Browse our anti-CDKN1B (CDKN1B) Antibodies

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

1. 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.

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

3. 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.

4. 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.

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

6. 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.

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

8. Rapamycin treatment increased the level of the p27(KIP1) cyclin-dependent kinase inhibitor, and rapamycin-induced ciliogenesis was abrogated in p27(KIP1)-depleted cells. These results indicate that mTORC1 inactivation induces ciliogenesis through p27(KIP1) upregulation, but not through autophagy.

9. we firstly demonstrate that BCRC-3 is down-regulated in BC tissues and cell lines for the first time. BCRC-3 is capable of functioning as ceRNA for miR-182-5p to regulate the expression of p27.

10. Our findings demonstrate that circYAP1 functions as a tumor suppressor in GC cells by targeting the miR-367-5p/p27 (Kip1) axis and may provide a prognostic indicator of survival in GC patients.

11. P27 expression is regulated by ARHGAP17 in cervical cancer.ARHGAP17 elevated P27 expression level through inhibiting PI3K/AKT signaling pathway.

12. MUC-1, CK7, and c-p27 immunostaining can be used as the predictive markers for esophageal cancer progression from Barrett's esophagus.

13. High KIP1 expression is associated with acute lymphoblastic leukemia.

14. c-Myc was demonstrated to drive OVAAL transcription, indicating a positive feedback loop between c-Myc and OVAAL in controlling tumor growth. OVAAL contributes to the survival of cancer cells through dual mechanisms controlling RAF/MEK/ERK signaling and p27-mediated cell senescence.

15. VEGF, COX-2, and p27 may be important biological markers that determine the angiogenic and lymphangiogenic potentials of papillary thyroid carcinoma, particularly between the follicular and classic variants.

16. expressions of p27(Kip1) and CaSR were decreased in primary hyperparathyroidism patients

17. the p27 gene rs34330 polymorphism might increase the cancer susceptibility, especially in Asians.

18. 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

19. Cholangiocarcinoma growth is associated with nuclear export of P27 that is due to AKT-mediated phosphorylation of P27 at T157.

20. 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.

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. 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.

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

3. 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.

4. 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.

5. 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.

6. 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

7. 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.

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

9. 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.

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

11. 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.

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

13. 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.

14. 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.

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

16. 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.

17. systems-level control of cell cycle arrest by pRB-E2F and p27-CDK regulation, is reported.

18. 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.

19. 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

20. Knockout of p27 enhances arterial collateralization in response to hindlimb ischemia through enlargement of a new collateral pathway.