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Tumor Suppressor Protein p53Tumor Suppressor ProteinsGenes, Tumor SuppressorCyclin D1Cyclin AVon Hippel-Lindau Tumor Suppressor ProteinCyclin ERetinoblastoma ProteinTumor Suppressor Protein p14ARFCell Line, TumorPhosphorylationMolecular Sequence DataProto-Oncogene Proteins c-mdm2Cell LineCyclin BMutationProtein BindingCell CycleCyclinsAmino Acid SequenceCyclin B1Nuclear ProteinsProtein-Serine-Threonine KinasesTransfectionApoptosisCell Cycle ProteinsDNA-Binding ProteinsCyclin A1Cyclin D2Cyclin D3Proto-Oncogene ProteinsTranscription FactorsCyclin DSerineGene Expression Regulation, NeoplasticSignal TransductionTumor Cells, CulturedGenes, p53Cyclin-Dependent KinasesBlotting, WesternCell ProliferationNeurofibromin 2Base SequenceCyclin-Dependent Kinase Inhibitor p21PhosphoproteinsCells, CulturedAdenomatous Polyposis Coli ProteinCell DivisionUbiquitin-Protein LigasesPromoter Regions, GeneticCyclin-Dependent Kinase Inhibitor p16Cyclin A2Protein Structure, TertiaryTranscription, GeneticCell Transformation, NeoplasticPTEN PhosphohydrolaseProteinsRNA, MessengerDown-RegulationProtein KinasesBinding SitesEnzyme ActivationDNA DamageGenes, SuppressorHeLa CellsCyclin G1Transcriptional ActivationNeoplasm ProteinsG1 PhaseCyclin GRecombinant Fusion ProteinsE2F Transcription FactorsCarrier ProteinsRepressor ProteinsCell NucleusGene Expression RegulationRNA, Small InterferingLigasesNeoplasmsFibroblastsCyclin-Dependent Kinase 2RNA InterferencePhosphoserineTrans-ActivatorsRecombinant ProteinsIntracellular Signaling Peptides and ProteinsCyclin-Dependent Kinase 4Precipitin TestsModels, BiologicalReverse Transcriptase Polymerase Chain ReactionTumor Markers, BiologicalE2F1 Transcription FactorImmunoblottingTyrosineGene SilencingEnzyme InhibitorsImmunoprecipitationMembrane ProteinsProto-Oncogene Proteins c-aktTranscription Factor DP1
KinasesProliferationMutationsSubstratesInactivationCdksApoptosisProgressionMutationRecombinant ProteinCDK4MalignantSerineImportant tumorTranscriptionInducesCdk2Kinase activityPathwaySpecificityCancersHuman tumorsRegulatorInhibitorsMicroenvironmentSuppressionPTENAntigensVivoRegulationContributesRegulatoryAntibodyComplexesMitosisDependentBreast tumorBindsTissueStructuralDifferentiationPosttranslational modificationsLocalizationInhibitoryHumansCarcinogenesisLungMitoticSequenceInteractionConcentrationCellular
Kinases11
Proliferation16
  • Binding of Cdks can lead to phosphorylation of other substrates at inappropriate time and unregulated proliferation. (wikipedia.org)
  • In mouse hepatocytes, p38γ induces proliferation after partial hepatectomy by promoting the phosphorylation of retinoblastoma tumour suppressor protein at known CDK target residues. (nature.com)
  • The N-terminal phosphorylation of RB by p38 bypasses its inactivation by CDKs and prevents proliferation in cancer cells. (nature.com)
  • The retinoblastoma tumor suppressor protein pRb is a master regulator of cellular proliferation, principally through interaction with E2F and regulation of E2F target genes. (bvsalud.org)
  • Low PDCD4 level was associated with reduced proliferation but not apoptosis or phosphorylation of endothelial nitric oxide synthase caused by pulsatile shear stress to help maintain the homeostasis of endothelial cells. (plos.org)
  • Introduction The commitment to cell proliferation is set up when extracellular signals converge on the cell cycle and induce the expression of D-type cyclins, their association with CDK4 and/or CDK6, as well as the activation from the holoenzyme complex [1C3]. (healthandwellnesssource.org)
  • Launch The dedication to cell proliferation is set up when extracellular indicators converge on the cell routine and stimulate the appearance of D-type cyclins, their association with CDK4 and/or CDK6, as well as the activation from the holoenzyme complicated [1C3]. (healthandwellnesssource.org)
  • Unchecked proliferation of Rb-positive tumor cells is often connected with mutations that dysregulate this pathway: like the overexpression of D-type cyclins, the overexpression or mutation of CDK4, or mutations in the Printer ink4 category of CDK inhibitors [3, 5, 6]. (healthandwellnesssource.org)
  • Recent studies have found that overexpression of the High-mobility group box-1 (HMGB1) protein, in conjunction with its receptors for advanced glycation end products (RAGEs) and toll-like receptors (TLRs), is associated with proliferation of various cancer types, including that of the breast and pancreatic. (biomedcentral.com)
