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Validated All-in-One™ qPCR Primer for CDKN1B(NM_004064.4) Search again
Product ID:
HQP071924
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CDKN4, KIP1, MEN1B, MEN4, P27KIP1
Gene Description:
cyclin dependent kinase inhibitor 1B
Target Gene Accession:
NM_004064.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a cyclin-dependent kinase inhibitor, which shares a limited similarity with CDK inhibitor CDKN1A/p21.
Gene References into function
- Rho activity can alter the translation of p27 mRNA and is important for RasV12-induced transformation in a manner dependent on p27 status
- Inhibition of bone marrow stem cell proliferation by retinol was mediated by the up-regulation of cyclin-dependent kinase inhibitors, p21(Cip1) and p27(Kip1).
- Retinoic acid-induced cell cycle arrest of human myeloid cell lines is associated with posttranscriptional up-regulation of p27(Kip1).
- p27Kip1 integrates mitogenic MEK kinase- and PI3-kinase-dependent signals from TCR and CD28 to regulate cell cycle progression in primary T lymphocytes.
- phosphorylation on serine 10 is required for its binding to CRM1 and nuclear export
- REVIEW: gene expression regulation and role CDK inhibitor P27 in cell survival and cell cycle control in early hematopoiesis.
- low expression may be significant and independent, unfavorable prognostic factor in renal cell carcinoma
- Interleukin-11 induction of proliferation of human T-cells is associated with downregulation of p27(kip1).
- Altered p27(Kip1) phosphorylation, localization, and function in human epithelial cells resistant to transforming growth factor beta-mediated G(1) arrest
- primary hepatoblastoma well-differentiated fetal tumors without mitotic activity are strongly p27 positive
- The COP9 signalosome inhibits p27(kip1) degradation and impedes G1-S phase progression via deneddylation of SCF Cul1.
- High p27 levels detected in a subset of advanced breast carcinomas correlate with lymph node metastasis, suggesting that other mechanisms may bypass the cell cycle inhibitory role of p27 and provide growth advantage in these tumores.
- Akt promotes cell-cycle progression through the mechanisms of phosphorylation-dependent 14-3-3 binding to p27(Kip1) and cytoplasmic localization.
- The combined evaluation of p27Kip1 and Ki-67 expression provides independent information on overall survival of ovarian carcinoma patients.
- Down-regulation of p27 is associated with malignant transformation and aggressive phenotype of cervical neoplasms.
- Cell attachment to the extracellular matrix induces proteasomal degradation of p21(CIP1) via Cdc42/Rac1 signaling (P21CIP1)
- P27KIP1 colocalizes with PGP9.5 in the nucleus
- BRCA1 transactivates p27(Kip1)depending on the presence of a functional C-terminal transactivation domain. Promoter-deletion analysis identified a putative BRCA1-responsive element at position -615 to -511 of the p27(Kip1) promoter.
- expression may be an indicator of poor prognosis in adenometroid adenocarcinoma of the uterine corpus
- reduction in p27 accelerates gastrointestinal tumorigenesis in APC mutant mice, but not in SMAD3 mutant mice
- p27(Kip1) is phosphorylated on serine 10 and threonine 187 by human kinase interacting stathmin, a nuclear protein that binds the C-terminal domain of p27(Kip1) and phosphorylates S10 in vitro and in vivo, promoting its nuclear export to the cytoplasm.
- inhibits phosphorylation of retinoblastoma protein and functions as negative control in cell cycle
- Kip1 inhibits Jab1 mediated c-Jun dependent transcription
- P21Waf1 immunoreactivity is higher in male breast cancers compared with female breast cancers.
- function and clinical value of cyclin E and p27 in adult acute leukemia (AL)
- P27/Kip.1 decreased with anaplasia and was absent in glioblastomas (GBM);Skp2 was absent in well differentiated astrocytomas but was expressed in GBM. Skp2 might denote dividing cells in anaplastic gliomas or be instrumental to p27/Kip.1 degradation.
- Androgen control of p27 stability in prostate cancer cells is mediated by F-box protein SKP2.
- P27 is required to maintain TGF-beta mediated G1 arrest in cancer cell line.
- exogenous p27kip1 overexpression results in cell cycle regulation in human prostate carcinoma cells; expression associated with increase in early apoptosis
- Has prognostic value in gastric cancer
- These data indicate that Akt may contribute to tumor-cell proliferation by phosphorylation and cytosolic retention of p27(kip1), thus relieving CDK2 from p27-induced inhibition.
- Data show that activation of protein kinase B (PKB)/Akt, contributes to resistance to antiproliferative signals and breast cancer progression in part by impairing the nuclear import and action of p27.
- Data show that cytoplasmic relocalization of p27(kip1), secondary to Akt-mediated phosphorylation, inactivates the growth inhibitory properties of p27(kip1) and sustains the proliferation of breast cancer cells.
- correlates with expression of Skp2 in malignant lymphoma: correlates with proliferation index
- This study represents the first demonstration of an increased expression of p27 in cleavage-stage human arrested embryos.
- upregulation by Muc4/sialomucin
- Data show that PAX3-FKHR-expressing cells had reduced expression of p27(Kip1) protein, a key cell cycle regulator.
- The results indicate that the cell shape change caused by staurosporine correlates with the accumulation of p27kip1 and that staurosporine interferes with the p27kip1-specific proteolysis activity.
