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Human Cyclin-Dependent Kinase Inhibitor 1B (p27, Kip1) (CDKN1B) interaction partners

1. we have analyzed p27 protein expression in early stage HER2-positive breast cancers from women who had been enrolled into the HERA trial. We have demonstrated that, by using a predefined cutoff, low p27 expression may be associated with benefit from adjuvant trastuzumab treatment.

2. The knockdown of cyclin-dependent kinase inhibitor p27 (p27kip1) relieves the suppression of cell migration in triple-negative breast cancer(TNBC). The up-regulated expression of LAPTM4B together with the down-regulated expression of p27kip1 classifies a group of breast cancer patients with poor prognosis, consequently considered as a potentially prognostic marker and candidate target for therapeutic intervention of TNBC.

3. Cyclin-dependent kinase inhibitor 1B (CDKN1B) was identified as a direct target of negative regulation by miR-222-3p in NP cells, and expression of miR-222-3p was found to be negatively correlated with that of CDKN1B in intervertebral disc degeneration tissue.

4. Results indicated that WAVE2 and ACTN4 were necessary for the regulation of p27 phosphorylation. Also, WAVE2 and p27 cooperatively promote the motility and invasiveness of pancreatic ductal adenocarcinoma cells.

5. p27 regulated the cell cycle and inhibited cell proliferation by affecting formation of the cell cycle-dependent complex CDK6/CCND1, but did not directly affect the expression of CDK6 and CCND1.

6. HuD enhanced p27 mRNA translation by interacting with both the 5'-untranslated region (UTR) and the 3'-UTR of p27 mRNA, and consequently suppressed cell cycle progression and growth of pancreatic neuroendocrine tumors.

7. ER stress treatment generates a marginal increase in Gp78 endogenous levels, and this elevation effect was prominent for intracellular accumulation of p27 in cells. Taken together, our current findings suggest a valuable multifactorial regulatory mechanism and linkage of p27 with UPS pathway

8. genetic polymorphism of GAS5 may influence the development of gastric cancer and so could be a new marker of this disease. The link with disease may involve p27Kip1 expression.

9. This is the first report of AC026166.2-001 acting as a tumor suppressor in laryngeal squamous cell carcinoma by regulating the miR-24-3p/p27 axis.

10. UBCH7/UBE2L3 catalyzes the conjugation of heterotypic ubiquitin chains on p27(Kip1) that are proteolytically incompetent

11. our findings suggested that miR-222 may promote the progression of polycystic ovary syndrome by targeting p27 Kip1.

12. These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)

13. Study found that PSMD2 was markedly upregulated in breast cancer. High PSMD2 expression was significantly correlated with poor prognosis. PSMD2 knockdown inhibited cell proliferation and arrested cell cycle at G0/G1 phase in vitro, as well as suppressed tumor growth in vivo. Mechanically, PSMD2 physically interacted with p21 and p27 and mediated their ubiquitin-proteasome degradation with the cooperation of USP14.

14. BAP31 levels were significantly increased in tumor tissues from patients with gastric intestinal-type adenocarcinoma. Study in gastric cancer cell lines and mouse xenograft model found that BAP31 could combine with p27kip1 and regulate its proteasome degradation.

15. PHLPP2 stabilization by p27 mediates its inhibition of bladder cancer invasion by promoting autophagic degradation of MMP2 protein.

16. Theaflavin-3,3'-digallate (TF3) up-regulated the expression of p27 to induce G0/G1 cell cycle arrest in OVCAR-3 cells. Our study indicated that Chk2 and p27 were vital anticancer targets of TF3 and provided more evidence that TF3 might be a potent agent to be applied as adjuvant treatment for ovarian cancer.

17. Global analysis of p27 and cJun chromatin binding and gene expression shows that cJun recruitment to many target genes is p27 dependent, increased by p27 phosphorylation, and activates programs of epithelial-mesenchymal transformation and metastasis.

18. our results suggest that p27 may participate in the regulation of mitotic progression in a CDK-independent manner by modulating PRC1 activity.

19. Study shows that Cdk2/cyclin A-bound p27 samples lowly-populated conformations that provide access to the BCR-ABL and Src kinases promoting intra-assembly phosphorylation of p27 on distal T187. Even when tightly bound to Cdk2/cyclin A, intrinsic flexibility enables p27 to integrate and process signaling inputs, and generate outputs including altered Cdk2 activity, p27 stability, and, ultimately, cell cycle progression.

20. HP plays an important role in the development and progression of GC through silencing of CDH1, RUNX3, p21WAF and p27 expression

Zebrafish Cyclin-Dependent Kinase Inhibitor 1B (p27, Kip1) (CDKN1B) interaction partners

1. The retinoic acid pathway is activated in hair cell loss an regulates p27kip in hair cell regeneration.

Cow (Bovine) Cyclin-Dependent Kinase Inhibitor 1B (p27, Kip1) (CDKN1B) interaction partners

1. p27Kip1 inhibition has an effect on proliferation of bovine corneal endothelial cells by RNA interferenc

Pig (Porcine) Cyclin-Dependent Kinase Inhibitor 1B (p27, Kip1) (CDKN1B) interaction partners

1. FoxO1a can regulate p27kip nuclear localization

2. 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.

Mouse (Murine) Cyclin-Dependent Kinase Inhibitor 1B (p27, Kip1) (CDKN1B) interaction partners

1. p27(Kip1) stabilizes the alpha-tubulin acetyltransferase 1, thereby promoting the acetylation of microtubules, a post-translational modification required for proper axonal transport.

2. Study generated a knock-in mouse model in which T197 of p27 is replaced by an alanine (Cdkn1bT197A) to study the long-term effects of restoring p27 levels in vivo. Cdkn1bT197A/T197A mice present increased body size, organomegaly, and hyperplasia in multiple organs. This is an important model to study a variety of human proliferative disorders caused by increased turnover of p27 protein.

3. HuD enhanced p27 mRNA translation by interacting with both the 5'-untranslated region (UTR) and the 3'-UTR of p27 mRNA, and consequently suppressed cell cycle progression and growth of pancreatic neuroendocrine tumors.

4. the AMPK/p27(Kip1) pathway likely regulates the autophagy/apoptosis balance in aged MuSCs and may be a potential target for improving muscle regeneration in older individuals.

5. Findings indicate that p27Kip1 is central for the decreased proliferation at lower temperature, since p27Kip1 KO mouse embryonic fibroblasts (MEFs) hardly increased their doubling time in cold conditions, whereas wild-type MEFs significantly delayed proliferation in response to cold stress.

6. defective p27-phospho-S10 modifies endothelial behavior and promotes aneurysm formation via COX-2 activation.

7. Our results reveal both major pathways of p27(Kip1) degradation are required for the accelerated Burkitt lymphoma (BL) development driven by LMP2A in our BL model.

8. The data characterize mitochondrial p27 as a common denominator that improves mitochondria-dependent processes and define an increase in mitochondrial p27 as a new mode of action of caffeine.

9. 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.

10. 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

11. 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.

12. Specifically, the proteins p18INK4C, p21CIP1 and p27KIP1 seem to play an outstanding role in the maintenance of the differentiated state of adipocytes.

13. 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.

14. Our results revealed that CKS1 is involved in normal glutamatergic synapse development and dendritic spine maturation in adult hippocampus through modulating p27 stability.

15. 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.

16. p27(Kip1)-target genes are involved in cell adhesion and cell signaling in mouse embryonic fibroblasts.

17. 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.

18. 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.

19. Our findings demonstrate a direct role for microRNAs in controlling the rate of liver regeneration after injury.

20. 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.