Helicobacter pylori (H. pylori) -infected mice.
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Our results revealed that CKS1 is involved in normal glutamatergic synapse development and dendritic spine maturation in adult hippocampus through modulating p27 stability.
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p27kip1 is involved in the decisive step around cell-cycle exit and plays an important role in activity-regulated and functionally relevant adult hippocampal neurogenesis.
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p27(Kip1)-target genes are involved in cell adhesion and cell signaling in mouse embryonic fibroblasts.
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This study demonstrates that LMP2A uses the role of MYC in the cell cycle, particularly in the p27(kip1) degradation process, to accelerate lymphomagenesis in vivo.
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Study reports that p27 normally exerts a negative feedback on p21 expression: p27 directly represses the expression of the transcription factor Pitx2 which in turn maintains decreased p21 levels. Consequently, in cells lacking p27, de-repression of Pitx2 causes the up-regulation of p21 showing a new mechanism by which p27 regulates cell cycle progression by transcriptionally regulating the expression of Pitx2 and p21.
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Our findings demonstrate a direct role for microRNAs in controlling the rate of liver regeneration after injury.
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Fbxo7-deficient immature thymocytes failed to undergo expansion in the thymus due to a lack of Cdk6 activity, while mature T cells showed enhanced proliferative capacity upon T-cell receptor engagement due to reduced p27 levels. These studies reveal differential cell cycle regulation by Fbxo7 at different stages in T-cell development.
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systems-level control of cell cycle arrest by pRB-E2F and p27-CDK regulation, is reported.
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Results demonstrated that the addition of oncogenic mutations, such as loss of p27 or p53, promotes ovarian tumor development from the benign adenomas of germ cell-deficient ovaries.
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p27 inactivation promotes injury islet graft loss via the elevation of proliferation and inflammatory cytokines secretion in infiltrating macrophages which induced nonspecific inflammation independent of TNF-alpha/nuclear factor-kappa b pathway. T
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Knockout of p27 enhances arterial collateralization in response to hindlimb ischemia through enlargement of a new collateral pathway.
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These data illuminate a genetic pathway that initiates auditory HC regeneration and suggest p27(Kip1), GATA3, and POU4F3 as additional therapeutic targets for ATOH1-mediated auditory hair cells regeneration.
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Cdkn1b exert its effects via the inhibition of proliferation and is mediated by miR-24 and targeted by the transcription factors FOXO4 and AP4 in the peroxidasin (Pxdn) mutation-induced eye disorders, such as glaucoma.
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These results suggest that fad24 may have an important role in the S phase re-entry of quiescent C2C12 cells through the regulation of p27(Kip1) at the protein level
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The down-regulation of p27 and the activation of mTOR pathway may be involved in miR-222-induced heart failure and autophagy inhibition.
