• Mechanistically, overexpression of BCRC-3 induced the expression of cyclin-dependent kinase inhibitor 1B (p27). (biomedcentral.com)
  • Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. (thermofisher.com)
  • The activity of this kinase first appears in mid-G1 phase, which is controlled by the regulatory subunits including D-type cyclins and members of INK4 family of CDK inhibitors. (cancerindex.org)
  • AKT prevents cell death by inactivating proapoptotic factors including BAD, procaspase-9 and Forkhead transcription factor family proteins (FOXOs), activates transcription factors that upregulate antiapoptotic genes, including NF-kB, inactivates p53 through Mdm2, and phosphorylates the cell cycle inhibitors p21 CIP1/WAF1 and p27 KIP1 , thus increasing cell proliferation (Hennessy et al. (ebrary.net)
  • The cyclin-dependent kinase inhibitor, p21 cip1/waf1 (p21), maintains hematopoietic stem cell quiescence, and we evaluated its role in the regenerative response of neural tissue after ischemic injury using the mice deficient in p21. (rupress.org)
  • Although carcinogenic roles for the INK4B, INK4C, INK4D, CIP1, KIP1, and KIP2 genes appear to be limited, INK4A is among the most commonly mutated genes in human tumors. (medscape.com)
  • Up-regulation appears to be specific to p27 because expression of cyclin D1, E, and A, and p21Cip1/Waf1 was not modulated by these agents. (biomedcentral.com)
  • Preliminary studies using in vivo model of MNU-induced rat mammary cancer and in vitro model of cultured cells had suggested - but not proved - that various nutritional and chemopreventive anti-cancer agents, including moderate dietary restriction, up-regulated the expression of p27 (Fig. 1a ). (biomedcentral.com)
  • The cyclin-dependent kinase (CDK) inhibitors p21 and p16 inhibit the activity of CDKs, such as CDK4. (medscape.com)
  • Another important class of tumor suppressor genes involved in cell cycle control and in the generation of human cancers is the cyclin-dependent kinase (CDK) inhibitors. (medscape.com)
  • When up-regulated, p27 inhibits G1-to-S phase transition of the cell cycle. (biomedcentral.com)
  • 2005). AKT also phosphorylates and inhibits glycogen synthase kinase-3 (GSK3), thus enhancing p-catenin and cyclin D1 stabilization (Vivanco and Sawyers 2002). (ebrary.net)
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
  • While AKT phosphorylates multiple downstream targets (see above), the emerging picture is that the ability of AKT to coordinate mitogenic and nutrient-sensing pathways controlling protein synthesis is a key mechanism by which AKT regulates cell proliferation. (ebrary.net)
  • However, exact underlying mechanisms including signaling pathways downstream of receptor ligation are still under pursuit. (koreascience.kr)
  • We are investigating how Pbx and Meis proteins contribute to the specificity of Hox function in development and how disruption of their activities leads to neoplasia. (stanford.edu)
  • Our studies have demonstrated that several of the proteins encoded by cellular oncogenes function in fundamental aspects of gene regulation. (stanford.edu)
  • and group 4 (late-elderly, 75-85).Protein levels and deregulated protein phosphorylation linked to similar biological terms/functions, but involving different individual proteins, are found in FC with age. (ibecbarcelona.eu)
  • Mechanical force modulates the conformation and function of individual proteins, and this underpins many mechanically driven cellular processes. (ibecbarcelona.eu)
  • In turn, GTP-bound active GTPases can interact with a plethora of different effectors which mediate the different cellular functions of this family of proteins. (biomedcentral.com)
  • The activity of this kinase is restricted to the G1-S phase, which is controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16(INK4a). (thermofisher.com)
  • Transcriptional and translational control, sequestration in cyclin D1 complexes and localization all regulate p27 in G1 phase. (biomedcentral.com)