- induction of Skp2 may be causally linked with decreased levels of p27 in prostate cancer and implicate PTEN in the regulation of Skp2 expression
- These observations define a novel role for p27 in cell motility that is independent of its function in cell cycle inhibition.
- A low level of p27 expression was significantly correlated with loco-regional recurrence in nasopharyngeal carcinoma.
- Review focused on the regulation of p27 proteolysis and its consequences for tumorigenesis.
- Low p27 expression in colorectal carcinoma was significantly associated with late Dukes stage, high incidence of lymph metastasis, and distant metastasis, poor prognosis, and short survival time. p27 is an prognostic marker of colorectal carcinoma.
- In MCL lines, most p27 protein was sequestered into complexes containing cyclin D1, which renders p27 ineffective as an inhibitor of cellular growth & contributes to lymphomagenesis.
- Down-regulation of p27 is associated with early progression of head & neck squamous cell carcinoma.
- examination of protein-protein interactions involved in the recognition of p27 by E3 ubiquitin ligase
- in tumor-derived cells, p27(Kip1) could be degraded by calpains through a MAP kinase-dependent process, and abnormal cytoplasmic localization, linked to its phosphorylation state, could be involved in this alternative mechanism of degradation.
- Prolonged adenovirus-mediated expression of p27(Kip1) down-regulates integrin alphav beta5 expression on t(2;5)-anaplastic large cell lymphoma cells.
- Low expression is an independent adverse prognostic factor in patients with multiple myeloma
- Eight of 22 lymphomas with loss of p27 protein expression showed methylation in CpG island of 5' region of p27 gene. These findings suggested that gene methylation plays a role in loss of expression of p27, which gives the cells proliferative advantages.
- CDK2 activity was reduced dose-dependently after 24 h of ZD1839 treatment and this effect correlated with increased amount of p27(KIP1) and p21(CIP1/WAF1) associated with CDK2-cyclin-E and CDK2-cyclin-A complexes in head/neck squamous carcinoma cell line
- results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase
- deregulation of control mechanisms at G1/S transition by combination of high cyclin E levels in the absence of p27(Kip1) is sufficient to predispose mice to develop lymphoid malignancies and further support a role of p27(Kip1) as a tumor suppressor
- Skp2 mRNA expression level was high in squamous cell carcinomas of the lung and was inversely related with the p27(Kip1) protein level
- The sequences of p27(Kip1R) required for nuclear localization and growth inhibition were determined in HeLa cells using a green fluorescence protein (GFP) as a reporter molecule.
- PTEN and p27Kip1 have roles in tumor cell proliferation, and increased risk of recurrence
- p27Kip1 may play an important role in the invasion and metastasis of an oral cancer cell involved in regulation of E-cadherin and Tiam-1
- Inhibitor shows antitumor effect on glioma cells.
- Inducible p27(Kip1) expression inhibits proliferation of K562 cells and protects against apoptosis induction by proteasome inhibitors
- CDKN1A and CDKN1B variants are associated with advanced prostate cancer.
- results indicate that protein kinase CKII may control IkappaBalpha and p27Kip1 degradation and thereby G1/S phase transition through the phosphorylation of threonine 10 within CKBBP1 protein
- Reduced expression of p21 and p27, being VDR dependent, is major pathogenic factor for nodular parathyroid gland growth in advanced secondary hyperparathyroidism. Review.
- results show that cyclin D2 is complexed with p27, leading to a model for testicular germ cell tumors whereby the overexpression of cyclin D2 leads to the functional sequestration of p27 in the presence of CCNE and CCND2, favoring cell proliferation
- Patients with organ-confined disease but low p27 expression have a greater than fivefold risk of developing prostate-specific antigen recurrence than are men with high p27 expression; p27 may be a molecular marker associated with micrometastatic disease.
- ubiquitination is controlled by negatively charged amino acid in Skp2
- The abundance of p27 in oral leukoplakia may inhibit cell proliferation and lead premalignant tumor cells to apoptosis, and thus is concerned with prevention of tumor progression.
- Down-regulation of p27kip1 is associated with spindle-cell sarcoma
- Results suggest that p27(KIP1) contributes to the bone morphogenetic protein-induced growth arrest and neuronal differentiation of neuroblastoma cells.
- jab1 plays a role in the progression of thyroid carcinomas, especially those of aggressive phenotypes, and it may be responsible for p27 degradation in anaplastic and papillary carcinomas.
- Neuronal cytoplasmic P27 & phosphorylated p27 increase in Alzheimer's disease. Phosphorylated p27 overlaps with tau-positive neurofibrillary pathology. Dysregulation of the cell cycle plays a crucial role in the pathogenesis of Alzheimer's disease.
- hepatocyte growth factor suppresses HepG2 cell proliferation by directly increasing p27 expression and indirectly decreasing Skp2 expression.
