Search results for "DELETION"

showing 10 items of 383 documents

The DNA damage-induced decrease of Bcl-2 is secondary to the activation of apoptotic effector caspases.

2003

Apoptosis induced by DNA-damaging agents or radiation mainly proceeds through death receptor-independent caspase activation. The release of mitochondrial apoptogenic proteins, such as cytochrome c, into the cytoplasm leading to Apaf1-dependent activation of caspase-9 is a key event in this pathway. The permeability of the mitochondrial outer membrane is regulated by the various pro- and antiapoptotic Bcl-2 family proteins, and it is thought that DNA damage triggers apoptosis through the downregulation of antiapoptotic Bcl-2. Using murine embryonic fibroblasts (MEF) deficient and proficient in Apaf1, we show that DNA-damaging agents and radiation lead to a decline in Bcl-2 protein only in wt…

Cancer ResearchDNA damageCell TransplantationUltraviolet RaysTransplantation HeterologousApoptosisMice SCIDAdenocarcinomamedicine.disease_causeAdenoviridaeAmino Acid Chloromethyl KetonesMiceDownregulation and upregulationGeneticsmedicineTumor Cells CulturedAnimalsHumansAPAF1Enzyme InhibitorsMolecular BiologyCaspaseEtoposidebiologyDose-Response Relationship DrugCytochrome cProteinsDose-Response Relationship RadiationFibroblastsMolecular biologyCaspase InhibitorsCell biologyEnzyme ActivationPancreatic NeoplasmsApoptotic Protease-Activating Factor 1Proto-Oncogene Proteins c-bcl-2ApoptosisCytoplasmCaspasesbiology.proteinDactinomycinCarcinogenesisGene DeletionDNA DamageOncogene
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Novel insulin receptor substrate 1 and 2 variants in breast and colorectal cancer

2013

The insulin/insulin-like growth factor pathway is involved in breast and colorectal cancer (CRC) development. In the present study, we analyzed the coding region and short intron-exon borders of the insulin receptor substrate 1 and 2 (IRS‑1 and IRS‑2) genes in 12 cell lines derived from breast cancer (BC), 14 cell lines derived from CRC and 33 primary CRCs. The nucleotide variants identified in BC were 3 in IRS‑1, 1 of which (p.Arg267Cys) was novel and with a pathogenic potential as predicted by in silico analysis and 6 in IRS‑2. Twenty‑one variants in IRS‑1 and 18 in IRS‑2 were identified in the CRC samples. These included 11 novel IRS‑1 variants detected exclusively in CRCs, which include…

Cancer ResearchInsulin Receptor Substrate ProteinsSettore MED/06 - Oncologia MedicaIn silicoMutation MissenseBreast NeoplasmsColorectal NeoplasmBiologymedicine.disease_causeFrameshift mutationBreast cancerBreast cancerMCF-7 CellCell Line TumormedicineHumansMissense mutationFrameshift MutationInsulin Receptor Substrate ProteinSequence DeletionGeneticsMutationCaco-2 CellPolymorphism GeneticCancerGenetic VariationInsulin receptor substrate 1ArticlesGeneral MedicineInsulin receptor substrate 2HCT116 Cellsmedicine.diseaseColorectal cancerIRS1Mutagenesis InsertionalCell Transformation NeoplasticHT29 CellOncologyHCT116 CellBreast cancer; Colorectal cancer; Insulin receptor substrate 1; Insulin receptor substrate 2; Breast Neoplasms; Caco-2 Cells; Cell Line Tumor; Cell Transformation Neoplastic; Colorectal Neoplasms; Female; Frameshift Mutation; Genetic Variation; HCT116 Cells; HT29 Cells; Humans; Insulin Receptor Substrate Proteins; MCF-7 Cells; Mutagenesis Insertional; Mutation Missense; Polymorphism Genetic; Sequence Deletion; Signal Transduction; Cancer Research; OncologyInsulin Receptor Substrate ProteinsMCF-7 CellsFemaleCaco-2 CellsColorectal NeoplasmsHT29 CellsBreast NeoplasmHumanSignal Transduction
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Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