  • Our simulations show that, if HMGB1 is overexpressed, then the oncoproteins CyclinD/E, which regulate cell proliferation, are overexpressed, while tumor suppressor proteins that regulate cell apoptosis (programmed cell death), such as p53, are repressed. (biomedcentral.com)
  • Moreover, a number of extracellular proteins can bind to their receptors and activate signaling pathways that promote the proliferation of cancer cells. (biomedcentral.com)
  • The HMGB1 signal transduction can influence the cell's fate by two important processes - apoptosis and cell proliferation - which are regulated respectively by the proteins p53 and CyclinE, acting in two different signaling pathways. (biomedcentral.com)
  • CyclinE is a cell cycle regulatory protein which regulates the G1-S phase transition during cell proliferation. (biomedcentral.com)
  • To the best of the authors' knowledge, no computational model has been proposed to investigate the importance of HMGB1 in tumor proliferation. (biomedcentral.com)
  • The adenovirus E1A protein mimics the LxDLFD motif and competes with E2F for binding to Rb, promoting E2F activation and cell proliferation. (eu.org)
  • STAT3 is normally a well-characterized transcription aspect that is demonstrated to contribute to numerous processes of tumorigenesis such as MUC12 tumor cell survival and proliferation invasion angiogenesis and drug resistance [22]. (biosemiotics2013.org)
Mutations7
  • Scope includes mutations and abnormal protein expression. (cancerindex.org)
  • For example, studies suggest that ccRCC is closely associated with tumor suppressor von-Hippel Lindau ( VHL ) gene mutations that lead to stabilization of hypoxia inducible factors (HIF-1 α and HIF-2 α , also known as HIF1A and EPAS1) in both sporadic and familial forms [ 5 , 6 ]. (hindawi.com)
  • The majority of classical LFS families harbour germline mutations of the p53 tumour suppressor gene. (bmj.com)
  • Pediatric cancer retinoblastoma and the formation of other human tumors can be attributed to mutations in the retinoblastoma tumor suppressor gene(Rb). (affbiotech.com)
  • He found that RNR2 RNA levels increased dramatically, even more than the protein levels, upon exposure of cells to DNA damage and that mutations in RNR2 resulted in hypersensitivity to DNA damage. (the-scientist.com)
  • In this paper, we ask the following questions: How do these proteins and their mutations change the cell's fate - apoptosis or survival - when HMGB1 signal transduction is activated? (biomedcentral.com)
  • Expression of p63 is almost exclusively restricted to epithelial cells, mutations in this gene are infrequent, and its expression is increased in a variety of solid tumors, particularly those of the head and neck area 12,13 . (bvsalud.org)
Substrates5
  • Structural and biochemical data revealed that binding of phosphorylated p27 (phosp27) to CDK4 altered the kinase adenosine triphosphate site to promote phosphorylation of the retinoblastoma tumor suppressor protein (Rb) and other substrates. (rcsb.org)
  • Specific substrates for cdk-cyclin complexes include nuclear lamins, histones, oncogenes (e.g., c-abl and SV40 large T-Ag), tumor suppressor genes (e.g., retinoblastoma protein, Rb), nucleolin and others. (bdbiosciences.com)
  • Spy1 lacks the cyclin-binding site that mediates p27 and substrate affinity, explaining why Cdk-Spy1 is poorly inhibited by p27 and lacks specificity for substrates with cyclin-docking sites. (escholarship.org)
  • Binds to and inhibits cyclin-dependent kinase activity, preventing phosphorylation of critical cyclin-dependent kinase substrates and blocking cell cycle progression. (nih.gov)
  • HAUSP is normally a deubiquitinase that binds to gets rid of and MDM2 ubiquitin from Posaconazole it, stabilizing the proteins and and can ubiquitinate various other substrates [20, 21]. (healthandwellnesssource.org)
Inactivation5
  • p21 and other tumor suppressor genes' inactivation are therefore most likely involved in the first steps of the cancer model, with later stages possibly involving protooncogene activation and inflammation. (medscape.com)
  • Lundberg, A. S. & Weinberg, R. A. Functional inactivation of the retinoblastoma protein requires sequential modification by at least two distinct cyclin-cdk complexes. (nature.com)