  • The p16INK4A protein is a cell-cycle inhibitor that acts by inhibiting activated cyclin D:CDK4/6 complexes, which play a crucial role in the control of the cell cycle by phosphorylating Rb protein. (medscape.com)
  • b) 4-Hydroxytamoxifen (but not tamoxifen), genistein (but not genistin), daidzein, and probably other nutritional and chemopreventive anti-cancer agents could up-regulate expression of p27 via receptor protein tyrosine kinases (RPTKs), phosphoinositide 3-kinase (PI3K), phosphoinosite-dependent kinase (PDK), Akt/PKB and mTOR. (biomedcentral.com)
  • This report addresses the question of whether various nutritional and chemopreventive anti-cancer agents up-regulate the expression of p27 in preneoplastic and neoplastic cells. (biomedcentral.com)
  • Experimental evidence presented in the first half of this report shows that these agents fairly faithfully up-regulate expression of p27 in mouse epidermal (JB6) and human breast cancer (MCF7, MDA-MB-321, and AU565) cells. (biomedcentral.com)
  • Amino acid deficiencies also up-regulate the expression of p27 using some components of this pathway. (biomedcentral.com)
  • Finally, (d) global hypomethylation of 5'-m 7 G cap of mRNAs could also up-regulate expression of p27. (biomedcentral.com)
  • Based on these findings, we conclude that various nutritional and chemopreventive anti-cancer agents up-regulate expression of p27 in (pre)neoplastic cells. (biomedcentral.com)
  • Some circRNAs contain miRNA response elements (MREs) and function as competing endogenous RNAs (ceRNAs) to interact with miRNAs and regulate the expression of target mRNAs. (biomedcentral.com)
  • Up-regulation of the expression of p27 is likely due to the activation of translation rather than transcription of p27 because (a) up-regulation is mediated by the 5'-untranslated region (-575) of the p27 gene and (b) the antibiotic actinomycin D, an inhibitor of transcription, did not attenuate the up-regulation of p27. (biomedcentral.com)
  • This latter finding is likely to preclude the existence of cryptic transcription factor binding site(s) in the 5'-untranslated region of p27 gene. (biomedcentral.com)
  • The experimental evidence, presented in the second half of this report, was obtained using the 5'-untranslated region (-575) of p27 gene. (biomedcentral.com)
  • To address this question, the effects of various nutritional and chemopreventive anti-cancer agents on the activity of the proximal 5'-upstream region of p27 gene were investigated by transient transfection assay. (biomedcentral.com)
  • For example, the TP53 gene, located on chromosome 17, encodes a 53-kd nuclear protein that functions as a cell cycle checkpoint. (medscape.com)
  • Within each tissue, downstream PCP effectors link the signal to tissue specific readouts such as stereocilia orientation in the inner ear and hair follicle orientation in vertebrates or the polarization of ommatidia and wing hairs in Drosophila melanogaster. (uni-wuerzburg.de)
  • Two factors concur to determine specific Rho GTPase function: tissue specificity of GTPase effectors and distinct intracellular localizations of closely related Rho GTPases, due to different lipid modifications [ 1 ]. (biomedcentral.com)
  • Preliminary studies using either N -methyl- N -nitrosourea (MNU)-induced rat breast cancer model or human breast cancer cell lines in vitro had suggested, but not proved, that nutritional and chemopreventive anti-cancer agents increase p27 protein expression. (biomedcentral.com)
  • This apparent increase in p27 protein expression might have been due to either increased synthesis or decreased degradation, or a combination of both [ 1 ]. (biomedcentral.com)
  • This study provided evidence that the up-regulation of p27 protein expression is at least in part due to increased synthesis and that this increase fairly faithfully recapitulates the cancer preventive activity of nutritional and chemopreventive anti-cancer agents. (biomedcentral.com)
