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expressions of p27(Kip1) and CaSR were decreased in primary hyperparathyroidism patients
the p27 gene rs34330 polymorphism might increase the cancer susceptibility, especially in Asians.
our study identified that p27 expression was transcriptionally upregulated by enhancing the binding of FOXO1 to its promoter and post-transcriptionally induced through decreasing binding of miR-182 to its mRNA 3'-UTR upon isorhapontigenin treatment
Cholangiocarcinoma growth is associated with nuclear export of P27 that is due to AKT-mediated phosphorylation of P27 at T157.
Multiple function of p27 in cell cycle regulation, apoptosis, epigenetic modifications and post- translational modification are reviewed, and the mechanisms and factors that have important roles in p27 functions are briefly discussed.
Data show that fluid shear stress activates NOTCH signaling, which upregulates GJA4 (commonly, Cx37) 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-V109G and prostate cancer risk.
Data suggest a close association between the nonfunctionality of ATM/p53 pathway and accumulation of p27Kip1 in chronic lymphocytic leukemia (CLL) cells in response to DNA damage.
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.
FoxO3a overexpression increased the transcription and protein expression of Bcl2like protein 11 and cyclindependent kinase inhibitor 1B, and inhibited cyclin D1 transcription and expression.
Results suggest that CacyBP/SIP plays an important role in inhibiting glioma cell migration and invasion through promoting the degradation of cytoplasmic p27.
The functional variant rs34330 of CDKN1B is associated with risk of neuroblastoma.
FLT3 and FLT3-ITD can directly bind and selectively phosphorylate p27kip1 on tyrosine residue 88 in acute myeloid leukemia. Inhibition of FLT3-ITD in cell lines strongly reduced p27 tyrosine 88 phosphorylation and resulted in increased p27 levels and cell cycle arrest
Our results suggest that oxidised photoreceptor outer segments -induced retinal pigment epithelial cell cytokinesis failure is, at least in part, due to the upregulation of p27kip1 through activating the PKC, particularly PKCzeta pathway
p27Kip1-838C>A; rs36228499 is functional in human venous smooth muscle cells (SMCs) and in adventitial cells. The AA genotype is associated with stronger expression of the p27 gene and p27 protein. Only the adventitial cells, and not the SMCs, are responsive to the inhibitory effects of the protective AA genotype in cell growth.
Overview of CDKN1B mutations in MEN4 (review)
Expression of CIP/KIP proteins was found abundantly within the proliferative hair matrix, concomitant with a role in cell cycle checkpoint control. p21(CIP1), p27(KIP1) and cyclin E persisted within post-mitotic keratinocytes of the pre-cortex, whereas p57(KIP2) protein decreased but became nuclear.
Taken together, these data clearly show that FKBP3/Sp1/HDAC2/p27 control cell proliferation during non-small cell lung cancer development.
Sumoylation of K73 site of cyclin-dependent kinase inhibitor 1B (p27kip1) is critical to the nuclear-cytoplasmic translocation of p27kip1, which is mediated by RAN binding protein 2 and CRM1 protein. Sumoylation of p27kip1 promotes the proliferation of cholangiocarcinoma QBC939 cells
The retinoic acid pathway is activated in hair cell loss an regulates p27kip in hair cell regeneration.
p27Kip1 inhibition has an effect on proliferation of bovine corneal endothelial cells by RNA interferenc
FoxO1a 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.
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 signaling.
Specifically, the proteins p18INK4C, p21CIP1 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 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 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 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.
Our findings demonstrate a direct role for microRNAs in controlling the rate of liver regeneration after injury.
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.
systems-level control of cell cycle arrest by pRB-E2F and p27-CDK regulation, is reported.
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.
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
Knockout of p27 enhances arterial collateralization in response to hindlimb ischemia through enlargement of a new collateral pathway.
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.
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.
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
The down-regulation of p27 and the activation of mTOR pathway may be involved in miR-222-induced heart failure and autophagy inhibition.
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