- p27Kip1 is downregulated by estrogens in breast cancer cells through Skp2 and through nuclear export mediated by the ERK pathway
- Inhibition of Cdk2 by 1,25-(OH)2D3 may involve impairment of cyclin E-Cdk2-dependent p27Kip1 degradation through cytoplasmic mislocalization of Cdk2
- cyclin-dependent kinase inhibitor 1B plays dual role in the regulating apoptosis
- stability of p27(Kip1) by hepatitis C virus core is associated with blocking activated T cells for the G(1) to S phase transition and inhibiting T cell proliferation
- p27Kip1 levels are not affected by PTEN protein in the progression of ovarian carcinoma
- increased p27 degradation through the ubiquitin-proteasome pathway could be regulated in pituitary tumors by changes in Skp2 expression
- p27kip1 is down-regulated during rapamycin-resistant proliferation of CD8+ T cells
- TGF-beta induces apoptosis in normal thyrocytes via p27 reduction.
- Adenovirus-p27kip1 can inhibit the growth and multiplication of esophageal carcinoma cells and induce apoptosis.
- p27KIP1 has a role in down-regulation of telomerase activity
- Loss of p27 expression is associated with endometrial adenocarcinomas
- An inverse correlation between JUN and p27(Kip1) expression levels in breast cancer.
- JAB1 contributes to the progression of malignant lymphoma of the thyroid especially with aggressive phenotypes, possibly by degrading p27.
- p27kip1 protein and mRNA expression were up-regulated in myelocytes/metamyelocytes and reached peak levels in PMNs
- Overexpression of Skp2 and Jab1 is associated with the reduction of p27(KIP1) expression, and may have a role in the progression of Oral Squamous Cell Carcinoma.
- In conclusion, tissue expression of p27 is a significant predictor of 5-year survival in stage I-II pancreatic adenocarcinoma
- In various human cancers, the reduced p27Kip1 expression correlates well with poor prognosis
- regulated by Epstein-Barr virus nuclear antigen 3C (EBNA3c) during primary B cell transformation
- p27(Kip1) protein has a role in progression of Wilms' tumor
- p27kip1 has a role in progression of Ewing's family tumors
- Expression of p27Kip1 is down-regulated while oxidative DNA damage increases during cervical carcinogenesis. Both parameters are altered at early stages of the process and might help to predict patients at high risk of progression.
- p27(kip-1) is an indicator of poor prognosis in colorectal adenocarcinoma.
- p27 has nascent secondary structure that may have a function in molecular recognition
- A polymorphism in the CDKN1B gene is associated with increased risk of hereditary prostate cancer
- p27(KIP1) phosphorylation by CK2 probably involves a docking event mediated by the CK2beta subunit.
- The classical bipartite-type basic amino-acid cluster and the two downstream amino acids of the C-terminal region of p27 function as a nuclear localization signal for its full nuclear import activity.
- The expression patterns of cyclin D1, cyclin E, p21/waf1 and p27/kip1 in inflammatory bowel disease (IBD) may indicate their contribution in epithelial cell turnover and their possible implication in IBD-related dysplasia-carcinoma.
- Vitamin d3 receptor is involved in the induction of p27Kip1 by vitamin D3.
- the Skp2-p27kip1 pathway and the G1/S transition are regulated by RhoA, mDia, and ROCK
- results suggest that p27 underexpressing in patients with hepatocellular carcinoma is closely associated with infiltration, metastasis, and prognosis; alterations in the subcellular localization of p27 protein may occur early during hepatocarcinogenesis
- Low levels of p27 in primary and metastatic melanoma cases may explain the high proliferation rate of such lesions.
- VEGF together with pRb2/p130 may have a role in hepatocellular carcinoma in a p27((KIP1))-independent manner
- the role of p27 in at least some differentiation pathways of mES cells is to prevent apoptosis, and it is not involved in slowing cell cycle progression; also the pro-survival function of p27 is realized via regulation of metabolism of D-type cyclin(s).
- loss of p27 expression is associated with endometrial carcinogenesis
- cyclin A-cdk2 plays an ancillary noncatalytic role in the ubiquitination of p27(KIP1) by the SCF(skp2) complex
- the V109G polymorphism of the p27 gene may have a role in progression of oral squamous cell carcinoma
- hypoxia-mediated cell-cycle arrest may be mediated by p27 up-regulation
- v-cyclin and p27(KIP1) stably associate in primary effusion lymphoma cells
- Cytoplasmic mislocalization of p27Kip1 protein is associated with constitutive phosphorylation of Akt resulting in acute myelogenous leukemia
- Down Regulation of P27KIP1 is associated with benign prostatic hyperplasia
- The ad-p27wt induced cell cycle arrest at the G1-S transition point, whereas the ad-p27mt induced arrest at the G2-M point. Both ad-p27wt and ad-p27mt induced a growth-inhibiting effect, apoptosis, and suppression of in vitro tumorigenicity.
- p27 binds to tuberin and is regulated by SCFSkp2
- sequence requirement for N-terminal cleavage and the proteasomal degradation of p27Kip1 and their relationship was investigated
- Akt activation promotes cell cycle progression through inactivation of p27 in anaplastic large cell lymphoma.
- demonstrate genetically the oncogenic cooperation between defects on INK4a/ARF and p27, which are common alterations in human cancer
- Defect of spindle checkpoint gene Mad2 and mutation of p27 gene are involved mainly in colorectal carcinogenesis
- In contrast to some hematological malignancies p27KIP1 methylation does not appear to contribute significantly to T-LBL/ALL pathogenesis.
