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Protein CPorphyrinsOncogenesOncogene Proteins v-sisOncogene Protein tpr-metOncogene Protein v-mafProtein C DeficiencyOncogene Protein gp140(v-fms)Oncogene Protein p55(v-myc)Genes, mycOncogene Proteins v-mosProtein C InhibitorOncogene Protein p65(gag-jun)Oncogene Proteins v-rafOncogene Proteins v-fosActivated Protein C ResistanceOncogene Proteins v-erbBOncogene Proteins v-mybOncogene Protein v-crkOncogene Proteins v-ablProto-Oncogene Proteins c-mycOncogene Protein v-cblOncogene ProteinsCell Transformation, NeoplasticOncogene Protein p21(ras)Genes, rasOncogene Proteins v-relProtein SOncogene Proteins v-erbAThrombomodulinOncogene Proteins, ViralBlood Coagulation FactorsPulmonary Surfactant-Associated Protein COncogene Protein pp60(v-src)Factor VProto-OncogenesOncogene Proteins, FusionFactor VaThrombinGene Expression Regulation, NeoplasticMolecular Sequence DataBlood CoagulationBase SequenceOncogene Protein v-aktGene AmplificationMutationProto-Oncogene ProteinsCell LineProthrombinProtein S DeficiencyProto-Oncogene Proteins p21(ras)TransfectionCell Line, TransformedReceptors, Cell SurfaceCell Transformation, ViralAmino Acid SequenceReceptors, ThrombinSignal TransductionRNA, MessengerCell Line, TumorThrombophiliaBlood Coagulation DisordersGene Expression RegulationRetroviridae Proteins, OncogenicPapillomavirus E7 ProteinsTranscription, GeneticCell DivisionTranscription FactorsRecombinant ProteinsPartial Thromboplastin TimeMice, TransgenicDNA-Binding ProteinsCells, CulturedRetroviridaeDNA, NeoplasmGenes, Tumor SuppressorNeoplasmsTumor Cells, CulturedReceptor, PAR-1Protein BindingApoptosisAnticoagulants3T3 CellsGenes, srcFibroblastsras ProteinsGlycoproteinsTumor Suppressor Protein p53Translocation, GeneticFactor Xa1-Carboxyglutamic AcidGene ExpressionCell ProliferationPromoter Regions, GeneticBlood Coagulation TestsEnzyme ActivationNuclear ProteinsBinding SitesDisseminated Intravascular CoagulationRepressor Proteins
Genes have been identifiedTumor suppressorsTranscriptional activityMYCNEGFROverexpressionMutationsViralVitroPathwaysKinaseConstitutiveExpressionCyclinOncogenicTumourRegulatePhase ArrestMitochondriaTranscriptionCancersStabilityHumanRegulatoryCaspaseMicroenvironmentActivityTargetsProgressionGene activationReceptorOccursControlsServesCause cancerLevelsGenerallySpecificallyCellsRoleCell deathPositiveProductNormalLeadTypesNoteGrowthPatients
Genes have been identified2
Tumor suppressors1
Transcriptional activity1
  • This is because oncogenes can alter transcriptional activity, stability, or protein translation of another gene that directly or indirectly controls cell growth. (edu.vn)
MYCN5
  • This Recombinant Human MYCN protein is an essential resource for cancer researchers. (cusabio.com)
  • Equipped with an N-terminal 6xHis-tag, our Recombinant Human MYCN protein facilitates effortless purification and detection. (cusabio.com)
  • Choose between liquid and lyophilized powder forms to best suit your experimental requirements and elevate your research with our Recombinant Human MYCN protein. (cusabio.com)
  • Review: In vitro glutathione S-transferase (GST) pull-down assay with recombinant GST-CCNT1, GST-CDK9, and GST-EAF1 together with His-tagged MYCN proteins demonstrated that MYCN directly binds to EAF1 with the highest affinity. (cusabio.com)
  • Canonically, neuroblastomas can be classified according to the MYCN (N-myc proto-oncogene protein) gene amplification, a common marker of tumor aggressiveness and poor prognosis. (bvsalud.org)
EGFR1
  • EGFR downstream signaling promotes constitutive activation of TKIs domain due to the mutation in exon 19 and exon 21 (L858R point mutation), which leads to cell proliferation, invasion, metastasis, and angiogenesis, causing lung adenocarcinoma. (lidsen.com)
Overexpression3
  • Considering multiple signaling pathways converge on MYC it is not surprising that overexpression is frequently observed in multiple tumor types where elevated MYC levels are associated with malignant transformation and tumor proliferation [ 5 ]. (oncotarget.com)
  • Overexpression of the oncogene can lead to uncontrolled cell growth. (edu.vn)
  • Overexpression of myc transforms normal B cells into cancerous cells that continue to grow uncontrollably. (edu.vn)
Mutations5
  • A proto-oncogene is a gene that becomes an oncogene, a gene that has the potential to cause cancer, through mutations or an increase in expression. (shu.edu)
  • Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. (nature.com)
  • MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. (nature.com)
  • However, most lung adenocarcinomas either lack an identifiable driver oncogene, or harbour mutations in KRAS and are therefore still treated with conventional chemotherapy. (nature.com)
  • Different cancer types tend to depend on a limited number of 'driver' oncogene mutations. (cancerquest.org)
Viral3
  • The protein consists of four conserved domains (RNA-Binding Domain (TRBD), fingers, palm and thumb), organized into a "right hand" ring configuration that shares common features with retroviral reverse transcriptases, viral RNA replicases and bacteriophage B-family DNA polymerases. (wikipedia.org)
  • In a number of studies, it has been shown that while only a select number of cells are actually infected with the virus, numerous viral proteins are released into the cancer and stromal cells in the microenvironment and these viral proteins are known to affect tumor behavior and aggressiveness. (surgicalneurologyint.com)
  • Rather, only a few cells need to be infected, with the release of viral proteins from the viruses, which occupy most if not all of the tumor cells, including stromal cells. (surgicalneurologyint.com)
Vitro1
  • The c-myc protein is localized in the nucleus and can physically associate with RB protein in vitro, hence c-myc may functionally antagonize RB function. (wdv.com)
Pathways2
  • Stable monoubiquitinated form of wild type p53, accumulates in the cytoplasm and interacts with BAK or BAX proteins in mitochondria to induce apoptosis Thus Kevetrin activates both transcription dependent and transcription independent pathways to promote apoptosis. (shu.edu)
  • Additionally, scientists have found that this relationship is an important part of a number of complex cellular signaling cascade pathways, including Ras, β-catenin, myc, Rb, and many more. (shu.edu)
Kinase4
  • We investigated the mechanism of action and identified the activation of cell signaling that involves protein kinase C. (bvsalud.org)
  • 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)
  • Ras-dependent activation of MAP kinase pathway mediated by G-proteinβγ subunits. (gutkindlab.org)
  • Linkage of G protein-coupled receptors to the MAPK signaling pathway through PI 3-kinase g. (gutkindlab.org)
Constitutive1
  • It has been known for many years that the fundamental transforming event in BL is the translocation of the MYC gene, and the events that bring about this translocation and those that allow cells to survive with the constitutive expression of MYC have been the subject of intense investigation. (bmj.com)
Expression7
  • Zusammengefasst verhinderte das N. lobata Extrakt die Expression wichtiger Proto Onkogene, dessen exakten Mechanismus es noch zu klären gilt. (univie.ac.at)
  • The elevated expression of p53 leads to greater stability, which also induces the regulatory protein Mdm2. (shu.edu)
  • Perturbation of mitochondrial function using a number of conventional and novel inhibitors resulted in the decreased expression of MYC mRNA. (oncotarget.com)
  • Our data demonstrates the existence of a homeostasis mechanism whereby mitochondrial function controls MYC expression. (oncotarget.com)
  • The up-regulation of proto-oncogene may be the consequence of epigenetic control of gene expression by demethylase, and mbd2 is involved in the regulation of hMSH2 expression in human gastric cancer. (wjgnet.com)
  • As activation of c-myc expression promotes cell proliferation and blocks differentiation, it may positively regulate cell growth. (wdv.com)
  • Regulation of c-myc expression by PDGF through Rho GTPases. (gutkindlab.org)
Cyclin2
  • One example of a gene modification that alters the growth rate is increased phosphorylation of cyclin B, a protein that controls the progression of a cell through the cell cycle and serves as a cell-cycle checkpoint protein. (edu.vn)
  • Many proteins, including cyclin B, control these checkpoints. (edu.vn)
Oncogenic1
Tumour4
  • Specifically, the concepts of tumour heterogeneity, oncogene addiction, non-oncogene addiction, tumour initiating cells, tumour microenvironment, non-coding sequences and DNA damage response will be reviewed. (bmj.com)