  • 1. Rizzolio F, Lucchetti C, et al, Retinoblastoma tumor-suppressor protein phosphorylation and inactivation depend on direct interaction with Pin1. (signalchem.com)
  • 8 9 This lack of an absolute phenotype:genotype concordance could be attributed to incomplete screening of the p53 gene, inactivation of the p53 protein through interaction with other cellular proteins or viruses, or defects in other genes involved in p53 mediated cell cycle regulatory pathways. (bmj.com)
  • The need for cyclin D holoenzymes for inactivation of Rb as well as the advancement of cancers in mice prompted the introduction of CDK4/6 inhibitors to take care of a number of neoplasms [7, 8]. (healthandwellnesssource.org)
Cdks4
  • The role of cyclin B1 is to transition the cell from G2 to M phase but becomes unregulated in cancer cells where overexpression of cyclin B1 can lead to uncontrolled cell growth by binding to its partner Cdks. (wikipedia.org)
  • The activity of CDKs is controlled by their binding to coactivator subunits termed Cyclins, as well as by CDK inhibitory proteins termed CKIs. (intechopen.com)
  • Cyclins (regulatory subunits) bind to cdks (catalytic subunits) to form complexes that regulate the progression of the cell cycle. (bdbiosciences.com)
  • The main cyclin-cdks complexes formed in vertebrate cells are cyclin D-cdk4 (G0/G1), cyclin E-cdk2 (G1/S), cyclin A-cdk2 (S) and cyclin B1-cdk1 (G2/M). These complexes are regulated by activating and inhibitory phosphorylation events, as well as by interactions with small regulatory proteins including p21 and p27Kip1. (bdbiosciences.com)
Apoptosis4
Progression15
  • As a result, it negatively regulates cyclin-D-dependent phosphorylation of the retinoblastoma (pRb) gene product, thus blocking cell-cycle progression from G 1 -to S-phase ( 2 - 4 ). (iiarjournals.org)
  • The CDK4 activity associated with this cyclin was reported to be necessary for cell cycle progression through G2 phase into mitosis after UV radiation. (creative-biolabs.com)
  • Post-translational modifications (PTMs) of proteins are central to epigenetic regulation and cellular signalling, playing an important role in the pathogenesis and progression of numerous diseases. (bvsalud.org)
  • The retinoblastoma tumour suppressor protein (pRb) classically functions to regulate early cell cycle progression where it acts to enforce a number of checkpoints in response to cellular stress and DNA damage. (bvsalud.org)
  • At the molecular level, pitavastatin induced expression of the cyclin dependent kinase (CDK) inhibitor p21 in a cholesterol independent manner, blocked repressive phosphorylation of the Retinoblastoma tumor suppressor protein at CDK targeted sites, and reduced expression of E2F target genes required for progression through the G1/S boundary. (oncotarget.com)
  • The encoded protein binds to and inhibits the activity of cyclin-cyclin-dependent kinase2 or -cyclin-dependent kinase4 complexes, and thus functions as a regulator of cell cycle progression at G1. (nih.gov)
  • Although PDCD4 in general suppresses the development and progression of tumors, its specific biological functions differ by cell type [8] . (plos.org)
  • 18-20 p16 INK4a shares functional similarities with p53 in that it blocks progression through the cell cycle at G1/S by inhibiting CDK 4/6 mediated phosphorylation of Rb. (bmj.com)
  • proteins was connected with response, measured as both progression-free survival and general survival. (healthandwellnesssource.org)
  • Glycogen synthase kinase 3β (GSK-3β) represses cell cycle progression by directly phosphorylating cyclin D1 and indirectly regulating cyclin D1 transcription by inhibiting Wnt signaling. (elsevierpure.com)
  • Deregulation of proteins involved in these processes drive tumor progression and contributes to malignant phenotype. (oncotarget.com)
  • Pocket proteins Rb, p107 and p130 play central roles in cell cycle progression and differentiation. (eu.org)
  • Pocket proteins play essential roles in cell cycle progression, quiescence and differentiation, and their functional disruption is associated with human cancer. (eu.org)
  • The most studied function of the Rb protein is in the regulation of cell cycle progression at the G1/S boundary ( Giacinti,2006 ). (eu.org)
  • Conclusion: p63, p16, MIB, Cal A, Cys A are markedly expressed and p16 is strongly suppressed in oral cavity tumors, which suggests that the latter protein may play a role in negative regulation of cell cycle progression. (bvsalud.org)