- Trx may regulate cell cycle and growth through a novel modulation of AP-1 activity and p27Kip1 degradation with Jab1
- up-regulation of p27 and down-regulation of MAPK proteins were involved in atRA-induced apoptosis and cell cycle arrest in melanoma
- Thr-157 phosphorylation inhibits the association of p27 with importin alpha thus preventing its re-entry into the nucleus
- OxLDL has a dual effect on cell-cycle progression via regulation of p27(Kip1) expression, resulting in cellular proliferation and hypertrophy, involving activation of RhoA.
- Physiologic coupling of osteoblast differentiation to cell cycle withdrawal is mediated through runx2 and p27KIP1, and these processes are disrupted in osteosarcoma.
- The cytoplasmic localization of p27,Kip1 may be the molecular mechanism whereby breast cancer cells circumvent TNF-alpha-induced growth inhibition and apoptosis.
- Downregulation of both Skp2 and p27 increased apoptosis synergistically
- The targets and pathways affected by trastuzumab work in concert to maximize the expression and inhibitory effect of p27Kip1, which leads to cell cycle G1 arrest and growth inhibition.
- differentiation-inducing agents, particularly sodium butyrate, suppress growth of oral squamous carcinoma cells through apoptosis and induce cell differentiation possibly through mechanisms involving COX-2, p27Kip1 and/or p21WAF1/Cip1 in vitro and in viv
- p27Kip1 has a role in the decision of myoblasts to commit to terminal differentiation, distinct from the regulation of cell proliferation
- antisense oligonucleotides targeting the human ubiquitin-conjugating enzyme Cdc34 downregulate its expression, inhibit the degradation of p27Kip1, and prevent cellular proliferation
- p27Kip1 is upregulated by cycl AM when transfected into mouse cells.
- FOXO4A3 also can regulate p27 post-transcriptionally.
- High Cytoplasmic localization of p27(kip1) is associated with late-stage ovarian carcinomas
- low molecular weight forms of cyclin E may contribute to tumorigenesis through their resistance to the inhibitory activities of p21 and p27 while sequestering these CKIs from the full-length cyclin E
- p27Kip1 inhibits hTERT mRNA expression and telomerase activity through post-transcriptional up-regulation by IFN-gamma/IRF-1 signaling
- induction of p27 acts as a negative feedback mechanism for E2F1 and may also contribute to other functions of E2F1
- Altered response to contact inhibition exhibited by thyroid anaplastic cancer cells is due to the failure to upregulate p27(Kip1) in response to cell-cell interactions.
- P27KIP1 expression appears not to be predictive in poor survival outcome in patients with stage II or III colorectal cancer.
- expression of Skp2, p27KIP1 and Ki-67 in 10 naevi, 15 superficial spreading melanomas, 10 nodular melanomas and 14 melanoma metastases
- the PI3/AKT pathway and its effector p27(kip1) play major roles in thyroid carcinogenesis
- Ectopic expression of p27(Kip1) arrested cell proliferation, inhibited Cdk2 and Cdk4 activities, suppressed retinoblastoma phosphorylation and blocked the G(1)/S-phase transition.
- levels of cyclins and p27(Kip1) CDK inhibitor in hepatoma cells replated on fibronectin are regulated by TGF-beta1-mediated activations of c-Src and Rac1
- FOXO3a expression and reduced p27KIP1 promoter transactivation are seen in the progression of LNCaP human prostate cancer cells to androgen independence
- Inacativaton of this cell cycle regulatory genes by DNA methylation could be associated with tumorigenesis in NK cell disorders.
- Results suggest that BCR-ABL regulates cell cycle in CML cells at least in part by inducing proteasome-mediated degradation of the cell cycle inhibitor p27(Kip1) and provide a rationale for the use of inhibitors of the proteasome BCR-ABL leukemias.
- p21 and p27, related cyclin-dependent kinase (Cdk) inhibitors, select their cell cycle regulatory Cdk
- Results indicate that p27 serves as a regulator of drug resistance in ovarian tumors. ASON-mediated alteration of p27 reverses resistance of ovarian cancer to anticancer agents.
- The Cyclin-Dependent Kinase Inhibitor p27 plays key roles in cell cycle regulation, and was methylation-negative in myeloid neoplasia.
- N-Ras(L61) transformed cells lack a G0-G1 arrest upon TGF-beta treatment due to absence of p27. which is degraded through an SKP2-dependent pathwawy.
- analysis of a p27Kip1 mutant that causes growth arrest and apoptosis in breast cancer cells
- The 5'-UTR sequence of human p27 does not have internal ribosome entry site activities but contains promoters which may be involved in regulating p27 expression.
- T187-phospho-p27(KIP1) was correlated with M phase of the cell cycle in retinoblastoma.
- analysis of natural killer cell lymphoma/leukemia with homozygous loss of p27/kip1
- p27(kip1) protein downregulation is usually achieved by proteasomal degradation and is often correlated to a worse prognosis in several types of human cancers.
- p27 plays a role in terminal neuronal differentiation of human EC cells, but not in their initial commitment to differentiation
- study demonstrated the existence of a subtype of high-grade, negative estrogen receptor breast carcinomas with high S-phase kinase-associated protein Skp2 and low cdk-inhibitor p27 levels
- The codon 109 B allele of CDKN1B is associated with high-grade breast tumors.