  • 1 BL tumour cells usually express IgM, 13 - 15 B-cell markers such as CD19, CD20 and CD22 and markers of germinal centre (GC) centroblasts such as CD10, BCL6 4 and the human germinal centre-associated lymphoma (HGAL) protein. (bmj.com)
  • However, the tumour cells have undergone hypermutation, 21 23 a feature of the GC reaction during B-cell activation and differentiation. (bmj.com)
  • The c-myc does not inhibit the activity of another tumour supressor, p53 (ref. 12). (wdv.com)
Regulate4
  • Replacement of wild-type RB can suppress the tumorigenicity of some of these cells, suggesting that the RB protein (Rb) may negatively regulate cell growth. (wdv.com)
  • The small GTP-binding proteins Rac1 and Cdc42 regulate the activity of the JNK (SAPK) signaling pathway. (gutkindlab.org)
  • Some proto-oncogenes work to regulate cell death. (cancerquest.org)
  • The mutant proteins often retain some of their capabilities but are no longer sensitive to the controls that regulate the normal form of the protein. (cancerquest.org)
Phase Arrest2
  • Die Aktivierung des zellregulatorischen Proteins Chk2 und der damit korrelierende S Phase Arrest nach 24 Stunden wäre demnach durch DNA Schäden aufgrund des vorschreitenden Zelltod verursacht. (univie.ac.at)
  • Abrogation by c-myc of G1 phase arrest induced by RB protein but not by p53. (wdv.com)
Mitochondria3
  • Here we describe a novel link between mitochondria and MYC levels. (oncotarget.com)
  • Knockdown of let-7 family or miR-34a-5p could partially restore MYC levels following mitochondria damage. (oncotarget.com)
  • We also identified let-7 -dependent downregulation of the MYC mRNA chaperone, CRD-BP (coding region determinant-binding protein) as an additional control following mitochondria damage. (oncotarget.com)
Transcription6
  • In spite of such a broad range of potential targets, the MYC protein is surprisingly a relatively weak transcriptional activator and is presumed to function as a general enhancer of transcription [ 3 , 4 ]. (oncotarget.com)
  • Changes in epigenetic regulation, transcription, RNA stability, protein translation, and post-translational control can be detected in cancer. (edu.vn)
  • Therefore, changes in histone acetylation (epigenetic modification that leads to gene silencing), activation of transcription factors by phosphorylation, increased RNA stability, increased translational control, and protein modification can all be detected at some point in various cancer cells. (edu.vn)
  • The p53 protein itself functions as a transcription factor. (edu.vn)
  • Myc is a transcription factor that is aberrantly activated in Burkett's Lymphoma, a cancer of the lymph system. (edu.vn)
  • Transcription levels of Dnmt1, mbd2, MeCP2, p16 INK4A , hMSH2 and c-myc were detected by using real-time PCR or RT-PCR. (wjgnet.com)
Cancers1
  • Mdm2 is a proto-oncogene that is amplified in approximately 7% of cancers and is frequently seen in soft tissue tumors. (shu.edu)
Stability1
  • The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. (cusabio.com)
Human3
  • The human TERT gene (hTERT) is translated into a protein of 1132 amino acids. (wikipedia.org)
  • Oncomodulatory viruses, such as human cytomegaloviruses (HCMV), are known to release over 200 proteins, many of which can alter tumor behavior [ Table 1 ]. (surgicalneurologyint.com)
  • To explore the effect of DNA methyltransferase, demethylase and methyl-CpG binding protein MeCP2 on the expressions and methylation of hMSH2 and proto-oncogene in human gastric cancer. (wjgnet.com)
Regulatory1
  • Changes in the levels of cell regulatory proteins were observed thereafter, in particular, Chk2 was activated upon DNA cleavage initiated by the foregoing onset of apoptosis,and this correlated with the S phase cell arrest after 24 hours. (univie.ac.at)
Caspase2
  • The anti proliferative properties of the C. morifolia petroleum ether extract turned out to be attributable to the induction of cell death as the apoptotic executioner protein caspase 3 was already activated within 2 hours of incubation. (univie.ac.at)
  • Mechanism of action studies showed that Kevetrin strongly induced apoptosis by activation of Caspase 3 and cleavage of PARP. (shu.edu)
Microenvironment1
  • Activation of this factor occurs in the stromal cells, tumor cells, and invading immune cells within the tumor microenvironment. (surgicalneurologyint.com)
Activity4