Mutation2
  • Importantly, in the cohort studied, Ser312 mutation predisposes mice to develop thymic lymphomas and liver tumors, partly due to p53Ser312Ala's inability to fully induce a set of p53 target genes including p21 and cyclin G1. (ox.ac.uk)
  • Moreover, targeted mutation of Epm2a increased the phosphorylation of Ser9 on GSK-3β while having no effect on the phosphorylation of Ser21 on GSK-3α. (elsevierpure.com)
Recombinant Protein1
  • Anti-Cyclin A Antibody was produced by repeated immunizations with a recombinant protein corresponding to the human cyclin A. (signalchem.com)
CDK47
  • Palbociclib instead primarily targeted monomeric CDK4 and CDK6 (CDK4/6) in breast tumor cells. (rcsb.org)
  • This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activtiy is required for cell cycle G1/S transition. (creative-biolabs.com)
  • Cdk4-mediated phosphorylation of Rb protein is inhibited by p16, a product of a possible tumor suppressor gene. (nih.gov)
  • Functions in the nuclear localization and assembly of cyclin D-CDK4 complex and promotes its kinase activity towards RB1. (nih.gov)
  • At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D-CDK4 complex. (nih.gov)
  • Your choice of the tumor cell to senesce after CDK4/6 inhibition is manufactured following the cell provides withdrawn in the cell routine. (healthandwellnesssource.org)
  • This unrecognized transition previously, known as senescence after development arrest or SAGA today, is prompted in the CDK4/6 inhibitor-induced quiescent cell by the increased loss of MDM2 proteins and elevated focal localization from the chromatin-remodeling enzyme ATRX [17, 18]. (healthandwellnesssource.org)
Malignant3
  • Cyclin B1 can reside in the nucleus or the cytoplasm which can have an effect on the malignant potential of cyclin B1 when overexpressed in each location. (wikipedia.org)
  • Melanoma is the most malignant and lethal skin tumor owing to its high metastatic ability and the incidence of melanoma has been increasing over the years. (medsci.org)
  • Permissive histologic interpretation may result in the designation of some non-neoplastic Hürthle cell lesions as malignant tumors. (medscape.com)
Serine3
  • The protein encoded by this gene is a putative serine/threonine kinase that localizes to the mitotic apparatus and complexes with cell cycle controller CDC2 kinase in early mitosis. (cancerindex.org)
  • During G1, cyclin D-dependent kinase-mediated phosphorylation of Rb at Ser-795 marks the conversion of Rb from a transcriptionally repressive, hypophosphorylated state to an inactive, phosphorylated state, which may be sustained through mitosis by differential phosphorylation of up to 16 putative serine or threonine residues. (affbiotech.com)
  • In response to DNA double strand breaks, serine at position 15 of the TP53 (p53) tumor suppressor protein is rapidly phosphorylated by the ATM kinase. (reactome.org)
Important tumor1
  • Programmed cell death 4 (PDCD4) is an important tumor suppressor in the development of various human cancers [1] and inhibits translation rather than transcription. (plos.org)
Transcription5
  • The accumulation of both Cyclin and CKI proteins is tightly regulated at the level of transcription. (intechopen.com)
  • Cao L, Faha B, Dembski M, Tsai LH, Harlow E, Dyson N. Independent binding of the retinoblastoma protein and p107 to the transcription factor E2F. (bdbiosciences.com)
  • Protein arginine methyltransferase (PRMT) 5 is over-expressed in a variety of cancers and the master transcription regulator E2F1 is an important methylation target. (bvsalud.org)
  • Promotes G0-G1 transition when phosphorylated by CDK3/cyclin-C. Acts as a transcription repressor of E2F1 target genes. (abcam.cn)
  • Canonical Notch signaling activates the transcription of BMI1 proto‑oncogene polycomb ring finger, cyclin D1, CD44, cyclin dependent kinase inhibitor 1A, hes family bHLH transcription factor 1, hes related family bHLH transcription factor with YRPW motif 1, MYC, NOTCH3, RE1 silencing transcription factor and transcription factor 7 in a cellular context‑dependent manner, while non‑canonical Notch signaling activates NF‑κB and Rac family small GTPase 1. (spandidos-publications.com)
Induces2
  • Global CpG island hypermethylation, which induces epigenetic silencing of tumor suppressor genes, is also a unique feature of EBVaGC and is considered to be crucial for its carcinogenesis. (spandidos-publications.com)