- The reduction or loss of p27 protein and p27mRNA are potentially involved in hepatocarcinogenesis; hypermethylation of p27 might lead to the loss of p27mRNA transcription
- p27 may play a role in the prevention of differentiation of pancreatic cancer
- p27(kip1) and Ki-67 have roles in post-surgical disease progression of prostate cancer
- although a Cdc34 mutant bearing a deletion of the C-terminal 36 amino acids (Cdc34 1-200) was efficiently charged with ubiquitin by E1, it was severely reduced for the ability to ubiquitinate p27(Kip1) in vitro compared to wildtype Cdc34
- p27 is mislocalized in cytoplasm by oneractivated N-Ras61K via the Ral-GEF pathway.
- loss of phosphatase and tensin homolog is more frequent in anaplastic large cell lymphoma as compared to other mature T-/NK-cell lymphomas, which strongly correlates with the loss of p27 expression
- Tax1 induced transcriptional upregula inhibitors p21(cip1/waf1) (p21) and p27(kip1) (p27), and marked suppression of hematopoiesis in immature CD34 cells.
- Expression of p27 was associated with better overall survival.
- Aggressive acoustic neuromas show postoperative rapid growth and a decreased association with p27 expression.
- p27Kip1 binds the conserved minichromosome maintenance domain of MCM7 proteins in a growth factor-dependent manner, such that the carboxyl terminal domain of p27Kip1 inhibits DNA replication independent of its function as a cyclin-dependent kinase
- Jab1 promotes cell growth by decreasing p27 level p8-dependently.
- Loss of CUL4B causes the accumulation of cyclin E without a concomitant increase of p27
- These results suggest that the Bis induced growth inhibition of HL-60 cells promotes G0/G1 phase arrest via up-regulation of p27, which seems to be a prerequisite for differentiation.
- It is considered that tumorigenesis with UC-associated dysplasia is of the bottom-up type, related to altered expression of cyclin A and p27(Kip1).
- TIMP-1-mediates cell-cycle arrest via cyclin D1 downregulation & p27KIP1 upregulation.
- Data suggest that PTEN may regulate the expression of p27 by negatively regulating S phase kinase-associated protein 2 expression.
- These data indicate that p27-KID, which is intrinsically disordered in solution, acts as a thermodynamic tether when bound within the ternary complexes.
- These results suggest that p27(KIP1) interacts with cdc2 in the M-phase of human retinoblastoma cells.
- Expression of p27Kip1 is downregulated while oxidative DNA damage increases from early non-neoplastic epithelial alterations through vulvar intraepithelial neoplasias to invasive vulvar carcinomas.
- Mutations in the 3' untranslated region of Kip1 could provide an additional tool for risk classification in childhood leukemia.
- 14-3-3sigma stabilizes p27 Kip1 by inhibiting the activity of PKB/Akt
- Transfection of the pRb-defective SaOs-2 cells with the p27kip1 gene increases their susceptibility to paclitaxel-induced apoptosis. This promoting effect makes p27kip1 interesting tools for therapy in patients with pRb-defective cancers.
- Low expression for p27 is associated with breast cancer
- These data demonstrate a critical role for FAK in the regulation of cyclin-dependent kinase inhibitors (CDKIs) through two independent mechanisms: Skp2 dependent and Skp2 independent.
- Possible involvement of CDKN1A and CDKN1B variants in the etiology of breast cancer.
- Expression of AR protein in PC3-Lenti-AR cells resulted in transactivation of p21 and growth inhibition in culture and in mouse xenografts. Such inhibition was due to induced G1 arrest as documented by expression changes in p27 and p45(SKP2) proteins.
- expression of the p27(Kip1) double-mutant abolishes its cytoplasmic redistribution but does not abrogate G(0/1) phase arrest in the HepG(2) cell line
- These data suggest a key role for Ro52 RING finger protein in the regulation of p27 degradation and S-phase progression in mammalian cells.
- HBx mutant that did not interact with cyclin E/A failed to destabilize p27(Kip1) or deregulate the cell cycle.
- When 10% was used as a cutoff for p27 positivity, p27 was expressed in 11 of tumors; however, p27 expression was localized in the nuclei of tumor cells in only 4 of the samples.
- Results describe a previously unrecognized, SCFskp2-independent role for the control of p27 mRNA abundance in the development of non-small cell lung cancers.
- The variable expression levels of cell-cycle inhibitor genes CDKN2A, CDKN2B, and CDKN1B due to regulatory polymorphisms could indeed influence the risk of childhood pre-B ALL and contribute to carcinogenesis.
- p27Kip1 is required during induction of T cell tolerance.
- Data demonstrate that germ-line mutations in p27(Kip1) can predispose to the development of multiple endocrine tumors in both rats and humans.
- Phosphorylation of p27 at T198 prevents ubiquitin-dependent degradation of free p27
- p27 is widely expressed in gastric well differentiated endocrine tumors (GWDETs), while p21 expression is sparse and observed in two thirds of the cases. Loss of p21 and p27 expressions may be correlated with different carcinoid tumor subtypes.
- We identified a significant correlation between expression of cytoplasmic p27(kip1) and longer disease-specific survival times.
- altered expression of p27 may be part of the genetic pathway involving microsatellite instability, which is responsible for the development of some colorectal cancers
- Low p27 expression appears to be associated with poor prognosis, especially among patients with steroid receptor-positive breast tumors.