  • Mdm2 protein has the activity of an ubiquitin ligase, which allows for the targeted degradation of its substrates, including p53. (shu.edu)
  • There are many proteins that are turned on or off (gene activation or gene silencing) that dramatically alter the overall activity of the cell. (edu.vn)
  • In normal cells, both internal and external signals control the activity of the oncogenes. (cancerquest.org)
  • A key feature of oncogene activity is that a single altered copy leads to unregulated growth. (cancerquest.org)
Targets2
  • Genes encoding proteins involved in cell growth, metabolism, ribosome biogenesis, protein synthesis and mitochondrial function have all be defined as potential MYC targets. (oncotarget.com)
  • Illuminating the Onco-GPCRome: Novel G protein-coupled receptor-driven oncocrine networks and targets for cancer immunotherapy. (gutkindlab.org)
Progression1
  • The proto-oncogene c- MYC (referred to as MYC ) represents a master regulator via integration of external mitogenic signaling with the activation of genes required for cell cycle progression [ 1 ]. (oncotarget.com)
Gene activation1
  • Although inherently unstable, growth factor signaling leads to increased MYC levels and its association with MAX forming a transcriptional heterodimer complex that binds to conserved E-box elements (consensus CACGTG) in the promoters of target genes leading to gene activation [ 1 ]. (oncotarget.com)
Receptor2
  • Akt plays a central role in sarcomagenesis induced by Kaposi's sarcoma herpesvirus-encoded G protein-coupled receptor. (gutkindlab.org)
  • The TSC2/mTOR pathway drives endothelial cell transformation induced by the Kaposi's Sarcoma Associated Herpesvirus G Protein-Coupled Receptor. (gutkindlab.org)
Occurs1
  • Moreover, the breakpoint in the Ig gene to which MYC is transferred in eBL occurs at the V(D)J region, suggesting that translocation occurs during V(D)J recombination. (bmj.com)
Controls1
  • A Platform of Synthetic Lethal Gene Interaction Networks Reveals That the GNAQ Uveal Melanoma Oncogene Controls the Hippo Pathway Through FAK. (gutkindlab.org)
Serves2
  • This full-length protein (1-464aa) is expressed in yeast and serves as a powerful tool in various oncology applications. (cusabio.com)
  • The MYC proto-oncogene serves as a rheostat coupling mitogenic signaling with the activation of genes regulating growth, metabolism and mitochondrial biogenesis. (oncotarget.com)
Cause cancer1
Levels1
  • This decrease in MYC mRNA occurred concomitantly with an increase in the levels of tumor-suppressive miRNAs such as members of the let-7 family and miR-34a-5p . (oncotarget.com)
Generally1
  • 10 Genes that, when activated, contribute to the carcinogenesis are generally termed proto-oncogenes. (bmj.com)
Specifically1
  • Thus, c-myc and RB specifically antagonize one another in the cell. (wdv.com)
Cells2
  • Histone proteins that surround that region lack the acetylation modification that is present when the genes are expressed in normal cells. (edu.vn)
  • Genes whose protein products stimulate or enhance the division and viability of cells. (cancerquest.org)
Role1
  • Aberrations in NF1 , MET , ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. (nature.com)
Cell death1
Positive1
  • Proto-oncogenes are positive cell-cycle regulators. (edu.vn)
Product1
  • Phosphotyrosine-dependent activation of Rac-1 GDP/GTP exchange by the vav proto-oncogene product. (gutkindlab.org)
Normal2
  • The J segments flanking MYC translocated breakpoints typically exhibit deletions and/or additions of base pairs characteristic of normal Ig V(D)J segment rearrangement. (bmj.com)
  • The normal versions of genes in the first group are called proto-oncogenes. (cancerquest.org)
Lead1
  • Alterations on chromatin insulator elements (IEs) might lead to aberrant chromatin remodeling via DNA loop formation, causing oncogene reactivation in several types of cancer, including GBM. (biomedcentral.com)
Types1
  • Selected oncogenes that have been associated with numerous cancer types are described in more detail below. (cancerquest.org)
Note2
  • Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request. (cusabio.com)
  • Note that by convention gene names are italicized and the proteins they make are not. (cancerquest.org)
Growth1
  • The cell cycle is a finely orchestrated event dependent on the sequential activation of genes regulating cell growth and metabolism. (oncotarget.com)
Patients1