Database : MEDLINE
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[PMID]: 29524560
[Au] Autor:Khan AQ; Kuttikrishnan S; Siveen KS; Prabhu KS; Shanmugakonar M; Al Naemi H; Haris M; Dermime S; Uddin S
[Ad] Address:Academic Health System, Translational Research Institute, Hamad Medical Corporation, Doha, Qatar.
[Ti] Title:RAS-mediated oncogenic signaling pathways in human malignancies.
[So] Source:Semin Cancer Biol;, 2018 Mar 07.
[Is] ISSN:1096-3650
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Abnormally activated RAS proteins are the main oncogenic driver that governs the functioning of major signaling pathways involved in the initiation and development of human malignancies. Mutations in RAS genes and or its regulators, most frequent in human cancers, are the main force for incessant RAS activation and associated pathological conditions including cancer. In general, RAS is the main upstream regulator of the highly conserved signaling mechanisms associated with a plethora of important cellular activities vital for normal homeostasis. Mutated or the oncogenic RAS aberrantly activates a web of interconnected signaling pathways including mitogen-activated protein kinases (MAPK), phosphoinositide-3 kinase (PI3K)/AKT pathways, protein kinase C (PKC) and ral guanine nucleotide dissociation stimulator (RalGDS), etc., leading to uncontrolled transcriptional expression and reprogramming in the functioning of a range of nuclear and cytosolic effectors critically associated with the hallmarks of carcinogenesis. This review highlights the recent literature on how oncogenic RAS negatively use its signaling web in deregulating the expression and functioning of various effector molecules in the pathogenesis of human malignancies.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 109234 MEDLINE  
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[PMID]: 29524541
[Au] Autor:Lago S; Nadai M; Rossetto M; Richter SN
[Ad] Address:Department of Molecular Medicine, University of Padua, via Gabelli 63, 35121 Padua, Italy.
[Ti] Title:Surface Plasmon Resonance kinetic analysis of the interaction between G-quadruplex nucleic acids and an anti-G-quadruplex monoclonal antibody.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: G-quadruplexes (G4s) are nucleic acids secondary structures formed in guanine-rich sequences. Anti-G4 antibodies represent a tool for the direct investigation of G4s in cells. Surface Plasmon Resonance (SPR) is a high sensitive technology, suitable for assessing the affinity between biomolecules. We here aimed at improving the orientation of an anti-G4 antibody (1H6) on SPR sensor chip for optimizing the detection of binding antigens. METHODS: SPR was employed for the characterization of 1H6 interaction with G4 and non-G4 oligonucleotides. Dextran-functionalized sensor chips were used both in covalent coupling and capturing procedures. RESULTS: The use of two leading molecule for orienting the antibody of interest allowed to improve its activity form completely non-functional to 65% active. Thus, the specificity of 1H6 for G4 structures has been assessed with high sensitivity and reliability. CONCLUSIONS: The optimization of 1H6 immobilization protocol for SPR biosensing, allowed us to determine its affinity and specificity for G4 antigens with a higher sensitivity with respect to other in vitro assays such as ELISA. 1H6 specificity is a fundamental assumption for the future utilization of the antibody for monitoring G4s directly in cells. GENERAL SIGNIFICANCE: The heterogeneous orientation of amine-coupling immobilized ligands is a general problem that often leads to partial or complete inactivation of the molecules. Here we described a new strategy for improving ligand orientation: driving it from two sides. This principle can be virtually applied to each molecule which loses its activity or is poorly immobilized after standard coupling to SPR chip surface.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 109234 MEDLINE  
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[PMID]: 29524424
[Au] Autor:Shinohara Y; Tsukimoto M
[Ad] Address:Department of Radiation Biosciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda-shi, Chiba, Japan.