- Reduced expression of the cyclin-dependent kinase inhibitor p27(Kip1) is associated with increased tumor malignancy and poor prognosis in individuals with various types of cancer
- p53 and Ki-67 were expressed with increasing frequency, and bcl-2, p21, and mdm-2 with decreasing frequency in thyroid carcinoma progression. p27 and cyclin D1 were expressed in <15% of cases, with a trend toward decreasing expression.
- p21 and p27 in carcinoma of oral cavity have roles in progression of squamous cell carcinomas
- Results suggest that WDR6 is implicated in the cell growth inhibitory pathway of LKB1 via regulation of p27(Kip1).
- Phosphorylation of p27 at Thr 198 stabilizes p27 and permits cells to survive growth factor withdrawal and metabolic stress through autophagy. This may contribute to tumour-cell survival under such conditions.
- cytoplasmic p27 expression is inversely associated with microsatellite instability-high & CpG island methylator phenotype-high, especially in p53-negative tumors; suggests interplay of functional loss of p27 & p53 in colorectal cancer development
- This direct link between transforming tyrosine kinases and p27 may provide an explanation for Cdk kinase activities observed in p27 complexes and for premature p27 elimination in cells that have been transformed by activated tyrosine kinases.
- Phosphorylation by Src impairs the Cdk2 inhibitory action of p27 and reduces its steady-state binding to cyclin E-Cdk2 to facilitate cyclin E-Cdk2-dependent p27 proteolysis.
- Analysis of p27 and Ki-67 expression levels might indicate that low proliferating activity of desmoid fibroblasts is connected with another mechanism than the one, in which p27 takes part.
- CKS1B influences myeloma cell growth and survival through SKP2- and p27(Kip1)-dependent and -independent mechanisms
- A study evaluting the mechanism of differentiation in HT-29 cells, including the role of p27KIP1, is reproted.
- There was a highly significant positive association between p27(KIP-1) and estrogen receptor/progesterone receptor (ER/PR) status and with p27(KIP-1) and cyclin D1 expression in patients with DCIS
- Decreased expression of protein p27 Kip1 is related the c-myc amplification and is associated with prostate cancer
- Intensity of p27(Kip 1) gene expression in renal cell carcinoma is associated with clinical parameters: tumour size, stage, grade and disease presentation. Loss of p27 expression is a risk-factor for renal cell carcinoma disease progression.
- Down-regulation of p27(Kip 1) CDKI in prostate cancer is detected in epithelial, vascular and ductal, but not the stromal cells. The intensity of the expression in these cells is associated with tumor stage and grades.
- integrin beta1 has a role in inhibiting cell proliferation by preventing the Skp2-dependent degradation of p27(Kip1) via PI3K pathway
- The findings presented here suggest that Ca(2+)/CaM-dependent overactivation of PI3K/Akt signaling cascade in AD cells, plays an important role in regulating p27 abundance by increasing its degradation in the ubiquitin-proteasome pathway.
- Myc targets CKS1 to provoke the suppression of KIP1.
- p27 localization during the mammalian cell cycle is under the control of the tumor suppressor tuberin
- adhesion of mantle cell lymphoma and other non-Hodgkin lymphoma cells to bone marrow stromal cells resulted in a reversible G(1) arrest associated with elevated p27(Kip1) and p21 (WAF1) proteins
- germline CDKN1B/p27(Kip1) mutations predispose to a human multiple endocrine neoplasia type 1-like condition
- the G allele genotype was significantly associated with lymph node metastases of breast cancer but no significant correlation was noted between G allele genotype and breast cancer risk
- p15(INK4b), rather than p27(KIP1), is the cyclin-dependent kinase inhibitor responsible for G0/G1 arrest of human melanoma cells grown on fibrillar collagen
- pheochromocytomas display extreme reduction/loss of p27Kip1 expression at high frequency
- Data suggest that the aberrantly high Notch1 signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid cell cycle progression.
- No evidence is found to suggest that p27-Val109Gly alone or in combination with cMyc-Asp11Ser is associated with breast cancer survival.
- Low p27 protein expression is correlated with large tumor size, depth of invasion in squamous lesions, high stage, and poor survival in uterine cervix neoplasms.
- These results demonstrate that p27 is regulated by neutrophil elastase (NE) and is critical for NE-induced cell cycle arrest.
- p27 could be transformed from a native CDKI into a dynamic oncoprotein at the expense of its extranuclear localization in leukemic cells. Review.
- present study reviews the current state of knowledge regarding the genes associated to inherited pituitary neoplasia, with a particular focus on the novel pituitary adenoma predisposing genes, CDKN1B and AIP [review]
- inhibition of p27(Kip1) expression deregulates expresion of miR-221 and 222 which promotes cancer growth
- We conclude that Jab1 expression may lead to down-regulation of the negative cell cycle regulator p27(Kip1), pointing to a possible mechanism that promotes hepatocarcinogenesis.
- Spy1 expression enhances CDK2-dependent p27 degradation during late G1 and throughout S-phase
- Down-regulation of p27 Kip1 in papillary carcinoma of the thyroid may facilitate tumor cell growtn and disease progression.