2005

Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

Cancer ResearchLymphoma B-Cellbusiness.industrySuppressor of cytokine signaling 1HomozygoteIntracellular Signaling Peptides and ProteinsSuppressor of Cytokine Signaling ProteinsHematologymedicine.diseaseMediastinal NeoplasmsLymphomaRepressor ProteinsSuppressor of Cytokine Signaling 1 ProteinOncologyhemic and lymphatic diseasesmedicineCancer researchHumansPrimary mediastinal B-cell lymphomaDNA microarraybusinessGene DeletionOligonucleotide Array Sequence AnalysisLeukemia
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Deletion of the PER3 Gene on Chromosome 1p36 in Recurrent ER-Positive Breast Cancer

2010

El pdf del artículo es la versión de autor.-- et al.

Cancer ResearchMicroarrayGene DosageGene ExpressionEstrogen receptorBreast NeoplasmsGene dosageMiceBreast cancerOriginal ReportsAnimalsHumansMedicineGenetic Predisposition to DiseaseCopy-number variationskin and connective tissue diseasesSequence Deletionbusiness.industryCancerPeriod Circadian ProteinsPrognosismedicine.diseaseSurvival AnalysisDisease Models AnimalReceptors EstrogenOncologyChromosomes Human Pair 1Cancer researchFemaleBreast diseaseNeoplasm Recurrence LocalbusinessTamoxifenmedicine.drugJournal of Clinical Oncology
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Genomic Abnormalities Acquired in the Blastic Transformation of Splenic Marginal Zone B-cell Lymphoma

2003

Among 20 cases of typical splenic marginal zone lymphoma (SMZL), two cases had blastic transformation. The genetic mechanisms underlying the morphologic transformation were investigated by comparing genetic changes in initial and blastic phases. A complex karyotype including trisomy of 3q and genomic gain of 17q22-q24 was seen in both cases at diagnosis. However, the extra copy of 3q was lost during the transformation process in both tumors. Additionally, the Karpas 1718 cell line, which was derived from a patient with transformed SMZL and carried a trisomy of 3q, also evidenced the spontaneous loss of the extra 3q during the culturing process. Other acquired abnormalities observed exclusiv…

Cancer ResearchPathologymedicine.medical_specialtyLymphoma B-CellTrisomyChromosomal translocationBiologyComplex KaryotypeTumor Cells CulturedmedicineChromosomes HumanHumansSplenic marginal zone lymphomaChromosome AberrationsLymphoma Non-HodgkinSplenic NeoplasmsHematologymedicine.diseaseTransformation (genetics)OncologyKaryotypingDisease ProgressionB-Cell Non-Hodgkin LymphomaChromosomes Human Pair 3Chromosome DeletionAbnormalityBlast CrisisTrisomyChromosomes Human Pair 17Comparative genomic hybridizationLeukemia & Lymphoma
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Fulminant hepatic failure requiring liver transplantation in 22q13.3 deletion syndrome.

2010

We report on a 4-year-old girl with severe developmental delay, absent speech, and chromosome 22q13.3 deletion (Phelan-McDermid syndrome), karyotype 46,XX.ish del(22)(q13.31qter)(ARSA-,N85A-,SHANK3-). At the age of 3 years, she needed an emergency liver transplantation because of fulminant hepatic failure, most likely caused by hyperacute autoimmune hepatitis triggered by a viral infection. This is the second report of a patient with 22q13.3 deletion and fulminant liver failure. By array-CGH we identified in this patient a 5.675 Mb terminal deletion (22q13.31 --> qter; including approximately 55 genes; from NUP50 to RABL2B) and in the previous patient a 1.535 Mb deletion (22q13.32 --> qter;…