[Ti] Title:Guanine and inosine nucleotides/nucleosides suppress murine T cell activation.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Damaged tissues and cells release intracellular purine nucleotides, which serve as intercellular signaling factors. We previously showed that exogenously added adenine nucleotide (250 µM ATP) suppressed the activation of murine splenic T lymphocytes. Here, we examined the effects of other purine nucleotides/nucleosides on mouse T cell activation. First, we found that pretreatment of mouse spleen T cells with 250 µM GTP, GDP, GMP, guanosine, ITP, IDP, IMP or inosine significantly reduced the release of stimulus-inducible cytokine IL-2. This suppression of IL-2 release was not caused by induction of cell death. Further studies with GTP, ITP, guanosine and inosine showed that pretreatment with these nucleotides/nucleosides also suppressed release of IL-6. However, these nucleotides/nucleosides did not suppress stimulus-induced phosphorylation of ERK1/2, suggesting that the suppression of the release of inflammatory cytokines does not involve inhibition of ERK1/2 signaling. In contrast to ATP pretreatment at the same concentration, guanine or inosine nucleotides/nucleosides did not attenuate the expression of CD25. Our findings indicate that exogenous guanine or inosine nucleotides/nucleosides can suppress inflammatory cytokine release from T cells, and may be promising candidates for use as supplementary agents in the treatment of T cell-mediated immune diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 109234 MEDLINE  
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[PMID]: 29514977
[Au] Autor:Halaby SL; Fromme JC
[Ad] Address:Cornell University, United States.
[Ti] Title:The HUS-box is required for allosteric regulation of the Sec7 Arf-GEF.
[So] Source:J Biol Chem;, 2018 Mar 07.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Golgi complex is the central membrane and protein sorting station in eukaryotic cells. Activation of ADP ribosylation factor (Arf) GTPases is essential for vesicle formation via recruitment of cargo adaptors and coat proteins necessary for Golgi trafficking. Arf activation is spatially and temporally regulated by distinct guanine nucleotide exchange factors (GEFs) at different Golgi compartments. The yeast Arf-GEF Sec7 is a conserved and essential activator of Arf1 at the trans-Golgi network. Sec7 contains a highly conserved regulatory region, the HUSbox, with an unknown mechanistic role. In this study we explore how the HUS-box, which is N-terminal to the catalytic domain, acts together with C-terminal regulatory domains in the allosteric activation of Sec7. We report that mutation of the HUS-box disrupts positive feedback and allosteric activation of Sec7 by the GTPase Ypt31, a yeast Rab11 homolog. Taken together, our results support a model in which the inter- and intramolecular interactions of the HUS-box and C-terminus are necessary for the allosteric activation of Sec7.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  5 / 109234 MEDLINE  
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[PMID]: 29510672
[Au] Autor:Tokan V; Puterova J; Lexa M; Kejnovsky E
[Ad] Address:Department of Plant Developmental Genetics, Institute of Biophysics, Czech Academy of Sciences, Kralovopolska 135, 61200, Brno, Czech Republic.
[Ti] Title:Quadruplex DNA in long terminal repeats in maize LTR retrotransposons inhibits the expression of a reporter gene in yeast.
[So] Source:BMC Genomics;19(1):184, 2018 Mar 06.
[Is] ISSN:1471-2164
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Many studies have shown that guanine-rich DNA sequences form quadruplex structures (G4) in vitro but there is scarce evidence of guanine quadruplexes in vivo. The majority of potential quadruplex-forming sequences (PQS) are located in transposable elements (TEs), especially close to promoters within long terminal repeats of plant LTR retrotransposons. RESULTS: In order to test the potential effect of G4s on retrotransposon expression, we cloned the long terminal repeats of selected maize LTR retrotransposons upstream of the lacZ reporter gene and measured its transcription and translation in yeast. We found that G4s had an inhibitory effect on translation in vivo since "mutants" (where guanines were replaced by adenines in PQS) showed higher expression levels than wild-types. In parallel, we confirmed by circular dichroism measurements that the selected sequences can indeed adopt G4 conformation in vitro. Analysis of RNA-Seq of polyA RNA in maize seedlings grown in the presence of a G4-stabilizing ligand (NMM) showed both inhibitory as well as stimulatory effects on the transcription of LTR retrotransposons. CONCLUSIONS: Our results demonstrate that quadruplex DNA located within long terminal repeats of LTR retrotransposons can be formed in vivo and that it plays a regulatory role in the LTR retrotransposon life-cycle, thus also affecting genome dynamics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12864-018-4563-7

  6 / 109234 MEDLINE  
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[PMID]: 29444450
[Au] Autor:Burns MC; Howes JE; Sun Q; Little AJ; Camper DV; Abbott JR; Phan J; Lee T; Waterson AG; Rossanese OW; Fesik SW
[Ad] Address:Vanderbilt University School of Medicine, Department of Biochemistry, 2215 Garland Ave., 607 Light Hall, Nashville, TN, 37232-0146, USA.
