0000000000705001

AUTHOR

Alfredo Fusco

showing 3 related works from this author

The receptor protein tyrosine phosphatase PTPRJ negatively modulates the CD98hc oncoprotein in lung cancer cells.

2018

PTPRJ, a receptor protein tyrosine phosphatase strongly downregulated in human cancer, displays tumor suppressor activity by negatively modulating several proteins involved in proliferating signals. Here, through a proteomic-based approach, we identified a list of potential PTPRJ-interacting proteins and among them we focused on CD98hc, a type II glycosylated integral membrane protein encoded by SLC3A2, corresponding to the heavy chain of a heterodimeric transmembrane amino-acid transporter, including LAT1. CD98hc is widely overexpressed in several types of cancers and contributes to the process of tumorigenesis by interfering with cell proliferation, adhesion, and migration. We first valid…

0301 basic medicineCD98hcChemistryCell growthCellPTPRJProtein tyrosine phosphatasemedicine.disease_causeProtein tyrosine phosphatase03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structureProteasomal degradationOncologyMG132Cancer cellCancer researchmedicineProteasome inhibitorGene silencingLung cancerCarcinogenesismedicine.drugResearch Paper
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Role of PTPRJ genotype in papillary thyroid carcinoma risk

2010

The strong genetic predisposition to papillary thyroid carcinoma (PTC) might be due to a combination of low-penetrance susceptibility variants. Thus, the research into gene variants involved in the increase of susceptibility to PTC is a relevant field of investigation. The gene coding for the receptor-type tyrosine phosphatase PTPRJ has been proposed as a cancer susceptibility gene, and its role as a tumor suppressor gene is well established in thyroid carcinogenesis. In this study, we want to ascertain the role of PTPRJ genotype in the risk for PTC. We performed a case–control study in which we determined the PTPRJ genotype for the non-synonymous Gln276Pro and Asp872Glu polymorphisms by PC…

RiskOncologyCancer Researchmedicine.medical_specialtyGenotypeendocrine system diseasesEndocrinology Diabetes and MetabolismBiologyPolymerase Chain ReactionArticleSettore MED/13 - EndocrinologiaThyroid carcinomaEndocrinologyGene FrequencyInternal medicineGenotypeOdds RatiomedicineGenetic predispositionHumansGenetic Predisposition to DiseaseThyroid NeoplasmsAlleleAllele frequencyAllelesGenetic Association StudiesPapillay thyroid carcinomaGeneticsChi-Square DistributionPolymorphism GeneticReceptor-Like Protein Tyrosine Phosphatases Class 3ThyroidCase-control studyCarcinoma PapillaryGenotype frequencymedicine.anatomical_structureOncologyCase-Control Studies
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Mitochondrial G protein coupled receptor kinase 2 regulates proinflammatory responses in macrophages.

2013

G-protein-coupled receptor kinase 2 (GRK2) levels are elevated in inflammation but its role is not clear yet. Here we show that GRK2 expression is dependent on NFκB transcriptional activity. In macrophages, LPS induces GRK2 accumulation in mitochondria increasing biogenesis. The overexpression of the carboxy-terminal domain of GRK2 (βARK-ct), known to displace GRK2 from plasma membranes, in macrophages induces earlier localization of GRK2 in mitochondria in response to LPS leading to increased mt-DNA transcription, reduced ROS production and cytokines expression. Our study shows the relevance of GRK2 subcellular localization in macrophage’s biology and its potential therapeutic properties i…

LipopolysaccharidesG-Protein-Coupled Receptor Kinase 2BiophysicsβARK-ctGRK2InflammationMitochondrionBiochemistryArticleProinflammatory cytokineMiceStructural BiologyGeneticsmedicineAnimalsHumansReceptorMolecular BiologyInflammationG protein-coupled receptor kinasebiologyKinaseSubcellular localizationBeta adrenergic receptor kinaseMacrophagesCell BiologySubcellular localizationCell biologyMitochondriabiology.proteinmedicine.symptomReactive Oxygen SpeciesSignal Transduction
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