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Cholangiocarcinoma growth is associated with nuclear export of P27 (show PAK2 Proteins) that is due to AKT (show AKT1 Proteins)-mediated phosphorylation of P27 (show PAK2 Proteins) at T157.
Multiple function of p27 (show PAK2 Proteins) in cell cycle regulation, apoptosis, epigenetic modifications and post- translational modification are reviewed, and the mechanisms and factors that have important roles in p27 (show PAK2 Proteins) functions are briefly discussed.
Data show that fluid shear stress activates NOTCH (show NOTCH1 Proteins) signaling, which upregulates GJA4 (show GJA4 Proteins) (commonly, Cx37 (show GJA4 Proteins)) and downstream cell cycle inhibitor CDKN1B (p27).
High KIP1 expression is associated with multiple endocrine neoplasia type 1-related pancreatic neuroendocrine tumors.
Meta-analysis failed to validate any association between p27 (show PAK2 Proteins)-V109G and prostate cancer risk.
Data suggest a close association between the nonfunctionality of ATM (show ATM Proteins)/p53 (show TP53 Proteins) pathway and accumulation of p27Kip1 in chronic lymphocytic leukemia (CLL) cells in response to DNA damage.
after irradiation, loss of p27 (show PAK2 Proteins) is associated to accumulation of residual DNA damage and increased number of mitotic aberration. We show that p27 (show PAK2 Proteins) expression is necessary to preserve genomic integrity and for correct recognition and clearing-out of aberrant cells.
FoxO3a (show FOXO3 Proteins) overexpression increased the transcription and protein expression of Bcl2like protein 11 and cyclindependent kinase inhibitor 1B, and inhibited cyclin D1 (show CCND1 Proteins) transcription and expression.
Results suggest that CacyBP/SIP (show CACYBP Proteins) plays an important role in inhibiting glioma cell migration and invasion through promoting the degradation of cytoplasmic p27 (show PAK2 Proteins).
The functional variant rs34330 of CDKN1B is associated with risk of neuroblastoma (show ARHGEF16 Proteins).
p27Kip1 inhibition has an effect on proliferation of bovine corneal endothelial cells by RNA interferenc
FoxO1a (show FOXO1 Proteins) can regulate p27kip nuclear localization
the activation of Rac1 due to the cell-cell contact plays a critical role in the transcriptional up-regulation of p27Kip1 in vascular endothelial cells.
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.
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
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 (show RHOA Proteins) signaling.
Specifically, the proteins p18INK4C (show CDKN2C Proteins), p21CIP1 (show CDKN1A Proteins) and p27KIP1 seem to play an outstanding role in the maintenance of the differentiated state of adipocytes.
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.
Our results revealed that CKS1 (show CKS1B Proteins) is involved in normal glutamatergic synapse development and dendritic spine maturation in adult hippocampus through modulating p27 stability.
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.
p27(Kip1)-target genes are involved in cell adhesion and cell signaling in mouse embryonic fibroblasts.
This study demonstrates that LMP2A uses the role of MYC (show MYC Proteins) in the cell cycle, particularly in the p27(kip1) degradation process, to accelerate lymphomagenesis in vivo.
Study reports that p27 normally exerts a negative feedback on p21 expression: p27 directly represses the expression of the transcription factor Pitx2 (show PITX2 Proteins) which in turn maintains decreased p21 levels. Consequently, in cells lacking p27, de-repression of Pitx2 (show PITX2 Proteins) causes the up-regulation of p21 showing a new mechanism by which p27 regulates cell cycle progression by transcriptionally regulating the expression of Pitx2 (show PITX2 Proteins) and p21.
This gene encodes a cyclin-dependent kinase inhibitor, which shares a limited similarity with CDK inhibitor CDKN1A/p21. The encoded protein binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. The degradation of this protein, which is triggered by its CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes, is required for the cellular transition from quiescence to the proliferative state.
cyclin-dependent kinase inhibitor 1B
, cyclin-dependent kinase inhibitor 1b (p27, kip1)
, cyclin-dependent kinase inhibitor 1B (p27, Kip1)
, cyclin-dependent kinase inhibitor p27
, Cyclin-dependent kinase inhibitor 1B (p27 Kip1)
, Cyclin-dependent kinase inhibitor 1B (p27, Kip1)
, cyclin-dependent kinase inhibitor p27/Kip1
, Cyclin-dependent kinase inhibitor p27
, cyclin-dependent kinase inhibitor 1b, like