[Ti] Title:High-throughput screening identifies small molecules that bind to the RAS:SOS:RAS complex and perturb RAS signaling.
[So] Source:Anal Biochem;548:44-52, 2018 Feb 11.
[Is] ISSN:1096-0309
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:K-RAS is mutated in approximately 30% of human cancers, resulting in increased RAS signaling and tumor growth. Thus, RAS is a highly validated therapeutic target, especially in tumors of the pancreas, lung and colon. Although directly targeting RAS has proven to be challenging, it may be possible to target other proteins involved in RAS signaling, such as the guanine nucleotide exchange factor Son of Sevenless (SOS). We have previously reported on the discovery of small molecules that bind to SOS1, activate SOS-mediated nucleotide exchange on RAS, and paradoxically inhibit ERK phosphorylation (Burns et al., PNAS, 2014). Here, we describe the discovery of additional, structurally diverse small molecules that also bind to SOS1 in the same pocket and elicit similar biological effects. We tested >160,000 compounds in a fluorescence-based assay to assess their effects on SOS-mediated nucleotide exchange. X-Ray structures revealed that these small molecules bind to the CDC25 domain of SOS1. Compounds that elicited high levels of nucleotide exchange activity in vitro increased RAS-GTP levels in cells, and inhibited phospho ERK levels at higher treatment concentrations. The identification of structurally diverse SOS1 binding ligands may assist in the discovery of new molecules designed to target RAS-driven tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 109234 MEDLINE  
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[PMID]: 29306001
[Au] Autor:Zupancic E; Curato C; Kim JS; Yeini E; Porat Z; Viana AS; Globerson-Levin A; Waks T; Eshhar Z; Moreira JN; Satchi-Fainaro R; Eisenbach L; Jung S; Florindo HF
[Ad] Address:Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal; Department of Immunology, Weizmann Institute of Science, Rehovot, Israel; Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Faculty of Medicine (Polo I), Coimbra, Port
[Ti] Title:Nanoparticulate vaccine inhibits tumor growth via improved T cell recruitment into melanoma and huHER2 breast cancer.
[So] Source:Nanomedicine;14(3):835-847, 2018 Jan 03.
[Is] ISSN:1549-9642
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nanoparticulate vaccines are promising tools to overcome cancer immune evasion. However, a deeper understanding on nanoparticle-immune cell interactions and treatments regime is required for optimal efficacy. We provide a comprehensive study of treatment schedules and mode of antigen-association to nanovaccines on the modulation of T cell immunity in vivo, under steady-state and tumor-bearing mice. The coordinated delivery of antigen and two adjuvants (Monophosphoryl lipid A, oligodeoxynucleotide cytosine-phosphate-guanine motifs (CpG)) by nanoparticles was crucial for dendritic cell activation. A single vaccination dictated a 3-fold increase on cytotoxic memory-T cells and raised antigen-specific immune responses against B16.M05 melanoma. It generated at least a 5-fold increase on IFN-γ cytokine production, and presented over 50% higher lymphocyte count in the tumor microenvironment, compared to the control. The number of lymphocytes at the tumor site doubled with triple immunization. This lymphocyte infiltration pattern was confirmed in mammary huHER2 carcinoma, with significant tumor reduction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 109234 MEDLINE  
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[PMID]: 29523808
[Au] Autor:Vanshylla K; Bartsch C; Hitzing C; Krümpelmann L; Wienands J; Engels N
[Ad] Address:University Medical Center Goettingen, Institute of Cellular & Molecular Immunology, Humboldtallee 34, 37073, Goettingen, Germany.
[Ti] Title:Grb2 and GRAP connect the B cell antigen receptor to Erk MAP kinase activation in human B cells.
