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Fcp1-dependent dephosphorylation is required for M-phase-promoting factor inactivation at mitosis exitCell cycle checkpoint in cancer: a therapeutically targetable double-edged swordSTAT4 serine phosphorylation is critical for IL-12-induced IFN-gamma production but not for cell proliferationFunctional cloning of genes regulating apoptosis in neuronal cells.Different mutations of the RET gene cause different human tumoral diseases.Molecular aspects of primary immunodeficiencies: lessons from cytokine and other signaling pathways.FBXW7 and USP7 regulate CCDC6 turnover during the cell cycle and affect cancer drugs susceptibility in NSCLC.The Fcp1-Wee1-Cdk1 axis affects spindle assembly checkpoint robustness and sensitivity to antimicrotubule cancer drugs.New insights on oxidative stress in cancer.New therapeutic perspectives in CCDC6 deficient lung cancer cells.ATM controls proper mitotic spindle structureThe between Now and Then of Lung Cancer Chemotherapy and Immunotherapy.USP7 inhibitors, downregulating CCDC6, sensitize lung neuroendocrine cancer cells to PARP-inhibitor drugs.Transcriptional profile of Ki-Ras-induced transformation of thyroid cells.Sustaining the spindle assembly checkpoint to improve cancer therapy.Akt/protein kinase B promotes survival and hormone-independent proliferation of thyroid cells in the absence of dedifferentiating and transforming effects.Ret-mediated mitogenesis requires Src kinase activity.Molecular biology of the MEN2 gene.Glial cell line-derived neurotrophic factor differentially stimulates ret mutants associated with the multiple endocrine neoplasia type 2 syndromes and Hirschsprung's disease.Signalling of the Ret receptor tyrosine kinase through the c-Jun NH2-terminal protein kinases (JNKS): evidence for a divergence of the ERKs and JNKs pathways induced by Ret.The end of mitosis from a phosphatase perspective.Increased in vivo phosphorylation of ret tyrosine 1062 is a potential pathogenetic mechanism of multiple endocrine neoplasia type 2B.The platelet-derived growth factor controls c-myc expression through a JNK- and AP-1-dependent signaling pathway.Fighting tubulin-targeting anticancer drug toxicity and resistance.The highly malignant phenotype of anaplastic thyroid carcinoma cell lines is recessive.Block of c-myc expression by antisense oligonucleotides inhibits proliferation of human thyroid carcinoma cell lines.Retrospective Analysis of Coagulation Factor II Receptor ( F2R ) Sequence Variation and Coronary Heart Disease in Hypertensive PatientsThe expression of the high mobility group HMGI (Y) proteins correlates with the malignant phenotype of human thyroid neoplasiasType 1 IFNs and regulation of TH1 responses: enigmas both resolved and emerge
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P50
description
Forscher
@de
Italiaans onderzoeker
@nl
chercheur
@fr
forsker
@nb
investigador
@es
researcher
@en
հետազոտող
@hy
研究者
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name
R. Visconti
@ast
R. Visconti
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R. Visconti
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Roberta Visconti
@en
Roberta Visconti
@es
Roberta Visconti
@nb
Roberta Visconti
@sq
type
label
R. Visconti
@ast
R. Visconti
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R. Visconti
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Roberta Visconti
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Roberta Visconti
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Roberta Visconti
@nb
Roberta Visconti
@sq
altLabel
R. Visconti
@en
prefLabel
R. Visconti
@ast
R. Visconti
@nl
R. Visconti
@sl
Roberta Visconti
@en
Roberta Visconti
@es
Roberta Visconti
@nb
Roberta Visconti
@sq
P106
P27
P31
P496
0000-0001-7613-3801