0000000000725012

AUTHOR

Negusse Habtemichael

showing 2 related works from this author

The Mutation without childrenrgl Causes Ecdysteroid Deficiency in Third-Instar Larvae of Drosophila melanogaster

2000

Larvae homozygous for the recessive lethal allele without children(rgl) (woc(rgl)) fail to pupariate. Application of exogenous 20-hydroxyecdysone elicits puparium formation and pupation. Ecdysteroid titer measurements on mutant larvae show an endocrine deficiency in the brain-ring gland complex, which normally synthesizes ecdysone, resulting in a failure of the larvae to achieve a threshold whole body hormone titer necessary for molting. Ultrastructural investigation revealed extensive degeneration of the prothoracic cells of the ring gland in older larvae. The woc gene, located in polytene chromosomal region 97F, consists of 11 exons. A 6.8-kb transcript is expressed throughout development…

DNA Complementaryanimal structuresMolecular Sequence DataMutantwithout childrenmental retardation03 medical and health scienceschemistry.chemical_compoundExon0302 clinical medicineAnimalsDrosophila ProteinsHumansAmino Acid SequenceecdysoneMolecular BiologyAlleles030304 developmental biology0303 health sciencesEcdysteroidPolytene chromosomeBase Sequencezinc fingerbiologyHomozygotefungiEcdysteroidsCell Biologybiology.organism_classificationMolecular biology3. Good healthDNA-Binding ProteinsMicroscopy ElectronDrosophila melanogasterPhenotypechemistryMutagenesisLarvaring glandChromosomal regionInsect ProteinsSteroidsDrosophila melanogaster030217 neurology & neurosurgeryDrosophila ProteinEcdysoneTranscription FactorsDevelopmental BiologyDevelopmental Biology
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Inducible NO synthase confers chemoresistance in head and neck cancer by modulating survivin

2009

The dual role of the inducible NO synthase (iNOS) and NO signaling in head and neck squamous cell carcinoma (HNSCC) is a complex and can both promote or inhibit tumor progression. However, the underlying molecular mechanisms are not yet resolved in detail. We show for the first time that conditions, favoring low NO levels conferred resistance against cisplatin/taxol-induced apoptosis in HNSCC cell lines. Cytoprotection was mediated by survivin, because we observed its upregulation subsequent to low doses of the NO donors S-nitroso-N-acetyl-penicillamine (SNAP) and sodium nitroprusside (SNP) or ectopic expression of physiologic amounts of iNOS. Also, RNAi-mediated depletion of survivin block…

MaleUmbilical VeinsCancer ResearchSurvivinFluorescent Antibody TechniqueNitric Oxide Synthase Type IIApoptosisp38 Mitogen-Activated Protein KinasesInhibitor of Apoptosis ProteinsImmunoenzyme TechniquesPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundLY294002Enzyme InhibitorsRNA Small InterferingAged 80 and overReverse Transcriptase Polymerase Chain ReactionCell CycleMiddle AgedCell cycleOncologyHead and Neck NeoplasmsCarcinoma Squamous CellFemaleMicrotubule-Associated ProteinsNitroprussidePaclitaxelImmunoblottingAntineoplastic AgentsS-Nitroso-N-AcetylpenicillamineBiologyCell LineDownregulation and upregulationSurvivinmedicineHumansNitric Oxide DonorsRNA MessengerneoplasmsProtein kinase BNitritesPI3K/AKT/mTOR pathwayAgedmedicine.diseaseAntineoplastic Agents PhytogenicHead and neck squamous-cell carcinomachemistryDrug Resistance NeoplasmTumor progressionImmunologyCancer researchEndothelium VascularCisplatinProto-Oncogene Proteins c-aktInternational Journal of Cancer
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