  • A rise in the levels of the p53 protein induces the expression of p21 cyclin-dependent kinase inhibitor. (reactome.org)
Cdk27
  • Cyclin A is involved in both S-phase and G2/M transitions of the cell cycle through its association with cdk2 and cdk1, respectively. (bdbiosciences.com)
  • Cyclin A binds to S phase CDK2 and is required for the cell to progress through the S phase. (signalchem.com)
  • CDK2/Cyclin A is inhibited by the complex p21CIP. (signalchem.com)
  • We find that Spy1 confers structural changes to Cdk2 that obviate the requirement of Cdk activation loop phosphorylation. (escholarship.org)
  • Here, we show that cyclin E/Cdk2 phosphorylates and stabilizes the pro-survival Bcl-2 family protein Mcl-1, a key cell death resistance determinant to the small molecule Bcl-2 family inhibitors ABT-199 and ABT-737, mimetics of the Bcl-2 homology domain 3 (BH3). (oncotarget.com)
  • Cyclin E levels were elevated and there was increased association of cyclin E/Cdk2 with Mcl-1 in ABT-737-resistant compared to parental cells. (oncotarget.com)
  • Studies with Mcl-1 phosphorylation mutants show that cyclin E/Cdk2-dependent phosphorylation of Mcl-1 residues on its PEST domain resulted in increased Mcl-1 stability (Thr92, and Thr163) and Bim binding (Ser64). (oncotarget.com)
Kinase activity1
  • The N-terminal region of the protein binds CDC2 to form a complex showing reduced H1 histone kinase activity, indicating a role as a negative regulator of CDC2/cyclin A. In addition, the C-terminal kinase domain binds to its own N-terminal region, suggesting potential negative regulation through interference with complex formation via intramolecular binding. (cancerindex.org)
Pathway3
  • Defects of the retinoblastoma protein (pRb)/cyclin-D1/p16 pathway have been shown to play a critical role in the development of human malignancies. (iiarjournals.org)
  • We used a molecular pathway-based approach to analyze transcriptomic profiles of 59 colorectal tumors representing early and late preinvasive stages and the invasive stage of tumorigenesis. (biomedcentral.com)
  • We further revealed that chaetocin triggered the activation of Hippo pathway in ESCC cells, which is characterized by elevated phosphorylation levels of almost all core proteins in Hippo pathway, such as MST1 (Thr183), MST2 (Thr180), MOB1 (Thr35), LAST1 (Thr1079 and Ser909) and YAP (Ser127), ultimately leading to decreased nuclear translocation of YAP. (aging-us.com)
Specificity1
  • CRISPR/Cas gene editing depends on two components, a protein with DNA-nuclease activity (Cas) and a short RNA oligonucleotide (guide RNA, gRNA) that directs the nuclease activity of Cas enzymes to gRNA-complementary DNA sequences, thereby conferring specificity to the reaction. (biochem2.com)
Cancers7
  • Previous work has shown that high cyclin B1 expression levels are found in variety of cancers such as breast, cervical, gastric, colorectal, head and neck squamous cell, non-small-cell lung cancer, colon, prostate, oral and esophageal. (wikipedia.org)
  • High expression levels are usually seen before the tumor cells become immortalized and aneuploid which can contribute to the chromosomal instability and the aggressive nature of certain cancers. (wikipedia.org)
  • Mouse anti PTEN tumour suppressor antibody, clone A2b1, is specific for PTEN, a tumour suppressor protein located on the human chromosome 10 that is often mutated in various types of advanced cancers. (bio-rad-antibodies.com)
  • We examined the expression of p16 and Rb protein by means of immunohistochemistry in 61 non-small cell lung cancers and have demonstrated an inverse relationship between the expression of p16 and Rb protein: 28/30 specimens that did not stain for p16 stained for Rb and 21/31 p16-positive specimens did not stain for Rb. (nih.gov)
  • The PD0332991-induced downregulation of MDM2 and entrance into senescence is normally observed in a variety of types of cancers cell lines, including those produced from well-differentiated and dedifferentiated liposarcoma (WD/DDLS), breasts cancer tumor, non-small cell lung cancers, and glioma [18]. (healthandwellnesssource.org)
  • The crosstalk is regulated by tumor suppressor proteins, including ARF, P21 and FBXW7, which are also frequently mutated in many cancers. (biomedcentral.com)