- The apoptogenic activity of BM-ANF1 was mediated through p53 tumor-suppressor gene expression followed by the expression of p21(Cip1) and p27(Kip1)linking it with cell cycle arrest at G1 phase in cancer cells.
- Aberrations of the p53, Rb and p27 pathways are associated with aggressive clinical behavior in DLBCL.
- data suggest that p27 and p18 are unlikely to present classic tumor-suppressor genes in sporadic pancreatic endocrine tumors
- Data show that p27(Kip1) is a direct target for microRNAs 221 and 222, and suggest a role for these microRNAs in promoting the aggressive growth of glioblastoma.
- p27 plays an essential role in restriction of breast cancer progression.
- p27(Kip1) protein expression in tumor,invasive front and peritumoral tissues in patients diagnosed with renal cell carcinoma affects their long term survival
- caspase-like activity is implicated in the turnover of the mammalian cell cycle regulator p27(KIP1).
- miR-221 and miR-222 are endogenous regulators of p27(Kip1) protein expression, and thereby, the cell cycle.
- p27(Kip1) down-regulation seem to be early events in Fallopian tube carcinogenesis.
- Our study suggests that moderate hypoxia induces HPASMC proliferation, which is partially dependent of p27kip1 down-regulation probably via the induction of growth factors such inhibits both cell proliferation and p27kip1 mRNA degradation.
- present work reported that hepatic tissue expression of p27 both at mRNA and protein levels was significantly decreased in hepatocellular carcinoma group compared to other groups
- Pirh2 acts as a negative regulator of p27(Kip1) function by promoting ubiquitin-dependent proteasomal degradation
- The CDKIs p16 and p27 are associated with tumour progression in melanoma, but do not reliably predict recurrence or survival.
- Human thyroid carcinomas positive for MAP kinase, have high p27 degradative activity and low levels of p27 protein.
- A study evaluating the overexpression of p27(kip1) in urinary bladder urothelial carcinoma is reported; some urothelial carcinomas may tolerate this inhibitor of cell cycle progression.
- activation of PKCtheta inhibits the FOXO3a/ERalpha/p27(Kip1) axis that normally maintains an epithelial cell phenotype and induces c-Rel target genes, thereby promoting proliferation, survival, and more invasive breast cancer.
- data strongly implicate CDKN1B haploinsufficiency in the pathogenesis of T-cell prolymphocytic leukemia.
- Decreased p27kip1 expression in podocytes suggested a significant role in proteinuria among renal transplant recipients.
- Our results suggest p27 as a predictor of prognosis in patients with primary central nervous system lymphoma
- Equally a tumor suppressor and an additional predisposing system for tumorigenesis.
- The expression of p21(WAF1/Cip1) and p27(Kip1) was increased at both protein and mRNA levels by hydroxytyrosol, a main phenol of olive oil.
- Study shows that the 100-residue p27 C-terminal domain is extended and flexible when p27 is bound to Cdk2/cyclin A; this intrinsic flexibility of p27 provides a molecular basis for the signal transduction that regulates p27 degradation and cell division.
- alternatively spliced cyclin D1 modulates p27KIP1 binding and cell migration
- We immunohistochemically analyzed the expression of p21, p27, p14, p16, p53 and proliferation marker Ki67, in 67 low and high grade astrocytic tumors
- D-allose, a simple monosaccharide, may act to cause TXNIP induction and p27kip1 protein stabilization in tumor cells
- expression of p27 was similar in both Small-cell neuroendocrine carcinoma of the uterine cervix and squamous cell carcinoma
- Cleavage-stage human embryos exhibiting developmental arrest show increased p27 mRNA expression.
- the formation of adherens junctions in hepatocytes requires Ser-10 in p27
- Diindolylmethane modulates p27(kip) through transcription, prolongation of protein half-life, and nuclear localization.
- Jab1 protein may contribute to the tumor progression through Jab1-mediated p27kip1 degradation and that control of Jab1 expression is a novel therapeutic target in hon-Hodgkin's lymphoma.
- The absence of clonal inactivating mutations suggests that CDKN1B is not a classical tumor-suppressor gene in secondary/tertiary parathyroid tumors
- Only FIGO stage, cyclin D1, p27 (Kip1) and Ki-67 are independent prognostic factors that might help in predicting outcome of cervical cancer patients.
- hCaMKIINalpha suppresses tumor growth by inducing cell cycle arrest via p27 stabilization
- P27Kip1 is down-regulated in the endometrium of women with endometriosis.
- tumor cell incubation with pioglitazone results in increased levels of p53 and p27 and decreased levels of cyclin D1
- Large-scale analysis of cell cycle regulators in urothelial bladder cancer identifies p16 and p27 as potentially useful prognostic markers
- p16(INK4a), p21(WAF1/CIP1), p27(KIP1), and p53 are expressed in human corneal endothelial cells despite donor ages.
- expression of P27KIP1 in human hepatocellular carcinoma
- Review of molecular mechanisms underlying the functional loss of cyclindependent kinase inhibitors p16 and p27 in hepatocellular carcinoma.
- positive correlation between Foxo3a and p27(kip1)expression in non-Hodgkin's lymphomas
- These results identify p66Shc and FOXO3a as novel partners of beta(1)Pix and represent the first direct evidence of beta(1)Pix in cell proliferation via Erk/p66Shc-dependent and Akt-independent mechanisms.