  • The cyclin-dependent kinase (CDK) inhibitor p27(Kip1) is a key cell-cycle regulator of G1-to-S phase transition [ 1 ]. (biomedcentral.com)
  • In general, the circRNA-miRNA-mRNA axis may function as an extensive regulatory network in progression of some diseases. (biomedcentral.com)
  • Importantly, BCRC-3 could directly interact with miR-182-5p, and subsequently act as a miRNA sponge to promote the miR-182-5p-targeted 3'UTR activity of p27. (biomedcentral.com)
  • Our data indicate that Cmb is a novel PCP effector that promotes to wing hair formation, a function that is antagonized by Mwh. (uni-wuerzburg.de)
  • c) Expression of p27 could also be up-regulated via RPTKs followed by MAPKs - MEK, ERK and p38MAPK - and probably MNK. (biomedcentral.com)
  • Furthermore, MJ significantly increased the expression of BCRC-3, resulting in an obvious up-regulation of p27. (biomedcentral.com)
  • The polarization of cells is essential for the proper functioning of most organs. (uni-wuerzburg.de)
  • The exchange of GDP to GTP and thus the activation of Rho GTPases is catalyzed by guanine nucleotide exchange factors (GEFs), which act downstream of numerous growth factor receptors, integrins, cytokine receptors, and cadherins. (biomedcentral.com)
  • 9. Retinoic acid-mediated G1 arrest is associated with induction of p27(Kip1) and inhibition of cyclin-dependent kinase 3 in human lung squamous carcinoma CH27 cells. (nih.gov)
  • 13. Loss of the cyclin-dependent kinase inhibitor p27(Kip1) protein in human prostate cancer correlates with tumor grade. (nih.gov)
  • This protein kinase is activated by insulin and various growth and survival factors to function in a wortmannin-sensitive pathway involving PI3 kinase (2,3). (cellsignal.jp)
  • The cyclin-dependent kinase inhibitor p21 is induced by both p53-dependent and -independent mechanisms following stress, and induction of p21 may cause cell cycle arrest. (aacrjournals.org)
  • Surprisingly, p27 accumulation was not reversed by the protein kinase A (PKA) inhibitor H-89, but interestingly, was alleviated by the knockdown of β-arrestin 2. (ijbs.com)
  • In colon cancer suppression of BRAF in cell lines with BRAF V600E showed significant decreased proliferation through cyclin D1 and p27 Kip1 and induces apoptosis by a significant decrease in the levels of anti-apoptotic protein Bcl-2 [ 14 ]. (biomedcentral.com)
  • 5. Susceptibility of p27 kip1 knockout mice to urinary bladder carcinogenesis induced by N-butyl-N-(4-hydroxybutyl)nitrosamine may not simply be due to enhanced proliferation. (nih.gov)
  • 16. Genetic characterization of p27(kip1) and stathmin in controlling cell proliferation in vivo. (nih.gov)
  • 17. Nkx3.1 and p27(KIP1) cooperate in proliferation inhibition and apoptosis induction in human androgen-independent prostate cancer cells. (nih.gov)
  • 18. MiR-196a is upregulated in gastric cancer and promotes cell proliferation by downregulating p27(kip1). (nih.gov)
  • However, a number of recent studies have pointed out that in addition to being an inhibitor of cell proliferation, p21 acts as an inhibitor of apoptosis in a number of systems, and this may counteract its tumor-suppressive functions as a growth inhibitor. (aacrjournals.org)
  • Active cyclin/Cdk complexes phosphorylate and inactivate members of the retinoblastoma protein (Rb) family that are negative regulators of G 1 and S-phase progression, leading to induction of E2F-regulated gene expression and cell proliferation. (aacrjournals.org)
  • In glioma ( 28 ) and in vascular smooth muscle cells ( 29 ), p21 facilitates active cyclin-Cdk complex formation and induces cell proliferation. (aacrjournals.org)
  • Thus, our work provides a basis for β 2 -AR agonists inhibit myoblasts proliferation through signaling via β 2 -AR, β-arrestin 2, and p27. (ijbs.com)
  • In BRAF V600E mutated cells inhibition of BRAF pathway lead to a decrease in ERK1/2 phosphorylation and cyclin D1 levels and an increase in p27 Kip1 . (biomedcentral.com)