  • The enzyme phosphatase and tensin homologue (PTEN) gene is one of the most frequently inactivated tumor suppressor genes in a variety of cancers. (biosemiotics2013.org)
Human tumors1
  • We isolated CSCs from low passage PDAC cell lines derived from human tumors and commercially available cell lines. (amegroups.org)
Regulator1
Inhibitors2
  • Cdk enzymatic activity is tightly controlled through cyclin interactions, posttranslational modifications, and binding of inhibitors such as the p27 tumor suppressor protein. (escholarship.org)
  • Collectively, our findings identify a novel mechanism of cyclin E-mediated Mcl-1 regulation that provides a rationale for clinical use of Bcl-2 family and Cdk inhibitors for Mcl-1-dependent tumors. (oncotarget.com)
Microenvironment3
  • We also summarize the connections between m7G modifications and cancer development, drug resistance, and tumor microenvironment as well as we discuss the research's future directions and trends. (beds.ac.uk)
  • Notch signaling cascades crosstalk with fibroblast growth factor and WNT signaling cascades in the tumor microenvironment to maintain cancer stem cells and remodel the tumor microenvironment. (spandidos-publications.com)
  • Level of resistance to these medications, either innate or acquired, continues to be suggested to become due to failing from the tumor cell to leave in response towards the medication, linked to failing to mobilize cells from the tumor microenvironment, or from the inability from the tumor cell to advance from reversible quiescence into even more permanent senescence. (healthandwellnesssource.org)
Suppression5
  • Phosphorylation of Ser312 contributes to tumor suppression by p53 in vivo. (ox.ac.uk)
  • The cellular mechanism for its tumor suppression remains unknown. (elsevierpure.com)
  • These data provide a cellular basis for the tumor suppression activity of laforin. (elsevierpure.com)
  • Expression of EBF2 in the PDX1 and E-cadherin-expressing and organoid forming pancreatic epithelial CSCs indeed induced ductal and acinar-like structural differentiation in vivo in tumors resulting in tumor suppression. (amegroups.org)
  • This study reveals a previously unrecognized function of EBF2 in regulating PDAC progenitor cell differentiation and tumor suppression. (amegroups.org)
PTEN1
  • PTEN exhibits protein phosphatase activity and can suppress the growth of glioma cells. (bio-rad-antibodies.com)
Antigens1
  • Pharmacological inhibition of PRMT5 or adjusting E2F1 levels qualitatively altered the repertoire of lncRNA-derived peptide antigens displayed by tumour cells. (bvsalud.org)
Vivo5
  • To understand the biological importance of Ser312 phosphorylation in vivo, we generated p53Ser312Ala knock-in mice. (ox.ac.uk)
  • Thus, we demonstrate that phosphorylation of Ser312 is required for p53 to function fully as a tumor suppressor in vivo. (ox.ac.uk)
  • When presented to the immune system as either ex vivo-loaded dendritic cells or expressed from a viral vector, lncRNA-derived peptides drove a potent antigen-specific CD8 T lymphocyte response, which translated into a significant delay in tumour growth. (bvsalud.org)
  • The overexpression of miRNA-1908 significantly promoted anchorage-independent growth in vitro and significantly increased the tumor forming potential in vivo . (biomedcentral.com)
  • Using ex vivo thymocytes and primary embryonic fibroblasts from Epm2a -/- mice, we show here a general function of laforin in the cell cycle regulation and repression of cyclin D1 expression. (elsevierpure.com)
Regulation5
  • While the exact mechanism that explains how cyclin B1 becomes overexpressed is not very well understood, previous work has shown that down regulation of cyclin B1 can lead to tumor regression. (wikipedia.org)
  • Structural genes encode proteins that are not involved in gene regulation. (p450inhibitors.com)
  • He mentioned this to David Stillman , who was at Stanford to interview for a faculty position, and who studied cell cycle regulation of proteins as a postdoc in Kim Nasmyth 's lab at the MRC Laboratory of Molecular Biology in the U.K. Stillman pointed out that ribonucleotide reductase was cell cycle regulated-rather than remaining stable, the RNA and protein levels fluctuate throughout the cell cycle. (the-scientist.com)
  • If some important proteins are mutated or there are defects in the signaling mechanisms, normal cell growth regulation will break down, possibly leading to the occurrence of cancer in the future. (biomedcentral.com)