[So] Source:Sci Rep;8(1):4244, 2018 Mar 09.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The B cell antigen receptor (BCR) employs enzymatically inactive adaptor proteins to facilitate activation of intracellular signaling pathways. In animal model systems, adaptor proteins of the growth factor receptor-bound 2 (Grb2) family have been shown to serve critical functions in lymphocytes. However, the roles of Grb2 and the Grb2-related adaptor protein (GRAP) in human B lymphocytes remain unclear. Using TALEN-mediated gene targeting, we show that in human B cells Grb2 and GRAP amplify signaling by the immunoglobulin tail tyrosine (ITT) motif of mIgE-containing BCRs and furthermore connect immunoreceptor tyrosine-based activation motif (ITAM) signaling to activation of the Ras-controlled Erk MAP kinase pathway. In contrast to mouse B cells, BCR-induced activation of Erk in human B cells is largely independent of phospholipase C-É£ activity and diacylglycerol-responsive members of Ras guanine nucleotide releasing proteins. Together, our results demonstrate that Grb2 family adaptors are critical regulators of ITAM and ITT signaling in naïve and IgE-switched human B cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-22544-x

  9 / 109234 MEDLINE  
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[PMID]: 29523066
[Au] Autor:Chernikov AV; Gudkov SV; Usacheva AM; Bruskov VI
[Ad] Address:Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, 142292, Russia. anatole@inbox.ru.
[Ti] Title:Exogenous 8-Oxo-7,8-dihydro-2'-deoxyguanosine: Biomedical Properties, Mechanisms of Action, and Therapeutic Potential.
[So] Source:Biochemistry (Mosc);82(13):1686-1701, 2017 Dec.
[Is] ISSN:1608-3040
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:8-Oxo-7,8-dihydroguanine (8-oxo-G) is a key biomarker of oxidative damage to DNA in cells, and its genotoxicity is well-studied. In recent years, it has been confirmed experimentally that free 8-oxo-G and molecules containing it are not merely inert products of DNA repair or degradation, but they are actively involved in intracellular signaling. In this review, data are systematized indicating that free 8-oxo-G and oxidized (containing 8-oxo-G) extracellular DNA function in the body as mediators of stress signaling and initiate inflammatory and immune responses to maintain homeostasis under the action of external pathogens, whereas exogenous 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dGuo) exhibits pronounced antiinflammatory and antioxidant properties. This review describes known action mechanisms of oxidized guanine and 8-oxo-G-containing molecules. Prospects for their use as a therapeutic target are considered, as well as a pharmaceutical agent for treatment of a wide range of diseases whose pathogenesis is significantly contributed to by inflammation and oxidative stress.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process
[do] DOI:10.1134/S0006297917130089

  10 / 109234 MEDLINE  
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[PMID]: 29408272
[Au] Autor:Saif I; Kasmi Y; Allali K; Ennaji MM
[Ad] Address:Team of Virology, Oncology and Medical Biotechnologies, Laboratory of Virology, Microbiology, Quality and Biotechnologies/ETB, Faculty of Science sand Technologies-Mohammedia, Hassan II University of Casablanca, Morocco.
[Ti] Title:Prediction of DNA methylation in the promoter of gene suppressor tumor.
[So] Source:Gene;651:166-173, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The epigenetics methylation of cytosine is the most common epigenetic form in DNA sequences. It is highly concentrated in the promoter regions of the genes, leading to an inactivation of tumor suppressors regardless of their initial function. In this work, we aim to identify the highly methylated regions; the cytosine-phosphate-guanine (CpG) island located on the promoters and/or the first exon gene known for their key roles in the cell cycle, hence the need to study gene-gene interactions. The Frommer and hidden Markov model algorithms are used as computational methods to identify CpG islands with specificity and sensitivity up to 76% and 80%, respectively. The results obtained show, on the one hand, that the genes studied are suspected of developing hypermethylation in the promoter region of the gene involved in the case of a cancer. We then showed that the relative richness in CG results from a high level of methylation. On the other hand, we observe that the gene-gene interaction exhibits co-expression between the chosen genes. This let us to conclude that the hidden Markov model algorithm predicts more specific and valuable information about the hypermethylation in gene as a preventive and diagnostics tools for the personalized medicine; as that the tumor-suppresser-genes have relative co-expression and complementary relations which the hypermethylation affect in the samples studied in our work.
[Mh] MeSH terms primary: Computational Biology/methods
CpG Islands
DNA Methylation
Genes, Tumor Suppressor
Promoter Regions, Genetic
[Mh] MeSH terms secundary: Algorithms
DNA, Neoplasm
Datasets as Topic
Epistasis, Genetic
Humans
Markov Chains
Models, Genetic
Neoplasms/genetics
[Pt] Publication type:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Name of substance:0 (DNA, Neoplasm)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180207
[St] Status:MEDLINE


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