Candidate genemedicine.medical_specialtyFulminantmedicine.medical_treatmentChromosomes Human Pair 22Chromosome DisordersAutoimmune hepatitisDiseaseLiver transplantationGastroenterologyFulminant hepatic failureInternal medicineGeneticsmedicineHumansGenetics (clinical)In Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisComparative Genomic Hybridizationmedicine.diagnostic_testbusiness.industryKaryotypeSyndromeLiver Failure Acutemedicine.diseaseLiver TransplantationChild PreschoolFemaleChromosome DeletionLiver function testsbusinessAmerican journal of medical genetics. Part A
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Knockout of thep-Coumarate Decarboxylase Gene fromLactobacillus plantarumReveals the Existence of Two Other Inducible Enzymatic Activities Involved i…

2000

ABSTRACTLactobacillus plantarumNC8 contains apdcgene coding forp-coumaric acid decarboxylase activity (PDC). A food grade mutant, designated LPD1, in which the chromosomalpdcgene was replaced with the deletedpdcgene copy, was obtained by a two-step homologous recombination process using an unstable replicative vector. The LPD1 mutant strain remained able to weakly metabolizep-coumaric and ferulic acids into vinyl derivatives or into substituted phenyl propionic acids. We have shown thatL. plantarumhas a second acid phenol decarboxylase enzyme, better induced with ferulic acid than withp-coumaric acid, which also displays inducible acid phenol reductase activity that is mostly active when gl…

Carboxy-lyasesCoumaric AcidsCarboxy-LyasesMutantGenetics and Molecular Biologymacromolecular substancesCoumaric acidApplied Microbiology and BiotechnologyFerulic acidchemistry.chemical_compoundHydroxybenzoatesCloning Molecularchemistry.chemical_classificationEcologybiologyhemic and immune systemsMetabolismPhenolic acidHydrogen-Ion Concentrationbiology.organism_classificationLactobacillusElectroporationEnzymechemistryBiochemistryEnzyme InductionPropionatesOxidoreductasesGene DeletionLactobacillus plantarumFood ScienceBiotechnologyApplied and Environmental Microbiology
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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Termination of transcription in an ‘in vitro’ system is dependent on a polyadenylation sequence

1991

Using HeLa cell nuclear extract as a source of the different transcription and polyadenylation factors and reverse transcription to analyze the levels of RNA 5' and 3' to the cleavage-polyadenylation site, an in vitro assay has been established to study polyadenylation coupled to transcription directed by different adenovirus promoters. The levels of transcription 5' and 3' to the cleavage site in the L3 polyadenylation region are practically the same as described previously, however, the level of transcription 3' to the cleavage site in the SV40 early polyadenylation region decreases immediately after the cleavage site indicating a termination of the transcription.

Cell ExtractsTranscription GeneticPolyadenylationMolecular Sequence DataRNA polymerase IISimian virus 40BiologyCleavage (embryo)AdenoviridaeTranscription (biology)GeneticsRNA MessengerPromoter Regions GeneticBase SequenceRNARNA-Directed DNA PolymerasePromoterMolecular biologyReverse transcriptasebiology.proteinRNA Polymerase IIChromosome DeletionPoly ACytokinesisHeLa CellsPlasmidsNucleic Acids Research
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Cytotoxicity of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide in multidrug-resistant cancer cells through activation of PERK/eIF2α/AT…

2021

After decades of research, multidrug resistance (MDR) remains a huge challenge in cancer treatment. In this study, the cytotoxic of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide (MCC1734) has been investigated towards multidrug-resistant cancer cell lines. MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent. Interestingly, sensitive CCRF-CEM cells and multidrug-resistant P-gp-overexpressing CEM/ADR5000 cells represented similar sensitivity towards MCC1734, indicating MCC1734 can bypass P-gp-mediated resistance. Microarray-based mRNA expression revealed that MCC17…

Cell SurvivalEukaryotic Initiation Factor-2Antineoplastic AgentsMitochondrionBiochemistryFlow cytometryeIF-2 KinaseCell Line TumorOxazinesmedicineHumansCytotoxic T cellGene Regulatory NetworksCytotoxicityPharmacologyMolecular Structuremedicine.diagnostic_testChemistryCell cycleActivating Transcription Factor 4Gene Expression Regulation NeoplasticXanthenesDrug Resistance NeoplasmCell cultureApoptosisCancer cellCancer researchGene DeletionBiochemical Pharmacology
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