  • Another protein, calgranulin A (Cal A), is involved in the regulation of several cell processes, including the cell cycle and cell differentiation. (bvsalud.org)
Contributes1
  • Cyclin B1 contributes to the switch-like all or none behavior of the cell in deciding to commit to mitosis. (wikipedia.org)
Regulatory4
  • Cyclin B1 is a regulatory protein involved in mitosis. (wikipedia.org)
  • p16 Ink4a downregulation leads to an activation of PKA-CREB-PGC1α signaling through increased phosphorylation of PKA regulatory subunits. (diabetesjournals.org)
  • Spy1/RINGO (Spy1) proteins bind and activate Cdk but are resistant to canonical regulatory mechanisms that establish cell-cycle checkpoints. (escholarship.org)
  • Studying RNR2' s regulatory elements, he found those that were necessary to induce the production of higher protein levels in response to DNA damage and identified factors that bind these DNA elements to mediate the response of RNR2 to DNA damage. (the-scientist.com)
Antibody7
  • ATCC CCL-243) were probed with the mouse anti-human cyclin A antibody at concentration of 2.0 µg/mL (lane 1), 1.0 µg/mL (lane 2), and 0.5 µg/mL (lane 3). (bdbiosciences.com)
  • Both methods yield antibody in solution that is free of most other soluble proteins, lipids, etc. (bdbiosciences.com)
  • Immunohistochemistry using Rabbit Anti-Cyclin A antibody. (signalchem.com)
  • Fixation: formalin fixed paraffin embedded.Antigen retrieval: not required.Primary antibody: Anti-Cyclin A at 1:500 for 1 hr at RT. (signalchem.com)
  • Western Blot of Rabbit Anti-Cyclin A antibody. (signalchem.com)
  • Primary antibody: Anti-Cyclin A at 1:400 for overnight at 4°C. Predicted/Observed size: 60kDa for Cyclin A. (signalchem.com)
  • The Anti-Cyclin-A antibody is ideal for investigators involved in cell signaling, cell biology and signal transduction research. (signalchem.com)
Complexes1
  • The nuclear envelope is a membranous structure containing large protein complexes supported by a network of nuclear lamins. (wikipedia.org)
Mitosis6
Dependent10
  • The protein is phosphorylated in a cell-cycle dependent manner, with late prophase phosphorylation remaining through metaphase. (cancerindex.org)
  • The cell cycle is a tightly regulated process that is controlled by the conserved cyclin-dependent kinase (CDK)-cyclin protein complex 1 . (nature.com)
  • Concurrent deletion of cyclin E1 and cyclin-dependent kinase 2 in hepatocytes inhibits DNA replication and liver regeneration in mice. (nature.com)
  • In particular, the p16/cyclin-dependent kinase inhibitor 2A (CDKN2A) gene located on chromosomal region 9p21 frequently is altered in several types of cancer. (iiarjournals.org)
  • Methylation at lysine (K) 810, which occurs within a critical CDK phosphorylation site and antagonises a CDK-dependent phosphorylation event at the neighbouring S807 residue, acts to hold pRb in the hypo-phosphorylated growth-suppressing state. (bvsalud.org)
  • Studies with pitavastatin in primary patient derived tumor cells and established PDA lines, revealed dose dependent growth inhibition. (oncotarget.com)
  • This gene encodes a potent cyclin-dependent kinase inhibitor. (nih.gov)
  • The Notch signaling network exerts oncogenic and tumor‑suppressive effects in a cancer stage‑ or (sub)type‑dependent manner. (spandidos-publications.com)
  • 13 p16 INK4a is a cyclin dependent kinase inhibitor that is frequently mutated or deleted in many human cancer cell lines 14-16 and some sporadic malignancies, including sarcomas, breast cancer, leukaemia, and brain tumours, which are all component tumours of LFS. (bmj.com)
  • Cyclin E knock-down restored ABT-737 sensitivity to acquired and inherently resistant Mcl-1-dependent tumor cells. (oncotarget.com)
Breast tumor1
  • For example, an increase in expression of cyclin B1/cdc2 is significantly higher in breast tumor tissue and shown to increase lymph node metastasis in breast cancer. (wikipedia.org)
Binds2
  • The LxCxE motif binds to all pocket proteins and is present in chromatin regulators such as HDAC and KDM5A and in viral proteins. (eu.org)
  • A phosphorylation downstream to the core motif acts as a switch that binds to a positively charged pocket only present in p107/p130. (eu.org)
Tissue4
  • This is supported by studies in knockout mice showing development of soft-tissue sarcomas, ovarian stromal cell tumors and a high sensitivity to carcinogenic treatments. (cancerindex.org)