  • These three CKIs contain a conserved region of sequence at the NH 2 terminus that is required and sufficient for the inhibition of cyclin/Cdk complexes, whereas the COOH terminal regions are variable in length and function ( 12, 14 - 16 ). (aacrjournals.org)
  • 8. Induction of cell cycle arrest and apoptosis in human prostate carcinoma cells by a recombinant adenovirus expressing p27(Kip1). (nih.gov)
  • We show, for the first time, that CLB induces cell cycle arrest by repressing p27 degradation, via a pathway that depends on β 2 -AR and β-arrestin 2. (ijbs.com)
  • Another essential Akt function is the regulation of glycogen synthesis through phosphorylation and inactivation of GSK-3α and β (12,13). (cellsignal.jp)
  • 4. Reduced expression of the CDK inhibitor p27(KIP1) in rat two-stage bladder carcinogenesis and its association with expression profiles of p21(WAF1/Cip1) and p53. (nih.gov)
  • 6. Expression of p27/Kip1 is down-regulated in human prostate carcinoma progression. (nih.gov)
  • 14. [Correlation of Skp2 and P27kip1 protein expression and clinicopathological features of prostate cancer]. (nih.gov)
  • 15. Expression of p27((Kip1)), cyclin D3 and Ki67 in BPH, prostate cancer and hormone-treated prostate cancer cells. (nih.gov)
  • The two antibodies function as a capture-target-detection sandwich (#88800 and #98449, respectively) to detect endogenous protein expression in positive and negative controls. (cellsignal.jp)
  • However, the clinical significance of ENO1 expression remains unclear and its function and modulatory mechanisms have never been reported in endometrial carcinoma (EC). (oncotarget.com)
  • They also increase the expression levels of the cell cycle inhibitors (p53, p21, and p27) and the pro-apoptotic proteins (BAD, Bax, caspase 3, caspase 7, caspase 8, and caspase 9). (jcpjournal.org)
  • While dissecting the mechanism of action of PDBD on BCa, we found that PDBD inhibits Akt signaling and its downstream targets such as NF-κB activation, IAP proteins and Bcl-2 expression. (biomedcentral.com)
  • CKIs bind and inhibit the activity of cyclin/Cdk complexes and negatively regulate cell cycle progression (reviewed in Refs. (aacrjournals.org)
  • This in turn mediated inactivation of PI3K/AKT signaling and its downstream signals including glycolysis, cell cycle progression, and epithelial-mesenchymal transition (EMT)-associated genes. (oncotarget.com)
  • Both the N-terminal and C-terminal domains have been shown to mediate FAK interaction with a variety of other proteins critical for activation of FAK by integrins or other cell surface receptors as well as FAK regulation of different cellular functions [ 2 ]. (biomedcentral.com)
  • 1. p27(Kip1) deficiency promotes prostate carcinogenesis but does not affect the efficacy of retinoids in suppressing the neoplastic process. (nih.gov)
  • HDM2 is a hub protein with a large interactome and with different cellular functions. (silverchair.com)
  • Indeed, although the anabolic functions of CLB are well characterized, its potential role in muscle regeneration has not been fully explored. (ijbs.com)
  • 6 - 9 ) is the founding member of the Cip/Kip family of CKIs, which also includes p27 ( 10, 11 ) and p57 ( 12, 13 ). (aacrjournals.org)
  • p21 was shown to stabilize interactions between Cdk4 and cyclin D and promote the formation of active complexes in a concentration-dependent manner ( 27 ). (aacrjournals.org)
  • In this review article, we focus on the critical functions of AHR for DNA damage-dependent processes and immune responses which may contribute to the development of SCC in chronically UV- and/or PAH-exposed skin. (frontiersin.org)
  • Please note that while we are focusing on the mentioned aspects other functions of the AHR system might fall short, which may be also relevant for the process of skin cancer development. (frontiersin.org)
  • In this review, we summarize the functions and regulations of 3′UTRs and elaborate on the generation and functional consequences of 3′UTR diversity. (molcells.org)