- The inhibition of FOXO3a-mediated activation of the p27 gene by the high aberrant expression of c-Myc in many tumor cells likely contributes to their uncontrolled proliferation and invasive phenotype.
- Results suggest that GSK-3 regulates nuclear p27 Kip1 expression through downregulation of Skp2 expression and regulates p27 Kip1 assembly with CDK2, playing a critical role in the G0/G1 arrest associated with intestinal cell differentiation.
- The low to high grade dedifferentiation of prostate adenocarcinoma is accompanied with the down-regulation of p27(kip1) protein, which may be an important molecular sign of the lost cell cycle control.
- PTEN and p27Kip1 are not downregulated in the majority of renal cell carcinomas
- tetrandrine induces G(1) arrest and apoptosis through PI3K/kip1/AKT/GSK3beta pathway
- The expression of Skp2 and p27 proteins in 48 cases of Extranodal nasal-type natural killer cell lymphoma was studied and their correlations with Epstein-Barr virus status and clinical outcomes, was evaluated.
- miR-221 has an oncogenic function in hepatocarcinogenesis by targeting CDKN1B/p27 and CDKN1C/p57, hence promoting proliferation by controlling cell-cycle inhibitors.
- Show that p27KIP1 was up-regulated in topotecan-induced apoptosis in HepG2 cells.
- Simultaneous knock-down of both p21 and p27 significantly enhanced doubling time, clonogenicity and cell cycle progression in a prostate cancer cell line.
- Pim kinases directly phsophorylate p27Kip1 at threonine-157 and threonine-198 residues.
- Pim kinases promote cell cycle progression and tumorigenesis by down-regulating p27(Kip1) expression at both transcriptional and posttranslational levels.
- Activation of protein kinase G Increases the expression of p21CIP1, p27KIP1, and histidine triad protein 1 through Sp1.
- Antitumoral activities of argyrin A depend on the prevention of p27(kip1) destruction through a potent inhibition of the proteasome.
- cell cycle exit is preceded by p27-dependent inhibition of cyclin A-Cdk1/2, cyclin D1 downregulation and reduced pre-mitotic pRb pocket protein phosphorylation
- S10 phosphorylation of p27 mediates all trans retinoic acid induced growth arrest in ovarian carcinoma cell lines.
- CDKN1B V109G polymorphism may not have a role in prostate cancer among the Taiwanese population
- p27 has a role in salivary cancer
- These data suggest that a p27(Kip1)-driven checkpoint limits progression of prostatic intraepithelial neoplasia to prostate cancer.
- p27kip1 expression is frequently down-regulated in head and neck squamous cell carcinoma.
- MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1
- The present data support a role for p27 in the assembly of D-type cyclin-Cdk complexes and indicate that both cyclin D1-Cdk4-p27 assembly and kinase activation are regulated by p27 phosphorylation.
- down-regulated p27 protein expression is the possible underlying mechanism for the growth of uterine leiomyoma and over-expression of p27 induces cell death.
- the analysis of p21cip1, p27kip1, and p16INk4a by immunohistochemistry could be useful in the management of patients with papillary thyroid carcinoma
- p27 promotes cell migration in metastatic HCC cells through the regulation of RhoA activity.
- Pin1 is identified as a novel negative FOXO regulator, interconnecting FOXO phosphorylation and monoubiquitination in response to cellular stress to regulate p27(kip1).
- a high level of p27(Kip1) expression is evident from early stages of hepatocarcinogenesis.
- BCL2 and BCL-xL facilitation of G0 quiescence requires BAX, BAK, and p27 phosphorylation by Mirk
- Phosphorylation, half-life, and the nucleo-cytoplasmic traffic of p27 protein were altered by 15d-PGJ2 by mechanisms dependent on PI3K/Akt activity.
- Down-regulation of p27(Kip1) is a well-established feature of urothelial carcinoma. Probably, this down-regulation of cyclin-dependent kinase inhibitors supports the proliferation phase of oncogenesis.
- Low p27Kip1 expression were correlated with larger tumor size and higher stage, as well as tumor necrosis in renal cell carcinoma.
- forced VEGF overexpression or autocrine VEGF stimulation of VEGFR-2 triggers proliferation and migration/invasion of U-937 leukemic c
- Loss of p27 and overexpression of cyclin E play a critical role in the aggressiveness of gastroenteropancreatic neuroendocrine tumors
- p27Kip1 is regulated by serine 276 phosphorylation of the p65 subunit of NF-kappaB
- Proliferation parameters of differentiating cells correlate with the activity and structure of cyclin A/E-CDK2 but not of cyclin D-CDK4/6-p27 complexes.
- Reduced levels of p27Kip1 are assicuated with colorectal cancer.
- MG-123 induces apoptosis and G(1) arrest which is associated with upregulated p27kip1 expression in gastric carcinoma cells.
- These results showed that the expression of cyclin D1, p21 and p27, alone or in combination, are early events in gastric tumorigenesis and may serve as a candidate molecular marker for the early gastric carcinoma.
- A role for miR-221/222 in prostate carcinoma,with upregulation in patient-derived primary cell lines, and a significant inverse correlation with p27 expression.
- The E2 core of Cdc34 provides specificity to p27, and the residues 184-196 are required for possessive ubiquitination by Cdc34.