  • Tissue culture supernatant is purified by either protein A/G or affinity purification methods. (bdbiosciences.com)
  • Tissue specimens were collected from fresh surgically resected tumors in 27 cases and in one case, ascitic effusion was taken just before a surgery with fine-needle aspiration biopsy (FNA). (iiarjournals.org)
  • The p63 protein, a homologue of p53, may be associated with tumor formation in the epithelial tissue, acting as an oncogene 11,12 . (bvsalud.org)
Structural1
  • Phosphorylation of the lamins by cyclin B1-Cdk1 causes them to dissociate, compromising the structural integrity of the nuclear envelope so that it breaks down. (wikipedia.org)
Differentiation4
  • Clinicopathologic characteristics including gender age pathology differentiation and tumor-node-metastasis staging have. (biosemiotics2013.org)
  • Here we show that cell differentiation suppresses tumor formation. (amegroups.org)
  • therefore, definitive differentiation of Hürthle cell carcinoma from Hürthle-cell adenoma is based on vascular invasion and/or capsular invasion, as well as on permanent histologic sections or extrathyroidal tumor spread and lymph node and systemic metastases. (medscape.com)
  • Cystatin A (Cys A), a cysteine protease inhibitor, is a precursor of proteins involves in keratinocyte keratinization, and is expressed during the late phase of differentiation of these cells. (bvsalud.org)
Posttranslational modifications1
  • The tumor suppressor p53 is a master sensor of stress, and posttranslational modifications are key in controlling its stability and transcriptional activities. (ox.ac.uk)
Localization2
  • Another mechanism by which cyclin B1-Cdk1 activity is regulated is through subcellular localization. (wikipedia.org)
  • Localization: Cyclin A is nuclear and cytoplasmic.Staining: Cyclin A as precipitated red signal with hematoxylin purple nuclear counterstain. (signalchem.com)
Inhibitory2
  • p38γ and δ promote heart hypertrophy by targeting the mTOR-inhibitory protein DEPTOR for degradation. (nature.com)
  • We studied tumor cell signaling in the cell subsets to understand the tumor-inhibitory potentials of EBF2. (amegroups.org)
Humans1
  • G2/mitotic-specific cyclin-B1 is a protein that in humans is encoded by the CCNB1 gene. (wikipedia.org)
Carcinogenesis1
  • But the potential role of miR-1908 in the carcinogenesis and tumor development of glioblastoma is unknown. (biomedcentral.com)
Lung3
  • membranous co-expression of CADM1 and LATS2 in lung tumors predicts good prognosis. (cancerindex.org)
  • Cell adhesion molecule-1 (CADM1) is a member of the immunoglobulin superfamily that functions as a tumor suppressor of lung tumors. (cancerindex.org)
  • Phase III clinical trials of Rova‑T for patients with small‑cell lung cancer and a phase III clinical trial of nirogacestat for patients with desmoid tumors are ongoing. (spandidos-publications.com)
Mitotic1
  • Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. (creative-biolabs.com)
Sequence1
  • Analyzing preinvasive tumors of different sizes can therefore shed light on the sequence of these alterations. (biomedcentral.com)
Interaction5
  • The protein interaction landscape of the human CMGC kinase group. (nature.com)
  • Faha B, Ewen ME, Tsai LH, Livingston DM, Harlow E. Interaction between human cyclin A and adenovirus E1A-associated p107 protein. (bdbiosciences.com)
  • The objective of this work is to identify dysregulated genes and pathways of ccRCC temporally according to systematic tracking of the dysregulated modules of reweighted Protein-Protein Interaction (PPI) networks. (hindawi.com)
  • With the advances of high-throughput experimental technologies, large amounts of Protein-Protein Interaction (PPI) data are uncovered, which make it possible to study proteins on a systematic level [ 7 , 8 ]. (hindawi.com)
  • But it has been noticed that PPI data are often associated with high false positive and false negative rates due to the limitations of the associated experimental techniques and the dynamic nature of protein interaction maps, which may have a negative impact on the performance of complex discovery algorithms [ 11 ]. (hindawi.com)
Concentration1
  • These high levels of cyclin B1 can also be associated to the extent of tumor invasion and aggressiveness therefore concentration of cyclin B1 can be used to determine the prognosis of cancer patients. (wikipedia.org)
Cellular1